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Cardiology

  • Bryan Jonathan Har
Chapter
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Abstract

myocardial—myocardial infarction, angina, myocarditis

Keywords

Infective Endocarditis Valvular Heart Disease Peripheral Artery Disease Acute Management Specific Entity 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Aortic Dissection

Differential Diagnosis

CARDIAC

  • myocardial—myocardial infarction, angina, myocarditis

  • valvular—aortic stenosis, aortic regurgitation

  • pericardial—pericarditis

  • vascular—aortic dissection

RESPIRATORY

  • parenchymal—pneumonia, cancer

  • pleural—pneumothorax, pneumomediastinum, pleural effusion, pleuritis

  • vascular—pulmonary embolism, pulmonary hypertension

GI

—esophagitis, esophageal cancer, GERD, peptic ulcer disease, Boerhaave’s, cholecystitis, pancreatitis

OTHERS

—musculoskeletal, shingles, anxiety

Pathophysiology

ANATOMY

—layers of aorta include intima, media, and adventitia. Majority of tears found in ascending aorta at right lateral wall where the greatest shear force is produced

AORTIC TEAR AND EXTENSION

—aortic tear may produce a tearing, ripping sudden chest pain radiating to the back. Aortic regurgitation can produce diastolic murmur. Pericardial tamponade may occur, leading to hypotension or syncope. Initial aortic tear and subsequent extension of a false lumen along the aorta may also occlude blood flow into any of the following vascular structures:
  • coronary—acute myocardial infarction (usually RCA)

  • brachiocephalic, left subclavian, distal aorta—absent or asymmetric peripheral pulse, limb ischemia

  • renal—anuria, renal failure

  • carotid—syncope/hemiplegia/death

  • anterior spinal—paraplegia/quadriplegia, anterior cord syndrome

CLASSIFICATION SYSTEMS

  • StanfordA = any ascending aorta involvement, B = all others

  • D e B akeyI = ascending and at least aortic arch, II = ascending only, III = originates in descending and extends proximally or distally

RISK FACTORS

  • common—hypertension, age, male

  • vasculitis—Takayasu arteritis, giant cell arteritis, rheumatoid arthritis, syphilitic aortitis

  • collagen disorders—Marfan syndrome, Ehlers–Danlos syndrome, cystic medial necrosis

  • valvular—bicuspid aortic valve, aortic coarctation, Turner syndrome, aortic valve replacement

  • others—cocaine, trauma

Clinical Features

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC AORTIC DISSECTION?

 

LR+

LR–

H istory

Hypertension

1.6

0.5

Sudden chest pain

1.6

0.3

Tearing or ripping pain

1.2–10.8

0.4–0.99

Physical

Pulse deficit

5.7

0.7

Focal neurological deficit

6.6–33

0.71–0.87

Diastolic murmur

1.4

0.9

CXR/ECG

Enlarged aorta or wide mediastinum

2.0

0.3

LVH on ECG

0.2–3.2

0.84–1.2

  • APPROAC H—“presence of tearing, ripping, or migrating pain may suggest dissection. Pulse deficit or focal neurological deficits greatly increase likelihood of dissection. Absence of pain of sudden onset decreases likelihood of dissection. Normal aorta and mediastinum on CXR help to exclude diagnosis”

JAMA 2002 287:17

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, troponin/CK × 3, glucose, AST, ALT, ALP, bilirubin, albumin, lipase, INR/PTT

  • imaging—CXR, echocardiogram (TEE), CT chest or MRI chest

  • ECG

SPECIAL

  • aortography

Diagnostic and Prognostic Issues

CXR FINDINGS

—wide mediastinum (>6 cm [2.4 in.]), indistinct aortic knuckle, pleural cap, difference in diameter between ascending and descending aorta, blurring of aortic margin secondary to local extravasation of blood, pleural effusion or massive hemothorax, displaced calcification (separation of the intimal aortic calcification from the edge of the aortic shadow >1 cm [0.4. in.])

PROGNOSIS

  • type a—with surgery, 1-month survival 75–80%, 10-year survival 55%

  • type b—with aggressive hypertensive treatment, 1-month survival >90%, 10-year survival 56%

Management

ABC

O 2 to keep sat >95%, IV, antihypertensive therapy (keep HR <60 and SBP <120 mmHg. Labetalol 2 mg/min IV loading drip, then 2–8 mg/min (target heart rate 55–60) or 20–80 mg IV q10 min, maximum 300 mg, then 200–400 mg PO BID. If SBP still >120 mmHg, sodium nitroprusside 0.25–0.5 μg/kg/min IV initially, then 0.25–3 μg/kg/min, maximum 10 μg/kg/min)

TREAT UNDERLYING CAUSE

Type A (emergent surgical repair, endovascular stenting, long-term blood pressure control). Type B (medical blood pressure control). Monitor over time with serial CT/MR chest

Related Topics

Acute Coronary Syndrome (p. 28)

Stroke (p. 337)

Acute Coronary Syndrome

ACCF/AHA 2013 STEMI Guidelines

ACCF/AHA 2007 UA/NSTEMI Guidelines

ACCF/AHA UA/NSTEMI 2012 Focused Update

Differential Diagnosis of Chest Pain

CARDIAC

  • myocardial—myocardial infarction, angina (atherosclerosis, vasospasm), myocarditis

  • valvular—aortic stenosis

  • pericardial—pericarditis

  • vascular—aortic dissection

RESPIRATORY

  • parenchymal—pneumonia, cancer

  • pleural—pneumothorax, pneumomediastinum, pleural effusion, pleuritis

  • vascular—pulmonary embolism

GI

—esophagitis, esophageal cancer, GERD, peptic ulcer disease, Boerhaave’s, cholecystitis, pancreatitis

OTHERS

—musculoskeletal (costochondritis), shingles, anxiety

Pathophysiology

 

Pathologic changes

Clinical presentation

Pre-clinical

Atherosclerosis

Asymptomatic

Angina

Luminal narrowing

Central chest discomfort; worsened by exertion,emotion, and eating; relieved by rest and nitroglycerine

Unstableangina

Plaque ruptureor thrombus

Worsening pattern or rest pain; no elevation in troponin,with or without ECG changes of ischemia

NSTEMI

Partial occlusion

Non-ST elevation MI; elevation in troponin, with or withoutECG changes of ischemia

STEMI

Complete occlusion

ST elevation MI; elevation in troponin, with distinct ST segment elevation in ≥2 contiguous leads, new LBBB, or posterior wall MI with reciprocal ST depression in precordial leads on ECG

THIRD UNIVERSAL DEFINITION OF MYOCARDIAL INFARCTION (MI)

  • type 1—spontaneous MI due to a primary coronary event (atherosclerotic plaque rupture or erosion with acute thromboembolism)

  • type 2—MI secondary to an ischemic imbalance (supply demand mismatch)

  • type 3—MI resulting in death when biomarker values are unavailable (sudden unexpected cardiac death before serum biomarkers collected for measurement)

  • type 4—MI related to PCI (4A) or stent thrombosis (4B)

  • type 5—MI related to CABG

RISK FACTORS

  • major—diabetes, hypertension, dyslipidemia, smoking, family history of premature CAD, advanced age, male gender

  • associated—obesity, metabolic syndrome, sedentary lifestyle, high-fat diet

  • emerging—lipoprotein abnormalities, inflammation (↑ CRP), chronic infections, chronic kidney disease

POST–MI COMPLICATIONS

—arrhythmia (VT/VF, bradycardia), sudden death, papillary muscle rupture/dysfunction, myocardial rupture (ventricular free wall, interventricular septum), ventricular aneurysm, valvular disease (especially acute mitral regurgitation), heart failure/cardiogenic shock, peri-infarction pericarditis, post-cardiac injury pericarditis (Dressler’s syndrome)

Clinical Features

CHEST PAIN EQUIVALENTS

—dyspnea, syncope, fatigue, particularly in patients with diabetic neuropathy who may not experience chest pain

NEW YORK HEART ASSOCIATION (NYHA) CLASSIFICATION

  • I = no symptoms with ordinary physical activity

  • II = mild symptoms with normal activity (walking >2 blocks or 1 flight of stairs)

  • III = symptoms with minimal exertion

  • IV = symptoms at rest

CANADIAN CARDIOVASCULAR SOCIETY (CCS) CLASSIFICATION

  • I = angina with strenuous activity

  • II = slight limitation, angina with meals/cold/stress

  • III = marked limitation, angina with walking <1–2 blocks or 1 flight of stairs

  • IV = unstable angina
    • IV a = unstable angina resolves with medical treatment

    • IV b = unstable angina on oral treatment, symptoms improved but angina with minimal provocation

    • IV c = unstable angina persists, not manageable on oral treatment or hemodynamically unstable

KILLIP CLASS CLASSIFICATION

  • I = no evidence of heart failure

  • II = mild to moderate heart failure (S3, lung rales less than half way up, or jugular venous distension)

  • III = overt pulmonary edema

  • IV = cardiogenic shock

RATIONAL CLINICAL EXAMINATION SERIES: IS THIS PATIENT HAVING A MYOCARDIAL INFARCTION?

 

LR+

H istory

Pain radiation to the shoulderOR both arms

4.1

Pain radiation to right arm

3.8

Radiation to left arm

2.2

Radiation to both arms

9.7

Vomiting

3.5

Ex-smoker

2.5

Diaphoresis

2.0

Pleuritic chest pain

0.2

Sharp or stabbing chest pain

0.3

Positional chest pain

0.3

Chest pain reproducible by palpation

0.2–0.4

Physical

Hypotension

3.1

S3

3.2

Pulmonary crackles

2.1

EC G

New ST elevation ≥1 mm

5.7–53.9

New Q wave

5.3–24.8

Any ST elevation

11.2

New conduction defect

6.3

New ST depression

3.0–5.2

Any Q wave

3.9

Any ST depression

3.2

T wave peaking or inversion ≥1 mm

3.1

New T wave inversion

2.4–2.8

Any conduction defect

2.7

Multivariate Prediction Models

 

ACI-TIPI (Acute Cardiac Ischemia Time Insensitive Predictive Instrument)

3.9–12

Goldman Protocol

2.9–3.6

  • APPROAC H—“radiation of chest pain, diaphoresis, hypotension, and S3 suggest acute MI. Chest pain that is pleuritic, sharp or stabbing, positional or reproduced by palpation decreases likelihood of acute MI. On ECG, any ST ↑, new Q waves, or new conduction Δ make acute MI very likely. Normal ECG is very powerful to rule out MI”

JAMA 1998 280:14
  • UPDATE—“after clinical symptoms are used to identify patients with possible ischemia, the ECG and troponin results take precedence in making the diagnosis. The presence of diabetes, HTN, or dyslipidemia should not affect clinician’s probability estimate that an episode of chest pain represents an ACI”

The Rational Clinical Examination. McGraw-Hill, 2009

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, troponin/CK × 3 q6-8 h, BNP or NT-pro-BNP, AST, ALT, ALP, bilirubin, INR/PTT, Mg, Ca, PO4, albumin, lipase, fasting lipid profile, random and fasting glucose, HbA1C

  • imaging—CXR, echocardiogram (first 72 h), MIBI/thallium (>5 days later)

  • EC G—q8h × 3 or with chest pain

  • stress tests—ECG, echocardiogram, MIBI once stable (>48 h post-MI)

  • coronary catheterization

Diagnostic and Prognostic Issues

RISK STRATIFICATION FOR STABLE CORONARY DISEASE

  • EC G exercise stress test
    • absolute contraindications—recent myocardial infarction (<4 days), unstable angina, severe symptomatic LV dysfunction, life-threatening arrhythmia, acute pericarditis, aortic dissection, PE, severe symptomatic aortic stenosis

    • goal—keep on treadmill until subject reaches 85–90% of age-predicted heart rate (220–age)

    • ischemia criteria— ≥ 1 mm horizontal or down-sloping ST ↓ over multiple leads, or ST ↑ → myocardial ischemia (sens 68%, spc 77%) → proceed to angiogram

    • inconclusive—premature termination due to chest pain/poor exercise tolerance → proceed to pharmacological stress test

    • duke treadmill score—(exercise time in minutes) – 5 × (maximum ST ↓ in mm) – 4 × (treadmill angina index [0 = none, 1 = non-limiting, 2 = exercise limiting]). Low risk ≥ +5 (4-year survival 98–99%), moderate risk −10 to +4, high risk ≤ −11 (4-year survival 71–79%)

  • dipyridamole/adenosine MIBI—dipyridamole (Persantine) causes vasodilation. In CAD, the coronary artery is already maximally dilated to compensate, so addition of dipyridamole will not change perfusion to diseased vessel(s) further. This results in a relative perfusion mismatch compared to areas with normal dilatory reaction. Contraindicated in asthma/COPD. Antidote is aminophylline or caffeine

  • dobutamine echocardiography—assesses wall motion abnormalities. Compared to MIBI, echocardiogram is more specific and less sensitive. Contraindicated in severe hypertension and arrhythmias

APPROACH TO DIAGNOSIS OF STABLE CAD

—start with history, physical, rest ECG, and CXR. If low probability, do not investigate further. If high probability, proceed with management. If intermediate probability → stress test → cardiac CT, MIBI or stress echo → angiography

DIFFERENTIAL DIAGNOSIS OF TROPONIN ELEVATION

  • cardiac—myocardial infarction, myocarditis, congestive heart failure, pericarditis, vasospasm, tachycardia with supply–demand mismatch, drug/cocaine ingestion, stress (takotsubo) cardiomyopathy

  • pulmonary—pulmonary embolism

  • hepatic—liver failure

  • renal—chronic kidney disease

  • neurologic—stroke, intracranial hemorrhage

  • systemic—sepsis, prolonged strenuous exercise

SERUM MARKERS

  • troponin i/t—rises within 4–6 h, peaks at 18–24 h, remains elevated 7–10 days (sens 40% at presentation, 40–70% after 6–9 h of symptoms)

  • ck / ckmb—rises within 4–6 h, peaks at 18–24 h, remains elevated 3–4 days (sens 35–50% at presentation, 90% after 3 h in ER)

  • myoglobin—rises within 1–2 h, peaks in few hours

Therefore, measure markers (e.g., troponin) at least twice separated by 6–8 h with serial ECG. Despite all appropriate investigations, missed MI rate is 2–5%

ECG CHANGES IN ACUTE MI

—see APPROACH TO ECG p. 73

TIMI SCORE FOR PATIENTS WITH UNSTABLE ANGINA/NSTEMI

  • scoring (out of 7)—age ≥65, ≥3 CAD risk factors, known CAD (stenosis >50%), ASA use within prior 7 days, ≥2 angina episodes within 24 h, ↑ cardiac markers, ST deviation ≥0.5 mm

  • risk groupslow = 0–2, intermediate = 3–4, high = 5–7. Consider GPIIb/IIIa and early angiography with revascularization in intermediate or high-risk groups

  • risk of death, MI or revascularization in 14 days—0/1 = 4.7%, 2 = 8.3%, 3 = 13.2%, 4 = 19.9%, 5 = 26.2%, 6/7 = 40.9%

GRACE RISK SCORE FOR PATIENTS WITH UNSTABLE ANGINA/NSTEMI

Riskcategory

GRACErisk score

In-hospitaldeath (%)

Low

≤108

<1

Intermediate

109–140

1–3

High

>140

>3

Riskcategory

GRACErisk score

6-monthdeath

Low

≤88

<3

Intermediate

89–118

3–8

High

>118

>8

TIMI SCORE FOR PATIENTS WITH STEMI

  • scoring (out of 14)—age (3 points = ≥75, 2 points = 65–74), any of diabetes, hypertension, or angina (1 point), systolic BP ≤100 mmHg (3 points), HR >100 (2 points), Killip class II–IV (2 points), weight <67 kg (1 point), anterior ST elevation or LBBB (1 point), time to reperfusion >4 h (1 point)

  • risk of death in 30 days—0 = 0.8%, 1 = 1.6%, 2 = 2.2%, 3 = 4.4%, 4 = 7.3%, 5 = 12.4%, 6 = 16.1%, 7 = 23.4%, 8 = 26.8%, >8 = 35.9%

IN-HOSPITAL OUTCOMES

 

NSTEMI (%)

STEMI (%)

Death

4

6

Reinfarction

0.9

1.1

Cardiogenic shock

2.8

6.4

Stroke

0.7

0.8

Major bleeding

10

12

ACTION registry 2008/2009 data

Acute Management

ABC

—O2 to keep sat >95%, IVs, inotropes, consider balloon pump if hemodynamically unstable

PAIN CONTROL

nitroglycerin (nitro drip 25 mg in 250 mL D5W, start at 5 μg/min IV, then ↑ by 5–10 μg/min every 3–5 min to 20 μg/min, then ↑ by 10 μg/min every 3–5 min up to 200 μg/min, or until relief of pain, stop titration if SBP is <100 mmHg. Nitro patch 0.4 mg/h daily. Nitro spray 0.4 mg SL q5min × 3. Beware if suspect right ventricular infarction or if patients on sildenafil). Morphine 2–4 mg IV every 5–15 min PRN

CLOT CONTROL

  • antiplateletASA 162–325 mg PO chew × 1 dose, then 75–100 mg PO daily indefinitely. P2Y12 receptor blockade with clopidogrel 300–600 mg × 1 dose then 75 mg PO daily for 1 year; or ticagrelor 180 mg × 1 dose, then 90 mg PO BID for 1 year; or prasugrel (with PCI only; do not give if history of CVA or TIA, or age ≥75 years) 60 mg × 1 dose then 10 mg daily for 1 year. Combination ASA plus clopidogrel for minimum of 1 month (ideally 1 year)-post PCI with bare-metal stent, or minimum 12 months (possibly indefinitely) for drug-eluting stents. Consider G PIIb/IIIa inhibitor if intermediate/high-risk NSTEMI, treated with PCI, and pain unresponsive to nitroglycerin (tirofiban 0.4 μg/kg/min × 30 min IV, then continue 0.1 μg/kg/min × 18–24 h; eptifibatide 180 μg/kg IV bolus, then 2 μg/kg/min × 18–24 h; or, abciximab 0.25 mg/kg IV bolus, then 0.125 μg/kg/min × 12 h)

  • anticoagulation—options include LMW H (enoxaparin 30 mg IV bolus, then 1 mg/kg SC BID for STEMI [no IV bolus for NSTEMI], caution if renal failure or age >75) or unfractionated heparin (unfractionated heparin 70 U/kg [up to 4,000 U] IV bolus, then 18 U/kg/h [up to 1,000 U/h] and adjust to 1.5–2.5× normal PTT for 72 h). Factor Xa inhibitors (fondaparinux 2.5 mg SC daily until discharge or 8 days, caution if renal failure). Direct thrombin inhibitors (bivalirudin 0.1 mg/kg IV bolus then 0.25 mg/kg/h initially, followed by second 0.5 mg/kg bolus before PCI and 1.75 mg/kg/h during PCI, then continue infusion for up to 4 h post-PCI, if needed)

  • reperfusion therapy—see PCI for details. Fibrinolytics for STEMI (alteplase 15 mg IV over 2 min, then 0.75 mg/kg over 30 min [maximum 50 mg], then 0.5 mg/kg over 60 min [overall maximum 100 mg]; or tenecteplase IV bolus over 5 s, weight-based dosing: 30 mg for weight <60 kg, 35 mg for 60–69 kg, 40 mg for 70–79 kg, 45 mg for 80–89 kg, 50 mg for ≥90 kg])

RATE CONTROL

—start with metoprolol tartrate [immediate release] 25 mg PO q6-12 h. Titrate as tolerated up to maximum dose of metoprolol tartrate [immediate release] 100 mg PO q12h or metoprolol succinate [extended release] 200 mg PO daily. Alternatively, carvedilol 6.25 mg PO BID and titrate as tolerated up to 25 mg PO BID. The goal heart rate is 50–55 with normal activity. If ongoing ischemia or refractory hypertension at the time of presentation, may also consider metoprolol tartrate 5 mg IV q5min, up to 3 doses. Avoid if HF, low-output state, presence of prolonged first-degree or high-grade AV block, history of reactive airways disease, or MI precipitated by cocaine use. If β-blocker contraindicated, consider non-dihydropyridine calcium channel blockers (diltiazem 30–120 mg PO QID or verapamil 80–120 mg PO TID [contraindicated if LV dysfunction])

LIPID CONTROL

—high-intensity statin such as atorvastatin 80 mg PO daily or rosuvastatin 40 mg PO daily

BLOOD PRESSURE SUPPORT

—for patients with cardiogenic shock, consider IV fluids, inotropes (dobutamine/dopamine), balloon pump, and early revascularization

OVERALL APPROACH

 

Stable angina

Unstable angina or NSTEMI

STEMI

ASA

Nitrates

Morphine

±

β-blockers

ACE inhibitors or ARBs

HMG-CoA inhibitors

Heparin or antithrombin

NO

P2Y12 inhibitors

NO

GPIIb/IIIa inhibitors

NO

✓ (consider)

NO

Fibrinolytics or PCIa

NO

NO

Cardiology consult

Outpatientb

CCUc

CCUc

aIf initial presentation is to a PCI-capable hospital, then primary PCI should be performed within 90 min from time of first medical contact (FMC). If initial presentation is to a non-PCI-capable hospital, then arrange urgent transfer to PCI-capable hospital if primary PCI can be performed within 120 min from time of FMC. If timely PCI cannot be provided, administer fibrinolytic within 30 min of FMC. Urgent CABG is also an option post-catheterization

bOutpatient cardiology for stress test

cCCU consult for risk stratification, monitoring, PCI, and/or CABG

CAUTIONS IN TREATMENT OF ACUTE MYOCARDIAL INFARCTION

—avoid negative inotropic agents such as β-blockers and non-dihydropyridine calcium channel blockers if clinical heart failure. Avoid administration of nitroglycerin, morphine, and diuretics to patients with right ventricular infarction as these medications can cause venodilation and decrease preload, leading to hypotension

Long-Term Management of Coronary Artery Disease

ANTIANGINAL

nitroglycerin (nitro patch 0.4–0.8 mg/h daily; nitro spray 0.4 mg SL q5 min × 3; isosorbide mononitrate 30 mg PO daily, maximum 240 mg), β-blocker (metoprolol tartrate [immediate release] 25–100 mg PO BID, metoprolol succinate [extended release] 50–200 mg PO daily, carvedilol 6.25–25 mg PO BID, bisoprolol 5–10 mg PO daily), calcium channel blocker (amlodipine 5–10 mg PO daily)

ACE INHIBITOR

ramipril 2.5–10 mg PO BID, lisinopril 2.5–10 mg PO daily, trandolapril 0.5–4 mg PO daily, perindopril 2–8 mg PO daily. If ACE inhibitor not tolerated, use ARB

ANTIPLATELET

ECASA 81 mg PO daily indefinitely. P2Y12 receptor blockade (clopidogrel 75 mg PO daily; ticagrelor 90 mg PO BID, or prasugrel 10 mg PO daily) generally for 1 year after ACS. Combination ASA plus clopidogrel for minimum of 1 month (ideally 1 year)-post PCI with bare-metal stent, or minimum 12 months (possibly indefinitely) for drug-eluting stents. Consider ticagrelor or prasugrel if received PCI

ANTICOAGULATION

—controversial especially in combination with ASA and/or P2Y12 inhibitor. May be considered for patients post-STEMI or NSTEMI with one of the following criteria: (1) atrial fibrillation, (2) left ventricular thrombus, (3) significant left ventricular dysfunction with extensive regional wall motion abnormalities. Start warfarin 5 mg daily within 72 h and continue heparin/LMWH until INR is between 2 and 3 (unless planning angioplasty). Beware bleeding risk. If possible, minimize duration of “triple therapy” (i.e., ASA, P2Y12 inhibitor, and warfarin), consider GI protection with proton-pump inhibitor, and target lower INR (e.g., 2.0-2.5)

RISK REDUCTION ★ABCDEFG

  • ASA/ACE INHIBITOR / ARB

  • B lood pressure control (see HYPERTENSION p. 65)

  • C holesterol control (see DYSLIPIDEMIA p. 70)

  • D iabetic control (see DIABETES p. 381)

  • E xercise (30 min of moderate-intensity exercise 3–4×/week)

  • F at reduction (see OBESITY ISSUES p. 457)

  • Get going to quit smoking! (see SMOKING ISSUES p. 480)

DRIVING POST-MYOCARDIAL INFARCTION

—see p. 490 for details

Treatment Issues

RIGHT VENTRICULAR INFARCTION

—evidence of inferior MI should automatically trigger one to check right-sided leads (V4R) to assess for the possibility of RV infarction, which occurs in about 50% of patients with inferior MI. May see increased JVP, Kussmaul sign, and clear lungs clinically. ST elevation in V4R is diagnostic and prognostic. Hypotension should be treated with fluid bolus to ensure good preload

POSTERIOR INFARCTION

—ST depression in V1–V2 in a regular ECG should automatically trigger one to request for posterior (V7–V9) leads to check for posterior MI. Posterior infarct may be associated with inferior infarcts (90%) and lateral infarcts (10%) as the PDA may be supplied by the right or left circumflex coronary artery

POST-MI RISK STRATIFICATION

  • extent of infarct / residual function—assessment is based on clinical factors (↑ HR, ↓ BP, Killip class, diabetes, renal failure, ↑ WBC, GRACE risk score, TIMI risk score), ECG, biomarkers (CK, troponin), imaging (echocardiogram, MIBI, cardiac MRI), and angiography. Early measurement of LV function, although of prognostic importance, is misleading as myocardium function may improve in first 2 weeks. Medical management according to risk

  • extent of myocardium at risk—assessment is based on exercise stress test, stress echocardiogram, stress sestamibi (ischemic tissue), thallium scan (viable tissue), PET scan, cardiac MRI, angiography. Angioplasty or CABG should be considered

  • risk of arrhythmia—high risk of VF/VT within the first 48 h, therefore monitor with telemetry. If it occurs after 48 h, consider antiarrhythmics and early ICD

BALLOON PUMP

—a long balloon in the descending aorta that deflates during systole and inflates during diastole to augment coronary perfusion and cardiac output as well as decrease afterload. Reasonable for severe refractory ischemia and hemodynamic instability. May be used in conjunction with inotropes. Contraindicated in aortic regurgitation, AAA, aortic dissection, uncontrolled sepsis bleeding disorder, and severe PVD

FIBRINOLYTICS USE

  • indications—>120 min anticipated delay from first medical contact to primary PCI, ≥30 min of chest pain, patient presentation within 12 h (ideal door to needle time <30 min), ECG criteria (>1 mm ST ↑ in ≥2 contiguous leads, or new LBBB with suggestive history, age <75)

  • absolute contraindications—any intracranial hemorrhage; ischemic stroke within 3 months (except acute ischemic stroke within first 4.5 h); structural cerebral vascular lesion; malignant intracranial neoplasm; closed-head or facial trauma within 3 months; intracranial or intra spinal surgery within 2 months); severe uncontrolled hypertension (unresponsive to emergency therapy); suspected aortic dissection; bleeding diathesis or active bleeding (excluding menses)

  • relative contraindications—chronic, poorly-controlled, severe hypertension; severe hypertension on presentation (>180/110 mmHg); ischemic stroke >3 months; dementia; other intracranial pathology (not already specified above); internal bleeding within 2–4 weeks; active peptic ulcer; major surgery within 3 weeks; non-compressible vascular punctures; use of anticoagulation therapy; pregnancy; traumatic CPR >10 min; prior exposure to streptokinase (if planning to use this fibrinolytic again)

  • risk of bleeding—average risk of severe bleed is 1.8%. Increased risk with women, BP >165/95 mmHg, age >65, weight <70 kg [<154 lbs], and lysis with TPA (+0.5% absolute risk/factor)

  • persistent ST elevation—look for resolution of symptoms and ST elevation to decrease by >50% within 90 min of fibrinolytic therapy. Persistent ST elevation may suggest failed fibrinolytic therapy, and requires urgent rescue catheterization. Other causes of ST elevation include pericarditis, ventricular aneurysm, hyperkalemia, LBBB, and early repolarization abnormality

Related Topics

Aortic Dissection (p. 27)

Asystole (p. 495)

Diabetes Mellitus (p. 381)

ECG (p. 73)

Hyperlipidemia (p. 70)

Hypertension (p. 65)

Pericarditis (p. 35)

Shock (p. 108)

Smoking Cessation (p. 480)

PERCUTANEOUS CORONARY INTERVENTION (PCI, PTCA)

  • indications for acute STEMI—patient presents within 12 h of chest pain (at a PCI-capable hospital, ideal time from first medical contact to device or “FMC-to-device time” ≤90 min; if at a non-PCI-capable hospital requiring transfer for primary PCI, then ideal “FMC-to-device time” ≤120 min), ECG criteria (>1 mm ST ↑ in ≥2 contiguous leads, new or presumed new left bundle branch block), contraindications to fibrinolysis, or in patients in cardiogenic shock irrespective of time of MI onset

  • indications for chronic stable CAD—single/double vessel disease refractory to medical therapy. Decision for revascularization (PCI vs. CABG) should follow assessment by heart team (interventional cardiology and cardiac surgery)

  • adverse events—access site (bleeding, hematomas, arteriovenous fistulae, pseudoaneurysms), contrast nephropathy, arrhythmia (VT, VF), stroke, dissection, myocardial infarction, death

  • bare metal stents vs . drug - eluting stents—in-stent restenosis is due to fibrosis of coronary vasculature and usually happens 3 months post-procedure. Drug-eluting stents (sirolimus, paclitaxel, everolimus, or zotarolimus) are designed to inhibit cell proliferation and decrease the risk of in-stent restenosis. There has been some controversy regarding higher adverse events in patients with first generation drug-eluting stents (sirolimus or paclitaxel). The most recent outcomes research analysis suggests that newer-generation drug-eluting stents (everolimus or zotarolimus) are associated with a decreased rate of repeat revascularization, stent thrombosis, and no significant difference in mortality

  • benefits—primary PCI is generally preferred given the superior outcomes compared to fibrinolysis, particularly if (1) fibrinolysis contraindicated, (2) previous history of CABG, or (3) cardiogenic shock. However, patients who are able to seek medical attention within 1 h of chest pain onset, have allergy to contrast dye, or do not have access to PCI in a timely fashion should consider fibrinolytics

OUTCOMES FOR FIBRINOLYTICS VS. PRIMARY PCI

 

Fibrinolytics (%)

PrimaryPCI (%)

Non-fatal reinfarction

7

3

Stroke

2

1

Death (4–6 weeks)

7–9

5–7

Combined endpoint of death–fatal reinfarctionand stroke

14

8

NEJM 2007 356:1; NEJM 2007 356:10; NEJM 2007 357:16

CORONARY ARTERY BYPASS GRAFT SURGERY

  • coronary anatomy
    • right coronary (RCA)—gives rise to right marginal (RMA), right posterior descending (RPDA), and right posterolateral branches (RPL 1, 2, 3)

    • left main (LM)—gives rise to left anterior descending (LAD) → diagonal (D1, 2 3) and septals; ramus intermediate (Ram Int); and left circumflex (LCX) → obtuse marginal (OM 1, 2, 3)

    • dominant artery—defined as the artery that supplies PDA and at least one posterolateral (PL) artery

  • indications—studies suggest CABG provides mortality benefit for specific subgroups, including patients with (1) left main disease >50% occlusion, (2) two vessel disease with significant involvement of proximal left anterior descending, and (3) diffuse triple vessel disease. Diabetic patients and those with reduced left ventricular function derive more benefit from bypass surgery. Angiographic disease severity should be assessed using the SYNTAX score. Decision for revascularization (PCI vs. CABG) should follow assessment by heart team (interventional cardiology and cardiac surgery)

  • morbidity benefit—95% have improvement of symptoms immediately after surgery, 75% symptom free at 5 years. Recurrent disease more common in vein grafts than artery grafts

  • grafts—saphenous veins from calf or thigh (SVG), internal mammary arteries (LIMA/RIMA), radial arteries (RA), and gastroepiploic artery from stomach (GA). A total of 90% of arterial graft and 50% of vein graft remain patent by 10 years

  • complications
    • cardiac—MI 2–4%, arrhythmia (AF 40%, sustained VT/VF 2–3%), AV block requiring pacemaker 0.8–4%, pericarditis/tamponade, aortic dissection

    • neurological—stroke, postoperative delirium, cognitive impairment, depression, phrenic nerve damage, intercostal nerve damage

    • others—renal failure, bleeding, infection, pleural effusions, death

  • medications—hold clopidogrel or ticagrelor 5–7 days prior to CABG. Continue ASA before and after surgery

Pericardial Diseases: Pericarditis and Tamponade

Differential Diagnosis

★MINT★

  • Metabolic—uremia, dialysis, hypothyroidism

  • Medications—procainamide, hydralazine, INH, phenytoin, penicillin

  • Infarction—MI (early, late)

  • Infectious—HIV, Coxsackie, echovirus, adenovirus, TB

  • I nflammatory—psoriatic arthritis, enteric arthritis, rheumatoid arthritis, SLE, mixed connective tissue disease

Idiopathic

  • Neoplastic—primary (mesothelioma), metastasis (breast, lung, melanoma), leukemia, lymphoma

  • Trauma—stab, gunshot wound, blunt, CPR, postpericardiotomy

Clinical Features

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT WITH A PERICARDIAL EFFUSION HAVE CARDIAC TAMPONADE?

 

Sens (%)

H istory

 

Dyspnea

87–89

Fever

25

Chest pain

20

Cough

7–10

Physical

Tachycardia

77

Pulsus paradoxus >10 mmHga

82

Elevated JVP

76

↓ heart sounds

28

Hypotension

26

Hypertension

33

Tachypnea

80

Peripheral edema

21–28

Pericardial rub

19–29

Hepatomegaly

28–55

Kussmaul sign

26

EC G

Low voltage

42

Atrial arrhythmia

6

Electrical alternans

16–21

ST elevation

18–30

PR depression

18

aPulsus paradoxus LR+ 3.3, LR– 0.03

  • APPROAC H—“among patients with cardiac tamponade, a minority will not have dyspnea, tachycardia, elevated JVP, or cardiomegaly on chest radiograph. A pulsus paradoxus >10 mmHg among patients with a pericardial effusion helps distinguish those with cardiac tamponade from those without. Diagnostic certainty of the presence of tamponade requires additional testing”

JAMA 2007 297:16

DISTINGUISHING FEATURES OF ACUTE TAMPONADE AND CHRONIC CONSTRICTIVE PERICARDITIS

 

Acute tamponade

Constrictive pericarditis

Vitals

Tachycardia, hypotension+++, pulsus paradoxus

Hypotension, pulsus paradoxus (rare)

JVP

Elevated, Kussmaul (rare)

Elevated, Kussmaul

Prominent x′ descentbut blunted y descent

Prominent x′ and y descent (Friedrich’s sign)

Apex beat

Impalpable

Impalpable

Heart sounds

Distant

Distant, early S3/knock

Other features

Dullness and bronchial breath sounds over left base (Ewart sign)

Hepatosplenomegaly, edema

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, troponin, CK

  • imaging—CXR (calcification if constrictive disease), echocardiogram

  • EC G—may have sinus tachycardia, low voltages, and electrical alternans in tamponade/effusion; diffuse ST elevation (concave up) and PR depression may be seen in pericarditis

SPECIAL

  • pericardiocentesis—diagnostic or therapeutic (for tamponade, TB/bacterial pericarditis, or large persistent effusion)

  • pericardioscopy

  • CT/MRI chest—if suspect constrictive pericarditis

Management

ACUTE PERICARDITIS

NSAIDs (indomethacin 25–50 mg PO TID, ibuprofen 600–800 mg PO TID × 2–4 weeks, or until resolution of pain) for most cases of idiopathic or viral pericarditis, but avoid after acute MI. If post-MI, ASA 650 mg PO TID × 3–4 weeks. Adjuvant colchicine 0.6 mg PO BID × 3 months in addition to NSAID/ASA to reduce risk of recurrence. Prednisone 0.25–0.5 mg/kg PO daily × 2 weeks (followed by taper) may be considered for connective tissue-mediated disease, although symptoms may recur upon withdrawal

RECURRENT PERICARDITIS

ASA 650 mg PO TID × 4–8 weeks or NSAIDs (indomethacin 25–50 mg PO TID, ibuprofen 600–800 mg PO TID × 4–8 weeks). Add colchicine (0.6 mg PO BID × 3–6 months) for longterm prophylaxis. Avoid anticoagulation as risk of hemopericardium. Prednisone 0.25–0.5 mg/kg PO daily may also be useful, although symptoms may recur upon withdrawal

TAMPONADE

—ABC, O 2 , IV’s, bolus IV fluids, pericardiocentesis (subxyphoid blind approach, echocardiogram-guided parasternal or apical approach), pericardiectomy, pericardial window if recurrent/malignant effusion. Avoid nitroglycerin and morphine if tamponade as they may decrease preload, leading to worsening of cardiac output

CONSTRICTIVE PERICARDITIS

—complete pericardiectomy

Specific Entities

ACUTE PERICARDITIS

—may be preceded by upper respiratory tract infection. Diagnosis is based on any two of the following inflammatory signs (LR+ 5.4): fever, pericardial friction rub (three components), characteristic chest pain (better with upright position and leaning forward, or pleuritic), PR depression, and diffuse ST elevation. Large effusion without inflammatory signs or tamponade suggests chronic idiopathic pericardial effusion (LR+ 20)

RECURRENT PERICARDITIS

—returns in days to weeks upon stopping medications. Likely causes include rheumatologic disorders, Dressler’s syndrome, and post-pericardiotomy syndrome

TAMPONADE

—a clinical diagnosis based on dyspnea, tachycardia, hypotension, pulsus paradoxus, and elevated JVP. Tamponade causes restriction in left or right ventricular diastolic filling. Tamponade with inflammatory signs suggests malignant effusion (LR+ 2.9)

CONSTRICTIVE PERICARDITIS

—contraction of pericardium due to chronic inflammation, leading to left and/or right heart failure. May follow pericarditis or radiation. May be difficult to distinguish from restrictive cardiomyopathy clinically

Heart Failure

NEJM 2003 348:20

Canadian Heart Failure Guidelines 2006

Canadian Heart Failure Guidelines Updates 2017–2013

Differential Diagnosis of HF Exacerbation/Dyspnea

CARDIAC

  • myocardial—HF exacerbation, myocardial infarction

  • valvular—aortic stenosis, acute aortic regurgitation, mitral regurgitation/stenosis, endocarditis

  • pericardial—tamponade

  • dysrhythmia

RESPIRATORY

  • airway—COPD exacerbation, asthma exacerbation, acute bronchitis, bronchiectasis, foreign body obstruction

  • parenchyma—pneumonia, cryptogenic organizing pneumonia, ARDS, interstitial lung disease exacerbation

  • vascular—pulmonary embolism, pulmonary hypertension

  • pleural—pneumothorax, pleural effusion

SYSTEMIC

—sepsis, ARDS, metabolic acidosis, anemia, neuromuscular, psychogenic, anxiety

Pathophysiology

ANATOMIC/PHYSIOLOGIC CLASSIFICATION OF CARDIOMYOPATHY

  • dilated (dilatation and impaired contraction of one or both ventricles)—idiopathic, ischemic, valvular, viral, genetic, late manifestation of hypertrophic heart disease, tachycardia induced, alcohol induced, peripartum

  • hypertrophic (disorder with disproportionate hypertrophy of the left ventricle and occasionally right ventricle)—idiopathic (autosomal dominant inheritance with incomplete penetrance), storage disease (Fabry’s disease, Pompe disease, Hurler’s syndrome, Noonan’s syndrome), athlete’s heart, obesity, amyloid

  • restrictive (non-dilated ventricles with impaired ventricular filling)—idiopathic familial, infiltrative (amyloidosis, hemochromatosis, sarcoidosis), drugs, radiation, endomyocardial fibrosis

  • arrhythmogenic right ventricular (replacement of right ventricular free wall with fatty tissue)—arrhythmogenic right ventricular dysplasia

  • unclassifiable—endocardial fibroelastosis, left ventricular non-compaction

ETIOLOGIC CLASSIFICATION OF CARDIOMYOPATHY

  • ischemic cardiomyopathy (mostly dilated)—varying degrees of persistent ischemia, infarction, and left ventricular remodeling

  • valvular cardiomyopathy (mostly dilated)—abnormal loading conditions and secondary left ventricular remodeling and dysfunction

  • hypertensive cardiomyopathy (dilated, restrictive)—left ventricular hypertrophy and dysfunction

  • diabetic cardiomyopathy (dilated)—left ventricular dysfunction in the absence of atherosclerosis or hypertension

  • inflammatory cardiomyopathy (mostly dilated)—infectious (diphtheria, rheumatic fever, scarlet fever, typhoid fever, meningococcal, TB, Lyme disease, Leptospirosis, RMSF, poliomyelitis, influenza, mumps, rubella, rubeola, variola, varicella, EBV, Coxsackie virus, echovirus, CMV, hepatitis, rabies, mycoplasma, psittacosis, arboviruses, histoplasmosis, cryptococcosis, Chagas disease), autoimmune, idiopathic myocardial inflammatory diseases

  • metabolic cardiomyopathy (dilated, restrictive, and/or hypertrophic)—endocrine (thyrotoxicosis, hypothyroidism, acromegaly, pheochromocytoma), storage diseases (glycogen storage disease, Fabry’s disease, Gaucher’s disease, Niemann–Pick disease), nutritional deficiencies (Beriberi, Kwashiorkor, pellagra), deposition (amyloidosis, hemochromatosis, sarcoidosis)

  • muscular dystrophies (mostly dilated)—Duchenne, Becker’s, myotonic dystrophy

  • neuromuscular—Friedreich’s ataxia (hypertrophic), Noonan’s syndrome, lentiginosis

  • general systemic disease (mostly dilated)—connective tissue diseases (rheumatoid heart disease, ankylosing spondylitis, SLE, scleroderma, dermatomyositis), granulomatous (sarcoidosis, Wegener’s granulomatosis, granulomatous myocarditis), other inflammatory (giant cell myocarditis, hypersensitivity myocarditis), neoplasm (primary, secondary, restrictive pattern)

  • sensitivity and toxic reactions (mostly dilated)—alcohol, amphetamine, arsenic, catecholamines, cocaine, anthracyclines, zidovudine, radiation (restrictive as well)

  • peripartum (dilated)—see p. 471

FUNCTIONAL CLASSIFICATION OF HEART FAILURE

  • systolic dysfunction (↓ LVEF <45%)—S3 (dilated ventricle with volume overload). Mechanisms include decreased contractility and increased afterload. Causes include MI, cardiomyopathy (dilated, infiltrative), valvular (aortic regurgitation, mitral regurgitation, “burned out” aortic stenosis), “burned out” hypertension and myocarditis

  • diastolic dysfunction (normal LVEF)—S4 (stiff ventricle), LVH, ↓ ventricular relaxation, normal LVEF, ↑ chamber pressures. Mechanisms include decreased active relaxation and passive relaxation (stiff ventricle). Causes include ischemia, hypertension, valvular (aortic stenosis), cardiomyopathy (restrictive, hypertrophic), and pericardial disease

  • mixed dysfunction—in many cases, diastolic dysfunction is present with systolic heart failure

PRECIPITANTS OF HF ★FAILURE★

  • Forget to take medications (non-adherence)

  • Arrhythmia, anemia

  • Infection, ischemia, infarction

  • Lifestyle change

  • Upregulators (thyroid, pregnancy)

  • Rheumatic heart disease, acute valvular disease

  • Embolism

Clinical Features

DISTINGUISHING FEATURES BETWEEN COPD AND HEART FAILURE

 

COPD

Heart Failure

History

Previous COPD

Previous HF

 

Medications

Medications

Inspect

Nicotine stain, barrel chest

 

Laryngeal height <4 cm

Cardiac exam

Subxyphoid cardiac pulse

Elevated JVP, S3, S4

Resp. exam

Hyperresonance

Bilateral crackles

Prolonged expiratory time

Investigations

CXR shows hypeinflation

CXR shows redistribution and cardiomegaly

 

ABG shows hypercapnia and hypoxemia

ABG shows hypoxemia

Elevated BNP

LEFT HEART FAILURE

—left-sided S3, rales, wheezes, tachypnea. Causes include previous MI, aortic stenosis, and left-sided endocarditis

RIGHT HEART FAILURE

—right-sided S3, ↑ JVP, ascites, hepatomegaly, peripheral edema. Causes include left heart failure, pulmonary hypertension, right ventricular MI, mitral stenosis, and right-sided endocarditis

GRADING OF PITTING EDEMA

0 = no edema, 1 = trace edema, 2 = moderate edema disappears in 10–15 s, 3 = stretched skin, deep edema disappears in 1–2 min, 4 = stretched skin, fluid leaking, very deep edema present after 5 min

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS DYSPNEIC PATIENT IN THE EMERGENCY DEPARTMENT HAVE CONGESTIVE HEART FAILURE?

 

Sens (%)

Spc (%)

LR+

LR–

History

Initial clinical judgment

61

80

4.4

0.45

Hx heart failure

60

90

5.8

0.45

Myocardial infarction disease

40

87

3.1

0.69

Coronary artery

52

70

1.8

0.68

Dyslipidemia

23

87

1.7

0.89

Diabetes

28

83

1.7

0.86

Hypertension

60

56

1.4

0.71

Smoker

62

27

0.84

1.4

COPD

34

57

0.81

1.1

PND

41

83

2.6

0.70

Orthopnea

50

77

2.2

0.65

Edema

51

76

2.1

0.64

Dyspnea on exertion

84

34

1.3

0.48

Fatigue and weight gain

31

70

1.0

0.99

Cough

36

61

0.93

1.0

Physical

S3

13

99

11

0.88

AJR

24

96

6.4

0.79

JVD

39

92

5.1

0.66

Rales

60

78

2.8

0.51

Any murmur

27

90

2.6

0.81

Lower extremity edema

50

78

2.3

0.64

Valsalva maneuver

73

65

2.1

0.41

SBP <100 mmHg

6

97

2.0

0.97

S4

5

97

1.6

0.98

SBP ≥150 mmHg

28

73

1.0

0.99

Wheezing

22

58

0.52

1.3

Ascites

1

97

0.33

1.0

CXR

Pulmonary venous congestion

54

96

12

0.48

Interstitial edema

34

97

12

0.68

Alveolar edema

6

99

6.0

0.95

Cardiomegaly

74

78

3.3

0.33

Pleural effusions

26

92

3.2

0.81

Any edema

70

77

3.1

0.38

Pneumonia

4

92

0.50

1.0

Hyperinflation

3

92

0.38

1.1

ECG

Atrial fibrillation

26

93

3.8

0.79

New T wave changes

24

92

3.0

0.83

Any abnormal finding

50

78

2.2

0.64

ST elevation

5

97

1.8

0.98

ST depression

11

94

1.7

0.95

BNP

BNP ≥ 250 pg/mL

  

4.6

 

BNP ≥ 100 pg/mL a

  

2.7

 

BNP ≥ 50 pg/mL

  

1.7

0.06

aFor patients with an estimated GFR of 15–60 mL/min/1.73 m2, a threshold of 201 pg/mL can be used

  • APPROAC H—“the features evaluated in more than one study with the highest LRs (>3.5) for diagnosing heart failure were the following: the overall clinical judgment, history of heart failure, S3, jugular venous distension, pulmonary venous congestion or interstitial edema on CXR, and atrial fibrillation on ECG. The features evaluated in more than one study with the lowest LRs (<0.60) for diagnosing of heart failure were the following: the overall clinical judgment, no prior history of heart failure, no dyspnea on exertion, the absence of rales, and the absence of radiographic pulmonary venous congestion, or cardiomegaly. The single finding that decreased the likelihood of heart failure the most was a BNP <100 pg/mL. While the findings of this study are useful when assessing dyspneic patients suspected of having heart failure, no individual feature is sufficiently powerful in isolation to rule heart failure in or out. Therefore, an overall clinical impression based on all available information is best. If the appropriate constellation of findings with high LRs for heart failure are present, that may be sufficient to warrant empirical treatment without further urgent investigations”

JAMA 2005 294:15

The Rational Clinical Examination. McGraw-Hill, 2009

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE ABNORMAL CENTRAL VENOUS PRESSURE?

  • JVP VS. CAROTID—JVP has biphasic waveforms, is non-palpable, is occludable, decreases with inspiration, changes with position, and increases with abdominojugular reflux (AJR). To perform the AJR, the blood pressure cuff is pumped 6× and then pressed against the abdomen at 20–35 mmHg for 15–30 s. Normal = no change in JVP, or transient increase of >4 cm that returns to baseline before 10 s, or sustained increase <3 cm throughout. Positive AJR occurs when abdominal compression causes a sustained increase in JVP >4 cm (sens 24%, spc 96%, LR+ 4.4)

JAMA 1996 275:8
  • UPDATE—a JVP height ≥3 cm above the sternal angle in any position indicates an abnormal CVP. Clinical assessment of high JVP has a LR+ for high CVP of 3.1. An assessment of low JVP has a LR+ for low CVP of 3.4

The Rational Clinical Examination. McGraw-Hill, 2009

RATIONAL CLINICAL EXAMINATION SERIES: CAN THE CLINICAL EXAMINATION DIAGNOSE LEFT-SIDED HEART FAILURE IN ADULTS?

INCREASED FILLIN G PRESSURE—very helpful findings are radiographic redistribution and jugular venous distension. Somewhat helpful findings are dyspnea, orthopnea, tachycardia, decreased systolic or pulse pressure, S3, rales, and abdominojugular reflux. Edema is helpful only when present

SYSTOLIC DYSFUNCTION—very helpful findings are radiograph (cardiomegaly, redistribution), anterior Q waves, LBBB, and abnormal apical impulse (especially if sustained). Somewhat helpful findings are tachycardia, decreased blood pressure or pulse pressure, S3, rales, dyspnea, previous infarction other than anterior, and high peak CK (post-infarct). Edema and increased jugular venous pressure are helpful if present

DIASTOLIC DYSFUNCTION—very helpful finding is elevated blood pressure during the episode of increased filling pressure. Somewhat helpful findings are obesity, lack of tachycardia, older age, and absence of smoking or CAD. Normal radiographic heart size is helpful if present

APPROAC H—“in patients without known systolic dysfunction, ≤1 finding of increased filling pressure can exclude diagnosis, ≥3 findings suggests increased filling pressure. In patients with known systolic dysfunction, absence of finding of increased filling pressure can exclude diagnosis, ≥1 finding suggests increased filling pressure. For systolic dysfunction, can exclude diagnosis if no abnormal findings, including no sign of increased filling pressure are present (LR– 0.1). ≥3 findings are needed to confirm the diagnosis (LR+ 14)”

JAMA 1997 277:21

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, troponin/CK × 3, BNP or NT-pro-BNP, D-dimer, TSH, albumin

  • imaging—CXR, echocardiogram (check E/A ratio if diastolic dysfunction)

  • EC G

SPECIAL

  • further imaging—MIBI, MUGA

  • stress test—to assess ischemic heart disease

  • cardiac catheterization

  • AB G—if severe dyspnea

Diagnostic and Prognostic Issues

B-TYPE NATRIURETIC PEPTIDE/N-TERMINAL PROHORMONE OF BRAIN NATRIURETIC PEPTIDE

  • diagnosis—BNP and NT-proBNP levels are elevated with HF, PE, pulmonary hypertension, LVH, ACS, AF, renal failure, overload, and sepsis. Generally, can rule-out HF if BNP <100 pg/mL or NT-proBNP <300 pg/mL; may rule-in if BNP >500 pg/mL, NT-proBNP >900 pg/mL (if age 50–75 years), or NT-proBNP >1,800 pg/mL (if age >75 years). Best used in combination with clinical scoring system when diagnosis is uncertain

  • Baggish clinical scoring system—elevated NT-proBNP [>450 pg/mL if age <50 years, or >900 pg/mL if age ≥50 years] (+4), interstitial edema on CXR (+2), orthopnea (+2), lack of fever (+2), age >75 years (+1), lack of cough (+1), use of loop diuretic prior to presentation (+1), rales (+1). If score 0–5, low likelihood of HF; if 6–8, intermediate likelihood of HF; if 9–14, high likelihood of HF

  • prognosis—BNP >80th percentile is associated with a >50% increase in long-term mortality

HF PROGNOSIS

—33% 1-year mortality, 75% 6-year mortality

Acute Management

ABC

—O2 to keep sat >95%, IV’s

SYMPTOM CONTROL

—★LMNOPL asix/furosemide 20–120 mg IV PRN, M orphine 2–5 mg IV PRN, N itroglycerin 0.4 mg SL PRN, O2, Position (upright)

Long-Term Management

★DDDD★

  • DIETlow salt (<100 mmol/day, 1.5–2 g/day), fluid restriction (1.5–2 L/day)

  • DIURETICSfurosemide 20–120 IV/PO daily-BID with daily adjustments (try to use smallest dose possible to allow ACE inhibitor) ± metolazone 2.5–5 mg PO 30 min before furosemide, spironolactone 12.5–50 mg PO daily or eplerenone 25–50 mg PO daily VASODILATORSACE inhibitor (captopril 6.25–50 mg PO TID, enalapril 1.25–10 mg PO BID, ramipril 2.5–10 mg PO BID, lisinopril 2.5–20 mg PO daily, perindopril 2–8 mg PO daily). ARB (valsartan 40–160 mg PO BID, candesartan 8–32 mg PO daily). Hydralazine 10–50 mg PO QID and nitrates (nitropatch 0.4 mg topical daily or isosorbide mononitrate 30–90 mg PO daily). β-blockers (metoprolol tartrate 50–100 mg PO BID, carvedilol 3.125–25 mg PO BID, bisoprolol 2.5–10 mg PO daily)

  • DI G ITALISdigoxin 0.0625–0.25 mg PO daily

  • TREAT UNDERLYIN G CAUSECAD (PCI/CABG), aortic stenosis (AV replacement), sleep apnea (CPAP)

  • DEVICES—if ejection fraction <30–35%, consider cardiac resynchronization therapy (CRT/biventricular pacing) ± implantable cardioverter defibrillators (ICD). Ventricular assist devices may also be considered in selected cases of refractory HF

Treatment Issues

ACE INHIBITOR

(Garg, JAMA 1995)—hazard ratios for total mortality 0.77 and mortality/hospitalization 0.65 for any patients with LVEF <40%. Target dose = maximum tolerated. Contraindications include SBP <80 mmHg, bilateral renal artery stenosis, severe renal failure, and hyperkalemia

ARB

(CHARM)—consider substitution with ARB if ACE inhibitor not tolerated (e.g., cough). May also be used as adjunct to ACE inhibitor if β-blocker not tolerated. Contraindications similar to ACE inhibitor

HYDRALAZINE/NITRATES

(VHEFT I and II, A-HeFT)—less effective than ACE inhibitor. Particularly useful for pregnant patients, African Americans, or those who developed renal insufficiency while on ACE inhibitor, or as add-on therapy

ANGIOTENSIN RECEPTOR–NEPRILYSIN INHIBITOR

(McMurray, NEJM 2014, PARADIGM-HF)—combination sacubitril-valsartan demonstrated 16% reduction in all-cause mortality, 20% reduction in death from cardiovascular causes, and 21% reduction heart failure hospitalizations compared to enalapril

β-BLOCKERS

(Foody JAMA 2002)—hazard ratios for total mortality 0.65 and mortality/hospitalization 0.64. May worsen symptoms in first few weeks and may take up to 1 year to see full effect in LVEF. Useful for patients with NYHA II–III (and stable IV) and LVEF <40%, also NYHA I, LVEF <40%, and post-MI. Contraindications include fluid overload and severe asthma. Start only when patient euvolemic

SPIRONOLACTONE

(RALES 1999, EPHESUS 2003, EMPHASIS-HF 2011)—hazard ratios for all-cause mortality 0.7 and hospitalization for HF, 0.65 for patients with NYHA III–IV, LVEF <35%, and already on maximum medical therapy. Hazard ratios for cardiovascular death/HF hospitalization 0.63 and cardiovascular mortality 0.76 for patients with NYHA II and LVEF ≤30% (or LVEF 31–35% plus QRS duration >130 msec), and already on maximum medical therapy. Caution in elderly and renal failure patients as higher risk of hyperkalemia

DIGOXIN

(DIG 1997)—hazard ratios for total mortality 0.99 and mortality/hospitalization 0.92. Particularly useful for patients with both HF and atrial fibrillation, or symptomatic HF despite maximum medical therapy

OVERALL APPROACH

—treat underlying cause if possible. Non-pharmacological treatments (diet, exercise, smoking cessation) → add ACE inhibitor if LVEF ≤40% (or hydralazine/nitrates if renal failure, ARB if cough secondary to ACE inhibitor) → add β-blocker when euvolemic if LVEF ≤40% → add spironolactone/eplerenone if NYHA II-IV if LVEF ≤30% (or ≤35% and QRS duration >130 msec) → add digoxin ± ARB if still symptomatic. If ejection fraction is <30–35% despite optimal medical therapy, consider revascularization, implantable cardioverter defibrillator, cardiac resynchronization (if QRS is wide), and ventricular-assist device/heart transplant

Specific Entities

CAUSES OF FLASH PULMONARY EDEMA

cardiac (ischemic heart disease, acute aortic regurgitation, acute mitral regurgitation, mitral stenosis/obstruction, arrhythmia), pulmonary (pulmonary embolism, pneumonia), renal (bilateral renal artery stenosis), systemic (hypertension crisis, fever, sepsis, anemia, thyrotoxicosis)

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HOCM)

  • pathophysiology—autosomal dominant condition with mutated cardiac sarcomere, leading to massive ventricular hypertrophy (particularly septum). This results in left ventricular outflow tract obstruction, mitral regurgitation, diastolic dysfunction, and subsequently myocardial ischemia and overt heart failure. Cardiac arrhythmias may lead to sudden death (<1%/year). Other complications include atrial fibrillation and infective endocarditis

  • risk factors for sudden death—major risk factors include history of cardiac arrest (VF), sustained VT, unexplained syncope, non-sustained VT on Holter, abnormal BP response on exercise test, left ventricular wall thickness >30 mm, and family history of sudden death. Minor risk factors include left ventricular outflow obstruction (gradient ≥30 mmHg), diastolic dysfunction, microvascular obstruction, late gadolinium enhancement on cardiac MRI, and high-risk genetic defect

  • clinical features—most are asymptomatic although dyspnea, chest pain, syncope, and sudden death may develop. Family history should be obtained. Physical findings include brisk carotid upstroke, bifid carotid pulse, double apical impulse, systolic ejection murmur (LLSB, louder with standing and Valsalva) ± mitral regurgitation murmur

  • diagnosis—echocardiogram (septal thickening, systolic-anterior motion of mitral valve). Further workup includes 48 h Holter monitor and exercise testing annually

  • treatmentsavoidance (dehydration and strenuous exercise), medical (β-blockers and non-dihydropyridine calcium channel blockers as first line, disopyramide as second line), interventional/surgical (septal myomectomy, alcohol septal ablation, dual-chamber pacing), prophylaxis (implantable cardioverter defibrillator for high-risk patients to prevent sudden cardiac death, anticoagulation if atrial fibrillation)

NEJM 2004 350:13

Digoxin Intoxication

Circulation 2004 109:24

Causes

OVERDOSE

—intentional, accidental (digoxin, foxglove, yellow oleander)

DRUG INTERACTIONS

—quinidine, amiodarone, verapamil, diltiazem, tetracycline, erythromycin, rifampin, cyclosporine, SSRIs

PHARMACOKINETICS (see precipitants below)

  • old age , renal failure

  • cardiac—ischemia, myocarditis, cardiomyopathy, amyloidosis, cor pulmonale

  • metabolic—hypokalemia, hypomagnesemia, hypernatremia, hypercalcemia, hypoxemia, acid–base imbalance

Pathophysiology

DIGOXIN LEVEL

—measurement of serum levels is not routinely necessary as dosing can usually be titrated according to clinical and hemodynamic effects. When measured, serum level should be collected at 12–24 h after the last dose (post-distribution phase). While the upper normal limit is 2.6 nmol/L [2.0 ng/mL], higher digoxin levels may be seen in asymptomatic patients. Low-dose digoxin, resulting in serum levels 0.5–0.9 nmol/L [0.4–0.7 ng/mL] is associated with possible survival benefit compared to ≥1 nmol/L [≥0.78 ng/mL] in HF patients

MECHANISM

—digitalis acts by inhibiting the membrane-bound Na/K ATPase transport system. This leads to intracellular loss of K and gain of Na. Increase in intracellular Ca leads to ↑ cardiac contractility. Digoxin also exerts a vagotonic action, which slows conduction through the SA and AV node and helps to control heart rate

PRECIPITANTS OF DIGOXIN TOXICITY

—toxicity is not merely related to serum levels, but also digoxin dosing (e.g., acute overdose), other medications (e.g., non-potassium sparing diuretics), and conditions (e.g., renal insufficiency, acute coronary syndromes, cardiac amyloidosis, hypothyroidism). For instance, hypokalemia, hypernatremia, hypomagnesemia and acidosis predispose to toxicity even at low-serum digoxin levels because of their depressive effects on the Na/K ATPase pump. In contrast, hyperkalemia occurs in acute toxicity and is directly related to prognosis

Clinical Features

SIGNS AND SYMPTOMS

  • neurological—delirium, hallucination, blurred vision with altered color perception, headaches, dizziness

  • cardiac—bradycardia, high-degree AV block, paroxysmal atrial tachycardia (often 2:1 AV conduction), unifocal or multifocal PVCs, bidirectional ventricular tachycardia, accelerated junctional tachycardia

  • G I—anorexia, N&V, diarrhea, abdominal pain

  • metabolic—hyperkalemia

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, Ca, Mg, albumin, serum digoxin level

  • EC G

  • AB G

Diagnostic Issues

ECG CHANGES ASSOCIATED WITH DIGOXIN

  • therapeutic levels—sagging of ST segments, flattened T waves, U waves, and shortened QT. Not to be confused with digoxin toxicity

  • toxic levels—first degree heart block, paroxysmal atrial tachycardia (often 2:1 AV conduction), regularized atrial fibrillation (i.e., with complete heart block), unifocal or multifocal PVCs, ventricular bigeminy, bidirectional VT

Management

ACUTE

—ABC, O 2 , IV, treat arrhythmia

TREAT UNDERLYING CAUSE

observe, cardiac monitoring, activated charcoal (if ingestion within 4 h). Correct electrolyte disturbances and reverse acidosis. Atropine for bradycardia. Digibind/purified antidigoxin FAB fragments (if acute ingestion of 10 mg or more in adults, or digoxin level >13 nmol/L [10 ng/mL], K >5 mM and life-threatening arrhythmia, hemodynamic instability, unstable arrhythmia [e.g., symptomatic bradycardia], or end-organ hypoperfusion [e.g., acute renal failure]). May see response in 20 min and complete response up to 4 h. Monitor potassium levels after treatment with Digibind)

Treatment Issues

AVOID

  • IV calcium—indicated for other causes of severe hyperkalemia, calcium may precipitate VT/sudden death and should NOT be given for hyperkalemia of digoxin toxicity

  • cardioversion—relatively contraindicated because asystole or ventricular fibrillation may be precipitated

  • transvenous pacing—can precipitate arrhythmias and deterioration

HALF-LIVES

—plasma t½ for digoxin 1.6 days, digitoxin 5 days

INDICATIONS FOR DIGOXIN THERAPY

—in patients with symptomatic systolic H F and sinus rhythm (digoxin may be especially useful in patients with severe symptoms despite standard medical therapy, LVEF <25%, or cardiomegaly), diastolic H F (with rapid atrial fibrillation or severe symptoms despite standard medical therapy), and rapid atrial fibrillation (with or without heart failure). Use with extreme caution or avoid in the elderly, patients with severe conduction abnormalities, acute coronary syndromes, or renal failure

Atrial Fibrillation

NEJM 2001 344:14; NEJM 2004 351:23

AHA/ACC/HRS 2014 Atrial Fibrillation Guidelines

Canadian Cardiovascular Society 2014 Atrial Fibrillation Guidelines

Differential Diagnosis of Palpitations

★PPP★

  • P H YSIOLO G IC (high output states)—anemia, pregnancy, fever, exercise, stress

PATHOLOGIC★CDE★

  • C ardiacarrhythmia (see tachycardia below), myocardial (cardiomyopathy, atrial myxoma, shunts), valvular, transplanted heart

  • D rugs—sympathomimetic agents, vasodilators, anticholinergic agents, β-blocker withdrawal, illicit (cocaine, amphetamines)

  • E ndocrine—hypoglycemia, hyperthyroidism, pheochromocytoma

PSYCHIATRIC

—panic attack/disorder, generalized anxiety disorder, somatization disorder

Differential Diagnosis of Narrow Complex Tachycardia

REGULAR NARROW COMPLEX TACHYCARDIA

—sinus tachycardia, atrial flutter with fixed block (rate 300, 150, 100), supraventricular tachycardia (atrial tachycardia, AV nodal reentry, orthodromic AV reentrant/WPW), accelerated junctional tachycardia

IRREGULAR NARROW COMPLEX TACHYCARDIA

—sinus tachycardia/arrhythmia, premature atrial contractions, multifocal atrial tachycardia, atrial flutter with variable block, atrial tachycardia with variable block, atrial fibrillation

Differential Diagnosis of Irregularly Irregular Rhythm

ATRIAL

—sinus arrhythmia (rate 60–100), wandering pacemaker (rate 60–100), premature atrial rhythm/beat, multifocal atrial tachycardia (rate >100), ectopic atrial tachyarrhythmia with variable block, atrial flutter with variable block, atrial fibrillation

VENTRICULAR

—premature ventricular contraction, polymorphic ventricular tachycardia, ventricular fibrillation

Pathophysiology

CAUSES OF ATRIAL FIBRILLATION

  • cardiovascularmyocardial (hypertension, CAD, HF, hypertrophic cardiomyopathy, dilated cardiomyopathy, myocarditis, infiltration [amyloidosis, sarcoidosis, hemochromatosis], ASD), valvular (rheumatic, acquired, endocarditis), arrhythmia (WPW, SSS), pericardial (pericarditis), cardiac surgery

  • pulmonary—COPD, pulmonary embolism, pleural effusion

  • metabolic—thyrotoxicosis, obesity

  • drugs—theophylline, adenosine, digitalis, β-agonists, alcohol

  • idiopathic (10%)

CLASSIFICATION OF ATRIAL FIBRILLATION

  • paroxysmal atrial fibrillation—episodes of AF last <7 days (usually <24 h). Terminates spontaneously or with intervention. May variably recur

  • persistent atrial fibrillation—continuous AF sustained >7 days

  • long - standing persistent atrial fibrillation—continuous AF >12 months

  • permanent atrial fibrillation—a classification determined by clinician and patient to stop further attempts to restore and/or maintain sinus rhythm. A therapeutic attitude rather than inherent pathophysiological attribute of AF

  • nonvalvular atrial fibrillation—AF in the absence of rheumatic mitral stenosis, mechanical or bioprosthetic heart valve, or mitral valve repair

  • lone atrial fibrillation—AF in patients <60 years, no structural heart disease or risk factors, including hypertension

Clinical Features of Narrow Complex Tachycardia

HISTORY

—palpitations, chest pain, dyspnea, dizziness, syncope, past medical history (AF, SVT, WPW, CAD, HF, hypertension, diabetes, stroke, TIA, thyroid dysfunction), medications (antihypertensives, antiarrhythmics), DVT/PE risk factors

PHYSICAL

—vitals (pulse rate and rhythm, BP), cardiac and pulmonary examination for heart failure

CAROTID SINUS MASSAGE, VALSALVA, OR ADENOSINE

—SVT may spontaneously terminate, while AF or atrial flutter may slow down. Avoid adenosine if suspect pre-excitation syndrome (atrial fibrillation or atrial flutter with WPW)

Clinical Features

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT WITH PALPITATIONS HAVE A CARDIAC ARRHYTHMIA?

 

Any arrhythmia

Significant arrhythmia

LR+

LR–

LR+

LR–

H istory

Cardiac disease

2.03

0.71

0.42

1.07

Male sex

1.63

0.76

1.20

0.90

Age >60

1.70

0.83

1.89

0.77

Smoking >11/day

0.78

1.03

0.77

1.03

Anxiety disorder

0.98

1.01

0.92

1.04

FH of palpitations

0.86

1.04

1.07

0.98

EtOH >10 days/week

0.76

1.05

1.02

1.00

Panic disorder

0.26

1.30

Any psychiatric disorders

0.67

1.12

Palpitations

Regular

1.66

1.38

0.55

Irregular

1.65

0.62

1.23

Duration >5 min

1.52

0.38

0.79

0.95

Duration >60 s

1.15

0.69

1.17

0.63

Continuous symptoms

1.06

0.93

1.20

HR >100/min

0.91

1.08

0.86

Precipitating factors

Affected by sleep

2.29

0.70

2.44

0.63

Occurring at work

2.17

0.76

1.54

0.86

Caffeine

1.84

0.91

2.06

0.89

Occurs holiday

1.56

0.92

0.79

1.04

Occurs weekend

1.43

0.90

0.72

1.08

Alcohol

1.36

0.96

1.94

0.90

Lying in bed

1.30

0.61

1.02

0.97

Exercise

0.74

1.09

0.78

1.07

Breathing

0.52

1.23

0.52

1.20

While resting

1.02

0.97

Associated symptoms

Regular rapid poundingsensation in neck

177

0.07

Neck fullness

0.85

1.04

Visible neck pulsations

2.68

0.87

Dizzy spells

0.93

1.08

1.34

0.67

Chest pain

0.81

1.07

0.92

1.02

Dyspnea

0.31

0.27

1.12

Vasovagal symptoms

1.72

0.63

Presyncope

1.04

0.95

Physical examination

HR <60 or >100

3.00

0.78

Obesity

1.55

0.93

Hypertension

1.01

1.00

  • APPROAC H—“while the presence of a regular rapid-pounding sensation in the neck or visible neck pulsations associated with palpitations makes the diagnosis of atrioventricular nodal reentry tachycardia likely, the reviewed studies suggest that the clinical examination is not sufficiently accurate to exclude clinically significant arrhythmias in most patients. Thus, prolonged electrocardiographic monitoring with demonstration of symptom-rhythm correlation is required to make the diagnosis of a cardiac arrhythmia for most patients with recurrent palpitations”

JAMA 2009 302:19

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, Mg, TSH, INR, PTT, D-dimer, troponin

  • imaging—CXR, echocardiogram (enlarged left atrium)

  • EC G

  • 24-h holter

  • exercise stress test

SPECIAL

  • electrophysiology studies

Acute Management

ABC

O 2 to keep sat >95%, IV

SYNCHRONIZED CARDIOVERSION

—premedicate if possible with midazolam 1–2 mg IV q2–3 min, fentanyl 50–150 μg IV × 1, shock 50, 100, 200, 300, 360 J, prepare to intubate and give IV anti-arrhythmics PRN

AV NODAL BLOCKING AGENTS ★ABCD★

  • A miodaroneamiodarone 150 mg IV bolus over 10 min, q10–15 min. Alternatively, infusion 60 mg/h over 6 h, then 30 mg/h over 18 h. Maximum 2.2 g/day

  • β-blockersmetoprolol 5 mg IV over 1 min q5min × 3 PRN, esmolol 500 μg/kg IV over 1 min, maintenance dose 50–200 μg/kg/min IV

  • C alcium channel blockersdiltiazem 15–20 mg IV over 2 min, repeat in 15 min at 20–25 mg PRN, maintenance dose 5–20 mg/h IV; verapamil 2.5–5.0 mg IV over 1–2 min, followed by 5–10 mg in 15–30 min PRN with maximum of 30 mg, maintenance dose 0.05–0.2 mg/min IV

  • Digitalisdigoxin 0.25–0.5 mg IV q6h to a total dose of 1 mg, maintenance dose 0.125–0.25 mg PO/IV daily

OVERALL APPROACH

  • unstable atrial fibrillation—perform cardioversion immediately

  • stable atrial fibrillation <48hrate control (β-blockers, calcium channel blockers, digoxin) and consider rhythm control (DC cardioversion, amiodarone, propafenone, flecainide). Anticoagulate at least × 4 weeks post-cardioversion

  • stable atrial fibrillation >48h or unknown durationrate control (β-blockers, calcium channel blockers, digoxin) and consider rhythm control (IV unfractionated heparin → TEE to exclude atrial thrombus → cardioversion within 24 h → anticoagulate × 4 weeks; ALTERNATIVELY anticoagulate × 3 weeks → cardioversion → anticoagulate at least × 4 weeks)

  • treat underlying cause/precipitant—infection, myocardial infarction, ischemia, drugs, pulmonary embolism, thyrotoxicosis

Long-Term Management

RATE CONTROL

—target resting HR <80 and exercise HR <110 in patients with significant symptoms. (Consider target resting HR <110 in asymptomatic patients with preserved LVEF). β-blocker (metoprolol tartrate [immediate release] 50–100 mg PO BID, metoprolol succinate [extended release] 100–200 mg PO daily, carvedilol 6.25–50 mg PO BID, bisoprolol 5–10 mg PO daily). Calcium channel blockers (diltiazem CD 120–480 mg PO daily). Digitalis (digoxin 0.5 mg PO × 1 dose, then 0.25 mg × 2 doses q6–12 h, then 0.0625–0.25 mg daily)

RHYTHM CONTROL

elective cardioversion (only after a 3-week course of therapeutic anticoagulation or atrial thrombus excluded by TEE. Cardioversion should be followed by 4 weeks of anticoagulation). Antiarrhythmics (amiodarone 200–400 mg PO daily, sotalol 40–160 mg PO BID, especially if CAD; flecainide 50 mg PO q12h, especially if no structural heart disease; propafenone 150 mg PO q8h, especially if no structural heart disease)

CLOT CONTROL

ASA 81 mg daily if low-risk (nonvalvular disease and CHADS2 = 0). Otherwise, anticoagulation (warfarin 5 mg PO daily to target INR between 2–3, dabigatran 110–150 mg PO BID, rivaroxaban 15–20 mg PO daily, apixaban 2.5–5 mg PO daily). Warfarin for AF with valvular disease. Novel anticoagulants (dabigatran, rivaroxaban, and apixaban) should not be used in patients with severe renal impairment, prosthetic heart valves, mitral stenosis, or valvular lesions associated with moderate to severe heart failure. Patients at higher risk of bleeding may require lower doses. Bridging anticoagulation (for initiation/interruption of warfarin therapy) not routinely required but should be considered in those at high risk for acute thrombosis (e.g., mechanical heart valves)

PROCEDURES

radiofrequency ablation of the pulmonary veins (PVI). Radiofrequency ablation of AV node with insertion of a permanent pacemaker and long-term anticoagulation as last resort. Surgical (corridor and maze procedures)

NEJM 2002 347:23; NEJM 2009 361:12; NEJM 2010 362:15; NEJM 2011 365:10; NEJM 2011 365:11

Treatment Issues

STROKE RISK FACTORS IN PATIENTS WITH ATRIAL FIBRILLATION

  • ★CHADS2★
    • C H F (any history, 1 point)

    • Hypertension (any history, 1 point)

    • A ge ≥75 (1 point)

    • D iabetes (1 point)

    • S troke or TIA (2 points)

    • risk of stroke ( if untreated )—0 points = 1.9%/year, 1 = 2.8%, 2 = 4.0%, 3 = 5.9%, 4 = 8.5%, 5 = 12.5%, 6 = 18.2%

  • ★CHA2DS2-VASc★
    • C H F (any history, 1 point)

    • Hypertension (any history, 1 point)

    • A ge ≥75 (2 point)

    • D iabetes (1 point)

    • S troke or TIA (2 points)

    • V ascular disease (coronary, aortic, or peripheral) (1 point)

    • A ge 6574 (1 point)

    • S ex, female (1 point)

    • risk of stroke ( if untreated )—0 points = 0%/year, 1 = 1.3%, 2 = 2.2%, 3 = 3.2%, 4 = 4.0%, 5 = 6.7%, 6 = 9.8%, 7 = 9.6%, 8 = 6.7%, 9 = 15.2%

    • other risk factors—CAD, echocardiography abnormalities (atrial size >5 cm, LV dysfunction), thyrotoxicosis, rheumatic valvular disease (RR 17). All mitral stenosis and HOCM patients with AF should have chronic anticoagulation (regardless of CHADS2 or CHA2DS2-VASc score)

    • risk reduction—ASA decreases risk by ~30%. Anticoagulation decreases risk of stroke by ~60%

    • factors increasing risk of bleeding with warfarin use—advanced age, female sex, diabetes, prior hemorrhage, uncontrolled hypertension, alcoholism or liver disease, cancer, bleeding disorder, chronic kidney disease, ASA/clopidogrel/NSAIDs (including COX-2 inhibitors). Note that risk of fall by itself is not a contraindication to warfarin use

    • risk of bleeding on anticoagulation—as CHADS2 score increases so does risk of major bleeding (but risk of stroke usually remains higher than risk of bleeding). Benefit-to-risk ratio for anticoagulation generally becomes even more favorable as risk factors for stroke accumulate. Risk calculation for bleeding usually unnecessary. Existing risk models do not reliably predict individual risk. Use clinical judgment

  • ★HASBLED★
    • Hypertension, SBP >160 mmHg (1 point)

    • Abnormal liver function (1 point)

    • Abnormal renal function (1 point)

    • Stroke (1 point)

    • Bleeding tendency/predisposition (1 point)

    • Labile INR on warfarin (1 point)

    • Elderly, age >65 (1 point)

    • Drugs (ASA, clopidogrel, NSAIDS) (1 point)

    • Drugs (alcohol abuse) (1 point)

    • risk of bleeding—0 = 1.13 bleeds/100 patient-years, 1 = 1.02, 2 = 1.88, 3 = 3.74, 4 = 8.70, 5 = 12.50, insufficient data for scores ≥6

IMPORTANT TOXICITIES OF AMIODARONE

  • cardiac (5%)—sinus bradycardia and AV nodal block. QT prolongation leading to torsades de pointes may rarely occur

  • thyroid—amiodarone-induced thyrotoxicosis (3%). Type 1 from increased thyroid hormone synthesis from excess iodine (usually with underlying multinodular goiter or Graves’ disease). Type 2 from destructive thyroiditis and thyroid hormone release. Doppler US showing goiter and ↑ vascularity favors type 1 (hyperthyroidism), but normal sized gland and normal/↓ vascularity favor type 2 (thyroiditis). Presence of (any) radioiodine uptake favors hyperthyroidism (type 1), but absence of uptake does not reliably differentiate between type 1 or type 2. Patients on amiodarone may not develop classic symptoms of thyrotoxicosis; however, recurrence of AF should prompt investigation. Discontinuing amiodarone MAY paradoxically worsen thyrotoxicosis; treatment includes anti-thyroid drugs and steroids (for type 2). Hypothyroidism also common (20%)

  • pulmonary (<3%)—chronic interstitial pneumonitis (most common), cryptogenic organizing pneumonia, ARDS, and solitary pulmonary nodule. Histologically characterized by foamy macrophages in the air space. DLCO is often decreased. CT chest may show diffuse/localized interstitial or alveolar opacities. Treat with steroids and stop amiodarone

  • hepatic (15%)—non-alcoholic steatohepatitis which in severe cases may lead to cirrhosis

  • neurologic (30%)—ataxia, tremor, peripheral polyneuropathy, insomnia, and impaired memory

  • vision (100%)—corneal microdeposits may result in halo vision, photophobia, and blurred vision. Optic nerve injury (1–2%) may cause blindness

  • dermatologic (25–75%)—photosensitivity, gray-bluish discoloration (blue man syndrome), and alopecia. This is reversible upon discontinuation of amiodarone, but may take a few years

  • monitoring—baseline TSH, LFTs, PFT and CXR. TSH and LFTs every 6 months, CXR yearly, and PFT as needed

NEJM 2007 356:9

Related Topics

ACLS (p. 495)

Digoxin (p. 43)

ECG (p. 73)

Wolff–Parkinson–White Syndrome (p. 76)

Syncope

See SYNCOPE (p. 353)

Cardiac Examination

Pulse

PULSUS TARDUS ET PARVUS

(low carotid upstroke and amplitude)—aortic stenosis

BRISK PULSE

(rapid carotid upstroke)—hypertrophic cardiomyopathy

BOUNDING PULSE

(rapid carotid upstroke and descent)—↑ left ventricular volume (aortic regurgitation, mitral regurgitation, VSD, PDA, severe bradycardia), ↓ peripheral resistance (fever, anemia, thyrotoxicosis, rigid arteries, pregnancy)

PULSUS BISFERIENS

(double-peaked)—combination aortic stenosis and regurgitation

REGULARLY IRREGULAR PULSE

—sinus arrhythmia, pulsus bigeminus (PVC, PAC)

IRREGULARLY IRREGULAR PULSE

—atrial fibrillation, premature atrial or ventricular contractions

Blood Pressure

CORRECT CUFF SIZE

—width of bladder ≥40% of arm circumference and length of bladder ≥80% of arm circumference

AUSCULTATORY GAP

—defined as the gap between the first Korotkoff sound (which may disappear briefly) and its reappearance. Missing the higher reading can lead to an underestimation of systolic blood pressure. Thus, the systolic blood pressure should always be palpated first before auscultation

WIDE PULSE PRESSURE

—isolated systolic hypertension, aortic regurgitation, hyperdynamic states (sympathetic hyperactivity, fever/sepsis, anemia, thyrotoxicosis, large AV fistula, PDA, beriberi, pregnancy)

PSEUDOHYPERTENSION

—false elevation of systolic blood pressure secondary to rigid arteries. The Osler’s maneuver may be useful for determining the presence of pseudohypertension

PULSUS ALTERNANS

(alternating fluctuation in pulse pressure)—initially hear only the more prominent beats. As cuff pressure decreases, start to hear the less intense beats (1:1 ratio). This may be detected in severe LV dysfunction and aortic stenosis

PULSUS PARADOXUS

—inspiratory drop in systolic blood pressure >10 mmHg. Causes include asthma, COPD, tamponade, restrictive cardiomyopathy, constrictive pericarditis, hypovolemic shock, and rarely pulmonary embolism, SVC obstruction, and morbid obesity

Jugular Venous Pressure

A WAVE

—atrial contraction
  • prominent a wave—tricuspid stenosis, pulmonary stenosis, pulmonary hypertension, hypertrophic cardiomyopathy, and Ebstein’s anomaly

  • cannon a wave—AV dissociation (complete heart block, ventricular tachycardia) (right atrium contracts against closed tricuspid valve)

  • decreased a wave—dilated right atrium

  • absent a wave—atrial fibrillation

X DESCENT

—atrial relaxation. S1 starts
  • decreased x descent—atrial fibrillation

  • x descent deeper than y descent—tamponade

C WAVE

—bulging of tricuspid valve into right atrium during ventricular isometric contraction

X’ DESCENT

—descent of the base of the heart during systole

V WAVE

—atrial filling. S2 just before peak of v
  • dominant v wave—tricuspid regurgitation (cv wave), right heart failure, atrial septal defect

Y DESCENT

—opening of tricuspid valve/atrial emptying
  • rapid steep y descent—constrictive pericarditis (square root sign), severe right heart failure

  • decreased y descent—tricuspid stenosis

  • blunted/absent y descent—tamponade

ABDOMINOJUGULAR REFLUX (AJR)

—blood pressure cuff pumped 6×, then pressed against abdomen at 20–35 mmHg for 15–30 s. Positive AJR occurs when abdominal compression causes a sustained increase in JVP >4 cm [>1.6 in.] and predicts elevated left atrial pressure (≥15 mmHg, LR+ 8.0, LR– 0.3)

KUSSMAUL SIGN

—paradoxical increase in JVP during inspiration. Causes include right ventricular failure, restrictive cardiomyopathy, constrictive pericarditis, SVC obstruction, and pulmonary embolism

Precordial Examination

INSPECTION

—apex, right ventricular heave

PALPATION

—apex, heaves, thrills, palpable heart sounds
  • displaced apical beat (lateral to mid-clavicular line)—left ventricular dilatation, LR+ 8.0

  • enlarged apical beat (≥2.5 cm)—left ventricular dilatation, LR+ 4.7

  • sustained apical beat (outward impulse extends to, or past, S2)—left ventricular pressure overload (aortic stenosis), volume overload (aortic regurgitation, VSD), severe cardiomyopathy, or ventricular aneurysm

  • retracting apical beat (retraction during systole; inward motion begins at S1, outward impuse after S2)—constrictive pericarditis (up to 90%), tricuspid regurgitation

  • sustained left parasternal movement (“lift/heave”)—tricuspid regurgitation, mitral regurgitation

  • palpable P2—pulmonary hypertension in mitral stenosis, LR+ 3.6

Heart Sounds

TECHNIQUE

—S1, S2, and physiological splitting of S2 are best heard over the base. Identification of S3 and S4 requires conscious effort listening for low pitched sounds over the apex (using the bell)

DISTINGUISHING S1 FROM S2

—time with carotid pulse, diastole longer than systole, S2 louder than S1 at the base, S1 is low pitched and longer while S2 is high pitched and shorter, S2 often split

INTENSITY OF S1 AND S2

  • loud P2 >A2 at pulmonic area—increased pulmonary pressure (left ventricular failure, mitral stenosis, pulmonary hypertension), increased pulmonary flow (atrial septal defect)

  • loud S2 at aortic area—hypertension, hyperdynamic states (fever, hyperthyroidism, anemia)

  • soft S2 over aortic area—severe aortic stenosis

  • loud S1 at mitral area—mitral stenosis

  • soft S1—mitral regurgitation, left bundle branch block, short PR interval

SPLITTING OF S2

  • fixed splitting (splitting same degree during both inspiration and expiration)—atrial septal defect, right ventricular failure

  • wide splitting (splitting greater during inspiration than expiration)—right bundle branch block, pulmonary stenosis, pulmonary hypertension

  • paradoxical (reversed) splitting (splitting only during expiration)—left bundle branch block, severe aortic stenosis, RV pacing

NORMAL AND EXTRA HEART SOUNDS

Sound

Heard

Pitch

Others

S1

LUSB

High

 

Early systolic click

RUSB

High

Aortic stenosis

Mid-systolic click

Apex

High

MVP, louder standing

S2

LUSB

High

Splitting

Opening snap (early diastolic)

Apex

High

Mitral stenosis

S3 (early diastolic)

Apex

Low

Heart failure

S4 (late diastolic)

Apex

Low

HTN, aortic stenosis

High pitch sounds are best heard with the diaphragm, while low pitch sounds are best heard with the bell

DISTINGUISHING FEATURES BETWEEN P2 AND OPENING SNAP

  1. 1.

    P2 is best heard at LUSB while opening snap is best heard at the apex

     
  2. 2.

    P2 separates from A2 on inspiration, while opening snap tends to move closer to S2 on inspiration

     

DISTINGUISHING FEATURES BETWEEN S4 AND S1

  1. 1.

    S4 is usually best heart at apex with the bell while S1 is best heard at base

     
  2. 2.

    S4 is usually more widely separated from S1 than splitting of S1

     
  3. 3.

    S4 is loudest at the start of expiration, softest at mid-inspiration

     
  4. 4.

    S4 may be accentuated by lying down, exercise, or forced inspiration with closed glottis

     
  5. 5.

    S4 has a lower pitch than S1

     

DISTINGUISHING FEATURES BETWEEN S3 AND OPENING SNAP

  1. 1.

    S3 has a lower pitch than opening snap

     
  2. 2.

    S3 occurs later than opening snap

     

DISTINGUISHING FEATURES BETWEEN S3 AND S4

  1. 1.

    S3 has a lower pitch than S4

     
  2. 2.

    S3 is closer to S2 while S4 is closer to S1

     
  3. 3.

    Left ventricular S3 is louder at the apex while right ventricular S3 or S4 is usually best heart at left sternal border or at the base

     

Murmurs

TIMING

  • mid-systolic—aortic stenosis, aortic sclerosis, pulmonary stenosis, hypertrophic obstructive cardiomyopathy, atrial septal defect, flow murmurs (fever, pregnancy, hyperthyroidism, anemia, aortic regurgitation due to high flow)

  • pansystolic—mitral regurgitation, tricuspid regurgitation, ventricular septal defect, aortopulmonary shunts

  • late systolic—mitral valve prolapse, papillary muscle dysfunction

  • early diastolic—aortic regurgitation, pulmonary regurgitation

  • mid-diastolic—mitral stenosis, tricuspid stenosis, atrial myxoma, Austin Flint murmur of aortic regurgitation, Carey Coombs murmur during acute phase of rheumatic fever

  • pre-systolic—mitral stenosis, tricuspid stenosis, atrial myxoma

  • continuous murmurs—patent ductus arteriosus, arteriovenous fistula, aortopulmonary connection, venous hum, mammary souffle

INTENSITY

—grade I (barely audible), grade II (faint but can be heard immediately), grade III (easily heard), grade IV (loud AND associated with palpable thrill), grade V (very loud, can be heard with the stethoscope half off chest), grade VI (very loud, can be heard with stethoscope off chest wall)

QUALITY

—depends on the pitch, may be musical, harsh, blowing, rumbling, scratchy, grunting, or squeaky

CONFIGURATION

—crescendo, decrescendo, crescendo–decrescendo, plateau, holosystolic

LOCATION

—aortic valve (RUSB), pulmonary valve (LUSB), tricuspid valve (LLSB), mitral valve (apex)

RADIATION

—aortic valve (carotids), pulmonary valve (left shoulder), tricuspid valve (xyphoid, right of sternum), mitral valve (axilla)

MANEUVERS

  • respirationright-sided murmurs typically increase with inspiration (except pulmonic click) or sustained abdominal pressure (↑ venous return), while left-sided murmurs are generally louder during expiration

  • V alsalva maneuver (↓ venous return and ↑ systemic arterial resistance)—most murmurs decrease in length and intensity during the Valsalva maneuver. Two exceptions are the systolic murmur of hypertrophic cardiomyopathy, which usually becomes much louder, and the systolic murmur of mitral valve prolapse, which becomes longer and often louder (click moves closer to S1)

  • positional changes—most murmurs diminish with standing due to reduced preload. However, the murmur of hypertrophic cardiomyopathy becomes louder and the murmur of mitral valve prolapse lengthens and often is intensified. Squatting (or usually passive leg raising, both ↑ venous return and ↑ systemic arterial resistance) produces opposite effect

  • isometric exercise (↑ systemic arterial resistance)—murmurs caused by blood flow across normal or obstructed valves (e.g., mitral or pulmonic stenosis) become louder. Murmurs of mitral and aortic regurgitation and ventricular septal defect also increase with handgrip exercise

  • transient arterial occlusion (↑ systemic arterial resistance)—transient external compression of both arms by bilateral cuff inflation to 20 mmHg greater than peak systolic pressure augments the murmurs of mitral regurgitation, aortic regurgitation, and ventricular septal defect, but not murmurs due to other causes

DISTINGUISHING FEATURES AMONG COMMON SYSTOLIC AND DIASTOLIC MURMURS

Systolic murmurs

Diastolic murmurs

Findingsa

Tricuspid regurgitation

Mitral valve prolapse

Mitral regurgitation

Aortic sclerosis

Aortic stenosis

Hypertrophic cardiomyopathy

Tricuspid stenosis

Pulmonary regurgitation

Mitral stenosis

Aortic regurgitation

Inspection

Dyspnea

Cyanosis

Cachexia

Jaundice

Pectus excavatum

Marfan’s scoliosis

Dyspnea

Normal

Dyspnea

Sustained apex

Dyspnea

Double apex

Normal

Dyspnea

Mitral facies

Cyanosis

Dyspnea

Argyll

Robertson

Marfan’s

Ank. Spond

Radial pulse

Irregular (AF)

Normal

Irregular (AF)

Normal

Brachio-radial delay

Brisk

Irregular (AF)

Normal

Irregular (AF)

Water-hammer

BP

Normal

Normal

Normal

Normal

Narrow PP

Normal

Normal

Normal

Narrow PP

Wide PP

Carotid

Normal

Normal

Bounding

Irregular (AF)

Normal

Pulsus parvus et tardus

Brisk bifid

Irregular (AF)

Normal

Irregular (AF)

Bounding/collapsing pulse

JVP

Increased V wave Prominent a wave (pul. HTN), no a wave (AF)

Normal

Absent a wave (AF)

Normal

Normal

Prominent a wave

Prominent a wave, slow y descent, absent a wave (AF)

Prominent a wave (pul. HTN)

Absent a wave (AF) Prominent a wave (pul. HTN), cv wave (TR)

Normal

Palpation

Palpable P2 (pul. HTN), thrill

RV heave

Normal

Enlarged, displaced apex, thrill

RV heave

Normal

Sustained apex, thrill

LV heave

Double apical impulse

Thrill

LV heave

Normal

Palpable P2 (pul. HTN), thrill

RV heave

RV heave

Palpable P2 (pul. HTN)

Sustained, displaced apex, thrill

LV heave

S1b

Soft

Normal

Soft

Normal

Normal

Normal

Wide splitting S1

Normal

Loud S1

Split (chronic) Absent (acute)

S2b

Loud (pul. HTN)

Normal

Normal

Normal

Paradoxical split, soft

Paradoxical split

Normal

Loud (pul. HTN)

Palpable P2 (pul. HTN)

Soft

S3

R sided

Normal

L sided

Normal

Normal

L sided

Normal

R sided

Absent

L sided

S4

None

Normal

Normal

Normal

L sided

L sided

Normal

R sided

Normal

L sided

Clicks or snaps

None

Mid-systolic click

None

None

Early systolic click

None

Opening snap (LLSB)

None

Opening snap (apex)

None

Murmurc

LLSB

High pitch

Holosystolic

Apex

High pitch

Late systolic

Apex

High pitch

Holosystolic

RUSB

High pitch

Mid-systolic

RUSB

High pitch

Mid-systolic

LLSB, apex

High pitch

Mid-systolic

LLSB

Low pitch

Mid-diastolic

LUSB

High pitch

Early diastolic

Apex

Low pitch

Mid-diastolice

RUSB

High pitch

Early diastolic

Radiation

Xyphoid

None

Axilla

None

Clavicle

Carotids

Base of heart

None

None

None

Apex

Sternum

Maneuvers

inspiration, sustained

Abdominal pressure

standing, Valsalvadsquatting

↑ isometric, transient art. occlusion

None

↑ squatting, leg raise ↓ standing, Valsalva, isometric

standing, Valsalvasquatting

↑ inspiration

↑ inspiration

↑ isometric ↓ standing, Valsalva

↑ isometric, transient art. occlusion, Best heard sitting up in end expiration

Other associated murmurs/clinical features

Graham Steell murmur (pul. HTN) Ascites, pulsatile liver, edema

Mitral regurgitation (holosystolic at apex)

Pulmonary edema

None

Gallavardin phenomenon (mid-systolic murmur at apex)

Mitral regurgitation (mid-systolic at apex)

Mitral stenosis may also be present

PR murmur called Graham Steell m. if secondary to pul. HTN

Pulmonary and tricuspid regurg. Murmurs (pul. HTN)

Austin Flint Murmur (mid-diastolic over apex) Mid-systolic flow m. Other signsf

aNot all findings listed for each condition may be present on examination

bLoud heart sounds are usually due to mild-moderate stenotic lesions, while light heart sounds are usually due to regurgitant or severe stenotic lesions

cRegurgitant murmurs usually start early, while stenotic murmurs tend to start mid-way

dFor mitral valve prolapse, maneuvers that increase murmur intensity also move both the click and murmur closer to S1

eFor mitral stenosis, the murmur is classically described as mid-diastolic with presystolic accentuation

fAll the following special signs for aortic regurgitation are related to increased pulse pressure. These include Quincke’s sign (pulsatile refill in capillary bed of finger nails), Becker’s sign (pulsatile retinal artery), deMusset’s sign (head bob), Mueller's sign (pulsatile uvula), Mayne’s sign (DBP ↓ 15 mmHg with arm raised), Gerhardt's sign (pulsatile spleen), Rosenbach’s sign (pulsatile liver), Traube’s sign (pistol shot sound over femoral arteries), Duroziez’s sign (femoral artery bruit with compression), Hill's sign (popliteal SBP > brachial SBP by 60 mmHg)

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ABNORMAL SYSTOLIC MURMUR?

  • AORTIC STENOSIS—“presence of any of following significantly increases the likelihood of aortic stenosis: effort syncope, slow carotid upstroke, late or mid peaking systolic murmur, decreased or absent S2, apical-carotid delay, brachioradial delay.” “The presence of AS requires detection of a systolic murmur, generally radiating to the right clavicle.”

Update for Clinical Signs for Detecting Aortic Stenosis

 

LR+

LR−

Slow carotid upstroke

9.2

0.56

Murmur radiating to right carotid

8.1

0.29

Reduced or absent S2

7.5

0.50

Murmur over the right clavicle

3.0

0.10

Reduced carotid volume

2.0

0.64

The Rational Clinical Examination. Mcgraw-Hill, 2009
  • MITRAL RE G UR G ITATION—“for cardiologists, absence of a mitral area murmur or a late systolic/holosystolic murmur significantly reduces the likelihood of mitral regurgitation, except in the setting of acute MI. Cardiologists can accurately distinguish left-sided regurgitant murmurs, such as mitral regurgitation and ventricular septal defect, using transient arterial occlusion”

  • TRICUSPID RE G UR G ITATION—“cardiologists can accurately detect the murmur of tricuspid regurgitation. Cardiologists can accurately rule in and rule out tricuspid regurgitation using the quiet inspiration and sustained abdominal pressure maneuvers”

  • H YPERTROP H IC CARDIOMYOPAT H Y—“cardiologists can rule in or rule out hypertrophic cardiomyopathy by evaluating for decreased murmur intensity with passive leg elevation or increased murmur intensity when the patient goes from a squatting to standing position

  • MITRAL VALVE PROLAPSE—“a systolic click, with or without systolic murmur, is sufficient for the diagnosis of mitral valve prolapse. The absence of both a systolic click and murmur significantly reduces the likelihood of echocardiographic mitral valve prolapse. In patients with echocardiographic mitral valve prolapse, a holosystolic murmur without a systolic click significantly increases the likelihood of long term complications, whereas absence of both a systolic click and murmur significantly reduces the likelihood of long term complications”

JAMA 1997 277:7

INNOCENT MURMURS

—in otherwise healthy younger patients. Systolic murmurs tend to be mid-systolic, grade 1 or 2 (possibly 3), loudest over LUSB, and do not radiate. Murmurs that are associated with systolic thrill (LR+ 12), holosystolic (LR+ 8.7), loud (LR+ 6.5), or plateau-shaped (LR+ 4.1) are more likely to be significant. Diastolic murmurs are always abnormal

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AORTIC REGURGITATION?

  • AORTIC RE G UR G ITATION—“when a cardiologist hears the typical murmur of aortic regurgitation, the likelihood of mild or greater aortic regurgitation is increased significantly. The absence of a typical diastolic murmur significantly reduces the likelihood of aortic regurgitation”

  • MITRAL STENOSIS—“presence of a mid-diastolic murmur significantly increases the likelihood of mitral stenosis, while absence of a mid-diastolic murmur significantly reduces the likelihood of mitral stenosis”

  • PULMONARY RE G UR G ITATION—“when a cardiologist hears a typical pulmonary regurgitation murmur, the likelihood of pulmonary regurgitation increases significantly. Absence of a typical murmur does not alter the likelihood of pulmonary regurgitation”

JAMA 1999 281:23

Investigations

ECHOCARDIOGRAM

—if cardiac symptoms, murmur grade ≥3, diastolic murmur, or when other cardiac findings are present

Aortic Stenosis

AHA/ACC Valvular Heart Disease 2014 Guidelines

Lancet 2009 373:9667; NEJM 2002 346:9

Differential Diagnosis

VALVULAR

  • congenital malformations—unicuspid, bicuspid

  • calcification—degenerative or senile, atherosclerosis, Paget’s disease, chronic renal failure

  • infections—rheumatic fever, Chlamydia pneumoniae

  • rheumatoid arthritis

SUBVALVULAR

  • discrete lesions—membranous diaphragm, fibromuscular ring

  • obstructive—hypertrophic cardiomyopathy

SUPRAVALVULAR

—localized or discrete narrowing of the ascending aorta (Williams’ syndrome)

LOW GRADIENT AORTIC STENOSIS

—resulting from low cardiac output

Pathophysiology

COMPLICATIONS ★BEE★

  • Bleeding (angiodysplasia + aortic stenosis + acquired vWD type IIa = Heyde’s syndrome)

  • Endocarditis

  • Embolic events (cerebral, systemic)

Clinical Features

PHYSICAL

—tachypnea, decreased pulse pressure, brachioradial delay, pulsus parvus et tardus (slow rise and low amplitude), apical-carotid delay, hyperdynamic apical beat, systolic thrill at the base of heart, narrowly split or paradoxical splitting of S2 or absent S2, harsh mid-systolic ejection murmur (radiation to carotids), Gallavardin phenomenon

GALLAVARDIN PHENOMENON

—aortic stenosis murmur is usually harsh and loudest over the right upper sternal border, whereas a Gallavardin murmur is musical and may be heard over apex. It is due to radiation of the high-frequency components of the aortic stenosis murmur to the apex

DISTINGUISHING FEATURES BETWEEN AORTIC SCLEROSIS AND AORTIC STENOSIS MURMUR

 

Aortic sclerosis

Aortic stenosis

Pathophysiology

Abnormally thickened valve leaflets but minimal outflow obstruction

Decreased functional area of valve to cause decreased outflow

Carotid pulse

Normal

Pulsus parvus et tardus

S2

Normal

Soft single S2 (P2)

Murmur

Mid-systolic murmur

Late peaking of systolic murmur

DISTINGUISHING FEATURES BETWEEN AORTIC STENOSIS, MITRAL REGURGITATION, AND HYPERTROPHIC CARDIOMYOPATHY

 

Aortic stenosis

Mitral regurgitation

HOCM

Carotid upstroke

Slow, low amplitude

Normal or low amplitude

Brisk

S1

Normal

Soft

Normal

S2

Single if severe

Normal

Often reversed

S3

No

Loud

No

S4

If severe

No

Yes

Loudest murmur

RUSB

Apex

LLSB and apex

Maneuvers

 Standing

 Squatting

 Valsalva

Investigations

BASIC

  • CXR

  • echocardiogram—transthoracic

  • EC G—left ventricular hypertrophy

  • exercise testing

SPECIAL

  • cardiac catheterization

Diagnostic and Prognostic Issues

AORTIC VALVE AREA AND SEVERITY

  • normal = peak velocity <2 m/s, area = 3–4 cm2

  • mild = peak velocity 2.0–2.9 m/s, mean gradient <20 mmHg, area = 1.5–2 cm2

  • moderate = peak velocity 3.0–3.9 m/s, mean gradient 20–39 mmHg, area = 1–1.5 cm2

  • severe = peak velocity ≥4 m/s, mean gradient >40 mmHg, area = ≤1 cm2 (or indexed area ≤ 0.6 cm2/m2)

  • symptoms—usually do not appear until valve ≤1 cm2. The significance of valve area depends on patient size (larger patient = more severe for same valve area)

  • progression—valve area decreases by ~0.1 cm2/year and the mean gradient increases by 7 mmHg/year (particularly if cardiac risk factors)

PROGNOSIS OF AORTIC STENOSIS ★ASH

  • (Angina, Syncope, Heart failure)
    • severe aortic stenosis with no symptoms —1–2% die in short period

    • severe aortic stenosis with angina presentation—50% die in 5 years

    • severe aortic stenosis with syncope presentation—50% die in 3 years

    • severe aortic stenosis with heart failure presentation—50% die in 2 years

    • severe aortic stenosis after valve replacement—survival similar to normal individuals

Management

MILD OR MODERATE AORTIC STENOSIS

—follow clinically and with echocardiogram (every 3–5 years for mild, every 1–2 years for moderate, every year for severe)

SEVERE OR SYMPTOMATIC AORTIC STENOSIS

aortic valve replacement (transcatheter or surgical, see criteria below), balloon valvuloplasty (offers no survival benefit and is only a temporizing measure until surgical or percutaneous aortic valve replacement can be performed)

VASODILATORS

—use with caution in the setting of hypertension or HF. ACE inhibitors preferred over β-blockers because of risk of reduced inotropy; start low dose and titrate slowly; risk of hypotension and syncope

Treatment Issues

AORTIC VALVE REPLACEMENT (AVR)

  • recommended indications ( class I )—if severe AS with symptoms of HF, syncope, exertional dyspnea, angina, or presyncope (by history or on exercise testing); asymptomatic severe AS and LVEF <50%; or severe AS and undergoing cardiac surgery for other reasons

  • reasonable indications ( class II a )—if asymptomatic but very severe AS (i.e., peak velocity ≥5 m/s or mean gradient ≥60 mmHg); severe AS and exercise test with ↓ exercise tolerance or ↓ in SBP; symptomatic low-flow/low-gradient severe AS (i.e., valve area ≤1 cm2) with LVEF <50%, and severe/high gradients on dobutamine stress test; symptomatic low-flow/low-gradient severe AS (i.e., valve area ≤1 cm2) with normal LVEF ≥50% and valve obstruction as most likely cause of symptoms (based on clinical, hemodynamic, and anatomic data); or moderate AS and undergoing cardiac surgery for other reasons

  • possible indications ( class II b )—if severe AS and rapid disease progression and low surgical risk

  • preoperative consult—AVR should be done before elective non-cardiac surgeries in symptomatic patients

  • risk of AVR—mortality 1–2%, morbidity 1%/year (venous thromboembolic disease, bleeding, deterioration of prosthetic valve, endocarditis)

SURGICAL VS. TRANSCATHETER VALVE

—transcatheter aortic valve replacement (TAVR) should be considered for patients with an indication for AVR who have high or prohibitive surgical risk for surgical AVR. A multidisciplinary heart valve team should collaborate in the decision making process

MECHANICAL VS. BIOPROSTHETIC VALVE

—compared to human tissue valves, mechanical valves have prolonged durability, but higher chance of thromboembolism and bleeding from chronic anticoagulation. Overall, long-term outcomes are better with a mechanical valve. Main indications for bioprosthesis valve include patients who cannot or will not tolerate warfarin or for whom compliance is uncertain, patients ≥65 years of age who do not have risk factors for thromboembolism, and women of childbearing age

Aortic Regurgitation

AHA/ACC Valvular Heart Disease 2014 Guidelines

Differential Diagnosis

VALVE ABNORMALITY

—rheumatic heart disease, infective endocarditis, SLE, calcifications, congenital (bicuspid or unicuspid aortic valve), flail leaflet, osteogenesis imperfecta, drugs (fenfluramine)

AORTIC DILATION

—aortic dissection, ankylosing spondylitis, syphilis, Marfan’s, Ehlers Danlos, hypertension, bicuspid aortic valve, cystic medial necrosis

Pathophysiology

PATHOPHYSIOLOGY

—leaky aortic valve → initial compensation with left ventricular dilatation and eccentric hypertrophy (palpitations, atypical chest pain), wide pulse pressure (due to increased stroke volume with elevation in SBP and regurgitation with rapid collapse of the arteries and a low diastolic blood pressure) → eventually decompensation leading to left ventricular dysfunction (heart failure)

Clinical Features

PHYSICAL

  • general appearance—Marfan’s syndrome, ankylosing spondylitis, Argyll Robertson pupils, Quinckes sign (pulsatile refill in capillary bed of finger nails), digital throb, Beckers sign (visible pulsations of the retinal arteries and pupils), deMussets sign (head bob occurring with each heart beat), Muellers sign (systolic pulsations of the uvula)

  • vitals—wide pulse pressure, water hammer (tapping impulse in forearm, especially when arm is raised vertically), Corrigans pulse, Maynes sign (>15 mmHg decrease in diastolic blood pressure with arm elevation)

  • cardiac—soft S1, left-sided S3 (heart failure), diastolic murmur (early diastolic or holodiastolic, blowing, over left upper sternal border), Austin Flint murmur (mid/late diastolic rumble, over apex) and mid-systolic flow murmur

  • othersG erhardts sign (systolic pulsations of the spleen), Rosenbachs sign (systolic pulsations of the liver), Traubes sign (pistol shot pulse with systolic and diastolic sounds heard over the femoral arteries), Duroziezs sign (systolic and diastolic bruit heard when the femoral artery is partially compressed), H ills sign (popliteal cuff systolic pressure exceeding brachial pressure by >60 mmHg). Note that all the special signs are due to increased pulse pressure

DISTINGUISHING FEATURES BETWEEN AORTIC REGURGITATION AND PULMONARY REGURGITATION MURMUR

  • pulmonary regurgitation murmur—high pitch decrescendo diastolic murmur (Graham Steell murmur) loudest over left upper sternal border. Increases with inspiration. May be associated with signs of pulmonary hypertension

  • aortic regurgitation murmur—early diastolic decrescendo murmur loudest over right and/or left upper sternal border. No change or decreases with inspiration. May be associated with Austin Flint murmur and the other signs of aortic regurgitation

DISTINGUISHING FEATURES BETWEEN AUSTIN FLINT AND MITRAL STENOSIS MURMUR

 

Austin Flint

Mitral stenosis

Gender

M > F

F > M

Hemoptysis

Almost never

Likely mitral stenosis

Rhythm

Sinus

Atrial fibrillation

M1

Usually faint

Usually loud

P2

Normal or ↑

Usually loud

Ventricular gallop/S3

Always present

Absent

Diastolic murmur

Usually early or mid-diastolic

Often presystolic accentuation (if in sinus rhythm)

Opening snap

Absent

Present

CXR

Boot shaped

LAE

ECG

Sinus, LVH, prolonged PR

Atrial fibrillation, P mitrale

Investigations

BASIC

  • CXR—cardiomegaly

  • echocardiogram

  • EC G—LVH

  • exercise testing

SPECIAL

  • cardiac catheterization

Prognostic Issues

ASYMPTOMATIC WITH NORMAL LV SYSTOLIC FUNCTION

  • prognosis—development of symptoms and/or LV dysfunction <6%/year; asymptomatic LV dysfunction <3.5%/year; sudden death <0.2%/year

ASYMPTOMATIC WITH LV DYSFUNCTION

  • prognosis—progression to cardiac symptoms >25%/year

SYMPTOMATIC

  • prognosis—mortality >10%/year

Management

LIFESTYLE CHANGES

—salt restriction/diuretics

MEDICATIONS

—afterload reduction with vasodilators (nifedipine, ACE inhibitors, ARBs) indicated for severe AR with symptoms, LV dysfunction, or LV dilatation, but not for long-term management of asymptomatic mild to moderate AR and normal LV function

FOLLOW-UP

—asymptomatic mild AR with normal LV function and little/no LV dilatation can be followed annually with clinical exam and echocardiogram every 2–3 years (sooner if symptoms emerge). Asymptomatic severe AR with normal LV function and LV dilatation (>60 mm) should be seen every 6 months with echocardiogram every 2–3 years

PROCEDURES

—intraaortic balloon pumps should be avoided

AORTIC VALVE REPLACEMENT (AVR)

  • recommended indications ( class I )—if symptomatic severe AR; asymptomatic chronic severe AR (regurgitant fraction ≥50%, regurgitant volume ≥60 mL/beat, Doppler jet width ≥65% of LVOT) and LVEF <50%; or severe AR and undergoing cardiac surgery for other reasons

  • reasonable indications ( class II a )—if asymptomatic severe AR with normal LVEF ≥50% but severe LV dilatation (LVESD >50 mm); or moderate AR and undergoing other cardiac surgery

  • possible indications ( class II b )—if asymptomatic severe AR and normal LVEF ≥50% but with progressive severe LV dilatation (LVEDD >65 mm) and low surgical risk

Mitral Stenosis

Circulation 2009 119:11

AHA/ACC Valvular Heart Disease 2014 Guidelines

Differential Diagnosis

  • R H EUMATIC H EART DISEASE

  • MITRAL ANNULAR CALCIFICATION

  • CON G ENITAL

  • ENDOCARDITIS

  • ATRIAL MYXOMA

  • PROST H ETIC VALVE DYSFUNCTION

  • COR TRIATRIATUM

Pathophysiology

STENOTIC MITRAL VALVE

—left ventricular inlet obstruction → left atrial overload and left ventricle output failure → atrial fibrillation, pulmonary hypertension and eventually right heart failure

Clinical Features

HISTORY

—symptoms related to pulmonary hypertension (dyspnea, hemoptysis, chest pain), symptoms related to right heart failure (hepatomegaly, ascites, edema), hoarseness (Ortner’s syndrome, due to enlarged left atrium compressing on recurrent laryngeal nerve), complications (endocarditis, thromboembolism), past medical history (rheumatic fever), medications

PHYSICAL

  • general appearance—tachypnea, peripheral cyanosis, mitral facies (purple patches on cheeks secondary to vasoconstriction)

  • vitals—decreased pulse volume

  • jvp—prominent a wave (pulmonary hypertension), absent a wave (atrial fibrillation), cv wave (tricuspid regurgitation)

  • cardiac—right ventricular heave, palpable P2 (pulmonary hypertension), loud S1 (valve cusps widely apart at the onset of systole) in early disease, soft S1 in severe disease (valves rigid), loud S2, absent S3, opening snap (over apex and left lower sternal border; the earlier the opening snap, the more severe the stenosis), low pitch diastolic rumble (over apex, left decubitus position in expiration) ± pre-systolic accentuation, tricuspid regurgitation

  • abdominal—hepatomegaly, ascites, edema

Investigations

BASIC

  • CXR—left atrial enlargement, splaying of carina

  • echocardiogram—TEE to exclude left atrial thrombus before treatment

  • EC G—P mitrale, RVH

SPECIAL

  • cardiac catheterization

Diagnostic and Prognostic Issues

MITRAL STENOSIS AND SEVERITY

  • progressive—mitral valve area (MVA) >1.5 cm2, diastolic pressure half-time <150 ms

  • severe—MVA ≤1.5 cm2 (MVA ≤1.0 cm2 with very severe MS), diastolic pressure half-time ≥150 ms (diastolic pressure half-time ≥220 ms with very severe MS); associated with severe left atrial enlargement and pulmonary artery systolic pressure >30 mmHg. Note, transmitral mean gradient often >5–10 mmHg but mean pressure gradient varies greatly according to heart rate

  • symptoms—often present when MVA ≤1.5 cm2 (i.e., with severe MS). Onset of symptoms may be precipitated by exercise, emotional stress, infection, pregnancy, or rapid atrial fibrillation

PROGRESSION

—approximately 0.1–0.3 cm2/year. Initially slow stable course (latent period) of 20–40 years between rheumatic fever and symptoms. From onset of symptoms (accelerated period), around 10 years until disability. Overall 10-year survival is 50–60% in untreated symptomatic MS, >80% in asymptomatic. Median survival <3 years with severe pulmonary hypertension

Management

LIFESTYLE CHANGES

—salt restriction/diuretics

MEDICATIONS

negative chronotropic agents and HR control to prolong diastolic filling (β-blockers, non-dihydropyridine calcium channel blockers). Anticoagulation for patients with concomitant atrial fibrillation (irrespective of CHADS2 score), left atrial thrombus, or prior embolic event (even if in sinus rhythm). Prophylaxis for rheumatic fever (secondary prevention)

FOLLOW-UP

—any change in symptoms warrant reevaluation and echocardiogram. Otherwise, yearly evaluation in asymptomatic patients including CXR and ECG. Yearly echocardiogram for severe MS

PROCEDURES

—indicated when symptomatic severe mitral stenosis. Percutaneous balloon mitral valvuloplasty (particularly for patients with non-calcified mitral valve, no left atrial thrombus, mild mitral regurgitation, and no other cardiac interventions) is equivalent to surgical valvuloplasty in terms of success. Average increase in valve area is 1.0 cm2

Specific Entities

ACUTE RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

  • pathophysiology—group A Streptococcus infection → non-suppurative inflammation with cardiac, joints, and CNS manifestations 2–4 weeks later. Post-Streptococcus glomerulonephritis and scarlet fever may also occur separately as complications of group A Streptococcus infection

  • jones criteria for acute rheumatic fever
    • major criteriaJNES
      • Joint - migratory polyarthritis

      • carditis (pericarditis, myocarditis, valvulitis)

      • N odules (subcutaneous)

      • Erythema marginatum

      • Sydenham chorea

    • minor criteria—clinical (fever, polyarthralgias), laboratory (↑ ESR, prolonged PR interval)

    • diagnosis—either two major criteria or one major criterion and two minor criteria, plus evidence of antecedent streptococcal infection (e.g., positive throat culture or rapid antigen detection test or elevated streptococcal antibody test)

  • investigations—anti-Streptolysin O antibodies, anti-DNase B, antihyaluronidase, positive throat culture, echocardiogram

  • treatments—patients with rheumatic disease are at high risk of recurrent rheumatic fever. Recurrent disease causes additional valve damage, and thus these patients should receive secondary prophylaxis for rheumatic fever (benzathine penicillin G 1.2 M U IM q4weeks, penicillin V 250 mg PO BID, or azithryomycin 250 mg PO daily if allergic to penicillin). For patients with valvular involvement, therapy should continue for at least 10 years, or until age 40 (whichever is longer). With a history of carditis in the absence of persistent valvular disease, treat for 10 years, or until age 21 (whichever is longer)

Mitral Regurgitation

AHA/ACC Valvular Heart Disease 2014 Guidelines

Differential Diagnosis

PRIMARY MR (VALVE ABNORMALITY)

—rheumatic heart disease, infective endocarditis, mitral valve prolapse, myxomatous degeneration (Barlow’s valve), fibroelastic deficiency disease, mitral annular calcification, ruptured chordae tendineae, drugs (fenfluramine)

SECONDARY MR (LEFT VENTRICULAR DILATATION)

—myocardial infarction, dilated cardiomyopathy

Pathophysiology

LEAKY MITRAL VALVE

—left atrial and ventricle volume overload → atrial fibrillation and left heart failure

Clinical Features

CLINICAL FEATURES

—exertional dyspnea, fatigue, decreased S1, widely split S2, S3, holosystolic murmur (over apex), displaced and enlarged apex

Investigations

BASIC

  • CXR—cardiomegaly, LAE

  • echocardiogram

  • EC G—P mitrale, LVH

SPECIAL

  • cardiac catheterization

Management

MEDICATIONS

—no specific therapy for MR. Treat concomitant atrial fibrillation if present

FOLLOW-UP

—asymptomatic mild MR with normal LV function and no LV dilatation can be followed annually. Asymptomatic severe MR should be seen every 6–12 months with echocardiogram at the time of assessment

PROCEDURES

mitral valve repair (generally better outcome if technically possible) or replacement if symptomatic, atrial fibrillation, pulmonary hypertension, end-systolic dimension ≥40 mm, or LVEF 30–60%. Transcatheter mitral valve repair may be considered for severely symptomatic, severe primary MR with prohibitive surgical risk

Specific Entities

TRICUSPID REGURGITATION

  • pathophysiology—leaky tricuspid valve → right atrium and ventricle volume overload → eventually decompensation leading to right heart failure (hepatosplenomegaly, ascites, peripheral edema)

  • causes—right ventricular dilatation (left heart failure, pulmonary hypertension, Eisenmenger syndrome, pulmonic stenosis), valve abnormality (rheumatic heart disease, infective endocarditis, Ebstein’s anomaly). Rarely is it due to isolated tricuspid valve abnormality

  • clinical features—cachexia, jaundice (congestive hepatomegaly), JVP cv wave, RV heave, S3 (with dilated RV), S4 (with stiff RV), holosystolic murmur (over left lower sternal border), edema

  • investigations—ECG (P pulmonale, RVH), CXR (cardiomegaly), echocardiogram, cardiac catheterization, rule out intracardiac shunts

  • treatments—valve repair or replacement if severe symptoms

MITRAL VALVE PROLAPSE

  • pathophysiology—prevalence 0.6–2.5% of population. May be sporadic or familial connective tissue disorder with morphologic abnormalities of the mitral valve (increased leaflet thickness and redundancy, chordal elongation, and sagging of the leaflets into the left atrium in systole)

  • treatmentsASA 75–325 mg PO daily for history of transient ischemic attacks, atrial fibrillation (age <65 years, no MR, no HTN, no HF). Anticoagulation with warfarin for atrial fibrillation (if age >65, MR, HTN, or HF), history of stroke/TIA, or left atrial thrombus

TWO SUBTYPES OF MITRAL VALUE PROLAPSE

 

Mild subtype

Severe subtype

Demographics

Mainly women (age 20–50)

Mainly men (age 40–70)

Pathology

Mild leaflet abnormalities

Myxomatous disease

Minimal MR

Considerable leaflet thickening and MR

Symptoms

Orthostatic hypotension

Atrial fibrillation

Palpitations

Physical findings

Mid-systolic click with or without a late systolic murmur

MR murmur

Chordal rupture may lead to sudden worsening of MR

Prognosis

Few patients have progressive MR

Progressive MR requiring surgery

Increased risk of sudden death

Endocarditis

ACC/AHA Infective Endocarditis 2008 Focused Update

AHA Infective Endocarditis 2005 Guidelines

NEJM 2001 345:18

Differential Diagnosis

INFECTIVE ENDOCARDITIS

  • commonStreptococcus viridans (S. sanguis, S. mutans, S. mitis), Streptococcus pneumoniae, Streptococcus bovis, Enterococcus (E. faecalis, E. faecium), Staphylococcus aureus, Gram-negative bacilli

  • long incubation time (721) daysH ACEK
    • H aemophilus

    • A ctinobacillus

    • C ardiobacterium

    • E ikenella

    • K ingella

  • special mediaMycoplasma, Chlamydia, Legionella, Brucella, Bartonella, Coxiella burnetii (Q fever), Histoplasma, Tropheryma whippelii

MARANTIC ENDOCARDITIS

—non-bacterial thrombotic endocarditis secondary to malignancy (usually adenocarcinoma) or SLE (Libman–Sacks endocarditis)

Pathophysiology

SUBTYPES

—classified as acute vs. subacute, native valve vs. prosthetic valve, and right sided vs. left sided
  • native heart valve—usually S. viridans, S. bovis, enterococci

  • prosthetic heart valve—<2 months (usually coagulase negative staphylococci, may need to treat surgically), >1 year (usually S. viridans, S. bovis, enterococci)

  • injection drug use—usually S. aureus and Gram negative rods. Tricuspid valve most commonly affected

  • cancer—about 50% of patients with S. bovis endocarditis also have neoplasms of the GI tract

RISK FACTORS FOR ENDOCARDITIS

  • high risk—complex cyanotic congenital heart disease (unrepaired or incompletely repaired cyanotic congenital heart disease, including palliative shunts and conduits; completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure; repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device), surgically constructed systemic pulmonary shunts, previous infective endocarditis, prosthetic heart valve, cardiac transplantation recipients who develop cardiac valvulopathy

  • moderate risk—most other congenital heart diseases, acquired valvular disease (rheumatic heart disease, mitral/aortic/pulmonary/tricuspid stenosis or regurgitation), mitral valve prolapse with valvular regurgitation or leaflet thickening, hypertrophic cardiomyopathy

  • low or no risk—secundum ASD or surgically repaired ASD, VSD, PDA, mitral valve prolapse with thin leaflets in the absence of regurgitation, ischemic heart disease, previous CABG

  • non-cardiac—IDU, poor dental hygiene, longterm hemodialysis, long-term indwelling catheter, procedures (GU, GI, surgical wound infection), diabetes, HIV

Clinical Features

HISTORY

—fever, murmur, dyspnea, chest pain, anorexia, weight loss, malaise, night sweats, complications (painful nodules, rash, stroke, myocardial infarction, any infections), past medical history (structural heart disease, recent procedures [dental, GI, GU], IDU, SLE, malignancy), medications

PHYSICAL

—fever, splinter hemorrhages, clubbing, Osler nodes (tender, subcutaneous nodules in pulp of digits or thenar eminence), Janeway lesions (nontender, erythematous, hemorrhagic pustular lesions on palms or soles), needle track marks, petechiae over conjunctivae and oral mucosa, Roth spots (pale areas surrounded by hemorrhage on fundoscopic examination), lymphadenopathy, respiratory examination (HF), murmur (regurgitant), splenomegaly, petechiae over legs

HIGH INDEX OF SUSPICION

—always consider endocarditis in the differential when dealing with fever of unknown origin, persistent bacteremia, HF, MI, myocarditis, pericarditis, stroke, pneumonia, pulmonary embolism, splenic infarction, glomerulonephritis, septic arthritis, and osteomyelitis. All patients with S. aureus bacteremia should undergo echocardiography (25% have IE)

Investigations

BASIC

  • labs—CBCD, lytes, urea, Cr, AST, ALT, ALP, bilirubin, LDH, ESR, ANA, serology (HBV, HCV, HIV), urinalysis

  • microbiology—blood C&S × 3 (endocarditis protocol and blood C&S × 2 daily until culture negative), sputum Gram stain/AFB/C&S, urine C&S, stool C&S, O&P, C. diff toxin A/B

  • imaging—CXR, echocardiogram (TEE >TTE), CT chest/abd

  • EC G—heart block

Diagnostic and Prognostic Issues

MODIFIED DUKE’S CRITERIA

  • major—positive blood culture × 2 (or positive blood culture × 1 for C. burnetii), echocardiographic evidence (oscillating intracardiac mass, abscess, new partial dehiscence of a prosthetic valve), new murmur

  • minorfever (>38 °C [100.4 °F]), risk factor (cardiac conditions, IDU), vascular phenomena (major arterial emboli, septic pulmonary infarct, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions), immunologic phenomena (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor), positive blood culture not meeting major criteria

  • diagnosis—likely endocarditis if 2 major, 1 major plus 2 minor, or 5 minor criteria

ECHOCARDIOGRAM

—transesophageal echocardiogram (TEE sens 90–100%, spc 95–100%) preferred over transthoracic echocardiogram (TTE sens 50–80%, spc 90%) for detecting vegetations, perivalvular extension of infection and abscesses, diagnosing prosthetic valve endocarditis, and for differentiating between uncomplicated Staphylococcus aureus bacteremia and endocarditis

PROGNOSIS

—mortality of 25–50% for prosthetic valve endocarditis, 35% for Staphylococcal endocarditis and 10% for Streptococcal endocarditis

Related Topics

Aortic Regurgitation (p. 56)

Mitral Regurgitation (p. 59)

Tricuspid Regurgitation (p. 59)

Management

EMPIRIC ANTIBIOTIC THERAPY

native valve and non-IDU (ampicillin 2 g IV q4h or cloxacillin 2 g IV q4h plus gentamicin 1 mg/kg IV q8h, or vancomycin 1 g IV q12h plus gentamicin 1 mg/kg IV q8h), native valve and IDU (cloxacillin 2 g IV q4h plus gentamicin 1 mg/kg IV q8h or vancomycin 1 g IV q12h plus gentamicin 1 mg/kg IV q8h), prosthetic valve (vancomycin 1 g IV q12h plus gentamicin 1 mg/kg IV q8h plus rifampin 600 mg PO daily)

TARGETED ANTIBIOTIC THERAPY

(please refer to the Sanford Guide to Antimicrobial Therapy for up to date recommendations)—Streptococci (penicillin G 2–3MU IV q4h or ceftriaxone 2 g IV/IM q24h × 4 weeks. Gentamicin 1 mg/kg IV q24h × 2 weeks may be added in certain circumstances to shorten the course by 2 weeks). Penicillin-sensitive Enterococci (ampicillin 2 g IV q4h or vancomycin 1 g IV q12h × 4–6 weeks, plus gentamicin 1 mg/kg IV q8h × 4–6 weeks for native valve). Penicillin-resistant Enterococci (vancomycin 1 g IV q12h × 6 weeks, plus gentamicin 1 mg/kg IV q8h × 6 weeks for native valve). S . aureus (cloxacillin 2 g IV q6h or nafcillin or oxacillin 3 g IV q6h or cefazolin 2 g IV q8h × 2–6 weeks [depending on right- or left-sided valve] ± gentamicin 1 mg/kg IV q8h × 3–5 days: for native valve). MRSA (vancomycin 1 g IV q12h × 6 weeks for native valve). H ACEK (ceftriaxone 2 g IV/IM q24h or ampicillin-sulbactam 3 g IV q6h or ciprofloxacin 500 mg PO BID × 4 weeks). For prosthetic valve infection, therapy is usually longer (by 2–4 weeks) with gentamicin

SURGERY

valvular replacement (<10% reinfection rate. See indications below)

Treatment Issues

INDICATIONS FOR SURGERY

—in the acute period, refractory congestive heart failure is the most important indication. Other indications include perivalvular extension of infection with abscess, fistula, or heart block; failure of antibiotic therapy with persistent bacteremia; infection with fungi or untreatable pathogens; Staphylococci on a prosthetic valve; or recurrent embolic events with persistent vegetation(s) despite appropriate antibiotic therapy. Consider early surgical consult for mobile vegetation(s) >10 mm with or without emboli

OVERALL RECOMMENDATIONS FOR ENDOCARDITIS PROPHYLAXIS

—only given to patients with the highest risk of developing endocarditis, which include the following:
  • high - risk conditions—prosthetic valve, prosthetic material used for valve repair, unrepaired cyanotic congenital heart defect, repaired cyanotic congenital heart defect with residual defects at the site or adjacent to the site of the prosthetic device, completely repaired cyanotic congenital heart defect with prosthetic material or device during first 6 months after procedure, cardiac transplant recipients with valvulopathy, previous endocarditis

  • procedures
    • oral cavity—dental procedures that involve manipulation of gingival or peripical region of teeth, perforation of oral mucosa

    • respiratory tract—tonsillectomy, adenoidectomy, bronchoscopy with a rigid bronchoscope, or flexible bronchoscopy if biopsied

    • gi / gu tract—prophylaxis generally not recommended

  • prophylaxis regimens—give one of the following 30–60 min prior to procedure: amoxicillin 2 g PO, ampicillin 2 g IM/IV, cefazolin 1 g IV/IM, ceftriaxone 1 g IV/IM, cephalexin 2 g PO, clindamycin 600 mg PO/IM/IV, azithromycin 500 mg PO, clarithromycin 500 mg PO

Peripheral Vascular Disease

NEJM 2007 356:12

ACCF/AHA Peripheral Artery Disease 2005 and 2013 Guidelines

Differential Diagnosis of Claudication

ARTERIAL

  • atherosclerosis

  • intraluminal occlusion—embolism, thrombosis, dissection, adventitial cystic disease, arterial fibrodysplasia, arterial tumor, occluded limb aneurysm

  • vasculitis—Takayasu’s arteritis, temporal arteritis, thromboangiitis obliterans

  • vasospasm

  • drugs—ergot

  • fibrosis—iliac endofibrosis, radiation fibrosis, retroperitoneal fibrosis

  • trauma

VENOUS

—DVT, thrombophlebitis, venous congestion

NEUROPATHIC

—spinal stenosis, peripheral neuropathy

OTHERS

—arthritis (hips, knees), compartment syndrome

Clinical Features

HISTORY

—pain, discomfort, or fatigue that occurs in leg muscle with exercise and improves with resting (ischemic intermittent claudication is NOT sensitive for peripheral vascular disease), maximum walking distance, non-healing wounds, trauma, DVT risk factors, past medical history (CAD, HF, AF, stroke, TIA, renal disease, hypertension, cholesterol), medications

PHYSICAL

—comprehensive pulse examination of lower extremity
  • ankle brachial index (ABI)—abnormally high measurement >1.40 associated with non-compressible calcified vessel (and unreliable), 1.00–1.40 normal, 0.91–0.99 borderline, and ≤0.90 abnormal. If ≤0.90 significant narrowing of one or more blood vessels in the legs likely present, <0.8 intermittent claudication, <0.4 resting claudication, <0.25 critical limb ischemia. An ABI that ↓ by 20% following exercise is diagnostic of peripheral vascular disease, while a normal ABI following exercise eliminates the diagnosis

  • Buerger s test—raise legs to 90° with patient in supine position. Check for return of rubor as the legs are lowered. Abnormal if angle of circulation <0° i.e., legs below table)

  • De W eeses test—disappearance of previously palpable distal pulses after walking exercise

VENOUS INSUFFICIENCY EXAMINATION

—hemosiderin deposit, pitting edema, dermatitis, cellulitis, ulcer (with prominent granulation tissue over medial malleolus), superficial venous collaterals (DVT), varicose vein (palpate for tenderness or hardness that may suggest thrombophlebitis), Trendelenburg test (helps to determine whether venous reflux is related to the superficial or deep venous system. Occlude a collapsed superficial vein just below the site of suspected reflux from deep to superficial system. With patient standing, observe refilling of vein. Rapid refilling despite occlusion suggests incompetence of valves in the deep venous system, while slow refilling with occlusion and rapid refilling after occlusion is removed suggests incompetence of valves in the superficial venous system)

RATIONAL CLINICAL EXAMINATION SERIES: DOES THE CLINICAL EXAMINATION PREDICT LOWER EXTREMITY PERIPHERAL ARTERIAL DISEASE?

 

LR+

LR–

H istory

Claudication

3.3

0.89

Inspection

Wounds (ischemic ulcers and gangrene over lateral malleolus, tips of toes, metatarsal heads, bunion)

5.9

0.98

Discolouration

2.8

0.74

Atrophy

Absence of hair

Palpation

Any palpable pulse abnormality (femoral, popliteal, posterior tibial, dorsalis pedis)

4.7

0.38

Coolness

5.9

0.92

Capillary refill time (firm pressure to planter aspect of great toe for 5 s. Abnormal if >5 s for normal skin)

1.9

Auscultation

Any bruit (iliac, femoral, popliteal)

5.6

0.39

  • SPECIAL TESTSankle brachial index (ankle SBP by palpation/Doppler of posterior tibial or dorsalis pedis pulse divided by brachial SBP), venous filling time (raise leg to 45° for 1 min with patient supine position for vein to collapse. With patient then sitting up and legs dangling, determine the time for vein to refill. Abnormal if >20 s) (LR+ 3.6, LR– 0.8)

  • APPROAC H—“for screening patients who require further testing to diagnose peripheral arterial disease, the most useful individual symptoms and signs are: claudication, femoral bruit and a pulse abnormality on palpation. The absence of claudication and the presence of normal pulses decrease the likelihood of moderate to severe disease. When considering patients who are symptomatic with leg complaints, the most useful individual findings are the presence of cool skin, the presence of at least 1 bruit and any palpable pulse abnormality. The absence of any bruit (iliac, femoral and popliteal) and the presence of normal peripheral pulses reduce the likelihood of peripheral arterial disease”

JAMA 2006 295:5

DISTINGUISHING FEATURES OF COMMON CAUSES OF LEG PAIN

 

Claudication

Spinal stenosis

Venous congestion

Pain

Cramp, tiredness

Cramp, tiredness, tingling

Tightness, bursting

Sites

Buttock, hip, thigh, calf, foot

Buttock, hip, thigh

Groin, thigh

Worse

Walking

Walking, standing

Walking

Better

Rest

Sitting or change in position

Leg elevation

Others

Vascular dx, ↓ pulse

Lower back pain

History of DVT

Investigations

BASIC

  • labs—CBC, lytes, urea, Cr, fasting glucose, fasting lipids, HbA1C

  • ankle brachial index—with or without exercise

  • duplex ultrasound

  • EC G

SPECIAL

  • CT/MR angiography

  • angiography

Diagnostic Issues

DIAGNOSTIC APPROACH

—ABI <0.90 is sufficient for the diagnosis of peripheral arterial disease as it suggests >50% stenosis of peripheral vasculature (sens 90%, spc 98%). Patients with large vessel disease (distal aorta or iliac arteries) may only have abnormal ABI after exercise. Patients with non-compressible vessels (as suggested by ABI >1.30–1.40) should have toe-brachial index done. Perform duplex US or CT/MR angiogram if the diagnosis is uncertain or if revascularization is being considered. Digital-subtraction angiograph remains the gold standard

Management

RISK REDUCTION ★ABCDEFG

  • ASA

  • B lood pressure control (see HYPERTENSION p. 65)

  • C holesterol control (see DYSLIPIDEMIA p. 70)

  • D iabetic control (see DIABETES p. 381)

  • E xercise (30 min of moderate-intensity exercise 3–4×/week)

  • F at reduction (see OBESITY ISSUES p. 457)

  • Get going to quit smoking! (see SMOKING ISSUES p. 480)

MEDICAL

antiplatelet (ASA 75–325 mg PO daily, clopidogrel 75 mg PO daily), high-intensity statin (atorvastatin 80 mg PO daily, rosuvastatin 40 mg PO daily). Consider cilostazol 100 mg PO BID for life-limiting claudication (in the absence of heart failure), but treatment with pentoxifylline 400 mg PO TID is of dubious benefit

SURGICAL

revascularization (surgery or percutaneous transluminal angioplasty)

Treatment Issues

REVASCULARIZATION

—indicated for patients with significant functional limitations (lifestyle or jobs) despite maximal lifestyle and medical treatment. Not optimal for patients <40 with atherosclerosis obliterans, with non-disabling symptoms, diabetes, significant coronary risk factors, or other diseases associated with high mortality

Specific Entities

VASCULAR DISEASE FAMILY

—CAD, CVD, PVD, AAA, renal artery stenosis, chronic mesenteric ischemia

ABDOMINAL AORTIC ANEURYSM

—U.S. Preventative Services Task Force recommends one-time screening with abdominal US for men 65–75 who have ever smoked. Repair is controversial for 4–5 cm [1.6–2 in.]; >5 cm [>2 in.] warrants surgical intervention (risk of spontaneous rupture is 22%/year). Monitor lesions ≤5 cm [≤2 in.] with ultrasound regularly (every 6 months if lesions 4 cm [1.6 in.], more frequent for bigger lesions). Operative mortality is 4–6% for elective repair, 19% for urgent repair, and 50% for repair of a ruptured aneurysm. No driving if AAA >6 cm [2.4 in.] in men, >5.5 cm [2.2 in.] in women

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE ABDOMINAL AORTIC ANEURYSM?

  • PALPATION—to detect abnormal widening of the aortic pulsation (sens 50% for AAA 4–4.9 cm [1.6–1.9 in.], sens 76% for AAA ≥5 cm [≥2 in.], LR+ 12 and LR– 0.72 for AAA ≥3 cm [≥1.2 in.], LR+ 15.6 and LR– 0.51 for AAA ≥4 cm [≥1.6 in.])

  • APPROAC H—“abdominal palpation will detect most AAAs large enough to warrant surgery, but it cannot be relied on to exclude the diagnosis. The sensitivity of palpation appears to be reduced by abdominal obesity. When a ruptured AAA is suspected, imaging studies such as ultrasound or computed tomography should be performed regardless of physical findings”

  • UPDATE—sensitivity for palpation of AAA improved among thinner patients, especially if abdominal girth is <100 cm

JAMA 1999 281:1

The Rational Clinical Examination. McGraw-Hill, 2009

Hypertension

CHEP Hypertension 2014 Guidelines

JNC8 Hypertension 2014 Guidelines

JNC7 Hypertension 2003 Guidelines

NEJM 2003 348:7; NEJM 2006 355:4; NEJM 2007 357:8

Differential Diagnosis

01-23-4

  1. 0

    ESSENTIAL H YPERTENSION

     
  2. 1

    ANATOMIC—aorta (coarctation, aortic dissection)

     
  3. 2

    RENAL—renal parenchymal disease (chronic renal failure, polycystic kidney disease), renal artery stenosis

     
  4. 3

    ADRENAL—pheochromocytoma, Conn’s syndrome, Cushing’s syndrome

     
  5. 4
    SCENTS
    • Super growth—acromegaly

    • C alcium—hypercalcemia (hyperparathyroidism)

    • E strogen or other drugs—NSAIDs, corticosteroids, anabolic steroids, oral contraceptives, cocaine, amphetamines, MAO inhibitors, SNRIs, SSRIs, erythropoietin, cyclosporine, tacrolimus, midodrine, alcohol excess, licorice root

    • N eurologic—Cushing’s triad (hypertension, bradycardia, and respiratory depression associated with increased intracranial pressure)

    • T hyroid—hyperthyroidism, hypothyroidism

    • S leep apnea

     

Pathophysiology

CLASSIFICATION OF HYPERTENSION

  • normal—SBP <120 mmHg and DBP <80 mmHg

  • prehypertension —SBP 120–139 mmHg or DBP 80–89 mmHg

  • stage 1 hypertension—SBP 140–159 mmHg or DBP 90–99 mmHg

  • stage 2 hypertension—SBP ≥160 mmHg or DBP ≥100 mmHg

  • masked hypertension—BP consistently elevated with out-of-office measurements, but normotensive when measured in office; associated with ↑ cardiovascular risk

  • white coat hypertension—BP consistently elevated with office measurements, but normotensive when out-of-office; possible slight ↑ cardiovascular risk (but still less than in masked or sustained hypertension)

  • hypertensive emergency—severe hypertension (usually SBP ≥220 and/or DBP ≥120 mmHg) with end organ damage such as pulmonary edema, aortic dissection, myocardial infarction, cerebrovascular hemorrhage, papilledema, fundoscopic hemorrhages or exudates, acute renal failure, eclampsia of pregnancy, and hypertensive encephalopathy

  • hypertensive urgency—severe hypertension (usually SBP ≥220 and/or DBP ≥120 mmHg) without findings of hypertensive emergency

ISOLATED SYSTOLIC HYPERTENSION

—younger people tend to have isolated diastolic hypertension (50–60% of patients under 40). With age, large arteries tend to stiffen with decreased elasticity secondary to a combination of atherosclerosis, calcification, and elastin degradation. Thus, isolated systolic hypertension predominates with age (over 90% of patients over 70)

HYPERTENSIVE END ORGAN DAMAGE

—ischemic heart disease, peripheral arterial disease, left ventricular hypertrophy, stroke, TIA, microalbuminuria or proteinuria, and chronic kidney disease

HYPERTENSIVE RETINOPATHY

  • mildfocal arteriolar narrowing (vasospasm), generalized arteriolar narrowing (increased vascular tone due to autoregulation, mild intimal hyperplasia, and hyaline degeneration in sclerotic stage). Subsequently, arteriovenous nicking (venous compression by a thickened arteriole, leading to dilation of vein around intersection) and opacity of arteriolar wall (widening and accentuation of the central light reflex leading to so-called copper wiring appearance)

  • moderatehemorrhages (blot, dot, or flame shaped due to disruption of the blood–retina barrier), microaneurysms (necrosis of the smooth muscles and endothelial cells), hard exudates (exudation of blood and lipids), and soft exudates (cotton wool spots, retinal ischemia)

  • malignant—signs of moderate retinopathy plus swelling of the optic disc

  • utility—the retina provides a window of cerebral circulation. Risk of stroke (and death) increases with degree of retinopathy. Note that the stages may not be sequential

NEJM 2004 351:22

Clinical Features

HISTORY

—blood pressure levels, ambulatory/home monitoring, complications and hypertensive end organ damage, other cardiac risk factors (smoking, diabetes, dyslipidemia, obesity), past medical history (thyroid, renal, or adrenal disorders), medications (antihypertensives, steroids, illicit drugs)

PHYSICAL

—vitals (heart rate, blood pressure), obesity (sleep apnea), moon facies and thoracocervical fat pad (Cushing’s), low-pitched voice and acral enlargement (acromegaly), upper body better developed and continuous murmur over precordium/back (coarctation), narrowed oropharynx and ↑ neck circumference (OSA), goiter (hyperthyroidism), aortic regurgitation (aortic dissection), striae, renal bruits (renal artery stenosis), abdominal masses (polycystic kidney disease, adrenal tumors), radiofemoral delay and weak femoral pulses (coarctation). Assess complications including retinopathy, stroke, HF, AAA, and PVD

MEASURING BLOOD PRESSURE

NEJM 2009 360:e6

Investigations

BASIC

  • labs—lytes, urea, creatinine, fasting glucose, HbA1C, fasting lipid profile, urinalysis, urine microalbumin

  • 24-h ambulatory blood pressure monitor

  • EC G

SECONDARY CAUSES WORKUP

  • hyperaldosteronism workup—if clinical features present (i.e., spontaneous hypokalemia <3.5 mmol/L; diuretic-induced hypokalemia <3.0 mmol/L; resistance to ≥3 antihypertensive drugs; adrenal incidentaloma with hypertension) then consider serum renin/aldosterone, saline infusion test, oral sodium loading test, adrenal vein sampling. Plasma renin activity is difficult to interpret in patients taking mineralocorticoid receptor antagonists (e.g., spironolactone)

  • pheochromocytoma workup—if clinical features present (i.e., paroxysmal and/or severe hypertension refractory to usual antihypertensive drugs; symptoms of catecholamine excess; hypertension triggered by β-blockers, MAO inhibitors, micturition, or Valsalva maneuver; adrenal incidentaloma with hypertension; genetic syndrome [MEN2A, MEN2B, von Hippel-Lindau, neurofibromatosis]) then consider 24-h urine metanephrine, plasma fractionated metanephrines

  • other endocrine workup (guided by clinical suspicion)—Ca, albumin, PTH, TSH, free T4, 24-h urine cortisol, 1 mg dexamethasone suppression test, late night salivary cortisol, IGF-1

  • renovascular workup—if ≥2 clinical features present (i.e., sudden-onset or worsening hypertension and age >55 or <30 years; presence of abdominal bruit; resistance to ≥3 antihypertensive drugs; ↑ serum Cr ≥30% with ACEi or ARB; other atherosclerotic disease; or recurrent flash pulmonary edema), then consider renal Doppler US, CT/MR angiogram, renal angiogram

  • sleep oximetry test—if suspect sleep apnea

Diagnostic Issues

CLINICAL DIAGNOSIS OF HYPERTENSION

  1. 1.
    H ypertensive urgency or emergency during first visit?
    • Yes → hypertension diagnosed

    • No → proceed to step 2

     
  2. 2.
    What is the blood pressure during initial visit?
    • SBP ≥180 mmHg and/or DBP ≥110 mmHg → repeat BP at least 2 more times at the same visit (discard first reading and average latter 2 readings). If mean BP 180/110 or greater, diagnosis of hypertension is confirmed

    • SBP 140–179 mmHg and/or DBP 90–109 mmHg (or mean automated office BP taken using an automated device that performs multiple readings with the patient alone in the room is SBP 135–179 and/or DBP 85–109 mmHg), then obtain out-of-office readings before second visit

    • SBP 130–139 and/or DBP 85–89 mmHg → annual follow-up

     
  3. 3.

    Out-of-office readings can be measured using 24-hour ambulatory monitoring (ABPM) or a home BP series (HBPM). ABPM is preferred. Further information on how to perform these can be found at www.hypertension.ca

     
  4. 4.
    What is the average blood pressure from the ambulatory BP monitor?
    • Mean awake SBP ≥135 mmHg or DBP ≥85 mmHg → hypertension diagnosed

    • Mean awake SBP <135 mmHg and DBP <85 mmHg → long-term follow-up

    • Mean 24-h SBP ≥130 mmHg or DBP ≥80 mmHg → hypertension diagnosed

    • Mean 24-h SBP <130 mmHg or DBP <80 mmHg → long-term follow-up

     
  5. 5.
    What is the average blood pressure from home BP monitoring?
    • Average SBP ≥135 or DBP ≥85 mmHg → hypertension diagnosed

    • Average SBP <135 or DBP <85 mmHg → repeat home BP monitoring (to confirm average BP <135/85 mmHg), or consider ambulatory BP monitoring (step 8), then long-term follow-up

     

CHEP Hypertension 2015 Guidelines

http://www.hypertension.ca

Acute Management

ACUTE

—ABC, O2, IV

HYPERTENSIVE EMERGENCY

labetalol 20 mg IV bolus initially, then 20–80 mg q10min, or 2 mg/min IV infusion (loading) then 2–8 mg/min, maximum total dose of 300 mg. Nitroprusside 0.25–0.5 μg/kg/min IV initially, increase by 0.5 μg/kg/min increments, to usually target 3 μg/kg/min (rarely >4 μg/kg/min, maximum 10 μg/kg/min). Nicardipine 5 mg/h IV initially, titrate to a maximum of 15 mg/h. Fenoldopam 0.1 μg/kg/min IV initially, titrate dose q15min. Consider ICU admission. Workup and treatment of underlying causes once stabilized

HYPERTENSIVE URGENCY

furosemide 20–40 mg PO/IV × 1 dose. Clonidine 0.1–0.3 mg PO BID. Captopril 25–50 mg PO TID. Labetalol 5–20 mg IV q15min or hydralazine 5–20 mg IV q15min to keep SBP <170 mmHg. Lower BP over hours to days, 25–30% lower than baseline; avoid lowering BP too rapidly (risk of stroke and MI if BP dropped to below minimum level required to maintain tissue perfusion). Workup and treatment of underlying cause once stabilized

Long-Term Management

LIFESTYLE CHANGES

healthy diet (high in fresh fruits, vegetables, and low fat dairy products; low in saturated fat and salt <100 mmol/day). Physical activity (optimum 30–60 min of moderate cardiopulmonary activity 4–7×/week). Reduction in alcohol (<2 drinks/day in men and <1 drink/day in women). Weight loss (in those with BMI >25 kg/m2, lose >5 kg). Smoke free environment

ANTIHYPERTENSIVES ★ABCD★

  • ACE inhibitorramipril 2.5–10 mg PO daily-BID, captopril 12.5–50 mg PO TID, perindopril 2–8 mg PO daily, lisinopril 2.5–10 mg PO daily, trandolapril 1–8 mg PO daily

  • ARBcandesartan 8–32 mg PO daily, losartan 50–100 mg PO daily, irbesartan 150–300 mg PO daily, valsartan 80–320 mg PO daily

  • β-blockers—not recommended as first-line agent for uncomplicated hypertension in those ≥60-years old. Metoprolol tartrate 50–100 mg PO BID, atenolol 50–100 mg PO daily, labetalol 100–400 mg PO TID, bisoprolol 5–10 mg PO daily

  • calcium channel blockersamlodipine 2.5–10 mg PO daily, diltiazem CD 180–360 mg PO daily

  • diureticschlorthalidone 12.5–25 mg PO daily, indapamide 1.25–2.5 mg PO daily, hydrochlorothiazide 12.5–25 mg PO daily, spironolactone 12.5–50 mg PO daily

  • α1 blockersterazosin 1–20 mg PO daily, doxazosin 1–16 mg PO daily

  • α1 agonistclonidine 0.1–0.5 mg PO BID

  • others—minoxidil, phentolamine, hydralazine

TREAT UNDERLYING CAUSE

Treatment Issues

ACE INHIBITORS/ANGIOTENSIN RECEPTOR BLOCKERS

  • indications—HF, post-MI, diabetes, proteinuria, renal failure (with caution), LVH

  • contraindications—pregnancy, ESRD, bilateral RAS

  • adverse effects—cough (with ACE inhibitor), angioedema, hyperkalemia

β-BLOCKERS

  • indications—resting tachycardia, HF, migraine, glaucoma, CAD/post-MI

  • contraindications—asthma, severe PVD, Raynaud’s phenomenon, depression, bradycardia, second or third degree heart block and hypoglycemia-prone diabetics

  • adverse effects—depression, ↓ exercise tolerance, bradycardia, hypotension

CALCIUM CHANNEL BLOCKERS

  • dihydropyridine (potent vasodilators)—nifedipine, amlodipine, felodipine, nicardipine

  • non-dihydropyridine (heart rate control)—verapamil (cardiac depressant activity), diltiazem (some cardiac depressant, some vasodilator)

  • indications—angina pectoris, recurrent SVT (verapamil), Raynaud’s phenomenon (dihydropyridine), migraine, heart failure due to diastolic dysfunction, esophageal spasm

  • contraindications—second or third degree heart block (non-dihydropyridine), HF with moderate to marked systolic dysfunction

  • adverse effects—nifedipine (dizziness, headache, flushing, and peripheral edema), verapamil (↓ cardiac contractility, conduction, and constipation), diltiazem (both side effects but a lot less severe)

DIURETICS

  • indications—most patients (particularly those of African descent)

  • contraindications—allergy

  • adverse effects—↓ K, ↑ Ca (thiazides), hyperuricemia, ↑ cholesterol, ↑ glucose, ↑ insulin resistance, impotence

BLOOD PRESSURE TREATMENT TRIGGERS AND TARGETS

 

Blood pressure (mmHg)

When to start therapy?

No macrovascular target organ damage or other independent cardiovascular risk factors

≥160/100

Macrovascular target organ damage or other independent cardiovascular risk factors

≥140/90

Very elderly

≥160

What should the targets be?

Diabetes

<130/80

All others (including non-diabetic chronic kidney disease)

<140/90

Very elderly (≥80-years old)

<150 (systolic)

CHEP Hypertension 2014 Guidelines

http://www.hypertension.ca

OVERALL APPROACH TO CHOICE OF THERAPY

Condition

Drug of Choice

HTN without other indications

A/B/C/D → AC/AD/BC/BD → ABC/ACD/BCD/ABD → ABCD

Avoid B as first line if age ≥60

ACEi may be less effective in those of African descent

Isolated systolic hypertension

ARB/C1/D → ARB plus either C1 or D → ARB plus C1 plus D

Avoid B

Angina

ACEi/B → ACEi plus B → add C1

Prior myocardial infarction

AB → ABC

Heart failure

AB → ABD (including spironolactone) → ACEi/ARB/B/D. Avoid hydralazine and minoxidil if LVH

Prior cerebrovascular disease

AD → add other agents

Peripheral vascular disease

A/B/C/D plus ASA.

Avoid B if severe PVD

Diabetes without nephropathy

A/C1/D → AC1/AD → add B or C2

Diabetes with nephropathy

A → AC/AB/AD

CKD ± proteinuria

A → AD → add other agents

Asthma

A/C/D. Avoid B

BPH

α-blockers

Migraine

B

Thyrotoxicosis

B

Essential tremor

B

Postural hypotension

Avoid vasodilators and diuretics

Raynaud’s

C (dihydropyridine)

Gout

Avoid D

Hyperkalemia

C/D. Avoid aldosterone antagonists

Hyponatremia

A/B/C. Avoid D

Pregnancy

Labetalol/methyldopa/nifedipine. Avoid ACE inhibitors and ARB (teratogenic)

where A ACE inhibitors/ARBs, B β-blockers, C calcium channel blockers, C1 long-acting dihydropyridine CCB, C2 non-dihydropyridine CCB, D diuretics

Specific Entities

RENAL ARTERY STENOSIS (RAS)

  • pathophysiology—causes include atherosclerosis and fibromuscular dysplasia

  • clinical features—systemic atherosclerosis, uncontrolled hypertension, flash pulmonary edema, asymmetrical kidneys, renal failure with ACE inhibitor, and renal bruits

  • diagnosis—MR angiogram (preferred as non-invasive and high sensitivity/specificity), CT angiogram (anatomical information), duplex US (anatomic and functional information), captopril-enhanced radioisotope renogram (functional information), contrast angiogram (gold standard)

  • treatmentsmedical (cornerstone of management of atherosclerotic disease; risk factor reduction with blood pressure control [avoidance of ACE inhibitors/ARBs in severe bilateral renal artery stenosis], statin therapy, and antiplatelet agent), angioplasty (not routinely recommended for atherosclerotic disease because outcomes similar to medical therapy alone; consider if fibromuscular dysplasia, severe or refractory hypertension, recurrent flash pulmonary edema, or acute decline in renal function due to renal artery stenosis. Unlikely to restore renal function if small kidneys or high creatinine >300 μmol/L [3.4 mg/dL]), surgery

NEJM 2001 344:6

NEJM 2009 361:20

NEJM 2014 370:1

DIFFERENTIAL DIAGNOSIS OF ABDOMINAL BRUITS

  • cardiovascular—abdominal aortic aneurysm, aortocaval fistula

  • renal vascular—renal artery stenosis

  • G I vascular—celiac artery compression syndrome, mesenteric ischemia

  • hepatic vascular—cirrhosis, hepatoma, AV malformation, arterioportal fistula, Cruveilhier–Baumgarten sign (cirrhosis, portal hypertension, and caput medusa)

  • splenic vascular—splenic AV fistula, splenic artery dissection, splenic enlargement

  • pancreatic vascular—pancreatic carcinoma

RATIONAL CLINICAL EXAMINATION SERIES: IS LISTENING FOR ABDOMINAL BRUITS USEFUL IN THE EVALUATION OF RENOVASCULAR HYPERTENSION?

 

LR+

LR–

Systolic and diastolic abdominal bruit

39

0.6

Any epigastric or flank bruit, including isolated systolic bruit

6.4

0.4

Systolic bruit

4.3

0.5

History of atherosclerotic disease

2.2

0.5

  • APPROACH—“given the high prevalence (7–31%) of innocent abdominal bruits in the younger age groups, it is recommended that if a systolic abdominal bruit is detected in a young, normotensive, asymptomatic individual, no further investigations are warranted. In view of the low sensitivity, the absence of a systolic bruit is not sufficient to exclude the diagnosis of renovascular hypertension. In view of the high specificity, the presence of a systolic bruit (in particular a systolic–diastolic bruit) in a hypertensive patient is suggestive of renovascular hypertension. In view of the lack of evidence to support characterizing bruits as to pitch, intensity and location, bruits should be reported only as systolic or systolic/diastolic”

JAMA 1995 274:16

The Rational Clinical Examination. McGraw-Hill, 2009

Related Topics

Aortic Dissection (p. 27)

Hyperaldosteronism (p. 398)

Pheochromocytoma (p. 398)

Hyperlipidemia

ACC/AHA 2013 Cholesterol Guidelines

Canadian Cardiovascular Society 2012 Dyslipidemia Guidelines

Differential Diagnosis of Hypercholesterolemia

PRIMARY

—polygenic, familial hypercholesterolemia (IIa; suspect when total cholesterol >6 mmol/L [>232 mg/dL], LDL >5 mmol/L [>193 mg/dL]), sitosterolemia

SECONDARY

—obesity, diabetes, hypothyroidism, nephrotic syndrome, medications (thiazides), cholestatic liver disease (primary biliary cirrhosis)

Differential Diagnosis of Hypertriglyceridemia

PRIMARY

—dietary, familial hypertriglyceridemia (IV; suspect when TGL >5 mmol/L [>440 mg/dL]), LPL deficiency (I), dysbetalipoproteinemia (III), ApoCII deficiency

SECONDARY

—obesity, diabetes, nephrotic syndrome, hypothyroidism, alcoholism, drugs (estrogen, tamoxifen, β-blockers, glucocorticoids, cyclosporine, glucocorticoids, novel antipsychotics, protease inhibitors, isotretinoin)

Differential Diagnosis of Combined Hypercholesterolemia and Hypertriglyceridemia

PRIMARY

—familial combined hyperlipidemia (IIb), mixed hypertriglyceridemia (V), dysbetalipoproteinemia (III)

SECONDARY

—diabetes, nephrotic syndrome, hypothyroidism, drugs (glucocorticoids, immunosuppressives, protease inhibitors), lipodystrophies

Differential Diagnosis of Low HDL

PRIMARY

—familial hypoalphalipoproteinemia, Tangiers disease, ApoAI mutation,

LCAT deficiency

SECONDARY

—drugs (anabolic steroids, isotretinoin)

Clinical Features

HISTORY

—past medical history (diabetes, CAD, HF, stroke, TIA, renal disease, hypertension, liver disease, gallstones, hypothyroidism, HIV), medications
  • hypertriglyceridemia—pancreatitis, chylomicronemia syndrome (dyspnea, confusion), hyponatremia, transaminitis, milky plasma (with blood work)

  • hypercholesterolemia—premature atherosclerosis, aortic sclerosis/stenosis

PHYSICAL

  • hypertriglyceridemia—lipemia retinalis (when TGL ≥22.6 mmol/L), eruptive xanthomas (commonly on buttocks, extensor surfaces of arms, back; when TG 11.3-22.6 mmol/L), hepatosplenomegaly

  • hypercholesterolemia—tendon xanthomas (most commonly in Achilles tendon and extensor surfaces of hands), xanthelasmas, tuberous xanthomas (over areas susceptible to trauma), corneal arcus (premature when <40-years of age)

Investigations

BASIC

  • labs—total chol, TGL, LDL, HDL, apoB, Lp(a), fasting glucose, HbA1C, Cr, TSH, hsCRP, CK, AST, ALT, ALP, bilirubin, LDH

Management

LIFESTYLE CHANGES

diet (↑ fruit and vegetable intake, ↑ mono- and polyunsaturated fats, ↓ saturated fats and trans-fatty acid to <7% of calories, ↑ omega-3 fatty acid from fish and plant sources, salmon oil 3–9 g can ↓TGL). Exercise, smoking avoidance

MEDICATIONS

  • H M G-CoA reductase inhibitors (↓↓ LDL ↑ HDL, ↓ TGL)—atorvastatin 10–80 mg PO daily, rosuvastatin 5–40 mg PO daily, simvastatin 10–80 mg PO daily, pravastatin 10–40 mg PO daily. Main side effects include myalgias, myopathy, and transaminitis

  • NPC1L1 transporter inhibitor (↓ LDL)—ezetimibe 10 mg PO daily

  • fibrates (↓ LDL ↑ HDL, ↓↓ TGL)—fenofibrate nanocrystallized tablet [Lipidil EZ] 145 mg PO daily without regard to meals (best oral absorption), fenofibrate micronized tablet [Lipidil Supra] 160–200 mg PO with dinner (moderate oral absorption and modestly improved with food), fenofibrate micronized capsule [Lipidil Micro] 200 mg PO with dinner (poor oral absorption but improved with food), gemfibrozil 600 mg PO daily (safe in pregnancy beginning in second trimester). Main side effects include rash, pruritis, GI upset, gallstones, and myalgia

  • bile - acid sequestrants (↓ LDL, ↑ cholesterol synthesis)—cholestyramine 2–24 g PO daily, colestipol 5–30 g PO daily in divided doses. Main side effects include constipation, vitamin K deficiency, and drug interactions (bind to other drugs and prevent absorption)

  • niacin (↓ TGL, ↓ LDL, ↑↑ HDL)—nicotinic acid 1–3 g PO daily. Main side effects include ↑ blood sugar, flushing (treat with ASA), hepatotoxicity, and gastric irritation

  • omega - 3 fatty acids (↓ TGL, ↑ LDL)—eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) 3–4 g PO daily. Main side effects include ↑ blood sugar; flushing, hepatotoxicity, and gastric irritation

  • PCSK9 inhibitor (↓↓↓ LDL)—evolocumab. Inhibits PCSK9 from binding to LDL receptor on hepatocytes, thus facilitating removal of LDL from circulation. Approved and possibly on market by 2016

  • aspirinASA 81 mg PO daily for secondary prevention

TREAT SECONDARY CAUSES/METABOLIC SYNDROME IF PRESENT

Treatment Issues

RISK CATEGORIES

  • high—10-year risk of cardiovascular event ≥20%, as estimated using validated risk calculator (Framingham Risk Score, Reynolds Risk Score); clinical vascular disease (e.g., CAD, CVA, TIA, PVD); abdominal aortic aneurysm; diabetes and age ≥40 years or >15 years duration and age ≥30 years or presence of microvascular disease; chronic kidney disease; high-risk hypertension. All high risk patients require treatment

  • moderate—10-year risk of cardiovascular event 10–19%. Consider initiating treatment if LDL ≥3.5 mmol/L [135 mg/dL]; or LDL <3.5 mmol/L [135 mg/dL] and ApoB ≥1.2 g/L [120 mg/dL]; or LDL <3.5 mmol/L [135 mg/dL] and non-HDL-C ≥ 4.3 mmol/L [166 mg/dL]; LDL <3.5 mmol/L [135 mg/dL] and hsCRP >2 mg/L in men age >50 or women age >60

  • low—10-year risk of cardiovascular event <10%. Consider initiating treatment if LDL ≥5.0 mmol/L [≥193 mg/dL]

HYPERCHOLESTEROLEMIA

  • American treatment guidelines—treat according to severity of cardiovascular risk with appropriate intensity of statin irrespective of actual lipid levels achieved

    INTENSITY OF STATIN THERAPY (ACC/AHA 2013 Guidelines)

    High-intensity

    Moderate-intensity

    Low-intensity

    ↓ LDL-C by approximately ≥50%

    ↓ LDL-C by approximately 30 to <50%

    ↓ LDL-C by approximately <30%

    Atorvastatin 40–80 mg PO daily

    Atorvastatin 10–20 mg PO daily

    Simvastatin 10 mg PO daily

    Rosuvastatin 20–40 mg PO daily

    Rosuvastatin 5–10 mg PO daily

    Pravastatin 10–20 mg PO daily

    Simvastatin 20–40 mg PO daily

    Lovastatin 20 mg PO daily

    Pravastatin 40–80 mg PO daily

    Fluvastatin 20–40 mg PO daily

    Lovastatin 40 mg PO daily

     

    Fluvastatin XL 80 mg PO daily

     

    Fluvastatin 40 mg PO BID

     
  • Canadian treatment guidelines—“treat to target” with specific lipid levels as goal of therapy

TREATMENT TARGETS BASED ON RISK CATEGORY (CCS 2012 Guidelines)

 

High risk

Moderate risk

Low risk

LDL

≤2 mmol/L [≤77 mg/dL] or ≥50% ↓ LDL

≤2 mmol/L [≤77 mg/dL] or ≥50% ↓ LDL

≥50% ↓ LDL

ApoB

≤0.80 g/L [<80 mg/dL]

≤0.80 g/L [≤80 mg/dL]

 

non-HDL-C

≤2.6 mmol/L [≤100 mg/dL]

≤2.6 mmol/L [≤100 mg/dL]

 

HYPERTRIGLYCERIDEMIA

  • treatment—dietary modification (with reduced fat, simple sugars, and calories) and alcohol abstinence. Severe cases (TG >11.3 mmol/L [1,000 mg/dL]) should be treated pharmacologically because of associated risk of pancreatitis. Target <4.5 mmol/L [<400 mg/dL]

SPECIAL CASES

  • familial hypercholesterolemia—lifestyle modification and pharmacologic therapy with potent statin (atorvastatin, rosuvastatin) plus add-on therapy with bile-acid sequestrant or ezetimibe, or both. Consider PCSK9 inhibitor when available. Homozygotes may require LDL apheresis or possible liver transplantation (to provide functional LDL receptors). Consider genetic counseling for affected family members

  • familial combined hyperlipidemia—lifestyle modification (weight reduction and dietary changes) and pharmacologic therapy with statin plus add-on therapy with ezetimibe or fibrate

  • dysbetalipoproteinemia—identify and treat comorbidities (diabetes, obesity, hypothyroidism). Pharmacologic therapy often unnecessary, but when needed, consider statin or fibrates. Consider genetic counseling (for apoE2 gene) for affected family members

  • chylomicronemia syndrome—dietary modification (total fat restriction initially until TG <11.3 mmol/L [1,000 mg/dL] then fat-limited diet), alcohol abstinence, optimize glycemic control, and discontinue offending medications. Pharmacologic therapy with fibrate plus add-on therapy with statin or orlistat

Specific Entities

METABOLIC SYNDROME

(syndrome X or insulin resistance syndrome)—National Cholesterol Education Program’s Adult Treatment Panel (ATP) III report criteria ≥3 of the following five features:
  • T G L— ≥ 1.7 mmol/L [≥150 mg/dL]

  • H DL—♀ <1.30 mmol/L [<50 mg/dL], ♂ <1.04 mmol/L [<40 mg/dL]

  • insulin resistance—fasting glucose ≥5.6 mmol/L [≥100 mg/dL] (modified; originally defined as fasting glucose ≥6.1 mmol/L [≥110 mg/dL])

  • waist circumference—♂ >102 cm [>40 in.], ♀ >88 cm [>35 in.]. May consider ethnic-specific cut-offs where appropriate (Europid ♂ ≥94 cm [≥37 in.], ♀ ≥ 80 cm [≥31.5 in.]; South Asian/Chinese: ♂ ≥90 cm [≥35.5 in], ♀ ≥80 cm [31.5 in.]; Japanese: ♂ ≥85 cm [33.5 in.], ♀ ≥90 cm [35.5 in.])

  • hypertension— ≥ 130/85 mmHg or on treatment

FAMILIAL DYSLIPIDEMIAS (FREDRICKSON CLASSIFICATION)

Type

Mechanism

Lipid profile

Tendon

xanthoma

Palmar

xanthoma

Eruptive

xanthoma

Xanthelasma

Tuberous

xanthoma

Cardiac

risk

Type I.

Hyperchylomicronemia

(LPL deficiency)

LPL deficiency resulting in chylomicron accumulation

↑↑ TGL

  

 

-

Type IIa.

Familial hypercholesterolemia

LDL receptor defect

↑ TC (LDL)

+/− ↑ TG

+/− ↑ apoB

  

++

Type IIb.

Familial combined hyperlipidemia

↑ hepatic production of VLDL

↑ apoB

+/− ↑ TG

+/− ↑ TC (LDL)

   

(sometimes)

+

Type III.

Dysbetalipoproteinemia

ApoE Δ (apoE2/E2); ↓ clearance of chylomicron and VLDL remnants

↑ TGL

↑ TC (VLDL, IDL)

(sometimes)

 

+

(and PVD)

Type IV.

Hypertriglyceridemia

↑ hepatic production of VLDL

↑ TC (VLDL)

↑ TGL

↓ HDL

  

 

+

Type V.

Mixed hypertriglyceridemia

↑ production and ↓ clearance of VLDL and chylomicrons

↑↑ TGL

↑ TC (VLDL)

  

 

-

Smoking Issues

See SMOKING ISSUES (p. 480)

Approach to ECG

AHA/ACCF/HRS 2009 Recommendations

Circulation 2007 115:10

Circulation 2009 119:10

Ten Steps to ECG

  1. 1.

    ID—name and age, date, technique (12 lead, calibration, paper speed)

     
  2. 2.

    rate—normal 60–100 beats/min. 300/150/100/75/60/50 rule

     
  3. 3.

    rhythm—regular/irregular, wide/narrow complex, sinus, atrial, atrioventricular, ventricular

     
  4. 4.

    axis—deviation, rotation

     
  5. 5.

    PR interval—normal 120–200 ms; first, second, third degree AV block

     
  6. 6.

    QRS interval—normal 80–110 ms, intraventricular conduction delay 110–120 ms, RBBB, LBBB, LAFB, LPFB

     
  7. 7.

    QT interval—QT <50% of RR interval; normal QTc 390–460 ms (women), 390–450 ms (men)

     
  8. 8.

    hypertrophy / enlargement—RAE, LAE, RVH, LVH

     
  9. 9.

    ischemia—ST elevation/depression, T wave inversion

     
  10. 10.

    infarction—Q waves

     
  11. 11.

    special conditions

     

Chest Leads Placement

  • V1—4th intercostal space, right sternal border

  • V2—4th intercostal space, left sternal border

  • V3—halfway between V2 and V4

  • V4—5th intercostal space, left mid-clavicular line

  • V5—5th intercostal space, left anterior axillary line

  • V6—5th intercostal space, left mid-axillary line

Rate and Rhythm

SINUS

—P before QRS, QRS after P, P upright I + II, P down aVR. Normal (rate 60–100), tachycardia (rate >100), bradycardia (rate <60), arrhythmia (variable)

ATRIAL

—rate 60–80 normally, variable P wave, short PR interval

JUNCTIONAL

(mid and distal region of AV node)—rate 40–60, no P wave or inverted P wave

VENTRICULAR

(His bundle, bundle branches, ventricle)—rate 20–40, no P wave

Tachycardia

REGULAR NARROW COMPLEX TACHYCARDIA

—sinus tachycardia, atrial flutter with fixed block (rate 300, 150, 100), supraventricular tachycardia (atrial tachycardia, AV nodal reentry, orthodromic AVRT (WPW), accelerated junctional tachycardia

IRREGULAR NARROW COMPLEX TACHYCARDIA

—sinus tachycardia/arrhythmia, premature atrial contractions, multifocal atrial tachycardia, ectopic atrial tachyarrhythmia with variable block, atrial flutter with variable block, atrial fibrillation

REGULAR WIDE COMPLEX TACHYCARDIA

—ventricular tachycardia, supraventricular tachycardia with aberrant conduction, pacemaker-mediated tachyarrhythmia, antidromic AVRT (WPW), metabolic abnormality (e.g., TCA overdose, hyperkalemia), artifact

IRREGULAR WIDE COMPLEX TACHYCARDIA

—monomorphic ventricular tachycardia (during “warm-up phenomenon”), polymorphic ventricular tachycardia, atrial fibrillation with pre-excitation (WPW), irregular supraventricular tachycardia with aberrant conduction, coarse ventricular fibrillation, artifact

DISTINGUISHING FEATURES SUGGESTIVE OF VT RATHER THAN SVT WITH ABERRANT CONDUCTION

—older age, history of coronary artery disease (>90% pre-test probability), history of structural heart disease (>90% pre-test probability), AV dissociation (dissociated P waves, fusion beats, capture beats), atypical bundle branch block morphology, concordance of precordial leads, QRS width >160 ms in LBBB or >140 ms in RBBB, extreme LAD (−90° to −180°). Hemodynamic stability (or instability) is not a useful distinguishing feature

Bradycardia and Prolonged PR

SINUS

—sinus bradycardia, sick sinus syndrome / sinus node dysfunction, sinus exit block, tachycardia-bradycardia syndrome (SSS + AF usually)

AV BLOCK

—prolonged PR interval
  • first degree—PR >200 ms constantly

  • second degree
    • mobitz type I (Wenckebach)—PR progressively longer and then dropped QRS

    • mobitz type II—PR constant and then sudden dropped QRS. When any but not all ventricular beats are dropped, second degree block exists

  • third degree—complete blockage with independent atrial and escape rhythms (junctional or ventricular escape)

Prolonged QRS—Bundle Branch Block and Hemiblock

ANATOMY

—SA node (RCA 59%, LAD 38%, both 3%) → AV node (RCA 90%, LCX 10%) → bundle of His (RCA) → right bundle (LAD), left anterior fascicle (LAD, RCA), and left posterior fascicle (RCA, LAD)

RBBB

—QRS ≥120 ms, slurred S wave in I and V6 and rSR’ in V1–3 with R’ taller than r. May also see QR’ complex in V1 (suggestive of old or new infarct). QRS polarity positive in V1–2. Causes include LAD involvement/anterior infarction, may be benign in young people

LBBB

—QRS ≥120 ms, broad notched or slurred R in I, aVL, V5, and V6, with no Q waves; broad monomorphic S in V1, may have small r wave. QRS polarity negative in V1–2. Causes include hypertension, CAD, dilated cardiomyopathy, rheumatic heart disease, infiltrative diseases, benign or idiopathic

LEFT ANTERIOR FASCICULAR BLOCK

—QRS <120 ms, left axis deviation −45° to −90°, qR in aVL, R-peak time in aVL of 45 ms or more. May be benign, LAD involvement/anterior infarction. Shortcut to diagnosis—I up, II down, aVF down

LEFT POSTERIOR FASCICULAR BLOCK

—right axis deviation 90–180°, QRS <120 ms, rS in I and aVL, and qR in III and aVF

Prolonged QT

NORMAL

—QTc = square root (QT in seconds/RR interval in seconds); QT <50% of RR interval; normal QTc 390–460 ms (women), 390–450 ms (men)

CAUSES

genetic, metabolic (hypokalemia, hypomagnesemia, hypocalcemia), antiarrhythmics (quinidine, procainamide, amiodarone, sotalol), antibiotics (macrolide, trimethoprim–sulfamethoxazole, fluoroquinolone), psychotropics (TCA, SSRI, haloperidol, risperidone), analgesics (methadone), structural heart disease (HF, LVH, acute ischemia), others (HIV, anorexia nervosa, stroke, brain injury)

PROGRESSION

—may result in torsades de pointes, VT, and sudden death (amiodarone less likely)

TREATMENTS

—remove offending agent(s), overdrive pacing, isoproterenol infusion, magnesium

Hypertrophy Criteria

RAE

—tall peaked P in II and aVF (>2.5 mm high); large initial component of biphasic P in V1 (p pulmonale)

LAE

—wide notched P in II (>2.5 mm long); biphasic P in V1 with broad negative phase; P wave duration >120 ms (p mitrale)

LVH

—tall R in aVL (>11 mm); R in V5 or V6 (whichever is taller) plus S in V1 >35 mm; R in V5 or R in V6 > 27 mm; poor R wave progression in precordial leads; ST depression and T wave inversion in lateral leads (I, aVL, V5–6) suggestive of ventricular strain; R in aVL plus S in V3 >28 mm in male or >20 mm in female (Cornell criteria). Diagnosis difficult with LBBB, consider LVH if S in V1 + R in V5 >45 mm (Klein criteria)

RVH

—right axis deviation (>110°); R > S wave in V1 and R >7 mm; persistent S waves V5–6; ST depression and T wave inversion V1–3

DIFFERENTIAL DIAGNOSIS FOR DOMINANT R WAVE IN V1

—RV hypertrophy, right bundle branch block, posterior myocardial infarction, pre-excitation (Wolff–Parkinson–White), dextrocardia, Duchenne muscular dystrophy, hypertrophic cardiomyopathy, normal variant, incorrect lead placement, juvenile pattern

Ischemia/Infarct Morphology

HYPERACUTE T WAVES

—starts in seconds

ST ELEVATION

—transmural injury, starts in minutes

ST DEPRESSION

—subendocardial infarction. Consider posterior infarct if in V1/V2

T WAVE INVERSION

—starts in hours, stays for weeks, and flips back in months

Q WAVES

—starts in 8 h. If no reperfusion, stays forever. Considered significant if >1 block wide and height >1/3 of QRS

ACCELERATED IDIOVENTRICULAR RHYTHM

—suggests reperfusion post-infarction (HR <100, intermittent)

Voltage Criteria

NORMAL

—QRS >5 mm high in limb leads, QRS >10 mm high in precordial leads

LOW

—thick chest wall, COPD, pericarditis, pleural effusion, amyloidosis, myxedema, hemochromatosis

Differential Diagnosis of ST Elevation

NORMAL MALE PATTERN

—1–3 mm elevation, concave, most marked in V2

ST ELEVATION OF NORMAL VARIANT

—seen in V4–5, short QT, high QRS voltage

BENIGN EARLY REPOLARIZATION

—most marked in V4 with notching at J point, upright T waves. Reciprocal ST depression in aVR, not in aVL, when limb leads are involved

ACUTE MI

—ST segment with a plateau of shoulder or upsloping, reciprocal behavior between aVL + III

PRINZMETAL

S AN G INA—same as MI but transient

ACUTE PERICARDITIS

—diffuse ST elevation, ST depression in aVR. Elevation seldom >5 mm, PR segment depression (best seen in II)

ACUTE MYOCARDITIS

—diffuse ST elevation, may simulate acute MI/pericarditis

AORTIC DISSECTION

—obstruction of right coronary artery by dissection flap

LV ANEURYSM

—persistent ST elevation after MI

PULMONARY EMBOLISM

—changes simulating MI seen often in both inferior and anteroseptal leads

STRESS (TAKOTSUBO) CARDIOMYOPATHY

—transient apical and/or mid LV systolic dysfunction that mimics myocardial infarction, in the absence of obstructive CAD

LBBB

—concave, ST segment deviation discordant from QRS. In the presence of LBBB, features suggestive of infarction include concordant ST segment changes (ST elevation ≥1 mm in leads with positive QRS complex and ST depression ≥1 mm in V1–3), disconcordant ST-segment changes (ST elevation ≥5 mm in leads with negative QRS complex) (Sgarbossa criteria)

LVH

—concave, other features of LVH

HYPERKALEMIA

—see below

HYPOTHERMIA

—Osborne waves may be seen

NEJM 2003 349: 22

Infarction Zones

Territory

Leads

Artery

Comment

Inferior

II, III, aVFa

RCA, LCXb

RV, SA, AV nodes

Lateral

I, aVL, V5, V6

LCX, RCA

 

Posterior

V1i, V2i, V8, V9c

RCA

 

Anterior

V1–V4d

LAD

May be massive LV

RV

R leads (V1), V4R

RCA

Preload

aEvidence of inferior MI should trigger one to automatically check V4R to assess for RV infarction, which occurs in up to 40% of patients with inferior MI. May see increased JVP and clear lung fields clinically. ST elevation in V4R is diagnostic and prognostic

bInferior infarcts may be related to either RCA (ST elevation in III > II and ST depression in I, aVL, or both >1 mm) or LCX (ST elevation in I, aVL, V5–6 and ST depression in V1–3)

ci = inverted. ST depression in V1–V2 in a regular ECG should trigger one to automatically request for posterior leads to check for posterior MI. Posterior infarct may be associated with inferior and lateral infarct as these territories are all supplied by RCA

dV1–V2 = septal, V3–V4 = anterior

Special Conditions

HYPERTHYROIDISM

—tachycardia, non-specific ST-T changes, biphasic T in V2–V6

DIGITALIS EFFECT

—slowing SA, AV. Gradual downward sloping/scooping of ST. ST depression in I, II, aVF, V2–V6

DIGITALIS TOXICITY

—unifocal or multifocal PVCs, first degree heart block, ventricular bigeminy, paroxysmal atrial tachycardia (often with 2:1 AV conduction), bidirectional VT, atrial fibrillation with complete heart block (regular escape rhythm)

HYPERKALEMIA

—tall, peaked T wave (especially precordial leads. Definitions of “tall T wave” include a height >5 mm in limb lead or 10 mm in precordial lead or a T wave height >50% of the entire QRS excursion in same lead), widened QRS, wide and flat P wave

HYPOKALEMIA

—flattened T wave/inversion, U wave

COPD

—RAD, ↓ amplitude, multifocal atrial tachycardia

HYPERCALCEMIA

—short QT

HYPOCALCEMIA

—prolonged QT

WOLFF–PARKINSON–WHITE SYNDROME

—short PR (<120 ms), delta wave, prolonged QRS (>120 ms), symptomatic tachycardia. Pharmacological treatments include amiodarone and procainamide. AV nodal blocking drugs (adenosine, β-blockers, verapamil/diltiazem, digoxin) are contraindicated in patients with WPW and AF as they may precipitate VF. Consider catheter ablation if symptomatic arrhythmias, AF, or atrial flutter. If failed, consider surgical ablation

BRUGADA SYNDROME

—type 1: high take-off and cove-shaped ST-segment elevation (≥2 mm) in V1–V2. Type 2: saddle-back ST-T pattern in V1–V2

Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  • Bryan Jonathan Har
    • 1
  1. 1.Interventional CardiologistCalgaryCanada

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