EMS World

DEC 2014

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CE ARTICLE hy p e r te n s i o n a n d h e a v y al c o h o l consumption. TREATMENT In the absence of AMI, there is no treatment for the ECG manifestations of SAH and increased ICP. Treatment of the patient in this case should focus on his increased ICP. ALS care is warranted. The patient in this case should receive oxygen if necessary via the appropriate device and flow rate to maintain an oxygen saturation of at least 94%, intra- venous access should be obtained and, if he exhibits signs of severe herniation (fxed and dilated pupil, severe hyper- tension and bradycardia, posturing, seizures), a fuid challenge could be administered in an attempt to increase preload and ultimately blood pressure to better maintain cerebral perfusion in the face of increased ICP. Place the patient on the cardiac monitor and obtain serial 12-lead ECGs en route to the emergency department (for medical emergencies) or trauma center (for trauma emergen- cies), as there is a risk of cardiac compli - cations secondary to increased ICP. Case #3: Left Ventricular Hypertrophy A 73 -year- old female presents conscious, alert and oriented to person, place, time and event, sitting on a chair in her backyard, complaining of dizzi- ness and weakness. She says she was working in her garden for the past two hours without rest, food or water. You note that it is 90ºF with high humidity. She describes a gradual onset of weakness over the past t wo hours, then experienced dizziness when she got up from her hands and knees to go into her home to escape the heat, which was, as she describes it, "really getting to me." She denies syncope, chest pain or discomfor t, dif ficult y breathing, abdominal or back pain, and headache. She has a histor y of hypertension and diabetes for which she takes metoprolol, diltiazem and glyburide. She has been compliant with her medications and has no known drug allergies. Your clinic al exam reveals dr y mucous membranes, lung sounds that are clear and equal bilaterally, and no jugular venous distention or peripheral edema. You observe no pronator drift, facial droop or slurred speech. All other findings are normal. Her blood glucose is 102 mg/dL. Other vitals: HR, 70/min.; BP, 98/52 mmHg; RR, 12/min. with good tidal volume; SpO 2 , 96% on room air; temperature, 98.6ºF (37ºC) tympanic. Per your protocol you perform a 12-lead ECG, shown in Figure 2. What is your interpretation of this ECG? Do you think the patient is having a STEMI? Left ventricular hypertrophy (LVH) is a condition in which there is an increase in the size of the myocar- dial fibers in the left ventricle of the heart. Any condition that impedes the forward movement of blood from the left ventricle will create a back pressure, requiring the heart to work harder to move blood forward into the aorta. As a result of the ventricular muscle working harder, it becomes larger. LVH is not an acute condition; it can take weeks to months to years to develop. Etiologies of LVH include hypertension (the most common cause), aortic stenosis (second most common), aortic regurgitation, mitral regurgitation, coarctation of the aorta and hypertro- phic cardiomyopathy. Patients with LVH from any of these etiologies are at increased risk for cardiovascular compli- cations including congestive hear t failure and cardiac dysrhythmias. 11 It is also a blood pressure-independent risk factor for sudden death, acute myocar- dial infarction and other cardiovascular morbidity and mortality. 12 ECG FINDINGS The ECG c an be useful but is not the best tool for diagnosing LVH; electrocardiography is the best and preferred method. ECG is a relatively insensitive method of detecting LVH, and patients with clinically significant LVH may have relatively normal ECGs. 13 This is not to say LVH is rare. In fact, one study concluded that LVH was the most common cause of ST-segment elevation in patients with chest pain presenting to the emergency department. 14 There is no single best ECG criteria for hypertrophy of any of the cardiac chambers (atria and ventricles). Several dif ferent sets of criteria have been proposed, with var ying sensitivities and specificities. The characteristics of LVH include: 11,12,15 • Increased QRS voltage: Scott criteria Limb leads: R in I plus S in 3 more than 25 mm; R in aVL more than 11 mm or greater than 18 mm if left axis is present; R in aVF more than 20 mm; S in aVR more than 14 mm; Precordial leads: S in V1 or V2 plus R in V5 or V6 more than 35 mm; R in V5 or V6 more than 26 mm; R plus S in any V lead more than 45 mm; • Increased QRS duration; • Left axis deviation; • ST-segment and T-wave abnor- malities in the left-sided leads, espe- cially V1–V3 (ST-segment elevation, downsloping ST-segment depression and T-wave inversion); • Left atrial abnormality/enlarge- ment. Another widely used criteria is the Sokolow-Lyon criteria, which states that LVH is present if the sum of the amplitude of the S-wave in lead V1 plus the amplitude of the R-wave in V5 or V6 (whichever is the tallest) is 35 mm or more, and/or the R wave in aVL is greater than or equal to 11 mm. The patient with ECG changes secondary to LVH will present with the characteristic clinical exam findings expected from the various etiologies of LVH, which include hypertension, aortic stenosis, aortic regurgitation, mitral regurgitation, coarctation of the aorta and hyper trophic cardiomyopathy. There are no clinical exam findings directly related to the ECG manifesta- tions of LVH. Figure 2: 12-lead ECG for the patient in case 3. 94 DECEMBER 2014 | EMSWORLD.com

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