Summary
Synopsis: The recently introduced preparation of intravenous glyceryl trinitrate1 (nitroglycerin) provides a rapid steady therapeutic blood concentration of nitrates during continuous infusion. Intravenous glyceryl trinitrate causes venodilation at low doses, but at higher doses dilates both arteries and veins. Its principal haemodynamic effects at therapeutic dosages include a decrease in blood pressure in preload (left ventricular filling pressure) and in determinants of afterload, and a decrease in myocardial oxygen demand. Human pharmacokinetic data are few and difficult to interpret due to wide interstudy and interindividual variation. There is no close correlation between infusion rate, blood concentration and haemodynamic effects.
The nature of the patient population treated with intravenous glyceryl trinitrate has largely precluded the use of a placebo, but in open trials the drug has been used successfully in the treatment of unstable angina, left ventricular failure accompanying acute myocardial infarction and in the control of hypertension associated with cardiac surgery at dosages titrated to achieve a specific end-point. Favourable haemodynamic responses have been achieved in very short term studies in congestive heart failure, and preliminary studies suggest that institution of intravenous glyceryl trinitrate early after acute myocardial infarction may limit ischaemic damage. However, use of the drug in acute myocardial infarction remains controversial. Intravenous glyceryl trinitrate is generally well tolerated, although hypotension and headache occur occasionally, and sinus tachycardia and bradycardia less frequently. Careful titration of dosage is required (beginning at 5 μg/min), and if the infusion sets contain polyvinylchloride, the delivered dose is lower than that calculated, because of adsorption of glyceryl trinitrate onto the plastic tubing.
Pharmacodynamic Studies: The effects of intravenous glyceryl trinitrate on cardiac haemodynamics, measured by invasive means such as arterial lines and Swan-Ganz catheters, appear to be related to dose, but not to blood concentrations. Venodilation predominates at lower infusion rates, while as the infusion rate increases, glyceryl trinitrate dilates both arterial and venous systems, leading to decreases in blood pressure. Decreases in systolic blood pressure have been noted to be greater than the decreases in diastolic blood pressure, which may be important in decreasing myocardial oxygen demand and preserving coronary perfusion. Heart rate response is a function of the left ventricular filling pressure and type of patient studied. A reflex increase in heart rate occurs in normal subjects, whereas in patients with heart failure who have a high systemic vascular resistance, heart rate is usually unchanged.
Intravenous glyceryl trinitrate significantly decreases both preload and afterload parameters, including left ventricular filling pressure, right atrial pressure, central venous pressure, mean arterial resistance and systemic vascular resistance. Indices of cardiac function — stroke volume and stroke work and cardiac output — are usually either unchanged or decreased. However, increases in cardiac output have occurred in patients with initially high left ventricular filling pressures and when decreased filling pressures were restored by fluid infusions.
Human studies of the effect of intravenous glyceryl trinitrate on coronary blood flow have reported variable findings, some indicating no change and others indicating a decrease which accompanies a reduction in preload and afterload. Intravenous glyceryl trinitrate has been shown to decrease myocardial oxygen consumption in patients with coronary artery disease or undergoing cardiac surgery, presumably due to the effect of the drug in decreasing preload parameters and diastolic wall tension. In patients with congestive heart failure, intravenous glyceryl trinitrate has been shown to decrease renal blood flow while having no effect on renal vascular resistance.
Glyceryl trinitrate, sodium nitroprusside and isosorbide dinitrate effect similar changes on many haemodynamic parameters. However, unlike glyceryl trinitrate, nitroprusside decreases diastolic blood pressure to a greater extent than systolic blood pressure.
When combined with dopamine or dobutamine, intravenous glyceryl trinitrate produces favourable haemodynamic effects in patients with left ventricular failure by increasing cardiac index and myocardial oxygen supply, while decreasing mean arterial and pulmonary arterial pressures.
Intravenous glyceryl trinitrate decreases pulmonary arterial pressures to a lesser degree than pulmonary vascular resistance, presumably by exerting a vasodilating effect on the pulmonary vessels. These changes may be accompanied by an increase in pulmonary shunting. In the brain, glyceryl trinitrate primarily dilates capacitance arteries, resulting in cerebral vasodilation. Increases in intracranial pressure have been reported, with and without associated decreases in mean arterial pressure.
Intravenous glyceryl trinitrate decreases blood pressure and systemic vascular resistance, though the mechanism by which it is achieved remains to be clarified. They may, however, include calcium ion efflux, α-adrenoceptor blockade, an effect on prostaglandin synthesis or on the production of cyclic guanosine monophosphate. Antianginal and antiischaemic effects produced by intravenous glyceryl trinitrate are thought to be due to the reduction of preload and afterload, leading to a reduction in myocardial size with resultant decreases in myocardial oxygen demand. The favourable effect on the myocardial oxygen supply/demand ratio in ischaemic myocardium appears to be responsible for the improvement of left ventricular function seen in patients with congestiv heart failure, with and without accompanying acute myocardial infarction.
Pharmacokinetic Studies: Pharmacokinetic data for intravenous glyceryl trinitrate in man are limited and difficult to interpret, as factors such as the assay procedure, interindividual variation, blood sampling site and adsorption of glyceryl trinitrate by some types of infusion sets may all affect interpretation of pharmacokinetic findings. There appears to be no close correlation between the infusion rate, blood concentration and haemodynamic effects. Glyceryl trinitrate is extensively distributed and is rapidly metabolised to less active metabolites which are excreted in the urine within 24 hours after a single dose. The elimination half-life of intravenous glyceryl trinitrate has ranged from less than 1 to 3 minutes. Impaired hepatic function may impair the clearance of the drug.
Therapeutic Trials: The nature of the patient population in which intravenous glyceryl trinitrate has been used has largely dictated that open trials be performed.
Intravenous glyceryl trinitrate has been used successfully in the treatment of refractory unstable angina pectoris in widely varying dosages, titrated to pain relief. The average number of anginal episodes has decreased by 70 to 92% and some patients may also require less narcotic supplementation for pain relief. Intracoronary glyceryl trinitrate has also been used successfully to treat naturally occurring or ergonovine-induced coronary artery spasm.
The effects of intravenous glyceryl trinitrate in decreasing infarct size associated with acute myocardial infarction have been measured by several different techniques, each varying with regard to sensitivity and specificity. Therefore, results must be interpreted with regard to the specific tests employed. Preliminary studies suggest that glyceryl trinitrate may reduce ischaemic injury and infarct size in patients with acute myocardial infarction and indicate that early administration after symptom onset may enhance the beneficial effects on infarct size. Since there is a danger of excessive reduction of coronary perfusion pressure, and because the results of studies on the effects of intravenous glyceryl trinitrate on infarct size are variable, the routine use of the drug in acute myocardial infarction remains controversial.
Trials of intravenous glyceryl trinitrate in congestive heart failure, with and without accompanying acute myocardial infarction, have been primarily haemodynamic assessments and were very short term. Intravenous glyceryl trinitrate has decreased left ventricular filling pressures and mean arterial pressures with associated increases in cardiac output. Patients having the most depressed left ventricular function appear to receive the greatest haemodynamic benefit.
Intravenous glyceryl trinitrate has been used effectively to lower blood pressure and prevent myocardial ischaemia in patients undergoing cardiac and non-cardiac surgery, with decreases of over 20% in blood pressure and indices of myocardial oxygen demand being achieved during myocardial revascularisation. In neuro- and orthopaedic surgery, decreases in mean arterial pressure of over 26% have been reported. As glyceryl trinitrate decreases diastolic blood pressure less than sodium nitroprusside, it may preserve myocardial perfusion to a greater extent than nitroprusside.
Side Effects: Intravenous glyceryl trinitrate, if judiciously monitored, is generally well tolerated. Hypotension, which is the most common and potentially serious side effect, occurs in approximately 18% of patients, but can be controlled by decreasing the rate of infusion or by drug withdrawal. Headaches occur in about 2% of patients, but are usually mild and do not require dosage reductions, although supplementary analgesia may be required in a few cases. Sinus bradycardia (4% incidence) due to either vagal or sympathetic dysfunction or volume depletion, nausea and/or vomiting (5% incidence) and sinus tachycardia (less than 1% incidence) have also been reported.
Dosage and Administration: The dosage of intravenous glyceryl trinitrate is usually titrated to the desired clinical effect, starting at 5 μg/min. While in the treatment of unstable angina an end-point in dosing may be pain relief, in acute myocardial infarction and congestive heart failure the reduction of pre- and afterload parameters with consequent improvements in haemodynamic parameters governing cardiac function and myocardial oxygen supply and demand, should be monitored closely until the preferred values and clinical effects are attained, although monitoring of arterial pressure may be satisfactory since venous effects precede arterial effects during dosage titration. In the prevention of hypertension associated with surgical procedures, dosage should be adjusted to reduce arterial pressures to ‘normal’ or to a predetermined level.
Since glyceryl trinitrate may adsorb to polyvinylchloride-type plastic intravenous bags and infusion sets, the drug should be mixed in glass or polyolefin containers and, ideally, administered via non-polyvinylchloride-type infusion sets. If polyvinylchloride-type infusion sets are used, dosage titrations to desired haemodynamic levels must be watched more carefully for up to 24 hours, until the plastic becomes ‘saturated’ with drug.
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Various sections of the manuscript reviewed by: P. W. Armstrong, Department of Medicine, Queen’s University, Kingston, Ontario, Canada; D.N. Bateman, Department of Pharmacological Sciences, University of Newcastle Upon Tyne, England, W.-D. Bussmann, Department of Cardiology, Clinic of the University of Frankfurt/Main, Federal Republic of Germany; J.T. Flaherty, Cardiology Division, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA; P. Harris, Cardiology Department, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia, E.F.McNiff, Pharmaceutical Research and Development Division, Bristol Myers, Buffalo, New York, USA; R.M. Norris, Coronary Care Unit, Green Lane Hospital, Auckland, New Zealand; R.E. Rude, Cardiopulmonary Division, University of Texas Health Science Center, Dallas, Texas, USA.
‘Nitro-Bid’(Marion Laboratories); ‘Nitroglycerin IV’ (Abbott); ‘Nitrostat-IV’ (Parke Davis); ‘Tridil’ (American Critical Care).
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Sorkin, E.M., Brogden, R.N. & Romankiewicz, J.A. Intravenous Glyceryl Trinitrate (Nitroglycerin). Drugs 27, 45–80 (1984). https://doi.org/10.2165/00003495-198427010-00003
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DOI: https://doi.org/10.2165/00003495-198427010-00003