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Anesth Analg 1999;89:962
© 1999 International Anesthesia Research Society

NEUROSURGICAL ANESTHESIA

An Association Between QTc Prolongation and Left Ventricular Hypokinesis During Sequential Episodes of Subarachnoid Hemorrhage

Daisuke Yoshikawa, MD, Testuya Hara, MD, Kenichiro Takahashi, MD, Toshihiro Morita, MD, and Fumio Goto, MD

Department of Anesthesiology and Reanimatology, Gunma University School of Medicine, Gunma, Japan


   Introduction
Top
 Introduction
Case Report
 Discussion
 References
 
The association of electrocardiographic abnormalities with central nervous system injuries is well recognized. Neurogenic changes in the electrocardiogram (ECG) are common after subarachnoid hemorrhage (SAH) (1,2). Echocardiographic studies have also demonstrated reversible left ventricular wall motion abnormalities in patients with SAH (3–7). We describe a patient with severe reversible left ventricular hypokinesis and QTc prolongation in the settings of two sequential episodes of SAH.


   Case Report
Top
 Introduction
 Case Report
Discussion
 References
 
A 64-year-old woman, without preexisting heart disease, had an acute onset of severe headache and vomiting. On arrival in the emergency room, she was lethargic and disoriented to time and place. Her systolic blood pressure was 60 mm Hg and her heart rate was 110 bpm. A dopamine infusion was started to maintain her systolic blood pressure above 90 mm Hg. There was evidence of QTc prolongation (463 ms) and T-wave inversion in leads V4–6 (Fig. 1A) on the ECG. The hematologic findings were normal, as were the serum electrolyte concentrations. The total serum calcium concentration was 9.0 mg/dL. SAH was demonstrated by computed tomography. Cerebral angiography revealed an internal carotid-posterior communicating artery aneurysm. Two-dimensional echocardiography revealed severe global left ventricular hypokinesis. The apical and mid-ventricular regions were akinetic. In contrast, the basal region was hyperkinetic. The estimated left ventricular ejection fraction (EF) was 30%. The serum creatine kinase (CK) activity was not elevated (peak activity: 170 IU/L, on day 1; normal <180 IU/L), although there was a borderline increase in the CK-MB fraction on SAH Days 1 (2.6%) and 2 (2.0%). The medical consultant advised that surgery should be delayed to minimize the risk of further cardiac complications.



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  		Figure 1. Electrocardiograms after first (A) and second (B) subarachnoid hemorrhage.

 
The patient was transferred to the neurosurgical intensive care unit. Her systolic blood pressure was maintained over 100 mm Hg without dopamine infusion after Day 3. The EF increased to 50% 5 days after SAH, and QTc normalized on Day 5 (Fig. 2). On Day 7, the patient experienced the sudden loss of consciousness and her trachea was intubated to prevent upper airway obstruction. Her systolic blood pressure decreased to <80 mm Hg and dopamine infusion was restarted. Echocardiography revealed severe global left ventricular hypokinesis and the EF decreased to 30% (Fig. 2). ECG revealed new T-wave inversions in leads II, III, aVF, and V3, as well as significant QTc prolongation (500 ms; Fig. 1B). An emergency craniotomy for aneurysm clipping was scheduled. On arrival in the operating room, the patient was comatose (Hunt and Kosnik grade IV). Radial arterial and pulmonary artery catheters were inserted under local anesthesia. Anesthesia was induced and maintained with 50% N2O, 1.5 mg fentanyl IV, and vecuronium IV, as required. Dopamine (3–5 µg · kg–1 · min–1) and olprinone hydrochloride (a phosphodiesterase III inhibitor, 0.2–0.4 µg · kg–1 · min–1) were infused IV continuously to maintain the patient’s blood pressure and cardiac output. The neurosurgical course was uncomplicated, and the patient was transferred to the intensive care unit, sedated, and maintained on a mechanical ventilator.



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  		Figure 2. Serial changes in the QTc (a) and left ventricular ejection fraction (b). SAH = subarachnoid hemorrhage.

 
On the first postoperative day, the patient’s level of consciousness was improved (Glasgow coma scale score: 13). Her EF was 50% and the QTc normalized. Her cardiac function gradually improved, and the EF was 64% on Day 18. The patient was tracheally extubated on the second postoperative day and transferred to the neurosurgical ward 2 days later. Unfortunately, 2 weeks after surgery, she suffered a hemorrhagic infarction of the left temporal lobe caused by vasospasm. Her cognitive function remained impaired after the infarction.


   Discussion
Top
 Introduction
 Case Report
 Discussion
References
 
Echocardiographic studies have demonstrated reversible left ventricular wall motion abnormalities in patients with SAH having no history of preexisting heart disease (3–7). Mayer et al. (5) have reported that abnormal left ventricular wall motion occurred in five (8%) of 57 patients with SAH. Four of these affected patients experienced hypotension (systolic blood pressure <100 mm Hg). Three previous echocardiographic studies of patients with SAH (3,4,6) have reported a similar cumulative frequency for abnormal wall motion (9%, 17 of 184 patients).

Hemodynamic instability and pulmonary edema occur frequently in patients with SAH and wall motion abnormalities (4,6,8), supporting the notion that such injuries may contribute to morbidity and mortality. Because echocardiography is not always performed in patients with SAH, it is important to determine specific markers of myocardial dysfunction in the settings of acute SAH. Mayer et al. (5) studied the relationship between serial ECG changes and left ventricular dysfunction in patients with acute SAH. They reported that the presence of either inverted T waves or severe QTc prolongation had 100% sensitivity and 81% specificity for left ventricular dysfunction. Pollick et al. (6) analyzed ECGs obtained during the first three hospital days in 13 patients with SAH. Inverted T waves were noted in all four patients with wall motion abnormalities compared with one of nine patients with normal echocardiograms (P < 0.01), although the QTc interval did not differ among the two groups. Kono et al. (7) reported that patients with SAH and ST segment elevation had wall motion abnormalities in the left ventricular apex.

In the present case, QTc prolongation and T-wave inversion were noted on the first ECG. As shown in Figure 2, as the patient’s EF increased the QTc normalized. Immediately after her cardiac function decreased with the rerupture of the aneurysm, the QTc increased. In contrast, the T-wave inversions persisted after the first SAH and new T-wave inversions appeared after the second SAH, when cardiac function again decreased. These data suggest that QTc prolongation and new T-wave inversions are good markers of cardiac dysfunction in patients with SAH.

The causes of acquired abnormal QT prolongation include myocardial ischemia, cardiomyopathy, hypokalemia, hypocalcemia, autonomic activity, drug effects, hypothermia, and cerebral lesions (9). Our patient had no previous history of cardiovascular disease. Furthermore, the electrolyte concentrations were normal and the patient received no drugs affecting the QT interval. Acute myocardial ischemia may induce QTc prolongation. Changes in the QT interval often accompany T-wave or U-wave inversions. ECG changes simulating a myocardial infarction pattern have been reported in association with SAH and intracranial hemorrhage (7,10,11). Therefore, it is sometimes difficult to distinguish ECG changes induced by SAH from those caused by ischemic heart diseases.

A sudden increase in intracranial pressure (ICP) stimulates the cortical and subcortical area of the brain, leading to autonomic instability (12,13). Myocardial damage in the setting of SAH frequently is associated with hypothalamic lesions (14). The posterior hypothalamus is responsible for sympathetic control, and its stimulation increases sympathetic tone in dogs (15). In experimental models, catecholamine infusions produce cardiac lesions that are histologically similar to myocardial lesions found at the time of autopsy in patients with SAH (16). Furthermore, in both experimental and clinical intracerebral hemorrhages, cardiac damage is prevented by ß-adrenergic blockade or complete cardiac denervation (17,18). Myocardial damage in the setting of SAH is believed to be a consequence of the massive sympathetic discharge and increase in peripheral vascular resistance that occur in response to increased ICP and/or hypothalamic ischemia.

A sudden increase in ICP induces abnormalities in ST–T-wave morphology and in cardiac rhythm. Furthermore, increases in ICP are associated with hypertension, increased sympathetic activity, and myocardial damage in rats (19). Hypothalamic (20) and cardiac nerve (21) stimulation both produce T-wave inversions and QT prolongation in animal models, indicating that these findings reflect intense myocardial sympathetic activation. Increased sympathetic activity and catecholamine surges are common factors that produce changes in depolarization on the surface ECG and myocardial dysfunction in patients with SAH.

Mayer et al. (5) also reported that peak preoperative CK, lactate dehydrogenase, and serum glutamic-oxaloacetic transaminase levels were significantly higher in patients with abnormal wall motion than in those with normal echocardiograms. They reported that a borderline increase in the serum CK-MB activity (2%–5%) had 100% sensitivity and 94% specificity for left ventricular dysfunction. The present patient had a borderline increase in the serum CK-MB activity on Days 1 and 2. These findings suggest that a borderline increase in the serum CK-MB activity may predict left ventricular dysfunction, although the usefulness of this test for predicting such dysfunction requires further study.

Unrecognized left ventricular wall motion abnormalities may contribute to morbidity and mortality in patients with SAH. These abnormalities are readily detected by two-dimensional echocardiography. T-wave inversion and QTc prolongation are sensitive markers of cardiac dysfunction in patients with SAH and, in addition to obvious ischemic ECG changes (such as abnormal Q waves or ST segment elevation), should be considered indications for echocardiography.


   Footnotes
 
Daisuke Yoshikawa, MD, Department of Anesthesiology and Reanimatology, Gunma University School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371, Japan.


   References
Top
 Introduction
 Case Report
 Discussion
 References
 

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Accepted for publication June 21, 1999.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1999 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press