Inhaled nitric oxide does not alter pulmonary or cardiac effects of fat embolism in dogs after cemented arthroplasty
Abstract
Purpose
We examined the effect of inhaled nitric oxide (NO) on the acute pulmonary hypertension and right ventricular (RV) dilation after fat embolism.
Methods
A bilateral cemented arthroplasty (BCA), created fat embolism in 20 dogs. In Part A, 12 dogs were randomized to an NO group (n = 6, inhaled NO 40 ppm before BCA and throughout the study) or a control group (n = 6). In Part B, a third group of dogs (n = 8) were given NO 20–40 ppm 2–3 min after BCA when pulmonary artery pressure (PAP) increased. Transesophageal echocardiography (TEE) and invasive hemodynamic monitoring evaluated the hemodynamic response to BCA. Postmortem, quantitative morphometry was used to estimate the number of fat emboli and diameter of lung vessel occluded by fat.
Results
Part A: The increase in PAP in the NO group (16 ± 1 to 34 ± 9 mmHg) within three minutes of BCA was not different from that in the control group (14 ± 4 to 35 ± 9 mmHg). Within three minutes of BCA, TEE demonstrated RV dilation in all groups (P < 0.05) but there was no difference in the change in RV area in the NO and control groups. When NO was given after BCA, no difference in PAP or RV dilation was noted from that in the control group. There were no differences, at post mortem, between the groups in the diameter of lung vessel occluded by fat
Conclusion
Whether given before the embolic insult or two to three minutes after the onset of pulmonary hypertension, inhaled NO did not attenuate the acute pulmonary hypertension or RV dilation after cemented arthroplasty.
Keywords
Nitric Oxide Right Ventricular Pulmonary Artery Pressure Pulmonary Artery Occlude Pressure Right Atrial PressureRésumé
Objectif
Étudier l’effet de l’oxyde nitrique inhalé (NO) sur l’hypertension pulmonaire aiguë et la dilatation du ventricule droit (VD) après une embolie graisseuse.
Méthode
Une arthroplastie bilatérale cimentée (ABC) a créé une embolie graisseuse chez 20 chiens. Dans la partie A de l’essai, 12 chiens ont été répartis de façon aléatoire vers un groupe NO (n = 6, 40 ppm de NO inhalé avant l’ABC et tout au long de l’étude) ou vers un groupe témoin (n = 6). Dans la partie B, un troisième groupe de chiens (n = 8) ont reçu 20]–40 ppm de NO, 2–3 min après l’ABC, au moment oú la pression de l’artère pulmonaire (PAP) s’est élevée. On a évalué la réponse hémodynamique à l’ABC par échocardiographie transœsophagienne (ETO) et par monitorage hémodynamique effractif. Après la mort, on a utilisé la morphométrie quantitative pour évaluer la proportion du système vasculaire pulmonaire obstruée par la graisse.
Résultats
Partie A: L’augmentation de PAP dans le groupe NO (16 ± I à 34 ± 9 mmHg), en moins de trois minutes suivant l’ABC, était semblable à celle du groupe témoin (14 ± 4 à 35 ± 9 mmHg). Moins de trois minutes après l’ABC, l’ETO a montré une dilatation du VD dans tous les groupes (P < 0,05) mais pas de différence intergroupe de changements survenus au VD. Aucune différence de PAP ou de dilatation du VD, en comparaison avec les chiens témoins, n’a été notée suivant l’administration de NO. À l’autopsie, il n’y avait pas de différence intergroupe quant au diamètre du vaisseau pulmonaire obstrué par la graisse.
Conclusion
Que le NO sort administré avant l’embolie ou deux ou trois minutes après le début de l’hypertension, il ne réduit pas l’hypertension pulmonaire aiguë ou la dilatation du VD à la suite d’une arthroplastie cimentée.
References
- 1.Ereth MH, Weber JG, Abel MD, et al. Cemented versus noncemented total hip arthroplasty — embolism, hemodynamics, and intrapulmonary shunting. Mayo Clin Pro 1992; 67: 1066–74.Google Scholar
- 2.Fitzgerald R, Mason L, Kanumilli V, Kleinhomer K, Sakamoto A, Johnson C. Transient cardiac standstill associated with embolic phenomena diagnosed by introperative transesophageal echocardiography during cemented total hip arthroplasty. Anesth Analg 1994; 79: 382–5.PubMedCrossRefGoogle Scholar
- 3.Pell ACH, Christie J, Keating JF, Sutherland GR. The detection of fat embolism by transoesophageal echocardiography during reamed intramedullary nailing. A study of 24 patients with femoral and tibial fractures. J Bone Joint Surg 1993; 75-B: 921–5.Google Scholar
- 4.Urban MK, Sheppard R, Gordon MA, Urquhart BL. Right ventricular function during revision total hip arthroplasty. Anesth Analg 1996; 82: 1225–9.PubMedCrossRefGoogle Scholar
- 5.Propst JW, Siegel LC, Schnittger I, Foppiano L, Goodman SB, Brock-Utne JG. Segmentai wall motion abnormalities in patients undergoing total hip replacement: correlations with intraoperative events. Anesth Analg 1993; 77: 743–9.PubMedCrossRefGoogle Scholar
- 6.Pietak S, Holmes J, Matthews R, Petrasek A, Porter B. Cardiovascular collapse following femoral prosthesis surgery for acute hip fracture. Can J Anaesth 1997; 44: 198–201.PubMedCrossRefGoogle Scholar
- 7.Murphy P, Edelist G, Byrick RJ, Kay JC, Mullen JB. Relationship of fat embolism to haemodynamic and echocardiographic changes during cemented arthroplasty. Can J Anaesth 1997; 44: 1293–300.PubMedGoogle Scholar
- 8.Byrick RJ, Mullen JB, Mazer CD, Guest CB. Transpulmonary systemic fat embolism. Studies in mongrel dogs after cemented arthroplasty. Am J Respir Crit Care Med 1994; 150: 1416–22.PubMedGoogle Scholar
- 9.Rossaint R, Falke KF, Lopez F, Slama K, Pison U, Zapol WM. Inhaled nitric oxide for the adult respiratory distress syndrome. N Engl J Med 1993; 328: 399–405.PubMedCrossRefGoogle Scholar
- 10.Pison U, Lopez FA, Heidelmeyer CF, Rossaint R, Falke KJ. Inhaled nitric oxide reverses hypoxic pulmonary vasoconstriction without impairing gas exchange. J Appl Physiol 1993; 74: 1287–92.PubMedCrossRefGoogle Scholar
- 11.Stewart TE, Valenza F, Ribeiro SP, et al. Increased nitric oxide in exhaled gas as an early marker of lung inflammation in a model of sepsis. Am J Respir Crit Care Med 1995; 151: 713–8.PubMedGoogle Scholar
- 12.Vedrinne JM, Curtil A, Martinot S, et al. The hemodynamic effects of hypoxemia in anesthetized pigs: a comparison between right heart catheter and echocardiography. Anesth Analg 1998; 87: 21–6.PubMedCrossRefGoogle Scholar
- 13.Treggiari-Venzi M, Ricou B, Romand J-A, Suter PM. The response to repeated nitric oxide inhalation is inconsistent in patients with acute respiratory distress syndrome. Anesthesiology 1998; 88: 634–41.PubMedCrossRefGoogle Scholar
- 14.Manktelow C, Bigatello LM, Hess D, Hurford WE. Physiologic determinants of the response to inhaled nitric oxide in patients with acute respiratory distress syndrome. Anesthesiology 1997; 87: 297–307.PubMedCrossRefGoogle Scholar
- 15.Galinier M, Rougé P, Fourcade J, et al. Lack of haemodynamic effects of nitric oxide on post-capillary pulmonary hypertension induced by acute sino-aortic denervation. Br J Pharmacol 1997; 120: 7–12.PubMedCrossRefGoogle Scholar
- 16.Mélot C, Vermeulen F, Maggiorini M, Gilbert E, Naeije R. Site of pulmonary vasodilation by inhaled nitric oxide in microembolic lung injury. Am J Respir Crit Care Med 1997; 156: 75–85.PubMedGoogle Scholar
- 17.Orsini EC, Byrick RJ, Mullen JBM, Kay JC, Waddell JP. Cardiopulmonary function and pulmonary microemboli during arthroplasty using cemented or noncemented components. J Bone Joint Surg 1987; 69A: 822–32.Google Scholar
- 18.Hopkins SR, Johnson EC, Richardson RS, Wagner H, De Rosa M, Wagner PD. Effects of inhaled nitric oxide on gas exchange in lungs with shunt or poorly ventilated areas. Am J Respir Crit Care Med 1997; 156: 484–91.PubMedGoogle Scholar
- 19.Young I, Mazzone RW, Wagner PD. Identification of functional lung unit in the dog by graded vascular embolization. J Appl Physiol 1980; 49: 132–41.PubMedGoogle Scholar
- 20.Fahmy NR, Head CA, Nathan N, Zapol WM. Inhaled nitric oxide reverses acute pulmonary hypertension and hypoxemia during orthopedic procedures. Anesthesiology 1997; 87: A1120.CrossRefGoogle Scholar
- 21.Byrick RJ, Forbes D, Waddell JP. A monitored cardiovascular collapse during cemented total knee replacement. Anesthesiology 1986; 65: 213–6.PubMedCrossRefGoogle Scholar