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CE ARTICLE so ALS transpor t would be prudent. The patient in this case should receive ox ygen if necessar y via the appro - priate device and flow rate to maintain an oxygen saturation of at least 94%. Intravenous access should be obtained, and the patient placed on a cardiac monitor and serial 12- le ad EC Gs performed en route to the emergency depar tment. Arguably, this patient could be transpor ted via basic life support, but his complaint of chest pain is a valid argument for ALS transport. Case #2: Subarachnoid Hemorrhage A 38-year-old male presents uncon- scious, supine on his bed with snoring respirations. He withdraws from painful stimuli and mutters incomprehensible sounds. His wife says he suffered an acute onset of a "really bad head- ache—he said it was the worst he'd ever had" about an hour ago during sexual intercourse, and the patient has become increasingly disoriented since and lost consciousness about five minutes ago, af ter which she called EMS. She says he complained of nausea and vomited twice, and also seemed to be intolerant of bright light, avoiding the brightly lit areas of his house and retreating to his bedroom, where he closed the window blinds. The patient has a history of hypertension treated with hydrochlorothiazide, and has no known drug allergies. In addi - tion, his wife reports he's an 18-pack-a- year smoker and a recovering alcoholic sober for a month. Your physical exam reveals no trauma to his head, ne c k , chest, abdomen or pelvis. His pupils are equal and reactive to light bilaterally, and he withdraws to painful stimuli, showing purposeful and equal movement to all of his extremities. His blood glucose is 133 mg/dL. Vital signs are: HR, 60/min.; BP, 168/110 mmHg; RR, 12/min. with shallow tidal volume; SpO 2 , 86% on room air; temperature, 98.8ºF (37.1ºC) tympanic. Per your protocol you perform a 12-lead ECG, which shows 2 mms of ST segment elevation in leads V1-V3 and deep, inverted T waves in leads II, III, aVF and V1-V6. What is your inter- pretation of this ECG? Do you think the patient is having a STEMI? T h e m o s t c o m m o n c a u s e o f subarachnoid hemorrhage (SAH) is the rupture of a cerebral arterial aneu- r ysm. The ruptured cerebral ar ter y then pumps high-pressure blood into the cerebrospinal fluid and the space between the surface of the brain and the subarachnoid membrane. SAH secondary to a ruptured arterial aneu- rysm tends to bleed rapidly, resulting in a fast increase in intracranial pres- sure (ICP). Other causes of SAH include bleeding diathesis (unusual suscepti- bility to bleeding), vascular malforma- tions, drug use, illicit drug use and trauma. These etiologies tend to bleed more slowly, and clinical manifestations may take days to weeks to appear. C ardiac c omplic ations are not uncommon in the time period imme- diately following subarachnoid hemor- rhage or ischemic stroke. In the dynamic prehospital environment, it can be diffi- cult to determine if the cardiac findings are caused by the intracranial event, the cause of the intracranial event or completely unrelated. 8 Intracranial hemorrhage (SAH or intracerebral hemorrhage) with increased ICP and other central ner vous system events such as traumatic brain injury and isch- emic stroke resulting in cerebral edema can produce ECG abnormalities that can mimic myocardial ischemia. 9 ECG FINDINGS The ECG findings associated with increased ICP include: 8–10 • Nonspecific ST changes; • Ischemic ST changes (depression and elevation); • Dif fuse T-wave inversion and enlargement, especially in precordial leads; • Prolonged QT interval; • Brady- and tachydysrhythmias. Intracranial bleeds can produce ischemic-looking ECGs. However, most patients will have an altered level of consciousness. In addition, intracra- nial events produce a prolonged QT and deep T-waves. Ischemic ST-segment elevation and flipped T-waves are usually not associated with QT prolon- gation, a finding that can help identify ECG changes associated with increased ICP and SAH. The exact reasons for the ECG c h a n g e s t h a t c a n a c c o m p a n y increased ICP are not well understood. One hypothesis is that increased ICP may result in a catecholamine surge, stressing the myocardium and resulting in ischemic changes. Vagus nerve stim- ulation may also play a role. In addition, elevated ICP and intracranial events may result in increased left ventricular pressure and subsequent subendocar- dial hemorrhage. As such, ICP and CNS events may actually induce myocardial damage, which produces the ECG abnormalities. 8 The patient with ECG changes secondary to SAH and increased ICP will present with the characteristic clinical exam findings expected from the various etiologies of increased ICP. There are no clinical exam findings directly related to the ECG manifesta- tions of increased ICP. DIFFERENTIATING BETWEEN SAH AND STEMI Differentiating between SAH and AMI can be difficult early in the progres- sion of SAH. Both etiologies can present with dizziness, nausea and vomiting, and altered mental status early in their progression. A rguably it bec omes easier to dif ferentiate AMI from SAH as SAH progresses, and AMI will not present with the neurologic findings (unequal pupils), bradycardia and hypertension characteristic of SAH and increased ICP. In the case above, the patient presented with a history and clinical exam find- ings that strongly suggested acute SAH and increased ICP as the etiology of his decreased level of consciousness. He had a history of acute onset of severe headache, nausea and vomiting, and photophobia. He was also exhibiting signs of increased ICP: bradycardia and hypertension. In addition, he had risk factors for SAH: cigarette smoking, EMSWORLD.com | DECEMBER 2014 93