Electrocardiographic changesand intracranial pathologyGERALDINE SYVERUD, CRNA, BSNCincinnati Ohio

A young woman who sustained severe headtrauma presented to the operating room foremergent surgical intervention. Herelectrocardiogram (ECG) exhibited signs ofmyocardial ischemia, which resolved severaldays postoperatively.

ECG changes suggestive of cardiacpathology can be associated withintracranial pathology, most notablysubarachnoid hemorrhage. Delay of operativetherapy may have catastrophic results.Experimental data indicates massivesympathetic outflow results from stimulationof the lateral and posterior hypothalamicregions. Large amounts of norepinephrine arereleased into the systemic circulation,resulting in hypertension, tachycardia,dysrhythmias and ECG changes. Myocardialischemia and injury can occur from theeffects of this excessive sympatheticstimulation. In certain case reports,neurologic patients who experiencedECG changes had normal hearts onpostmortem examination. This implies thatmyocardial recovery can occur despite theappearance of an abnormal ECG in theneurologic patient.

Anesthetic management of these patientsinvolves prevention of further increases inintracranial pressure and avoidance ofhyperventilation in the presence of

hypotension or vasospasm. Continuous ECGmonitoring is essential. Ventriculardysrhythmias may prove resistant toconventional pharmaceutical management.Beta blockade may be indicated to preventexcessive cardiac stimulation by endogenouscatecholamines, and, in addition, mayprevent the formation of the microscopiccardiac lesions typical of this hyperstimulation.

Key words: Electrocardiogram,myocardial ischemia, subarachnoidhemorrhage, torsade de pointe.

Patient presentationA 30-year-old woman was beaten with a lead pipeand sustained multiple facial and skull fracturesand a left subdural hematoma. An electrocardio-gram (ECG) was obtained soon after admission andrevealed sinus tachycardia with horizontal ST de-pression in leads III and AVF, consistent with myo-cardial ischemia. She was taken to the operatingroom shortly after admission for evacuation of thesubdural hematoma. A medical history was unavail-able on admission but was later obtained and notedto include no preexisting medical problems, with anegative review of systems. Three days later, a sec-ond ECG was obtained, which displayed sinusrhythm with accelerated A-V conduction (short PRinterval). The previously noted ischemic changeswere not present. The patient did well during her

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hospitalization and was allowed to go home ap-proximately five weeks postinjury.

DiscussionThe association between central nervous sys-

tem (CNS) disease and ECG changes was first de-scribed in 1938. These ECG changes were furtherdetailed and categorized, and their frequent associ-ation noted in the presence of spontaneous sub-arachnoid hemorrhage (SAH).1 It is estimated thatapproximately 50% of patients with aneurysmalSAH will have ECG abnormalities. 2 One case re-port describes a patient with a known aneurysmalSAH who had a preoperative ECG consistent withan anterior wall myocardial infarction. For this rea-son the operation was canceled, and the patientdied soon afterward of a second hemorrhage. Theautopsy revealed a normal heart with no evidenceof recent infarction. 3

The anesthesia team is responsible for the pre-operative assessment of all patients presenting forsurgery. The ECG is perhaps the primary instru-ment which is employed to evaluate the well-beingof the heart. Any patient with an abnormal ECG, ornew changes noted on ECG, warrants further car-diac work-up to determine the cause and signifi-cance of such findings; however, the neurologicpatient with subarachnoid hemorrhage who hassuch an ECG should not have surgery delayed. Theanesthetist must be aware of ECG findings whichcan occur in the presence of intracranial diseaseand should examine the origins and prognosticimplications such findings carry with them, since agood number of these patients require operativeintervention (Table I).

Table IConditions associated withsubarachnoid hemorrhage4

HypertensionCerebral aneurysmA-V malformationTraumaBrain tumorBlood dyscrasiasAngiopathiesSeptic emboliLeukemiaAnticoagulation therapyEclampsiaCocaine toxicity

Electrocardiographic changesThe most common abnormalities noted in the

ECG of the patient with CNS disease are prolonga-tion of the Q-T interval, large and often inverted Twaves and prominent U waves.' 4 The normal Q-Tinterval is defined as one-half of the preceding R-Rinterval. The risk of development of ventriculararrhythmias is increased in the presence of a pro-longed Q-T interval, because the delay in ventricu-lar repolarization predisposes to the developmentof reentrant arrhythmias. A particular form of ven-tricular tachycardia, known as torsade de pointe, hasbeen described in several case reports of patientswith SAH. This rhythm may either terminate spon-taneously or progress to ventricular fibrillation.Other ECG changes that are encountered in thesepatients include: peaked P waves, short P-R inter-vals, S-T segment depression and S-T segmentelevation.'. 2

Pathogenesis of ECG and myocardial findingsAn understanding of the role the CNS plays in

the genesis of ECG abnormalities has been obtainedthrough numerous animal studies.2 Apparently, thestimulation of certain central autonomic centersresults in a massive sympathetic outflow, with aconsequent release of large amounts of norepineph-rine from the adrenal medulla. These centers inhumans have been identified as lying in the lateraland posterior hypothalamic regions. These regionsare stimulated by increased intracranial pressure,the irritant effect of blood, ischemia or a combina-tion of these factors. Once stimulated, central effer-ent pathways produce norepinephrine release intothe general circulation, with resultant acute hyper-tension and cardiac manifestations (Table II).

Experimental evidence indicates that elevated

Table IISequence of events leading toelectrocardiographic changes followingneurologic insult4

1. Stimulation of central autonomic centers(lateral and posterior hypothalamic areas)

2. Massive release of norepinephrine

3. Tachycardia, hypertension, dysrhythmias,myocardial ischemia and pulmonary edema

myocardial levels of norepinephrine lead to a non-uniform rate of repolarization, which predisposesto ventricular arrhythmias. Experimental data alsosuggest that myocardial damage can result fromischemia, which involves primarily the subendo-cardium of the left ventricle. These changes include

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microscopic areas of focal necrosis, subendocardialpetechial hemorrhage, mononuclear infiltrates andmyofibrillar degeneration. Some researchers be-lieve that, in certain cases, this damage is reversible,and therefore may not be present on postmortemexamination. 2

Alpha-receptor stimulation from norepineph-rine may result in both peripheral and cerebralarterial spasm, This can increase the workload ofthe heart through a shift of blood volume to thecentral circulation.' A recent case series reportedthat 30-70% of patients with SAH developed pul-monary edema during their hospitalization. It hasnot been determined whether the appearance ofpulmonary edema is due to pump failure second-ary to left ventricular lesions, acute circulatory over-load, neurogenic pulmonary edema due to in-creased sympathetic or vagal tone or a combinationof these factors.

Pharmacologic treatmentPharmacological therapy involves the use of

sympathetic blocking agents. Alpha blockers maybe employed to prevent peripheral and cerebralarterial spasm. Beta-adrenergic blockade can beused to prevent or treat ventricular tachyarrhyth-mias which are produced by excessive sympatheticstimulation. Torsade de pointe ventricular tachy-cardia is resistant to or may even be aggravatedfurther by treatment with the Class I antiarrhyth-mic drugs, such as lidocaine, procainamide or quin-idine.5 One case report describes successful treat-ment of this dysrhythmia with propanolol, withoutrecurrence, in a patient with SAH, intracerebralhemorrhage and prolongation of the Q-T interval.-,

Evidence indicates that treatment with betablockers is effective in preventing the developmentof the characteristic subendocardial lesions. 2 In ani-mals, the ECG changes and ventricular arrhyth-mias produced by stimulation of specific brain areasare prevented by beta-adrenergic blockade. In addi-tion, one study in a human population demon-strated that in two groups of patients treated forSAH, the group who received propranolol had sig-nificantly fewer neurological deficits one-yearpostbleed.6 Propranolol may have a central effectwhich could account for these beneficial results.This hypothesis is supported by the fact that pro-pranolol readily crosses the blood-brain barrier andis known to decrease the cerebral oxygen require-ments in patients with stroke or cerebral ischemia.

Anesthetic considerationsNeurosurgical patients frequently present to

the operating room in a coma with no available

medical history, which limits the anesthetist'spreanesthesia assessment to information obtainedfrom physical examination and laboratory testing.The patient's past medical history should be ob-tained, if possible, prior to operation. It is difficultto determine the implications of abnormal labora-tory tests without information about the patient'sprevious medical history. For example, the neuro-surgical patient with symptomatic preexisting car-diac disease and the previously healthy patientwould show variation in their tolerance to sympa-thetic stimulation, i.e., tachycardia and hyperten-sion. A preoperative ECG suggesting myocardialischemia, even though the etiology of the changes isthought to be of neurologic origin, would be muchmore worrisome in the patient with preexistingcardiac disease.

The outcome of the patient with SAH is deter-mined primarily by the degree of intracranial hem-orrhage present, whether cerebral arterial vaso-spasm is present or if rebleeding occurs after theacute episode is successfully treated.

The anesthetic management of these patients istherefore directed toward prevention of further in-creases in intracranial pressure and systemic bloodpressure, which could worsen the bleed. These pa-tients should not be hyperventilated, especiallywhen hypotension or vasospasm is present preoper-atively, since this will reduce cerebral blood flowand oxygen delivery to the already hypoxic braintissue.7 Continuous intraoperative ECG monitoringis an established standard of care, and knowledge ofthe pathogenesis of ECG changes which may arisein the presence of SAH is important for propermedical management.8

Some authors suggest using morphine as ananalgesic for neurosurgical patients since there is apropensity for the development of pulmonaryedema. An increase in pulmonary vessel capaci-tance would tend to prevent extravascular fluidshifts which could occur due to an increase in vesseltone from excessive sympathetic stimulation.

In summary, ECG tracings suggestive of thepresence of myocardial ischemia or infarction canbe encountered in patients with intracranial pa-thology, most notably subarachnoid hemorrhage(Table I). Surgery is usually not delayed in order toobtain a full cardiac work-up on these patients, sincethese ECG findings are felt to be attributable to theeffects of a central neurogenic mechanism, ratherthan of cardiogenic origin.8 Whenever possible, thepast medical history should be obtained to deter-mine the status of the cardiovascular system prior tothe onset of neurological pathology. Postponementof operative intervention could result in further

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morbidity and mortality from progression of theCNS lesion.8,9

Patients with SAH also have a tendency to de-velop ventricular dysrhythmias when a prolongedQ-T interval is present, and these dysrhythmiasmay prove resistant to conventional antiarrhythmictherapy.4, 5' 10 Beta blockade appears to effectivelytreat and prevent these dysrhythmias by blockingthe cardiac stimulatory effects of endogenous cate-cholamines. Beta blockade also appears effective inpreventing the development of the microscopicmyocardial lesions which can form in response tohigh catecholamine levels.

REFERENCES(1) Melin J, Fogelholm R. Electrocardiographic findings in subarach-noid hemorrhage. Act Med Scand. 1983;213:5-8.(2) Marion D, Segal R, Thompson M. Subarachnoid hemorrhage andthe heart. Neurosurgery 1986;18:101-104.(3) Cropp GJ, Manning GW. Electrocardiographic changes simulat-ing myocardial ischemia and infarction associated with spontaneousintracranial hemorrhage. Circulation. 1960;22:25-38.

(4) Callaham M. Current Therapy in Emergency Medicine. Toronto andPhiladelphia: Decker Inc. 1987;302-305.(5) Carruth J, Silverman M. Torsade de pointe atypical ventriculartachycardia complicating subarachnoid hemorrhage. Chest. 1980;78:886-888.(6) Neil-Dwyer G, Walter P, Cruickshank J. Beta blockade benefitspatients following a subarachnoid hemorrhage. Eur J Clin Pharmacol.1985;28 (suppl):25-29.(7) Miller R. Anesthesia. New York: Churchill and Livingstone. 1986;1596-1597.(8) Samra S, Kroll D. Subarachnoid hemorrhage and intraoperativeelectrocardiographic changes simulating myocardial ischemia-Anesthesiologist's dilemma. Anesth Analg. 1985;64:86-89.(9) White J, Parker M, Rogers M. Preanesthetic evaluation of a patientwith pathologic Q waves following subarachnoid hemorrhage.Anesthesiology. 1985;62:351-354.(10) Taylor A, Fozzard H. Ventricular arrhythmias associated withCNS disease. Arch Intern Med. 1982;142:232-233.

AUTHORGeraldine Syverud, CRNA, BSN, received her BSN from the Col-

lege of Mount Saint Joseph-on-the-Ohio, Mt. St. Joseph, Ohio, in 1975.She graduated from the University Hospital School of Nurse Anesthe-sia, Cincinnati, in 1987. She is currently employed as a staff nurseanesthetist/clinical instructor at University Hospital, Cincinnati.

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