General chest ultrasound in neurocritical care

Published on 22/03/2015 by admin

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General chest ultrasound in neurocritical care


Neurocritical care patients often require hemodynamic monitoring to optimize cerebral blood flow and brain tissue oxygen delivery. Hemodynamic monitoring also aids in the management of usual coexisting disorders, such as acute lung injury and acute respiratory distress syndrome (ARDS), as well as shock states.1 General chest ultrasound (see Chapter 1), which consists of cardiovascular and lung ultrasound, is a noninvasive bedside tool that facilitates hemodynamic monitoring in modern neurocritical care. The manipulation of the cardiac output (CO), mean arterial pressure (MAP), systemic filling pressures and volumes, as well as the assessment of dynamic markers of fluid responsiveness and evaluation for pulmonary edema are all essential in optimizing cardiorespiratory function in the acutely brain- or spinal cord–injured patient. This chapter illustrates the role of general chest ultrasound in neurocritical care.

Cardiovascular evaluation in neurocritical care

Recommended transthoracic echocardiography (TTE) should include two-dimensional sector scanning, color Doppler flow mapping, as well as pulsed and continuous wave Doppler interrogation (see Chapter 26). The standard parasternal long-axis, short-axis, and apical two- and four-chamber views are used for analysis of left ventricular (LV) dysfunction. LV ejection fraction (EF) can be visually rated as normal (LVEF, 50%-55%) and mildly (LVEF, 40%-54%), moderately (LVEF, 30%-39%), or severely (LVEF < 30%) depressed.

In neurocritical care, patients with aneurysmal subarachnoid hemorrhage (SAH) and other neurologic events may be hemodynamically compromised. Many of these patients have electrocardiographic (ECG) abnormalities (ST-T-segment changes, QT prolongation, U-waves, and arrhythmias), variably elevated myocardial enzymes, and LV dysfunction. In such cases, TTE is essential in diagnosing a severely reduced CO on the grounds of neurogenic stunned myocardium (NSM). The latter has been reported in SAH, metastatic brain tumors, seizures, subdural hematoma, brain contusion, reversible posterior leukoencephalopathy syndrome, encephalitis, hydrocephalus, Guillain-Barré syndrome, acute myelitis, and ischemic strokes. Current pathophysiologic concepts suggest that the cardiac injury may be due to increments in the sympathetic stimulation of the myocardium. This concept is further supported by a characteristic histopathologic pattern of catecholamine-induced myocardial cell death that was retrieved from the autopsies in such cases; however, analyzing this further is beyond our scope.

An intriguing syndrome that overlaps substantially with NSM is takotsubo cardiomyopathy (TCM), also known as apical ballooning syndrome or “broken heart” syndrome.2 Originally described in the Japanese population, this syndrome is characterized by transient LV dysfunction that produces a distinctive configuration during systole on the ventriculogram that resembles a Japanese octopus catcher pot. The diagnostic features of takotsubo cardiomyopathy include reversible LV regional wall motion abnormalities beyond a single coronary artery distribution (typically involving the LV apex and midventricle, with relative sparing of the basal segment), ECG abnormalities, minor elevation in cardiac markers, and absence of significant coronary artery disease. LV ballooning depicted by TTE in TCM is usually apical, although midventricular and basal ballooning may be rarely observed. The terminology is still ambivalent because it was lately suggested that TCM should not be referred to as apical ballooning syndrome. Moreover, the overlapping with NSM is obvious. Outside of the neurocritical care setting, both syndromes may occur in postmenopausal women after a stressful event and are accompanied by a massive catecholamine surge.

Of note, the Mayo Clinic criteria for classifying a stress-induced cardiomyopathy consist of transient wall motion abnormalities of the LV midsegments (with the regional wall motion abnormalities extending beyond a single epicardial artery distribution in the absence of obstructive coronary artery disease, pheochromocytoma, or myocarditis), with or without apical involvement, and new ST-segment elevation and/or T-wave inversion or modest elevation in cardiac troponins. NSM fits these criteria with the exception that it allows global LV dysfunction without regional wall motion abnormalities as observed in TCM. Hence this remains largely an issue of classification of various echocardiographic findings. A summary of NSM features is presented in Table 7-1.


Neurogenic Stunned Myocardium

Clinical setting Acute brain insult
High intracranial pressure
Sudden emotional stress
Clinical presentation Biventricular failure
Cardiogenic shock
Echocardiography Apical hypokinesis/ballooning
Hypercontractile base
Dynamic left ventricular outflow obstruction
Mitral regurgitation
Coronary angiography Absence of occlusive coronary artery disease
Serum cardiac markers Troponin elevation of a lower degree than from coronary artery occlusion for similar cardiac function
Lung ultrasound and radiography Pulmonary edema (cardiogenic features)
Hemodynamic monitoring Depressed biventricular output
Elevated filling pressures
Dynamic preload variables suggesting plateaued ventricular function (Frank-Starling curve)
Clinical management Vasopressor and inotropic support guided by cardiac ultrasound and invasive hemodynamic monitoring
Intraaortic balloon pump to be considered in refractory cases
Prognosis Favorable

Despite the aforementioned terminology issues, in neurocritical care, both syndromes have a favorable prognosis because, with supportive measures, LV function spontaneously ameliorates within days, whereas in-hospital mortality remains less than 1%.35 However, cardiogenic shock requiring mechanical circulatory support and rare complications, including LV apical thrombus or fatal LV rupture, have been occasionally reported.6,7

Although uncommon, dynamic obstruction within the LV outflow tract should be evaluated because it has been described with apical ballooning syndrome and is believed to be caused by compensatory hyperkinesis of the basal segments. This obstruction can be exacerbated by low filling pressures or decreased afterload. Mitral valve regurgitation (MR) can be encountered, resulting from acceleration of blood through the dynamic obstruction, leading to a Venturi effect, with the anterior mitral leaflet being sucked into the LV outflow tract. As a result, significant hypotension could be expected secondary to both poor LV systolic function, as well as dynamic obstruction of the LV outflow tract. In this setting, avoiding the administration of systemic vasodilators and inotropic stimulation, which can worsen the outflow tract gradient, is a prudent therapeutic strategy. In addition, fluids should be cautiously used because patients often have elevated left-sided filling pressures and evidence of pulmonary edema.8

Preload and responsiveness

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