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Pulmonary Edema and Cardiac Dysfunction Following Subarachnoid Hemorrhage

  • Nancy McLaughlin (a1), Michel W. Bojanowski (a1), François Girard (a2) and André Denault (a3)

Abstract:

Background:

Pulmonary edema (PE) can occur in the early or late period following subarachnoid hemorrhage (SAH). The incidence of each type of PE is unknown and the association with ventricular dysfunction, both systolic and diastolic, has not been described.

Methods:

Retrospective chart review of 178 consecutive patients with SAH surgically treated over a three-year period. Patients with pulmonary edema diagnosed by a radiologist were included. Early onset SAH was defined as occurring within 12 hours. Cardiac function at the time of the PE was analyzed using hemodynamic and echocardiographic criteria of systolic and diastolic dysfunction. Pulmonary edema was observed in 42 patients (28.8%) and was more often delayed (89.4%). Evidence of cardiac involvement during PE varied between 40 to 100%.

Results and conclusions:

Pulmonary edema occurs in 28.8% of patients after SAH, and is most commonly delayed. Cardiac dysfunction, both systolic and diastolic, is commonly observed during SAH and could contribute to the genesis of PE after SAH.

RÉSUMÉ: Introduction:

L’oedème pulmonaire (OP) peut survenir précocement ou tardivement après une hémorragie sousarachnoïdienne (HSA). L’incidence de chaque type d’OP est inconnue et l’association à une dysfunction ventriculaire tant systolique que diastolique n’a jamais été décrite.

Méthodes:

Nous avons révisé les dossiers de 178 patients consécutifs atteints de HSA traitée par chirurgie sur une période de trois ans. Les patients ayant présenté un OP diagnostiqué par un radiologiste ont été inclus dans l’étude. L’OP était considéré comme précoce s’il survenait dans les 12 heures de l‘HSA. La fonction cardiaque au moment de l’OP a été analysée au moyen des critères hémodynamiques et échocardiographiques de la dysfonction systolique et diastolique. Un OP a été observé chez 42 patients (28,8%) et il était souvent tardif (89,4%). La fréquence de manifestations d’atteinte cardiaque pendant l’OP variait de 40% à 100%.

Résultats et conclusions:

Un OP survient chez 28,8% des patients suite à une HSA et il est souvent tardif. On observe fréquemment une dysfonction cardiaque tant systolique que diastolique pendant l’HSA, ce qui pourrait contribuer à la genèse de l’OP après l’HSA.

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References

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1. Ducker, TB. Central nervous system pressure and pulmonary edema. A clinical study. Trans Am Neurol Assoc 1967; 92:225227.
2. Fein, IA, Rackow, EC. Neurogenic pulmonary edema. Chest 1982; 81:318320.
3. Colice, GL. Neurogenic pulmonary edema. Clin Chest Med 1985; 6:473489.
4. Touho, H, Karasawa, J, Shishido, H, et al. Neurogenic pulmonaryedema in the acute stage of hemorrhagic cerebrovascular disease. Neurosurgery 1989; 25:762768.
5. Pender, ES, Pollack, CV Jr. Neurogenic pulmonary edema: casereports and review. J Emerg Med 1992; 10:4551.
6. Gomez, CM, Palazzo, MG. Pulmonary artery catheterization inanaesthesia and intensive care. Br J Anaesth 1998; 81:945956.
7. Zwissler, B, Rank, N, Jaenicke, U, et al. Selective pulmonaryvasodilation by inhaled prostacyclin in a newborn with congenital heart disease and cardiopulmonary bypass. Anesthesiology 1995; 82:15121516.
8. Hache, M, Denault, AY, Belisle, S, et al. Inhaled prostacyclin (PGI(2))is an effective addition to the treatment of pulmonary hypertension and hypoxia in the operating room and intensive care unit. [L’inhalation de prostacycline (PGI(2)) est un traitement complémentaire efficace de l’hypertension pulmonaire et de l’hypoxie observées en salle d’opération et à l’unite des soinsintensifs]. Can J Anaesth 2001; 48:924929.
9. Clements, FM, de Bruijn, NP. Perioperative evaluation of regionalwall motion by transesophageal two- dimensional echocardiography. Anesth Analg 1987; 66:249261.
10. Urbanowicz, JH, Shaaban, MJ, Cohen, NH, et al. Comparison oftransesophageal echocardiographic and scintigraphic estimates of left ventricular end-diastolic volume index and ejection fraction in patients following coronary artery bypass grafting. Anesthesiology 1990; 72:607612.
11. Brutsaert, DL, Sys, SU, Gillebert, TC. Diastolic failure:pathophysiology and therapeutic implications. J Am Coll Cardiol 1993; 22:318325.
12. Rakowski, H, Appleton, C, Chan, KL, et al. Canadian consensusrecommendations for the measurement and reporting of diastolic dysfunction by echocardiography: from the Investigators of Consensus on Diastolic Dysfunction by Echocardiography. J AmSoc Echocardiogr 1996; 9:736760.
13. Felman, AH. Neurogenic pulmonary edema. Observations in 6 patients. Am J Roentgenol Radium Ther Nucl Med 1971; 112:393396.
14. Wray, NP, Nicotra, MB. Pathogenesis of neurogenic pulmonaryedema. Am Rev Respir Dis 1978; 118:783786.
15. Carlson, RW, Schaeffer, RC Jr, Michaels, SG, Weil, MH. Pulmonaryedema following intracranial hemorrhage. Chest 1979; 75:731734.
16. Harari, A, Rapin, M, Regnier, B, et al. Letter: Normal pulmonary-capillary pressures in the late phase of neurogenic pulmonary oedema. Lancet 1976; 1:494.
17. Malik, AB. Mechanisms of neurogenic pulmonary edema. Circ Res 1985; 57:118.
18. Theodore, J, Robin, ED. Speculations on neurogenic pulmonaryedema (NPE). Am Rev Respir Dis 1976; 113:405411.
19. Malik, AB. Pulmonary vascular response to increase in intracranialpressure: role of sympathetic mechanisms. J Appl Physiol 1977; 42:335343.
20. Staub, NC. The pathogenesis of pulmonary edema. Prog Cardiovasc Dis 1980; 23:5380.
21. Warnell, P. The cardiopulmonary complications of aneurysmalsubarachnoid hemorrhage: current trends in management. Axone 1992; 14:2428.
22. Handlin, LR, Kindred, LH, Beauchamp, GD, et al. Reversible leftventricular dysfunction after subarachnoid hemorrhage. Am Heart J 1993; 126:235240.
23. Raymer, K, Choi, P. Concurrent subarachnoid haemorrhage andmyocardial injury. Can J Anaesth 1997; 44:515519.
24. Greenhoot, JH, Reichenbach, DD. Cardiac injury and subarachnoidhemorrhage. A clinical, pathological, and physiological correlation. J Neurosurg 1969; 30:521531.
25. Mayer, SA, Fink, ME, Homma, S, et al. Cardiac injury associatedwith neurogenic pulmonary edema following subarachnoid hemorrhage. Neurology 1994; 44:815820.
26. Graf, CJ, Rossi, NP. Catecholamine response to intracranialhypertension. J Neurosurg 1978; 49:862868.
27. Kolin, A, Norris, JW. Myocardial damage from acute cerebrallesions. Stroke 1984; 15:990993.
28. Hawkins, WE, Clower, BR. Myocardial damage after head traumaand simulated intracranial haemorrhage in mice: the role of the autonomic nervous system. Cardiovasc Res 1971; 5:524529.
29. Weir, BK. Pulmonary edema following fatal aneurysm rupture. J Neurosurg 1978; 49:502507.
30. Pollick, C, Cujec, B, Parker, S, Tator, C. Left ventricular wall motionabnormalities in subarachnoid hemorrhage: an echocardiographic study. J Am Coll Cardiol 1988; 12:600605.
31. Mayer, SA, Lin, J, Homma, S, et al. Myocardial injury and left ventricular performance after subarachnoid hemorrhage. Stroke 1999; 30:780786.
32. Mayer, SA, LiMandri, G, Sherman, D, et al. Electrocardiographicmarkers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage. J Neurosurg 1995; 83:889896.
33. Parekh, N, Venkatesh, B, Cross, D, et al. Cardiac troponin I predictsmyocardial dysfunction in aneurysmal subarachnoid hemorrhage. J Am Coll Cardiol 2000; 36:13281335.
34. Davies, KR, Gelb, AW, Manninen, PH, et al. Cardiac function inaneurysmal subarachnoid haemorrhage: a study of electrocardio-graphic and echocardiographic abnormalities. Br J Anaesth 1991; 67:5863.
35. Costachescu, T, Denault, AY, Guimond, JG, et al. The hemodynamically unstable patient in the intensive care unit: hemodynamic vs. transesophageal echocardiographic monitoring. Crit Care Med 2002; 30:12141223.
36. Vasan, RS, Benjamin, EJ. Diastolic heart failure-no time to relax. N Engl J Med 2001; 344:5659.
37. Vasan, RS, Larson, MG, Benjamin, EJ, et al. Congestive heart failurein subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort. J Am Coll Cardiol 1999; 33:19481955.
38. Vasan, RS, Benjamin, EJ, Levy, D. Prevalence, clinical features andprognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol 1995; 26:15651574.
39. Pinamonti, B, Di Lenarda, A, Sinagra, G, Camerini, F. Restrictive leftventricular filling pattern in dilated cardiomyopathy assessed by Doppler echocardiography: clinical, echocardiographic and hemo-dynamic correlations and prognostic implications. Heart Muscle Disease Study Group. J Am Coll Cardiol 1993; 22:808815.
40. Rihal, CS, Nishimura, RA, Hatle, LK, et al. Systolic and diastolicdysfunction in patients with clinical diagnosis of dilated cardiomyopathy. Relation to symptoms and prognosis. Circulation 1994; 90:27722779.
41. Giannuzzi, P, Temporelli, PL, Bosimini, E, et al. Independent andincremental prognostic value of Doppler-derived mitral deceleration time of early filling in both symptomatic and asymptomatic patients with left ventricular dysfunction. J AmColl Cardiol 1996; 28:383390.
42. Pinamonti, B, Zecchin, M, Di Lenarda, A, et al. Persistence ofrestrictive left ventricular filling pattern in dilated cardiomyopathy: an ominous prognostic sign. J Am Coll Cardiol 1997; 29:604612.
43. Sun, JP, James, KB, Yang, XS, et al. Comparison of mortality ratesand progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities. Am J Cardiol 1997; 80:15831587.
44. Redfield, MM, Jacobsen, SJ, Burnett, JC Jr, et al. Burden of systolicand diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA 2003; 289:194202.
45. Sandham, JD, Hull, RD, Brant, RF, et al. A randomized, controlledtrial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med 2003; 348:514.
46. Ducker, TB. Increased intracranial pressure and pulmonary edema. 1. Clinical study of 11 patients. J Neurosurg 1968; 28:112117.
47. Ciongoli, AK, Poser, CM. Pulmonary edema secondary tosubarachnoid hemorrhage. Neurology 1972; 22:867870.
48. Kosnik, EJ, Paul, SE, Rossel, CW, Sayers, MP. Central neurogenicpulmonary edema: with a review of its pathogenesis and treatment. Childs Brain 1977; 3:3747.
49. Fein, A, Grossman, RF, Jones, JG, et al. The value of edema fluidprotein measurement in patients with pulmonary edema. Am JMed 1979; 67:3238.
50. Eggleston, CA. Clinical correlation of neurogenic pulmonary edemato increased intracranial pressure. J Neurosurg Nurs 1982; 14:245254.
51. Lagerkranser, M, Pehrsson, K, Sylven, C. Neurogenic pulmonaryoedema. A review of the pathophysiology with clinical and therapeutic implications. Acta Med Scand 1982; 122:267271.
52. Melon, E, Bonnet, F, Lepresle, E, et al. Altered capillary permeabilityin neurogenic pulmonary oedema. Intensive Care Med 1985; 11:323325.
53. Schell, AR, Shenoy, MM, Friedman, SA, Patel, AR. Pulmonary edemaassociated with subarachnoid hemorrhage. Evidence for a cardiogenic origin. Arch Intern Med 1987; 147:591592.
54. Deehan, SC, Grant, IS. Haemodynamic changes in neurogenicpulmonary oedema: effect of dobutamine. Intensive Care Med 1996; 22:672676.
55. Smith, WS, Matthay, MA. Evidence for a hydrostatic mechanism inhuman neurogenic pulmonary edema. Chest 1997;111:13261333.
56. Kono, T, Morita, H, Kuroiwa, T, et al. Left ventricular wall motionabnormalities in patients with subarachnoid hemorrhage: neuro-genic stunned myocardium. J Am Coll Cardiol 1994; 4:636640.
57. Pinto, RJ, Goyal, V, Sharma, S, Bhagwati, SN. Transient myocardialdys function in a patient with subarachnoid haemorrhage. Int J Cardiol 1994; 46:289291.
58. Sakka, SG, Huettemann, E, Reinhart, K. Acute left ventriculardys function and subarachnoid hemorrhage. J Neurosurg Anesthesiol 1999; 11:209213.
59. Yasu, T, Owa, M, Omura, N, et al. Transient ST elevation and leftventricular asynergy associated with normal coronary artery in aneurysmal subarachnoid hemorrhage. Chest 1993;103:12741275.

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Pulmonary Edema and Cardiac Dysfunction Following Subarachnoid Hemorrhage

  • Nancy McLaughlin (a1), Michel W. Bojanowski (a1), François Girard (a2) and André Denault (a3)

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