Haven't read the initial case presentation? Read: Case 14: Heart-Felt Condolences

EKG Case Presentation:
You are alerted to the scene of a 41-year-old female with an altered level of consciousness. You arrive to find a female lying supine on a bed. According to her husband, she has been minimally responsive since the early morning after failing to wake up. The husband called 9-1-1 and continued to monitor his wife until you arrived.

The patient has an open airway and does not have labored breathing. The skin is warm and not diaphoretic. There is no evidence of trauma. A quick neurological exam reveals a Glasgow Coma Scale of 9 based on spontaneous eye opening, withdrawal to pain, and no verbal response. You record the following vital signs:

HR 57
RR 24
BP 160/100
SpO2 97%

Learning Objectives:

• Basic: Recognize the presentation of a subarachnoid hemorrhage
• Advanced: Identify potential non-specific EKG changes during a SAH

Expert Panel Discussion of the Case
Broad and deep T-wave inversions are often seen in patients who present with acute subarachnoid hemorrhage. Many ideas have been postulated to explain this phenomenon.

At quick glance, one must first recognize that this is an obtunded patient. The cause of the altered LOC could be potentially caused by one or several etiologies. One quick mnemonic to help recall common causes of altered LOC is to recite AEIOU TIPS:

Alcohol
Epilepsy (post-ictal state or non-convulsive status epilepticus)
Insulin (hypo- or hyperglycemia)
Overdose
Uremia (kidney failure)
Trauma
Infection (sepsis)
Psychiatric and
Stroke (Ischemic and hemorrhagic including subarachnoid hemorrhage)

A review of the history that was provided by the husband as well as the physical exam performed in the field (including finger-stick blood glucose), quickly eliminates several of the possible factors in the AEIOU TIPS mnemonic. The remaining areas of potential concern for this patient’s altered LOC is: Alcohol, Epilepsy, Overdose, Infection and Stroke. Further questioning of the husband and a cursory search may help to eliminate the potential for alcohol and overdose as causes as well.

This then leaves the field provider with concerns for Infection (meningitis, encephalitis) and Stroke. The neck rigidity found when moving the patient can be seen in both meningitis cases as well as subarachnoid hemorrhage from irritation of the meninges — the layers of tissue that surround the brain and spinal cord. The husband had stated that the patient had complained of a headache the night before. This could reflect early meningitis or may have been related to an initial small subarachnoid hemorrhage, often called a "sentinel bleed." About 40 to 50 percent of patients with an aneurysmal subarachnoid hemorrhage (SAH) have this sentinel bleed — or warning bleed — days to weeks prior to the second more massive SAH. This may have resulted in the occurrence of a headache the night before.

The EKG helps to make the final impression. Broad, deep precordial T-wave inversions are commonly seen in patients with SAH. EKG changes are seen in up to 90 percent of patients with SAH and include T-wave inversion, QT prolongation, U waves, tachycardias, bradycardias and life-threatening arrhythmias. The cause of this broad and deep precordial T-wave inversion is thought to be secondary to an intense catecholamine surge that occurs with the SAH. These circulating catecholamines are thought to affect the coronary microcirculation causing decreased flow and a change in the EKG.

Atraumatic SAH is most often caused by a ruptured aneurysm (80 percent). Most of these are saccular or berry aneurysms located in the Circle of Willis at the base of the brain. These aneurysms typically form at bifurcations of cerebral vessels. About 50 percent of ruptures occur at rest, while the remainder occurs with lifting, orgasm or brawling. The provider may wish to discreetly ask the husband if he and his wife had engaged in sexual activity the night before.

Treatment includes maintaining airway, breathing and circulation. Many patients have elevated blood pressure. However, aggressive lowering of BP should be discouraged until imaging studies (CT scan) have been performed to determine if the stroke is due to ischemia or hemorrhage.

A severly dramatic lowering of BP in acute ischemic stroke can worsen the outcome. Blood glucose levels should be obtained. Hypo- and hyperglycemia should be treated. Outcome from strokes are worse when blood sugar is not well controlled. Transport should be undertaken safely and promptly to a facility preferably with neurosurgical capability or with the ability to perform interventional radiology. Definitive treatment of an aneurysmal SAH involves either surgical clipping of the aneurysm by a neurosurgeon or placing coils into the aneurysm under angiographic guidance.

Additional Resources:
Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage Nader M. Banki, MD; Alexander Kopelnik, MD; Michael W. Dae, MD; Jacob Miss, BA; Poyee Tung, MD; Michael T. Lawton, MD; Barbara J. Drew, RN, PhD; Elyse Foster, MD; Wade Smith, MD, PhD; William W. Parmley, MD; Jonathan G. Zaroff, MD

From the Division of Cardiology (N.M.B., A.K., J.M., P.T., E.F., W.W.P., J.G.Z.), Department of Radiology (M.W.D.), Department of Neurosurgery (M.T.L.), Department of Physiological Nursing (B.J.D.), and Department of Neurology (W.S.), UCSF Medical Center, San Francisco, Calif.

Background on SAH
Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals.

Methods and Results
For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[123I] iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively. A blinded observer interpreted the scintigraphic images. Cardiac troponin I (cTI) was measured to quantify the degree of myocyte necrosis. Blinded observers calculated the LV ejection fraction and graded each LV segment as normal (score=1), hypokinetic (score=2), or akinetic (score=3). A wall-motion score was calculated by averaging the sum of the 16 segments. All subjects with interpretable scans (N=41) had normal MIBI uptake.

Twelve subjects had either global (n=9) or regional (n=3) absence of MIBG uptake. In comparison with patients with normal MIBG uptake, those with evidence of functional denervation were more likely to have LV regional wall-motion abnormalities (92% versus 52%, P=0.030) and cTI levels >1 µg/L (58% versus 21%, P=0.029).

Conclusions
LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation.
These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals.

• Br Med J. 1978 Oct 7;2(6143):990-2.s
Effect of propranolol and phentolamine on myocardial necrosis after subarachnoid hemorrhage.

A study was set up to assess the effect on the clinical course of subarachnoid haemorrhage (SAH) of giving propranolol 80 mg eight-hourly plus phentolamine 20 mg three-hourly by mouth for three weeks. Out of the 90 patients studied, 14 died. Two of the deaths occurred in an open pilot study of 10 patients, the remaining 12 deaths occurring in patients in a randomized double-blind placebo-controlled study. Postmortem examination was carried out on 12 of the patients, six of whom had been receiving placebo and six propranolol plus phentolamine. Necrotic myocardial lesions were present in the hearts of all six patients (age range 30-59 years) who died while taking placebo (all had had abnormal electrocardiograms (ECGs). In contrast, no necrotic lesions were found in the hearts of the six patients (age range 28-59) who died while receiving the drugs (all had previously had normal ECGs). We conclude that the necrotic myocardial lesions were induced by catecholamines and that propranolol had a cardioprotective effect. While death from a further haemorrhage in cases of SAH is not affected by propranolol and phentolamine, propranolol may have a beneficial effect in other potentially lethal stresses.

• From Emergency Medicine Clinics of North America, February 1996:
"In the post-stroke period, the most common injury pattern is a repolarization abnormality" (including) "large inverted T wave, ST depression, QT prolongation and U wave."

• Also in Case Studies in Neuroscience (Susan Johnson):
"The hyperactivity of the sympathetic nervous system that occurs after SAH produces an increased level of blood catecholamines. These may be responsible for hypertension and tachycardia...there are also EKG changes associated with SAH...including...T wave distortions, U waves, prolonged QT and arrhythmias."

• From Neurosurgical Emergencies, Volume I, from the American Association of Neurological Surgeons, page 141:
"Electrocardiographic changes are common after subarachnoid hemorrhage and include arrhythmias and waveform changes consistent with ischemia or infarction. It is believed that most of these abnormalities are the result of a massive rise in circulating catecholamine levels occurring at the time of hemorrhage."

Perhaps "most" of these patients also have a Cushing response going on, so that the rises in ICP are causing a normal-to-slowed heart rate in spite of catecholamine levels.

Case author: Gustavo E. Flores, Nick Nudell
Case discussion: Andrew Bowman, Nick Nudell

CALL FOR SUBMISSIONS! Do you have a cardiac-related case in your head that you think would challenge other responders? The EKG Club wants to hear from you. The EKG Club is currently looking for case submissions to be featured on EMS1. Don't worry about your writing skills — just send us the facts. To submit a cardiac case idea, email EKGcase@EMS1.com.