Hostname: page-component-cd9895bd7-jkksz Total loading time: 0 Render date: 2024-12-19T00:50:22.669Z Has data issue: false hasContentIssue false
  • English
  • Français

QTc dispersion as a marker for medical complications after severe subarachnoid haemorrhage

Published online by Cambridge University Press:  11 July 2005

C. S. A. Macmillan ,
P. J. D. Andrews  and
A. D. Struthers
C. S. A. Macmillan
Affiliation:
University of Edinburgh, Department of Anaesthetics, Western General Hospital, Edinburgh, UK
P. J. D. Andrews
Affiliation:
University of Edinburgh, Department of Anaesthetics, Western General Hospital, Edinburgh, UK
A. D. Struthers
Affiliation:
University of Dundee Medical School, Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital, Dundee, UK
Get access

Extract

Summary

Background and objective: Morbidity from subarachnoid haemorrhage is common and results from complications including myocardial dysfunction and neurogenic pulmonary oedema causing hypotension and hypoxia – both major causes of secondary brain injury. Predicting patients at risk of developing these complications may facilitate early intervention.

Methods: Using QTc dispersion to assess repolarization inhomogeneity, patients who had suffered severe acute subarachnoid haemorrhage were studied in an intensive care unit. Electrocardiograms were recorded within 24 h of ictus. Subsequent development of myocardial dysfunction was defined as a requirement for inotropes, and neurogenic pulmonary oedema as a PaO2 (kPa)/FiO2 ratio <40. Together they constituted cardiorespiratory compromise.

Results: Twenty-seven patients were recruited. QTc dispersion was greater in patients (74.1 ms, SD ± 26.1) than in controls (48.3 ms, 12.0) P < 0.0001, 95% CI 14.6, 37.0. Thirteen patients developed cardiorespiratory compromise and had greater QTc dispersion (84.5 ms, 26.2) than patients who did not develop cardiorespiratory compromise (64.5 ms, 22.7) P = 0.046, 95% CI 0.3, 39.6. There was no difference in QTc dispersion between patients who did and those who did not develop myocardial dysfunction alone. Similarly, there was no difference in QTc dispersion between patients who did and those who did not develop neurogenic pulmonary oedema alone.

Conclusions: Increased QTc dispersion is associated with the later development of cardiorespiratory compromise in poor-grade subarachnoid haemorrhage patients. QTc dispersion may be used as a marker to predict impending clinical deterioration, providing an opportunity for early intervention.

Keywords

HEART FUNCTION TESTS, electrocardiographyINTRACRANIAL HAEMORRHAGES, subarachnoid haemorrhageLUNG DISEASES, pulmonary oedema
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 20 , Issue 7 , September 2003 , pp. 537 - 542
Copyright
© 2003 European Society of Anaesthesiology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Andrews PJD. Medical management of complications following aneurysmal sub-arachnoid haemorrhage. In: Galley HF, ed. Critical Care Focus 1, Neurological injury. London, UK: BMJ Books, 2000: 28–38.
Solenski NJ, Haley ECJ, Kassell NF, et al. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med 1995; 23: 1007–1017.Google Scholar
Gentleman D, Jennett B. Audit of transfer of unconscious head-injured patients to a neurosurgical unit. Lancet 1990; 335: 330–334.Google Scholar
Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 1989; 298: 636–642.Google Scholar
Kassell NF, Haley EC Jr, Apperson-Hansen C, Alves WM. Randomized, double-blind, vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in Europe, Australia, and New Zealand. J Neurosurg 1996; 84: 221–228.Google Scholar
Gabrielli F, Balzotti L, Bandiera A. QT dispersion variability and myocardial viability in acute myocardial infarction. Int J Cardiol 1997; 61: 1–7.Google Scholar
Kelly RF, Parillo JE, Hollenberg SM. Effect of coronary angioplasty on QT dispersion. Am Heart J 1997; 134: 399–405.Google Scholar
Karpanou EA, Vyssoulis GP, Psichogios A, et al. Regression of left ventricular hypertrophy results in improvement of QT dispersion in patients with hypertension. Am Heart J 1998; 136: 765–768.Google Scholar
Kiely DG, Cargill RI, Grove A, Struthers AD, Lipworth BJ. Abnormal myocardial repolarisation in response to hypoxaemia and fenoterol. Thorax 1995; 50: 1062–1066.Google Scholar
Kiely DG, Cargill RI, Lipworth BJ. Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans. Chest 1996; 109: 1215–1221.Google Scholar
Randell T, Tanskanen P, Scheinin M, Kytta J, Ohman J, Lindgren L. QT dispersion after subarachnoid hemorrhage. J Neurosurg Anesthesiol 1999; 11: 163–166.Google Scholar
Gillespie ND, McNeill G, Pringle T, Ogston S, Struthers AD, Pringle SD. Cross sectional study of contribution of clinical assessment and simple cardiac investigations to diagnosis of left ventricular systolic dysfunction in patients admitted with acute dyspnoea. BMJ 1997; 314: 936–940.Google Scholar
Bernard GR, Artigas A, Brigham KL, et al. The American–European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Resp Crit Care Med 1994; 149: 818–824.Google Scholar
Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980; 6: 1–9.Google Scholar
Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; ii: 81–84.Google Scholar
Teasdale GM, Drake CG, Hunt W, et al. A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies. J Neurol Neurosurg Psychiatry 1988; 51: 1457.Google Scholar
Jennett B, Teasdale G, Knill-Jones R. Prognosis after severe head injury. Ciba Foundation Symposium 1975; 309–324.Google Scholar
Brouwers PJ, Wijdicks EF, Hasan D, et al. Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage. Stroke 1989; 20: 1162–1167.Google Scholar
Mayer SA, LiMandri G, Sherman D, et al. Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage. J Neurosurg 1995; 83: 889–896.Google Scholar
Lanzino G, Kongable GL, Kassell NF. Electrocardiographic abnormalities after nontraumatic subarachnoid hemorrhage. J Neurosurg Anesth 1994; 6: 156–162.Google Scholar
Andreoli A, di Pasquale G, Pinelli G, Grazi P, Tognetti F, Testa C. Subarachnoid hemorrhage: frequency and severity of cardiac arrhythmias. A survey of 70 cases studied in the acute phase. Stroke 1987; 18: 558–564.Google Scholar
Miller JA, Dacey RGJ, Diringer MN. Safety of hypertensive hypervolemic therapy with phenylephrine in the treatment of delayed ischemic deficits after subarachnoid hemorrhage. Stroke 1995; 26: 2260–2266.Google Scholar
Cruickshank JM, Neil-Dwyer G, Stott AW. Possible role of catecholamines, corticosteroids, and potassium in production of electrocardiographic abnormalities associated with subarachnoid haemorrhage. Br Heart J 1974; 36: 697–706.Google Scholar
Smith WS, Matthay MA. Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema. Chest 1997; 111: 1326–1333.Google Scholar
Davies KR, Gelb AW, Manninen PH, Boughner DR, Bisnaire D. Cardiac function in aneurysmal subarachnoid haemorrhage: a study of electrocardiographic and echocardiographic abnormalities. Br J Anaesth 1991; 67: 58–63.Google Scholar
Pollick C, Cujec B, Parker S, Tator C. Left ventricular wall motion abnormalities in subarachnoid hemorrhage: an echocardiographic study. J Am Coll Cardiol 1988; 12: 600–605.Google Scholar
Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 1994; 24: 636–640.Google Scholar
Deehan SC, Grant IS. Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. Int Care Med 1996; 22: 672–676.Google Scholar
Schell AR, Shenoy MM, Friedman SA, Patel AR. Pulmonary edema associated with subarachnoid hemorrhage. Evidence for a cardiogenic origin. Arch Int Med 1987; 147: 591–592.Google Scholar
Mayer SA, Fink ME, Homma S, et al. Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage. Neurology 1994; 44: 815–820.Google Scholar
Doshi R, Neil-Dwyer G. A clinicopathological study of patients following a subarachnoid hemorrhage. J Neurosurg 1980; 52: 295–301.Google Scholar
Marion DW, Segal R, Thompson ME. Subarachnoid hemorrhage and the heart. Neurosurgery 1986; 18: 101–106.Google Scholar
Todd GL, Baroldi G, Pieper GM, Clayton FC, Eliot RS. Experimental catecholamine-induced myocardial necrosis. I. Morphology, quantification and regional distribution of acute contraction band lesions. J Mol Cell Cardiol 1985; 17: 317–338.Google Scholar
Ferrans VJ, Hibbs RG, Weily HS, Weilbaecher DG, Walsh, JJ, Burch GE. A histochemical and electron microscopic study of epinephrine-induced myocardial necrosis. J Mol Cell Cardiol 1970; 1: 11–22.Google Scholar
Knudsen F, Jensen HP, Petersen PL. Neurogenic pulmonary edema: treatment with dobutamine. Neurosurgery 1991; 29: 269–270.Google Scholar
Reardon M, Malik M. QT interval change with age in an overtly healthy older population. Clin Cardiol 1996; 19: 949–952.Google Scholar
Pfeifer MA, Weinberg CR, Cook D, Best JD, Reenan A, Halter JB. Differential changes of autonomic nervous system function with age in man. Am J Med 1983; 75: 249–258.Google Scholar
Michaloudis D, Fraidakis O, Kanoupakis EW, Flossos A, Manios E. Idiopathic prolonged QT interval and QT dispersion: the effects of propofol during implantation of cardioverter-defibrillator. Eur J Anaesthesiol 1999; 16: 842–847.Google Scholar