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NEUROSURGICAL ANESTHESIA

Delayed Cardiogenic Shock and Acute Lung Injury After Aneurysmal Subarachnoid Hemorrhage

Division of Critical Care and Division of Critical Care Neurology, Mayo Medical Center, Saint Marys Hospital, Rochester, Minnesota

Address correspondence and reprint requests to Eelco FM Wijdicks, MD, Department of Neurology, 200 First Street SW, Rochester, MN 55901. Address e-mail to wijde{at}mayo.edu.

	Abstract

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Both cardiac and lung injury after aneurysmal subarachnoid hemorrhage has been attributed to an adrenergic surge. Cardiogenic shock is very uncommon. We describe a 55-yr-old woman with a delayed cardiogenic shock emerging within hours after aneurysmal rupture. Cardiac damage was documented by increased serum troponin T, CPK-mb fraction, and severe wall motion abnormality, which included an akinetic apex on echocardiography (ejection fraction of 33%). Her coronary angiogram was normal. Decreased cardiac index, increased systemic and pulmonary vascular resistance indices, and persistent oxygen desaturation despite improving ventricular contractility documented both cardiac and pulmonary injury. After treatment with dobutamine and milrinone all manifestations resolved.

	Introduction

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The coexistence of cardiac injury and aneurysmal subarachnoid hemorrhage (SAH) is well established. Cardiac injury ranges from insignificant electrocardiographic abnormalities to actual impaired pump function and shock. Patients in a poor grade SAH (World Federation of Neurological Surgeons [WFNS] grade 4 or 5) more commonly show cardiac injury, and the prevalence of poor ventricular function is frequent in patients progressing to brain death (1). True cardiac shock is much less common. We describe a delayed onset of cardiac shock with evolving pulmonary injury, reversed after treatment with positive inotropic drugs.

	Case Report

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A 55-yr-old woman was admitted in a hemodynamically stable condition but remained comatose (WFNS grade 4) after a rupture of an anterior communicating aneurysm. Eight hours later, she suddenly developed profound hypotension refractory to fluids and vasopressors (phenylephrine and norepinephrine).

On arrival to the neurological-neurosurgical intensive care unit, the patient was already tracheally intubated, had an external ventricular drain, the Glasgow Coma Scale score had decreased to 4, the systolic arterial blood pressure was 60 mm Hg, heart rate was regular 75 beats/min, and respiration was 20 breaths/min. Auscultation of the lungs now revealed bilateral crackles. A repeat head computed tomographic scan showed no rebleeding. The electrocardiogram revealed worsening and marked ST depression and the chest radiograph showed a rapid evolution of bilateral infiltrates (Fig. 1). Echocardiography showed multisegmental wall motion abnormalities and an akinetic apex. Her ejection fraction was 33% (Fig. 2, right). A coronary angiogram was normal with only minimal atherosclerotic disease.

View larger version (53K): [in this window] [in a new window]   Figure 1. Serial chest radiograph (taken within several hours from left to right) documenting development of marked pulmonary infiltrates ("whiteout") and enlarging heart shadow. Pulmonary infiltrates remained on follow-up despite improvement in heart shadow.

View larger version (10K): [in this window] [in a new window]   Figure 2. Left to right: Schematic drawing of echocardiographic abnormalities. The segments shown are at base, mid, and apex. Dark areas represent an akinetic segment; gray areas represent a hypokinetic segment. The marked improvement in ventricular function is notable. A third echocardiography performed 20 days later (not shown) showed completely normal function.

The initial pulmonary artery catheter measurements on norepinephrine were cardiac index (CI) 1.9 L/min/m², pulmonary artery occlusion pressure (PAOP) 10 mm Hg, systemic vascular resistance (SVRI) 2700 dynes · s/cm⁵ · m², and pulmonary vascular resistance (PVRI) 500 dynes · s/cm⁵ · m². Arterial oxygenation changed from a Pao₂ 242 mm Hg to 79 mm Hg on mechanical ventilation (MV) (intermittent MV/pressure support, fraction of inspired oxygen (Fio₂) of 100% and positive end-expiratory pressure of 10 cm H₂O). Her serum lactate was 6.3 mmol/L (0.5–2), troponin T 97 ng/mL (<0.03), and CK-mb 3.7 ng/mL.

Her hemodynamic state improved with the addition of IV dobutamine, allowing rapid discontinuation of norepinephrine and phenylephrine and liberation of MV. The bilateral pulmonary infiltrates and the requirement of Fio₂ of 50% with continuous positive airway pressure of 5 cm H₂O persisted. The Pao₂/Fio₂ ratio remained <250 for a week with gradual improvement thereafter.

On day 3, a decrease in systolic blood pressure to approximately 80 mm Hg led to the following hemodynamic measurements: CI, 2.01 L/min/m²; SVRI, 2738 dynes · s/cm⁵ · m²; and PVRI, 481 dynes · s/cm⁵ · m², which suggested both a cardiac and a pulmonary component as the patient was not receiving any pressors. IV milrinone was started, further improving the hemodynamic variables and resulting in the following readings: CI, 3.59 L/min/m²; SVRI, 1776 dynes · s/cm⁵ · m²; and PVRI, 156 dynes · s/cm⁵ · m²; however, there was limited Pao₂/Fio₂ ratio improvement, which slowly resolved.

A follow-up echocardiogram 1 wk later revealed resolution of the wall motion abnormalities and an improvement of the ejection fraction from 33% to 45% (Fig. 2, left). A third echocardiogram 20 days later was completely normal, with an ejection fraction of 60%.

The anterior communicating aneurysm was successfully treated with platinum coils. She was discharged home with some cognitive impairment.

	Discussion

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In the immediate aftermath of SAH, plasma troponin level can be increased, and a baseline electrocardiographic recording can clearly indicate myocardial injury. In clinical practice, the distinction between stress-induced myocardial infarction in a patient with undiagnosed coronary artery disease or pure catecholamine-induced myocytolysis attributable to contraction band necrosis is difficult, if not impossible, without a coronary angiogram (2). Such a finding has immediate repercussions for general anesthesia when clipping or coiling of the aneurysm is contemplated. However, very few reports have excluded large vessel coronary artery disease objectively, and none of them was in circumstances of shock in the context of SAH or had hemodynamic measurements (3–7). Moreover, the opportunity to study the development of cardiopulmonary injury after SAH in detail using pulmonary artery catheter measurements and serial echocardiography has not been reported. We believe our case report is thus unique and further adds to the understanding of this fascinating phenomenon.

Our patient had a severe myocardial injury and shock after aneurysmal subarachnoid hemorrhage with a level of troponin much higher than suggested for only stunning of the myocardium (2). Our case report clearly suggests that the degree of myocardial injury as measured by troponin (more than 3000-fold) and cardiogenic shock can be very profound but without coronary abnormalities and thus completely attributable to SAH.

After improvement of ventricular contractility, additional independent lung injury was suggested using pulmonary artery catheter measurements. Our observation suggests a dual impact rather than cardiogenic pulmonary dysfunction.

Sudden depression of the ventricular contractility has been reported in animal models (8) and in case series (9–11). Bombastic terms ("panic myocardium, stunning myocardium and catecholamine storm") have been used to denote the consequences of catecholamine surge after SAH (12). When available, pathological analysis points to myocardial injury that does not follow any particular coronary distribution, but the apex, as a result of its high adrenergic innervation, is preferentially involved (13,14).

Pulmonary edema in SAH can be secondary to cardiac failure (hydrostatic) and can also meet the criteria for acute respiratory distress syndrome (non-hydrostatic) (15,16). The mechanisms cannot be completely explained by inflammation; in fact, damage to the endothelium and basement membrane have been noted, and increased PVR could play a role (17,18). In our patient, the pulmonary artery catheter indicated a decreased CI, increased SVRI, and a PAOP of 10 mm Hg, suggesting cardiogenic shock, but the persistent hypoxemia, bilateral pulmonary infiltrates, a PAOP of <15 mm Hg, and the increased PVRI suggested an independent pulmonary injury. This was also supported by the observation that these indices improved with dobutamine and milrinone without significant improvement in the level of oxygenation.

The treatment of low cardiac output states warrants the use of inotropic drugs aiming at the increase of organ perfusion and tissue oxygen delivery. Drug treatment of critically ill patients with intrinsic myocardial failure includes primarily ß1-adrenergic stimulation (e.g., dobutamine) or phosphodiesterase inhibition (milrinone). Both dobutamine and milrinone, acting through different pathways, result in significant improvement of cardiac myocyte inotropy, chronotropy, dromotropy, and lucitropy (enhanced diastolic myocardial relaxation), along with enhanced peripheral and pulmonary vasodilatation. These drugs are therefore specifically indicated in cases of cardiogenic shock of any etiology.

	Footnotes

 
Accepted for publication September 27, 2004.

	References

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