Cardiac injury has been acknowledged as a consequence of acute brain injury and often is associated with clinical manifestations. The observation that electrocardiographic (EKG) abnormalities and even brief cardiac arrhythmias are common soon after the ictus may not necessarily cause concern. In fact, for many cardiologists the question of whether these changes either are typically fitting with the neurologic injury or signal a greater problem is not really a question—the changes are usually benign.1 Arrhythmias may arise from certain regions in the brain, including the insular cortex, cingulate cortex, and the amygdala, but the connection is not so clear in clinical practice, where there is often more widespread or multifocal hemispheric involvement (see volume Recognizing Brain Injury).17,30
The problem in part is that one should not accept that cardiac manifestations with acute brain injury are a minimal risk. Brief tachyarrhythmias causing demand ischemia—leading to serum troponin leak—are likely underrecognized. This may occur in previously healthy patients but is more likely in patients with prior (known or, more likely, previously unknown) coronary or myocardial disease.2,36
The question of whether the patient with acute brain injury is developing a cardiac syndrome is highly pertinent and urgent. The presentation usually includes new EKG changes, and these abnormalities could closely resemble acute ST-segment myocardial infarction (STEMI) or non-STEMI. In other patients, there are new cardiac arrhythmias such as supraventricular and ventricular ectopy, tachycardia, and atrial fibrillation.
Underlying heart failure or coronary syndrome is common in patients who are admitted after an ischemic stroke.5 Obesity, in itself, increases the risk of coronary artery disease and sleep apnea with or without pulmonary hypertension, deep vein thrombosis, and pulmonary emboli, all of which are more prevalent. Any patient with a history of ischemic heart disease, prior stroke, history of decompensated heart failure or prior heart failure, diabetes mellitus, or renal insufficiency may warrant further assessment, certainly if a major endovascular procedure under anesthesia or a surgical procedure is anticipated.3 Conditions that require intensive care management are: unstable coronary syndromes, including unstable or severe angina or a prior myocardial infarction; decompensated heart failure, supraventricular arrhythmias with a ventricular rate of >100 beats/min, symptomatic bradycardia, and newly recognized ventricular tachyarrhythmia. Any heart valve disease that includes severe aortic stenosis or symptomatic mitral stenosis also places the patient at increased risk during any procedure that may include surgery.
There are unique challenges when it comes to cardiac complications. How much is really within the provenance of an attending neurologist? When is a cardiologist urgently needed for advice? What can be expected in certain acute neurologic disorders, and which patients need more close monitoring? This involves a basic assessment but also recognition of acute coronary syndromes, treatment of acute atrial fibrillation, and evaluation for a temporary pacemaker. Full justice cannot be granted to this topic here, but this chapter highlights the most commonly encountered problems and frequent cardiac management concerns in acutely ill neurologic patients.
The first core principle is a comprehensive cardiac evaluation. Any physician should obtain a simple set of data that could classify the patient in a certain risk category. This includes a full “bare essentials” cardiac examination. History of unstable angina is important but likely not readily available or known. Cardiac auscultation may yield important findings. Specific attention should be directed toward new regurgitation murmurs, abnormal heart rhythms, and abnormal cardiac heaving or thrusting. Most patients with uncomplicated STEMI or non-STEMI have a normal blood pressure. With emerging cardiogenic shock and when systolic blood pressure declines below 90 mm Hg, the skin may become cool and clammy—due to global decrease in cerebral perfusion patients become disoriented and confused. The heart rate may increase or decrease, often depending on whether left ventricular failure is emerging. Respiratory rate is normal in most acute cardiac manifestations, but periodic breathing may signal the appearance of cardiac failure.
Auscultation of the heart is a specialized skill that only experienced cardiologists have, but there are simple observations that can be useful. Generally the clinical finding with the highest accuracy for predicting heart failure is a third heart sound. Appearance of a third sound (gallop rhythm) indicates left ventricular dysfunction—all best heard at the apex with a left recumbent turn of the patient—and a result of increased filling pressure of the left ventricle. Diffuse wheezing and rales are also signs of profound left ventricular failure. The cardiac evaluation is summarized in Table 4.1.
Table 4.1 Cardiac Evaluation
A second core principle is to assess the patient’s volume status. Is there volume overload or low cardiac output? Jugular venous pressure may be increased or normal in patients with heart failure and is not a useful test if not examined with assessment of the hepatojugular reflux (compression of the right upper quadrant for one minute with persistent rise of the jugular venous pressure after release). Its presence is highly indicative of increased cardiac filling pressures. Pulsus alternans (strong beat followed by a weak beat) is diagnostic of a low-output state, but most patients are also cool, dry, have facial pallor, and may have peripheral cyanosis.
A third core principle in early evaluation of a patient with a possible cardiac syndrome is to specifically look for high-risk electrocardiograms, those that predict serious cardiac arrhythmias. An admission electrocardiogram should be carefully scrutinized for the presence of Q waves, significant ST elevation or depression (deviation of 0.5 mm or more), increased QT interval, or a new bundle branch block. Any of these abnormalities should be explained and possible causes identified.
A fourth core principle is to know how and why to obtain more specific tests. This includes serum cardiac troponin and B-type natriuretic peptide (BNP). Cardiac troponins are proteins that control the calcium-mediated interaction between actin and myosin. The troponin complex consists of troponin C, which binds calcium; troponin I, which binds actin-myosin interactions, and troponin T, which attaches to the troponin complex by binding to tropomyosin and improves contraction. BNP is elevated in congestive heart failure. Of greater importance, a normal BNP virtually excludes heart failure and is useful if the diagnosis is uncertain.
If there is a serious evolving situation patients will need a bedside echocardiogram. This study provides information regarding left and right ventricular failure, ejection fraction, chamber size, regional wall motion, and estimation of right ventricular pressure to anticipate pending pulmonary hypertension. The presence of a thrombus, pericardial effusion, valvular dysfunction, or valvular strands is an important piece of information.
There are several clinical dilemmas that come up frequently. Many decisions are made on an ad hoc basis and may often early involve a cardiologist’s opinion. Further details can be found in the volume Recognizing Acute Brain Injury.
Approach to Myocardial Ischemia
Serum troponin can be used to exclude (“rule out”) myocardial infarction or diagnose (“rule in”) myocardial infarction. Common sense, however, dictates that it takes multiple parameters to diagnose myocardial infarction.7,11 One important lesson is not to get too intimidated by elevations of serum troponin in acutely ill neurologic patients.9,12,13,16 Troponin leaks do indicate myocardial injury and can be a result of any acute brain injury with hypertension causing acute ventricular strain.27,28 However, in itself, an isolated elevation of troponin level does not indicate an acute coronary syndrome. The significance of cardiac troponin increase is a commonly asked question. The serum cardiac troponin level in normal individuals is considered to lie within the range of 0.1–0.2 ng/L, and this is due to normal myocyte loss.31,35 The sensitivity of troponin T measurements has significantly improved, and this high-sensitivity of cardiac troponin I and T may cause difficulties with its interpretation. Usually cardiac troponin can be detected about 2 hours after onset of myocardial injury, but if the clinical suspicion is high, blood samples will have to be redrawn 3–6 hours later. Cardiac troponin levels can remain elevated up to 7 days for troponin I and 2 weeks for troponin T. Generally, peak troponin T indicates infarct size and is a reliable predictor of left ventricular function at 3 months and major adverse effects at 1 year.26 Elevated troponin T is also predictive of 30-day mortality in a patient with acute myocardial ischemia. But, if by 6 hours after the onset of symptoms the troponin is not elevated, the chance of a myocardial infarction is very low.
For neurologists, it is important to know that most patients with stress cardiomyopathy have only a modest rise in cardiac troponin that peaks within 24 hours. The magnitude of increase in cardiac troponin is much less than that measured in STEMI, and there is also a less steep rise. Troponin T, more than 0.6 ng/mL, or troponin I, more than 0.5 ng/mL does not fit with neurogenic stress cardiomyopathy.31 There are also many nonthrombotic causes of increased cardiac troponin, including demand ischemia in patients with supraventricular tachycardia or during atrial fibrillation with rapid ventricular response, significant anemia, hypotension, or hypovolemia. Cardiac troponin may also be increased by direct myocardial damage from contusion or chest trauma; and can be seen as a result of myocarditis, prior chemotherapy, direct-current cardioversion, or cardiac surgery. Pulmonary emboli or pulmonary hypertension may cause myocardiac strain and result in elevated troponin. Chronic (or acute on chronic) renal failure and sepsis are also well-known causes of an elevated cardiac troponin.11 Generally, increase in troponin can be seen in stable angina where the numbers are approximately 0.01 mcg/L. A small myocardial infarction or myocarditis or pulmonary emboli is typically in the 1 mcg/L range. A large territorial myocardial infarction is between 10 and 100 mcg/L.
Cardiac troponin has been found increased after every acute brain injury, but all studies have reported random values with wide intervals between measurement and ictus and no consistent correlations with outcome. Cardiac troponin can increase after any type of ischemic or hemorrhagic stroke and has been related to prognosis.22,24 Mostly the prevalence varies between 0% and 35% and contractile dysfunction and EKG changes such as ST depression and ST-wave inversion are also seen in these patients. Patients with increased troponin levels after an acute stroke additionally often have features of myocardial ischemia on EKG and a greater risk of mortality than patients who do not have a troponin rise.14,15
In general, a measurement of cardiac troponin within the first hour after presentation with evidence of a change (∆) within first hours, coupled with the clinical picture and abnormal echocardiogram, and certainly if troponin levels are sufficiently high, should warrant cardiologic consultation and appropriate medical therapy.
Approach to Stress Cardiomyopathy
Stress cardiomyopathy may present with “flash” pulmonary edema and relative hypotension progressing to severe hypotension. In these instances neurogenic pulmonary edema is often wrongly diagnosed, and cardiac failure is not considered. For most physicians more common considerations in acute cardiac failure, are acute systolic or diastolic dysfunction, acute valvular dysfunction, new cardiac arrhythmia, acute myocardial infarction, and free wall rupture or pericardial tamponade. Sepsis or long-standing cardiovascular surgery and prolonged cardiopulmonary bypass are other causes. Stress cardiomyopathy is common after a brain injury but often is not considered. Conditions predisposed to it are aneurysmal subarachnoid hemorrhage (SAH), status epilepticus and posterior reversible encephalopathy syndrome (PRES).
The diagnosis of stress cardiomyopathy is based on several criteria: (1) a major acute unexpected stressful event or acute brain injury; (2) transient left ventricular wall motion abnormalities involving the apical or midventricular myocardial segments but with wall motion abnormalities extending beyond the single epicardial coronary distribution; (3) absence of obstructive coronary artery disease or angiographic evidence of acute plaque rupture that could be responsible for the observable wall motion abnormality; and (4) new EKG abnormalities such as transient ST elevation or diffuse T-wave inversion or troponin elevations (Table 4.2).4 Clinical management includes consideration of early treatment with β-blockers, but also inotropes. The treatment of stress cardiomyopathy is largely determined by its presentation.18,19,20,38 Usually, patients have a decreased ventricular function but are not in shock. In these patients, close observation, avoidance of fluid overload, and cardiac rhythm control, if needed, is sufficient, and the abnormalities will reverse.
Table 4.2 Diagnostic Criteria Proposed by Mayo Clinic for Apical Ballooning Syndrome
Source: From reference 4.
If shock occurs, patients need to be treated immediately and aggressively. If the patient has developed acute heart failure with congestion, intravenous vasodilators are used with diuretics. Vasodilators, however, cannot be used if there is symptomatic hypotension. In patients with cardiogenic shock, defined as significant hypotension of systolic blood pressure <90 mm Hg due to impaired contractility, high intracardiac filling pressures, and marked tissue hyperperfusion, intravenous inotropes should be administered acutely. Mostly dopamine is administered at a dose of 5–20 mcg/kg/min. Dopamine increases contractility and heart rate through activation of the β-adrenergic receptors and also mediates vasoconstriction through the activation of α-receptors in the periphery.32,33 A much less attractive option is IV norepinephrine, which increases afterload without significantly increasing cardiac output.
In certain circumstances, dopamine and milrinone (a phosphodiesterase inhibitor) can significantly increase cardiac output through peripheral vasodilatation and reduction in cardiac afterload. Milrinone reduces right and left ventricular filling pressures but also mean arterial pressure. Therefore, there is a risk of hypotension with milrinone; moreover, the drug also has a long half-life, making it a somewhat complicated drug in this setting. In extreme instances, a severe stress cardiomyopathy with hypotension has been treated with an intraaortic balloon counterpulsation pump (IABP).25 These balloon pumps are based on counterpulsation, where blood pumped or displaced is synchronized with the normal cardiac cycle. It augments the diastolic pressure and reduces systolic pressure. It reduces left ventricular afterload and left ventricular wall tension and, through that, diminishes the oxygen demand. This will eventually lead to higher mean arterial pressures.
Another presentation of acute cardiac failure syndrome is severe hypertension with pulmonary congestion. Many of these patients have good left ventricular function but poor diastolic function, which results in acute pulmonary edema due to increased pulmonary capillary wedge pressure. Systolic heart failure is often associated with renal failure and a result of marked hypoperfusion. Worsening renal failure leads to fluid retention and worsening cardiac failure. Continuous renal replacement therapy allows both control of intravascular volume and correction of electrolytes.
To summarize, management of stress cardiomyopathy may involve hemodynamic augmentation, but exposing patients to a sympathetic pressor agent such as phenylephrine or norepinephrine to combat hypotensive effects should be considered counterintuitive given that catecholamine toxicity is likely a mechanism contributing to the original cardiac damage. Therefore these patients are better treated with inotropic medications such as dopamine or other inotropic agents such as milrinone. The mainstay of treatment of acute cardiac failure remains adequate oxygenation (may require noninvasive ventilation or endotracheal intubation), pain control with IV morphine, diuretics, and blood pressure control. Treatment of acute cardiac failure with pulmonary edema requires aggressive diuresis with IV furosemide but not exceeding 100 mg in the first 6 hours. Replacement of potassium and magnesium is needed. Vasodilators (sodium nitroprusside and nitrates) are only administered in patients with hypertensive type of congestive heart failure and have been controversial due to their potential for hypotension (and decrease in coronary perfusion) and reflex tachycardia. Inotropic support with dopamine or dobutamine and milrinone (in refractory cases) is needed in some patients, but vasopressors and vasopressin can be considered. Intraaortic balloon pump counterpulsation or extracorporeal membrane oxygenation are last-resort options.21,34
It is also often pertinent to improve fluid overload and congestion with loop diuretics such as furosemide infusion of 1 to 5 mg/h. Higher doses of furosemide may be needed but should not exceed 20 mg/h because of a considerable risk of permanent deafness from furosemide-induced cochlear damage. It also requires frequent electrolyte measurements and supplementation. Intravenous vasodilators such as nitroprusside decrease preload and afterload but can only be used if there is no evidence of hypotension or risk of hypotension. It also has been established that angiotensin-converting-enzyme (ACE) inhibitors cannot be used in these patients until at a later stage when the patient is more stabilized. It is equally important not to start or increase β-blockade in cases of decompensated heart failure.
Approach to an Acute Coronary Syndrome
The major proportion of acute coronary syndromes is non-STEMI in about 2/3 of all myocardial infarctions.10 STEMI is a life-threatening clinical syndrome that—in neurologic patients—may not be associated with chest pain or pressure but may manifest itself with shortness of breath, nausea, and vomiting in comatose patients with acute brain injury. Many EKG changes falsely suggest STEMI and turn out to be transient repolarization disturbances not related to myocardial injury. Patients with coronary artery disease who develop an acute brain injury, however, may have an acute or partial occlusion of the coronary artery as a result of activation of the sympathetic nervous system resulting in catecholamine circulation.
STEMI criteria are well defined by the American College of Cardiology and the American Heart Association (Table 4.3).3 After the diagnosis is established by EKG, troponin, echocardiography, or coronary angiogram, the therapy of acute coronary syndromes is reasonably well established and all patients should immediately receive 325 mg of chewable aspirin (Figure 4.1). Aspirin reduces mortality by 25% and blocks β-activation by limiting thromboxane production via the cyclooxygenase pathway.20 Current guidelines recommend against the routine use of β-blockers for acute STEMI. The administration of β-blockers to patients with acute coronary syndromes may lead to increased incidence of cardiogenic shock and may nullify the reduction of recurrent ischemia and reinfarction following reperfusion therapy.6,8,37 It is important to rapidly establish whether the patient is a candidate for revascularization either through administration of fibrinolytic therapy or primary percutaneous coronary intervention. In patients with acute neurologic disease, fibrinolytic therapy is often contraindicated because of the presence of an intracranial hemorrhage, recent ischemic stroke, recent traumatic brain injury, or even the presence of a brain tumor. The common presence of hypertension, with a diastolic blood pressure >100 mm Hg, in patients with acute brain injury is also a relative contraindication. Therefore, it is imperative in these patients to provide immediate reperfusion therapy and percutaneous coronary intervention (PCI) in a cardiac catheterization laboratory.23,29,33 PCI may be problematic in acute brain injury (recent cerebral hemorrhage, large territorial cerebral infarction, hemorrhagic contusions, ventriculostomy in situ, and so forth) given the need for anticoagulation or dual antiplatelet agents to maintain stent patency.
Table 4.3 American College of Cardiology/American Heart Association ST-Segment Elevation Myocardial Infarction (STEMI) Diagnosis Guidelines
Source: From reference 3.
Approach to Tachyarrhythmia
Cardiac arrhythmias are usually innocuous after acute neurologic illness but become concerning if patients have developed myocardial injury or have preexisting morbidity. A first important check is to see whether common causes for cardiac arrhythmias have been excluded. These are: drugs prolonging QTc interval (often haloperidol and atypical antipsychotics), antiepileptic drugs in high doses, therapeutic hypothermia or other cooling intervention, high doses of propofol, and displacement of a central catheter in the atrium. These are all correctable causes. The three most common tachyarrhythmias that are seen in a acutely ill neurologic patient are sinus tachycardia, supraventricular tachycardia and atrial fibrillation with rapid ventricular response (Figure 4.2). Sinus tachycardia is most common and mostly due to dehydration and a compensatory response to hypotension. It may be pain or agitation too. Fluid bolus are usually helpful and rate improves. Supraventricular tachycardia is often due to illness and improves with carotid massage or adenosine followed by metoprolol.
Atrial fibrillation with a subsequent development of rapid ventricular response is a quite common occurrence after acute brain injury.38 In some instances it may have been facilitated by discontinuation of medication to allow “permissive hypertension.” The main principle is to control the rapid ventricular rate, particularly if it results in a hemodynamic unstable arrhythmia. The approach is usually to slow the ventricular rate with either a β-blocker or a calcium channel blocker. Digoxin has a slow onset of action and therefore is not useful in acute treatment. Digoxin, however is a very useful long-term agent and should not be easily dismissed as treatment. Acute control of atrial fibrillation with rapid ventricular response can be attained with the use of metoprolol given as an intravenous bolus of 5 mg slowly over 2 minutes. (It may be repeated every 5 minutes to a total dose of 15 mg.) An alternative approach is to use an esmolol bolus of 5 mg/kg followed by an infusion starting at 100 mcg/kg/min and increasing to 200 mcg/kg/min. Calcium channel blockers have become most frequently used, and diltiazem given via intravenous bolus of 0.25 mg/kg followed by an infusion of 5–15 mg/h often will control the ventricular rate within a matter of minutes. Direct-current cardioversion may be indicated in unstable patients or those refractory to medical therapy.
Bradycardias are commonly seen in acute brain injury and may have no consequences if the patient remains asymptomatic. It is a common occurrence in patients with a new mass, acute hydrocephalus, crowded posterior fossa due to tumor, and in the setting of dysautonomia in acute neuromuscular disease. Symptomatic bradycardia (usually syncope with hypotension) is an indication for temporary pacing. It may particularly be needed if the patient has a reversible condition such as antiarrhythmic drug therapy overdose, or in the setting of acute myocardial infarction. IV atropine usually suffices, but if it reoccurs pacing may be needed. Indications for pacing are in Table 4.4.
Table 4.4 Recommendations for Temporary Transvenous Pacing
Cardiac arrhymias requires complete evaluation and this book cannot address management of cardiac arrhythmias in detail. Initial management of commonly seen arrhythmias is shown in Table 4.5.
Table 4.5 Guidance for the treatment of common Cardiac Arrhytmias
Atropine, cardiac pacing
Diltiazem, esmolol, amiodarone
Multifocal atrial tachycardia
Verapamil or metoprolol
Torsades de pointes
Adapted from Wijdicks EFM. The Practice of Emergency and Critical Care Neurology, Oxford University Press, New York, 2010.
Approach to Preoperative Risk Assessment
Older patients with preexisting medical conditions are at risk of postoperative cardiac complications. This risk is already increased in patients with two or more “cardiac medications” (β-blockers, diuretics, calcium channel blockers, ACE inhibitors, and any antiarrhythmic drugs). Common postoperative complications are atrial fibrillation with rapid ventricular rate and acute non-STEMI.
A detailed review of the perioperative cardiac risks and guidelines has been published by the American heart association. A procedure such as a craniotomy is at intermediate surgical risk with a reported cardiac arrest and nonfatal myocardial infarction rate of less than 5%. However, cardiac complications are up to five times more common in emergency neurosurgical procedures. Generally, the risk of perioperative myocardial infarction in patients with no evidence of coronary disease (defined by EKG, history of angina, or coronary angiogram) is low.
The risk of cardiac complications increases significantly in patients with unstable coronary syndromes, decompensated congestive heart failure, arrhythmias, and severe valvular disease. A full cardiologic evaluation, if time allows, is needed.
Putting it all Together
• In acute neurologic disease brief troponin rise without EKG changes may indicate insignificant myocardial injury
• STEMI may require immediate revascularization because fibrinolysis is often contraindicated in patients with acute brain injury
• New onset atrial fibrillation with rapid ventricular response is a common cardiac arrhythmia after acute brain injury and very responsive to β blockade or diltiazem
• Craniotomy has a low risk of perioperative myocardial infarction
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