Cardiovascular Aspects of Neurological Intensive Care

A number of interesting cardiovascular problems arise in relation to acute cerebral lesions. Although infrequent, they are unique to this setting and expose the mechanisms by which the brain participates in the control of the heart and vasculature. In addition, more mundane acute cardiovascular issues are frequent in the neurological intensive care unit (neuro-ICU); they include coronary ischemia, cardiac arrhythmias, and congestive failure that are seen in all general critical care settings. Management of these latter conditions in the neurocritical care setting must take into account the potential neurological complications of hypotension and hypertension, and the neurointensivist must establish strategies and priorities in their management.

ACUTE CORONARY ISCHEMIA

Atherosclerotic vascular disease causes a broad overlap between neurological and cardiac illnesses. Myocardial infarction (MI) is common in the stroke population, probably accounting for the most common causes of death in the weeks and months following stroke. Surgical and neurovascular interventional procedures also stress underlying coronary disease, which is why cardiac complications are frequently encountered in the neuro-ICU.

The diagnosis of acute coronary ischemia can be difficult in neurocritical care patients, as the classic complaint of chest pain may be masked by coma, intubation, and sedation. In patients with cardiac risk factors (including mainly ischemic and hemorrhagic strokes), surveillance should be heightened and routine screening with electrocardiogram (ECG) and serum markers should be part of the neuro-ICU protocol. Cardiac monitoring generally includes continuous ECG and invasive or noninvasive blood pressure monitoring. Twelve lead ECGs and serum markers such as troponin levels should be monitored after surgical or interventional procedures requiring general anesthesia. It is reasonable to “rule out MI” with ECG and serum for troponin level at admission to the neuro-ICU. Patients with risks for further myocardial injury, such as those with ECG changes, should have repeated screening for myocardial injury after major procedures such as craniotomy.

Treatment of acute coronary ischemia with nitrates, β-blockers, calcium antagonists, and analgesics usually can be undertaken without particular complication in neurological disease. Difficulty arises when the blood pressure falls as a result of treatment and reduces cerebral perfusion. As detailed in Chapter 2, cerebral perfusion pressure (CPP) is defined as the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). The CPP is usually well maintained through cerebrovascular autoregulation, but it can be compromised in the setting of recent acute stroke or vasospasm following subarachnoid hemorrhage (SAH). Although traditional clinical prioritization in coronary ischemic syndromes calls for preserving the myocardium, the neurointensivist must balance
risks in order to preserve brain viability. Lower levels of medication may be most appropriate in this set of patients. Doses can be titrated upward to just begin to lower MAP, rather than the more standard lowering of MAP by 20% or more. In the authors’ experience, it is usually possible to treat the coronary ischemia adequately without marked reductions in blood pressure.

Heparin and aspirin are standard treatments in the acute coronary syndromes, both unstable angina and MI. The use of these agents may pose additional risks in patients with recent craniotomy, intracerebral hemorrhage, and perhaps in cerebral infarction. Heparin usually can be used with low risk following ischemic stroke. Most clinicians are reluctant to use systemic anticoagulation with heparin within the first several days after a craniotomy. Antiplatelet drugs also may pose special risks in cases of acute hemorrhage, trauma, or acute craniotomy, although there are little data that quantify the actual risk, and decisions need to be made based on individual circumstances. Furthermore, thrombolytic therapy for acute MI is generally not an option in this patient population because of the increased risk of cerebral hemorrhage.

CARDIAC ARRHYTHMIAS

Arrhythmias occur in the neuro-ICU in patients with known cardiac disease as well as in those without apparent cardiac risk factors. Again, many neurocritical care patients have cardiac disease, and some of these disturbances are attributable to coronary artery insufficiency, whereas others have conduction disturbances that result from the neurological illness. In addition, a fair number of patients manifest atrial arrhythmias (mainly atrial fibrillation) while under observation in the first few days after stroke. The implication of this finding is generally held to be that there was a similar previous arrhythmia that created the substrate for the (embolic) stroke, but it may be that some rhythm disturbances arise as a result of infarction of brain areas that modulate cardiac conduction (see Tachyarrhythmias).

TABLE 5.1. Neuromuscular diseases involving myocardium and cardiac conduction

Neuromuscular disease	Common cardiac abnormality
Kearns-Sayre syndrome	Conduction block
Friedreich ataxia	Hypertrophic cardiomyopathy; subaortic stenosis
	Hypokinetic-dilated left ventricle; abnormal electrocardiogram
Charcot-Marie-Tooth disease	Conduction block
Myotonic dystrophy	Conduction defects; tachyarrhythmias ± cardiomyopathy
Fascioscapulohumeral dystrophy	Arrhythmia or conduction block
Limb girdle dystrophy	A-V conduction block; dilated cardiomyopathy
Multicore myopathy	Septal defects; conduction block; cardiomyopathy
Polymyositis	Arrhythmias; inflammatory cardiomyopathy

Animal models of cardiac changes in relation to acute brain injury have demonstrated some cerebral localization of these effects (1). Acute focal injuries to brain tissue, ischemic stroke, hemorrhage, and trauma lead to cardiac effects, as well as electrical activation of brain tissue as seen in epilepsy. Tachycardia and pressor responses are more common after stimulation of the right insular cortex and stimulation of the left vagus, which innervates the atrioventricular node and cardiac conduction system. Bradycardia seems to be more common after stimulation of the left insular cortex or the right vagus nerve, which innervates the sinoatrial node (2). Tachycardias are most commonly seen with seizure and epilepsy, although bradycardias and sinus arrest have been reported (3).

It should be emphasized also that certain neuromuscular diseases affect cardiac muscle and conduction pathways as a primary manifestation of the neurological disease, leading to cardiac dysfunction in a more direct fashion (Table 5.1) (4).

Bradycardias

Excepting the effects of β-adrenergic blocking drugs, a heart rate below 60 beats per minute (BPM) is usually the result of sinus node dysfunction or an atrioventricular conduction disturbance. Very acute cerebral diseases can also produce a vasovagal response that is pronounced enough to cause the heart rate to drop and blood pressure to fall to the point of causing syncope. Closed head injury is one setting that leads to bradycardia and conduction block, likely through a vagal mechanism (5). Whether similar mechanisms pertain in SAH and epilepsy is not known, although similar bradycardia is seen. Vagal influences inhibit sinus nodal activity but a sympathetic discharge of medullary origin probably accounts for the concurrent vasodepressor effect. When the vasodepressor component is prominent, even cardiac pacing may not eliminate hypotension but vasopressor drugs may reverse it. Atropine can be helpful in the reversing the bradycardic component in acute setting but, in extreme and protracted cases, external pacing may be necessary for short periods of time.

Some patients have similar responses after carotid angioplasty and stenting procedures (6). Stimulation of the carotid sinus by the angioplasty balloon can lead to profound bradycardia, including complete heart block. Pacing may be required for a brief period, although pretreatment with an anticholinergic usually is adequate. The stenting procedure may cause a more sustained stimulation of the carotid sinus, in which case hypotension and bradycardia may persist for 24 to 48 hours. Some of these patients require vasopressor therapy to maintain adequate perfusion (7). The vasovagal response is obviated during and after carotid endarterectomy by regional blockade of the carotid sinus, but other problems arise in the postoperative period, mainly hypertension.

Finally, bradycardia in a neuro-ICU raises concern as a possible indication of increased intracranial pressure. The Cushing reflex (bradycardia, hypertension, and respiratory depression) (Chapter 2) results from acutely increased intracranial pressure and diminished cerebral perfusion. Animal models demonstrate increases in circulating catecholamines as the probable cause of hypertension, possibly as a compensatory effect to increase cerebral perfusion (8,9). The bradycardia appears to be the result of pressure that is transmitted to mechanically sensitive centers in the floor of the fourth ventricle. However, it should be pointed out that in clinical circumstances tachycardia is as often observed as bradycardia with episodes of ICP elevation.

Tachycardias

Supraventricular tachycardias are common in all critical care settings. Sinus tachycardia is defined here as a heart rate exceeding 100 BPM, and usually represents a physiologic response to pain, stress, hypotension, congestive heart failure, or excessive catecholamine drive. It is generally not treated as a primary dysrhythmia, but rather the precipitating conditions are sought and corrected.

Paroxysmal supraventricular tachycardias (PSVT) related to a reentry or similar mechanism at the atrioventricular node are also common. Treatment with vagal stimulation maneuvers, especially carotid sinus massage, are useful. Low doses of verapamil, 2.5 to 10 mg, by intravenous (i.v.) injection or of adenosine, 6 to 12 mg, also can be used to “break” the tachycardia. Adenosine has a very short half-life, and in our experience is quite effective in this setting. β-Blockade reduces the risk of recurrent episodes of PSVT but there are a number of alternative approaches.

Atrial fibrillation with a rapid ventricular response is also very common in relation to neurological disease, particularly in older age groups. In the neuro-ICU, pain, infections, intravascular volume overload, and neurological injuries such as SAH are the most common precipitants. The rapid ventricular response is usually the most urgent issue, because the high rate may precipitate coronary ischemia or compromise cardiac function. Short-acting
β-adrenergic blockers such as labetalol and esmolol can be used by i.v. bolus or continuous infusion. Diltiazem also is quite effective as an infusion that can be titrated to achieve rate control and is the approach we have preferred. The major limitation of β-blockade and calcium channel antagonists in the neurological patients relates to the induced hypotension that often accompanies doses adequate to slow rate. There is also some concern that certain calcium antagonists may increase intracranial pressure; however, the clinical effects have been minor in our experience. When hypotension must be avoided in order to maintain tenuous cerebral perfusion (e.g., soon after an ischemic stroke), treatment with digoxin may be preferable. The effects of digoxin, of course, are slower, requiring several hours, and may not always be effective, but the lack of associated hypotension makes it valuable in care of the neurological patient.

Ventricular tachycardias are less frequent than are atrial ones in the neuro-ICU, but their implications and potential for severe hypotension underscores their importance. Isolated premature ventricular contractions (PVCs) are seen commonly in many monitored patients, and rarely require treatment. The use of dopamine as a vasopressor agent may be associated with more frequent PVCs and at some point the ventricular irritability mandates the use of alternate agents. The Lown classification (Table 5.2) has long been used to grade ventricular ectopy in terms of potential morbidity and risk of cardiac sudden death. Although much more sophisticated information can now be gathered by electrophysiologic studies, this classification still provides a simple and useful guide (10,11). Low-grade ectopy (grades I and II), usually are benign; treatment usually is considered in grade III and IV arrhythmias.

TABLE 5.2. Lown’s grading of cardiac arrhythmias

Grades	Frequency and forms of premature ventricular contractions (PVCs)
I	Isolated PVCs, <30/h
II	Frequent PVCs, >1/min or >30/h
III	Multifocal PVCs
IV	Repetitive multiform PVCs Couplets Salvos
Adapted from Lown B, et al. Monitoring for serious arrhythmias and high risk of sudden death. Circulation 1975;52:189-198.

Ventricular flutter and fibrillation are most commonly seen in patients with underlying ischemic heart disease. Prolonged Q-T intervals are a risk for ventricular ectopy. This circumstance arises with hypokalemia and in relation to some medications, including phenothiazines and tricyclic antidepressants. The ventricular tachycardias are emergent problems for which management protocols are essential.

A specific type of ventricular tachycardia, torsade de pointes, is also related to Q-T prolongation and deserves special mention because it has been reported in relation to acute neurological injuries such as SAH and cranial trauma (12,13). Repletion of potassium and magnesium is critical and low-dose β-blockade may be helpful. Careful monitoring and support are essential until the arrhythmia ceases and the Q-T interval shortens.

HYPERTENSIVE CRISIS

Markedly elevated blood pressure can be a reflection of accelerated hypertension. When it is associated with evidence of end-organ damage, the term malignant hypertension is applied and urgent intervention is necessary. Papilledema, retinal hemorrhages, and hematuria are indicative of malignant hypertension, and this clinical syndrome overlaps with hypertensive encephalopathy when cerebral features appear. The latter include headache, confusion, visual disturbances (cortical blindness and its variants), seizures, obtundation, and coma, and are usually associated with diastolic blood pressures of 130 mm Hg or greater. Most but not all affected patients have papilledema and retinal vascular changes. Cerebral hyperperfusion and pathologic changes of fibrinoid necrosis and microvascular thrombosis are felt to underlie the encephalopathy. Similar changes are seen in eclampsia
as well, although the precise mechanisms are not known in either circumstance. It has become apparent that changes in the appearance of the posterior cerebral white matter on magnetic resonance imaging and computed tomography scans are highly characteristic of hypertensive encephalopathy.

Hypertensive crisis represents a neurological emergency. Cerebral perfusion may be markedly increased initially, but the CPP can be quickly compromised as MAP drops. Monitoring of the intracranial pressure may be optimal, although in practice it is not always practical to monitor ICP, and therapy to lower ICP is often empiric. As a general guide, awake patients usually have an ICP less than 30 mm Hg, and the MAP can be lowered to approximately 100 mm Hg without compromising CPP. Intracranial pressure in patients in coma is uncertain, and lowering MAP significantly is most safely done after placement of an ICP monitoring device.

Treatment is optimally undertaken with central venous access and continuous blood pressure monitoring in the intensive care unit. The optimal pharmacologic agent should provide rapid, predictable control of blood pressure. Commonly used drugs are listed in Table 5.3. Intravenous bolus injection of labetalol can provide control in many cases and we usually resort to it first. Doses of 10 to 40 mg every 10 minutes can be used. Intravenous enalaprilat at 0.625 to 1.25 mg i.v. can be used, as well as sublingual captopril, 6.25 to 12.5 mg. Sublingual nifedipine has been associated with precipitous and profound drops in MAP, and other agents offer better control. Hydralazine, 10 to 40 mg i.v. every 4 to 6 hours also can be useful, but associated tachycardias can be seen. Nitroprusside remains the most rapidly effective and widely available agent for the control of profound hypertension, and can be used as a continuous infusion at 0.3 to 10 µg/kg per minute. The vasodilatory effect has the potential to exacerbate elevated ICP, but this is uncommon in practice and the effectiveness of the drug argues for its use in emergent situations. More conventional agents can be initiated for more prolonged effect once control is achieved.

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