Bundle-branch blocks Understanding the 12-lead ECG, part II Most common electrocardiogram (ECG) abnormality Appears as a wider than normal S complex Occurs when one of the two bundle branches can t conduct the impulse Most common cause: ischemic heart disease 2 ight bundle-branch branch block (BBB) Impulse conduction to right ventricle is blocked Examine lead V 1 to identify BBB ECG show delayed or positive wave Key identifier is S complex wider than 0.12 second, with positive wave in V 1 3 Left bundle branch block (LBBB) Electrical impulses don t reach left side of the heart S wider than 0.12 second Key to recognizing LBBB is a wide downward S wave or rs wave in leads V 1 and V 2 4 5 6
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13 What do you think? What do you think? Sinoatrial block, type II Second-degree atrioventricular (AV) block, type I Second-degree AV block, type II Nonconducted atrial premature impulse Sinoatrial block, type II Second-degree atrioventricular (AV) block, type I Second-degree AV block, type II Nonconducted atrial premature impulse 14 What do you think? Second-degree AV block, type II waves occur regularly in this tracing; Some of them are conducted to the ventricles while others are blocked; therefore, it is second-degree AV block. In this tracing, when the waves are conducted, the intervals do not lengthen; therefore, this is second-degree AV block, type II. 15 16 17 18
19 - pauses in the middle of a regular rhythm. - there are no extra waves during the pauses -- an indication that this is not AV block. - the pause is exactly twice the length of the shorter cycle, indicating regularly firing sinus impulses that fail to conduct to the atrium at times; his is SA block. Because the pause is twice the shorter cycle, it is type II. ecognizing myocardial infarction (MI) Series of predictable ECG changes occur in MI S-segment segment-elevation elevation MI (SEMI)-- --serious type of MI, associated with more complications, higher risk of death 20 Characteristic changes in AMI S elevation S segment elevation over area of damage S depression in leads opposite infarction athological waves educed waves Inverted waves S Occurs in the early stages Occurs in the leads facing the infarction Slight S elevation may be normal in V 1 or V 2 21 22 Deep wave wave changes S Only diagnostic change of myocardial infarction At least 0.04 seconds in duration Depth of more than 25% of ensuing wave S Late change Occurs as S elevation is returning to normal Apparent in many leads 23 24
25 Bundle branch block Anterior wall MI I II III av avl avf V1 V2 V3 V4 V5 V6 Left bundle branch block I II III av avl avf V1 V2 V3 V4 V5 V6 Sequence of changes in evolving AMI S S S 1 minute after onset 1 hour or so after onset A few hours after onset S S A day or so after onset Later changes A few months after AMI 26 Inferior wall SEMI Elevated S segments in leads II, III, and avf, which monitor the heart s inferior or bottom wall Inferior infarction Inferior infarction I II III av avl avf V1 V2 V3 V4 V5 V6 Area of the heart perfused by the right coronary artery 27 ight coronary artery 28 Septal MI erfused by the left anterior descending (LAD) coronary artery S-segment elevation seen in leads V 1 and V 2, the precordial or chest leads located on the anterior chest wall over the septum Anterior-wall SEMI Directly to the left of the septal area Also perfused by the LAD Most muscular, powerful pumping wall of the heart, responsible for large proportion of cardiac output S elevation seen in V 3 and V 4 29 30
31 Anterior infarction Lateral-wall SEMI Anterior infarction erfused by the circumflex artery I II III av avl avf V1 V2 V3 V4 V5 V6 Muscular, contributes significantly to the heart s pumping ability Monitored by precordial (chest) and frontal (limb) leads Left coronary artery S-segment elevation will appear in leads I, avl, V 5, V 6 32 Lateral infarction Lateral infarction I II III av avl avf V1 V2 V3 V4 V5 V6 Common dysrhythmias Left circumflex coronary artery 33 34 Sinus bradycardia Sinus rhythm slower than 60 beats per minute Commonly caused by ischemic heart disease causing sinoatrial (SA) node to malfunction Sinus bradycardia Signs and symptoms: hypotension, lethargy, fatigue, chest pain, difficulty breathing Also seen in MI, some medications (such as beta-blockers), blockers), and well-conditioned athletes 35 36
37 Sinus tachycardia Sinus rhythm faster than 100 beats per minute elated to physiologic cause: fever, infection, pain, physical exertion, anxiety, shock, hypoxia May need beta-blocker blocker if cause unknown 38 Atrial fibrillation (AF) Common dysrhythmia Irregular heart rhythm with no meaningful waves Atrial kick lost, atrias quiver due to depolarization of atrial cells Causes irregular ventricular rate, 40 to 180 beats per minute 39 40 remature ventricular contractions (VCs) Wide abnormal premature S complex Due to conduction through the ventricle instead of His-urkinje system S greater than 0.12 second 41 42
43 Ventricular tachycardia (V) apid rate, 100 to 250 beats per minute Wide, bizarre, S complex followed by large wave atient may be unconscious, pulseless, apneic-- --initiate C If patient awake, treat as medical emergency emergency 43 44 45 46 47 48
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55 56 Hypercalcemia Shortened interval (short/absent S segment) 57 58 Digitalis Scooping of S segment Shortening of interval Low amplitude of wave Elongation of interval High amplitude of U wave 59 60
61 Digitalis poisoning Atrial tachycardia with AV block Digitalis poisoning 1 st degree AV Block AF with accelerated junctional rhythm Mobitz I 62 Bidirectional V Digitalis poisoning Ventricular bigeminy 63 64 ricyclic antidepressants (AD) HYOHEMIA Sinus tachycardia with a prolonged S interval ightward axis Sinus bradycardia with first-degree AV block is evident. all wave in lead av Markedly abnormal repolarization changes suggests AD poisoning 65 he downstroke of each S complex is slurred and is typical of a J (Osborne) wave ( ). 66