EKGs ===== þ Hypertrophic Cardiomyopathy - Sharp narrow Qs in lateral leads, big voltage, inverted anterior Q waves þ EKGs in PE þ V Tach mimics þ EKG criteria for RV infarction: Leads Sensitivity (%) Specificity (%) V1 28 92 V3R 69 97 V4R 93 95 Roth A, Miller HI, Kaluski E: Early thrombolytic therapy does not enhance the recovery of the right ventricle in patients with acute inferior myocardial infarction and predominant right ventricular involvement. Cardiology 1990; 77(1): 40-9 A 1-mm elevation in the ST segment in lead V4R is 70% sensitive and 100% specific for RVI Madias JE, Mahjoub M, Wijetilaka R. Standard 12-lead ECG versus special chest leads in the diagnosis of right ventricular infarction. Am J Emerg Med. 1997;15:89–90. Fijewski TR, Pollack ML, Chan TC, Brady WJ. Electrocardiographic manifestations: right ventricular infarction. J Emerg Med. 2002;22:189–194. þ QT Intervals - normals are given in a table in Mariott - increased QT is a predictor for syncope caused by paroxysmal ventricular arrhythmias, especially in those with ischemic heat disease, hypokalemia, or hyomagnesemia or in those taking antiarrhythmic drugs. Abnormal morphology of the T wave in the presence of a prolonged QT interval is a strong predictor of arrhythmia. [Scientific American Medicine, Feb 1995 update.] - QT intervals are increased by many drugs: + Type Ia antiarrhythmics (e.g., quinidine, procainamide) + tricyclic antidepressants such as amitryptilene (Elavil) + Nonsedating antihistamines (e.g., terfenadine=Seldane, astemizole=Hismanal) + cisapride=Propulsid + Serentil (mesoridazine besylate) -- a phenothiazine antipsychotic/sedative (per letter from drug company 9/00) + arsenic [Tintinalli, 3rd ed. p 641.] - QT prolongation by these drugs increased, sometimes to point of causing arrhythmias such as Toursades de Pointes, by medications that inhibit the liver's cytochrome-450 enzyme system, such as erythromicin (and possibly other, newer macrolides such as clairithromycin=Biaxin, azithromycin=Zithromax) and IV antifungals and oral antifungals (e.g., ketoconazole, fluconazole=Diflucan), quinolones like Levaquin - hyperventilation can cause alkalosis that will prolong QT - acquired prolonged QT interval syndrome exists - asymptomatic but no complex ectopy, or FH of sudden death: nothing or beta blockers - asymptomatic but complex ectopy, or FH of sudden death: beta blockers þ Pericarditis EKG changes þ pediatric EKGs þ EKG Diagnosis of MI with LBBB on EKG: - ST elevation of 1 mm or more that is in same vector direction as QRS - ST elevation of 3 mm or more that is in opposite vector direction as QRS - ST _depression_ of 1 mm or more in V1, V2, or V3. [Sgarbossa EB, et al for GUSTO-1 Investigators. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med 1996;334(8): 481-528.] - focus on J point - if more than 5 mm discordant ST change, indicates MI (Amal Mattu, ACEP 2009) - simple ACEP criteria + concordant ST elevation or depression + opposite but more than 5 mm (not as specific as concordance) ALL these rules also apply with pacemaker Q wave in I or aVL or RsR' in lateral leads > not officially LBBB RBBB can have ST depression, but any ST elevation is pathologic þ Multi-lead EKG's þ Lead Placement þ EKG Changes in Elderly: following are normal variants - QRS widening up to 0.12 - QT prolongation up to normal top limits - Low QRS and P voltage in limb leads (up to 30% less than younger patients) - Left Axis Deviation without LVH - isolated first degree AV block - ST flattening - slight ST depression in left precordial leads - decreased T wave amplitude following are NOT normal variants - LBBB - QRS more than 0.12 - LVH consider LV hypertrophy in elderly only if RV5+SV1 more than 36 and RaVL at least 11. [Jones J, Srodulski AM, Romisher S. Am J Emerg Med 1990; 8:240.] þ Normal Sinus Rate - official designation is 60-100/min - should really be 50-90/min [Spodick DH, et al. Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined. Am Heart J 1992;124(4):1119.] þ Ventricular Hypertrophy: RVH: - R in V1 0.5 mV or more - S in V5-6 0.7 mV or more - QRS axis > 110 degrees LVH: - V2+V5 > 35 mm - any lead > 11 - Rosenbaum criteria: an S wave in lead III deeper than 15 mm - R in lateral chest leads more than 2.0 mV - QRS shifts to left in frontal plane (0 to -30, sometimes more negative) - S in V1-2 more than 2.5 mV * Sokolow + Lyon (Am Heart J, 1949;37:161) o S V1+ R V5 or V6 > 35 mm * Cornell criteria (Circulation, 1987;3: 565-72) o SV3 + R avl > 28 mm in men o SV3 + R avl > 20 mm in women * Framingham criteria (Circulation,1990; 81:815-820) o R avl > 11mm, R V4-6 > 25mm o S V1-3 > 25 mm, S V1 or V2 + o R V5 or V6 > 35 mm, R I + S III > 25 mm * Romhilt + Estes (Am Heart J, 1986:75:752-58) o Point score system # left ventricular hypertrophy * In the presence of left anterior hemiblock the diagnostic criteria of LVH are changed. Rosenbaum suggested that an S wave in lead III deeper than 15 mm as predictive of LVH. # long PR interval (also called first degree heart block) * PR interval longer than 0.2 seconds Young, healthy, thin-chested individuals often exceed the QRS voltage criteria for LVH. However, with ST and T changes of "strain" can definitiely diagnose LVH. Left atrial abnormality (dilatation or hypertrophy) * M shaped P wave in lead II * prominent terminal negative component to P wave in lead V1 (shown here) þ T wave changes with body position - Going from lying to sitting at 90 degrees will make lateral T waves flatten by 1 mm in lead V4, with concordant changes seen when sitting at 45 degrees. [Jolly BT, Sanford SM, Walton KA. Electrocardiographic T-wave changes caused by changes in body position [abstract]. Ann Emerg Med 1996;27(1):118-119.] þ Arrhythmias in Athletic Patients: - first degree heart block (prolongation of the P-R interval). - Wenkebach phenomenon (2nd degree block, Type 1)? In one series, 23% of athletes manifested Wenkebach phenomenon, compared with only a 6% incidence in controls. Ref: Marriott, Practical Electrocardiography 8th ed. p 364 Right Bundle Branch Block * wide QRS, more than 120 ms (3 small squares) * secondary R wave in lead V1 * other features include slurred S wave in lateral leads and T wave changes in the septal leads * 13% of healthy Air Force Academy cadets have this Rotman, M. and J. H. Triebwasser (1975). "A clinical and follow-up study of right and left bundle branch block." Circulation 51(3): 477-484. The experience with bundle branch block at the USAF School of Aerospace Medicine was reviewed. The clinical and follow-up status was evaluated in 394 subjects with right bundle branch block (RBBB) and 125 subjects with left bundle branch block (LBBB). The majority of subjects were asymptomatic at the time of bundle branch block diagnosis. The subjects were divided into subfroups based on electrocardiographic (EEG) findings to determine if any one subfroup was at higher risk for initial or follow-up morbidity of cardiobascular disease or follow-up mortality. At initial diagnosis and clinical evaluation, 94% of RBBB and 89% of LBBB subjects had no evidence of cardiobascular disease. In the RBBB group, 3 and 2% had cornary heart disease and hypertension, respectively; in LBBB subjects, 9 and 7% had cornary heart disease and hypertension, respectively. No one ECG subfroup in either the RBBB or LBBB group had a higher incidence of cardiobascular disease. Complete follow-up information was available in 94% of the RBBB subgroup subjects and 91% of the LBBB group. In the follow-up period, new cases of coronary heart disease and hypertension occurred in 6% of the RBBB group and 5 and 8%, respectively, in the LBBB group. Fourteen (4%) RBBB and nine (8%) LBBB subjects died during the follow-up period. No differences for follow-up groups. Progressive electrical dysfunction in the form of complete heart block occurred in one subject each absence, and degree of associated cardiobascular disease. Furthermore, within the age limits of the present aeromedical implications of bundle block are discussed. # left anterior hemiblock * QRS axis more left than -30 degrees * initial R wave in the inferior leads (II, III and aVF) * absence of any other cause of left axis deviation causes of a Northwest axis (no man's land) * emphysema * hyperkalaemia * lead transposition * artificial cardiac pacing * ventricular tachycardia causes of right axis deviation * normal finding in children and tall thin adults * right ventricular hypertrophy * chronic lung disease even without pulmonary hypertension * anterolateral myocardial infarction * left posterior hemiblock * pulmonary embolus * Wolff-Parkinson-White syndrome - left sided accessory pathway * atrial septal defect * ventricular septal defect causes of left axis deviation * left anterior hemiblock * Q waves of inferior myocardial infarction * artificial cardiac pacing * emphysema * hyperkalaemia * Wolff-Parkinson-White syndrome - right sided accessory pathway * tricuspid atresia * ostium primum ASD * injection of contrast into left coronary artery Posterior fascicular block - less common. You will see right axis deviation, an S in lead I and an Q in lead III (S1Q3). The QRS will be slightly prolonged (0.1 - 0.12 sec)