Hostname: page-component-78c5997874-94fs2 Total loading time: 0 Render date: 2024-11-16T15:08:47.025Z Has data issue: false hasContentIssue false
  • English
  • Français

Pulmonary Edema and Cardiac Dysfunction Following Subarachnoid Hemorrhage

Published online by Cambridge University Press:  02 December 2014

Nancy McLaughlin ,
Michel W. Bojanowski ,
François Girard  and
André Denault
Nancy McLaughlin
Affiliation:
Department of Neurosurgery, Centre Hospitalier de l'Université de Montréal (CHUM) - Hôpital Notre-Dame, Montreal, Qc, Canada
Michel W. Bojanowski
Affiliation:
Department of Neurosurgery, Centre Hospitalier de l'Université de Montréal (CHUM) - Hôpital Notre-Dame, Montreal, Qc, Canada
François Girard
Affiliation:
Department of Anesthesiology, CHUM - Hôpital Notre-Dame, Montreal, Qc, Canada
André Denault
Affiliation:
Department of Anesthesiology, Montreal Heart Institute, and the Department of Medecine - Critical Care Division, CHUM - Hôpital Notre-Dame, Montreal, Qc, Canada
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
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:

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.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 32 , Issue 2 , May 2005 , pp. 178 - 185
Copyright
Copyright © The Canadian Journal of Neurological 2005

References

1. Ducker, TB. Central nervous system pressure and pulmonary edema. A clinical study. Trans Am Neurol Assoc 1967; 92:225–227.Google ScholarPubMed
2. Fein, IA, Rackow, EC. Neurogenic pulmonary edema. Chest 1982; 81:318–320.CrossRefGoogle ScholarPubMed
3. Colice, GL. Neurogenic pulmonary edema. Clin Chest Med 1985; 6:473–489.CrossRefGoogle ScholarPubMed
4. Touho, H, Karasawa, J, Shishido, H, et al. Neurogenic pulmonaryedema in the acute stage of hemorrhagic cerebrovascular disease. Neurosurgery 1989; 25:762–768.Google Scholar
5. Pender, ES, Pollack, CV Jr. Neurogenic pulmonary edema: casereports and review. J Emerg Med 1992; 10:45–51.Google Scholar
6. Gomez, CM, Palazzo, MG. Pulmonary artery catheterization inanaesthesia and intensive care. Br J Anaesth 1998; 81:945–956.CrossRefGoogle ScholarPubMed
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; 82:1512–1516.Google Scholar
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; 48:924–929.Google Scholar
9. Clements, FM, de Bruijn, NP. Perioperative evaluation of regionalwall motion by transesophageal two- dimensional echocardiography. Anesth Analg 1987; 66:249–261.Google Scholar
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; 72:607–612.Google Scholar
11. Brutsaert, DL, Sys, SU, Gillebert, TC. Diastolic failure:pathophysiology and therapeutic implications. J Am Coll Cardiol 1993; 22:318–325.Google Scholar
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; 9:736–760.Google Scholar
13. Felman, AH. Neurogenic pulmonary edema. Observations in 6 patients. Am J Roentgenol Radium Ther Nucl Med 1971; 112:393–396.Google Scholar
14. Wray, NP, Nicotra, MB. Pathogenesis of neurogenic pulmonaryedema. Am Rev Respir Dis 1978; 118:783–786.Google Scholar
15. Carlson, RW, Schaeffer, RC Jr, Michaels, SG, Weil, MH. Pulmonaryedema following intracranial hemorrhage. Chest 1979; 75:731–734.CrossRefGoogle Scholar
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.Google Scholar
17. Malik, AB. Mechanisms of neurogenic pulmonary edema. Circ Res 1985; 57:1–18.Google Scholar
18. Theodore, J, Robin, ED. Speculations on neurogenic pulmonaryedema (NPE). Am Rev Respir Dis 1976; 113:405–411.Google Scholar
19. Malik, AB. Pulmonary vascular response to increase in intracranialpressure: role of sympathetic mechanisms. J Appl Physiol 1977; 42:335–343.Google Scholar
20. Staub, NC. The pathogenesis of pulmonary edema. Prog Cardiovasc Dis 1980; 23:53–80.Google Scholar
21. Warnell, P. The cardiopulmonary complications of aneurysmalsubarachnoid hemorrhage: current trends in management. Axone 1992; 14:24–28.Google Scholar
22. Handlin, LR, Kindred, LH, Beauchamp, GD, et al. Reversible leftventricular dysfunction after subarachnoid hemorrhage. Am Heart J 1993; 126:235–240.Google Scholar
23. Raymer, K, Choi, P. Concurrent subarachnoid haemorrhage andmyocardial injury. Can J Anaesth 1997; 44:515–519.CrossRefGoogle Scholar
24. Greenhoot, JH, Reichenbach, DD. Cardiac injury and subarachnoidhemorrhage. A clinical, pathological, and physiological correlation. J Neurosurg 1969; 30:521–531.Google Scholar
25. Mayer, SA, Fink, ME, Homma, S, et al. Cardiac injury associatedwith neurogenic pulmonary edema following subarachnoid hemorrhage. Neurology 1994; 44:815–820.CrossRefGoogle Scholar
26. Graf, CJ, Rossi, NP. Catecholamine response to intracranialhypertension. J Neurosurg 1978; 49:862–868.Google Scholar
27. Kolin, A, Norris, JW. Myocardial damage from acute cerebrallesions. Stroke 1984; 15:990–993.Google Scholar
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; 5:524–529.Google Scholar
29. Weir, BK. Pulmonary edema following fatal aneurysm rupture. J Neurosurg 1978; 49:502–507.Google Scholar
30. Pollick, C, Cujec, B, Parker, S, Tator, C. Left ventricular wall motionabnormalities in subarachnoid hemorrhage: an echocardiographic study. J Am Coll Cardiol 1988; 12:600–605.Google Scholar
31. Mayer, SA, Lin, J, Homma, S, et al. Myocardial injury and left ventricular performance after subarachnoid hemorrhage. Stroke 1999; 30:780–786.Google Scholar
32. Mayer, SA, LiMandri, G, Sherman, D, et al. Electrocardiographicmarkers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage. J Neurosurg 1995; 83:889–896.CrossRefGoogle ScholarPubMed
33. Parekh, N, Venkatesh, B, Cross, D, et al. Cardiac troponin I predictsmyocardial dysfunction in aneurysmal subarachnoid hemorrhage. J Am Coll Cardiol 2000; 36:1328–1335.Google Scholar
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; 67:58–63.Google Scholar
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; 30:1214–1223.Google Scholar
36. Vasan, RS, Benjamin, EJ. Diastolic heart failure-no time to relax. N Engl J Med 2001; 344:56–59.Google Scholar
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; 33:1948–1955.Google Scholar
38. Vasan, RS, Benjamin, EJ, Levy, D. Prevalence, clinical features andprognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol 1995; 26:1565–1574.Google Scholar
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; 22:808–815.Google Scholar
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; 90:2772–2779.Google Scholar
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; 28:383–390.CrossRefGoogle ScholarPubMed
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; 29:604–612.Google Scholar
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; 80:1583–1587.Google Scholar
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; 289:194–202.Google Scholar
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; 348:5–14.Google Scholar
46. Ducker, TB. Increased intracranial pressure and pulmonary edema. 1. Clinical study of 11 patients. J Neurosurg 1968; 28:112–117.Google Scholar
47. Ciongoli, AK, Poser, CM. Pulmonary edema secondary tosubarachnoid hemorrhage. Neurology 1972; 22:867–870.Google Scholar
48. Kosnik, EJ, Paul, SE, Rossel, CW, Sayers, MP. Central neurogenicpulmonary edema: with a review of its pathogenesis and treatment. Childs Brain 1977; 3:37–47.Google Scholar
49. Fein, A, Grossman, RF, Jones, JG, et al. The value of edema fluidprotein measurement in patients with pulmonary edema. Am JMed 1979; 67:32–38.Google Scholar
50. Eggleston, CA. Clinical correlation of neurogenic pulmonary edemato increased intracranial pressure. J Neurosurg Nurs 1982; 14:245–254.Google Scholar
51. Lagerkranser, M, Pehrsson, K, Sylven, C. Neurogenic pulmonaryoedema. A review of the pathophysiology with clinical and therapeutic implications. Acta Med Scand 1982; 122:267–271.Google Scholar
52. Melon, E, Bonnet, F, Lepresle, E, et al. Altered capillary permeabilityin neurogenic pulmonary oedema. Intensive Care Med 1985; 11:323–325.Google Scholar
53. Schell, AR, Shenoy, MM, Friedman, SA, Patel, AR. Pulmonary edemaassociated with subarachnoid hemorrhage. Evidence for a cardiogenic origin. Arch Intern Med 1987; 147:591–592.Google Scholar
54. Deehan, SC, Grant, IS. Haemodynamic changes in neurogenicpulmonary oedema: effect of dobutamine. Intensive Care Med 1996; 22:672–676.Google Scholar
55. Smith, WS, Matthay, MA. Evidence for a hydrostatic mechanism inhuman neurogenic pulmonary edema. Chest 1997;111:1326–1333.Google Scholar
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; 4:636–640.CrossRefGoogle Scholar
57. Pinto, RJ, Goyal, V, Sharma, S, Bhagwati, SN. Transient myocardialdys function in a patient with subarachnoid haemorrhage. Int J Cardiol 1994; 46:289–291.Google Scholar
58. Sakka, SG, Huettemann, E, Reinhart, K. Acute left ventriculardys function and subarachnoid hemorrhage. J Neurosurg Anesthesiol 1999; 11:209–213.Google Scholar
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;103:1274–1275.Google Scholar