EKG Mattu #1 Flashcards
1. Sinus rhythm (SR), rate 60, normal ECG. SR is generally defined as having an atrial rate of 60–100/minute and a P-wave axis +15 to +75 degrees. Sinus beats can be identified by upright P-waves in leads I, II, III, and aVF; if the P-waves are inverted in any of these leads, it implies an ectopic atrial origin for the P-waves. The PR interval should be >0·20 seconds; a shorter PR interval suggests either an atrioventricular (AV) junctional origin or the presence of a pre-excitation syndrome (for example Wolff-Parkinson-White syndrome). The normal ECG often will demonstrate inverted T-waves in leads aVR and V1.
2. SR with sinus arrhythmia, rate 66, benign early repolarization (BER). Sinus arrhythmia is defined as sinus rhythm with slight variation (>0·16 seconds) in the sinus cycles. This produces mild irregularity in the rhythm and usually occurs at lower heart rates (<70/minute). BER is a normal variant often found in young healthy adults, especially men. Patients will have ST-segment elevation in many leads, although not in aVR or V1. The absence of reciprocal ST-segment changes helps distinguish this entity from acute myocardial infarction. Acute pericarditis can be difficult to distinguish from BER. The presence of PR-segment depression in various leads favors the diagnosis of acute pericarditis; however, the distinction between these two entities often must be made based on the patient history and physicial examination: acute pericarditis is classically associated with pleuritic sharp chest pain that changes with body position, and these patients may have a pericardial friction rub heard during cardiac auscultation.
- SR, rate 91, with first degree AV block. The normal PR-interval is 0·12–0·20 seconds. This patient has a marked first degree AV block with a PR-interval of 0·32 seconds.
4. Ectopic atrial rhythm, rate 82, otherwise normal ECG. P-waves in leads I, II, and aVF are inverted suggesting an ectopic origin of the atrial beats. The normal PR-interval (0·16 seconds) implies that the origin is in the atrium rather than in the AV junction.
5. AV junctional rhythm, rate 50. AV junctional rhythms are usually associated with a rate of 40–60/minute and narrow QRS complexes (unless there is a conduction abnormality, for example bundle branch block). If an AV junctional rhythm has a rate 61–100/minute, it is referred to as an “accelerated AV junctional rhythm;” if the rate is >100/minute, it is referred to as an “AV junctional tachycardia.” In AV junctional rhythms, P-waves may be hidden or may precede or follow the QRS complex. When these “retrograde” P-waves precede the QRS, they will be associated with a short PR-interval (<0·12 seconds). This patient had recently started taking a calcium channel blocking medication for hypertension. When the medication was discontinued, SR returned and the ventricular rate increased.
6. Accelerated idioventricular rhythm (AIVR), rate 65. Ventricular escape rhythms are usually associated with rates 20–40/minute. When a ventricular rhythm is 40–110/minute, it is referred to as an “accelerated ventricular rhythm” or “accelerated idioventricular rhythm.” When the rate exceeds 110/minute, “ventricular tachycardia” is diagnosed. This patient’s rhythm strip demonstrates evidence of AV dissociation, easily seen in the latter portion of the strip. AIVR is commonly seen in the setting of AMI, especially after the administration of thrombolytic agents. AIVR is thought to be a marker of reperfusion. This patient’s dysrhythmia resolved in minutes without therapy, typical of post-thrombolytic AIVR.
7. SR, rate 100, right bundle branch block (RBBB). RBBB is typically associated with an rSR’ pattern in the right precordial leads, although a single, wide R-wave or a qR pattern may be seen instead. The S-wave in the lateral leads (I, aVL, V5, V6) is slightly wide, and the QRS duration is ≥0·12 seconds. If all the criteria are met except the QRS duration is ≤0·12 seconds, an incomplete RBBB is diagnosed. Leads V1−V3 often demonstrate ST-segment depression and inverted T-waves. Any ST-segment elevation should alert the healthcare provider to the possibility of AMI.
8. SR, rate 80, first degree AV block, left bundle branch block (LBBB). LBBB is characterized by prolonged QRS duration ≥0·12 seconds, leftward QRS axis, a broad monophasic R-wave in leads I and V6, and a deep wide S-wave in lead V1 (often times without any R-wave). The ST-segments and the T-waves are directed in an opposite direction to the main QRS vector in all leads (the rule of “appropriate discordance”). This patient had a pre-existing LBBB and borderline first degree AV block. The increased dose of the beta-receptor blocking medication caused a significant increase in the PR-interval. See figure on p. 55.
9. SR, rate 81, left anterior fascicular block (LAFB). LAFB is associated with a leftward QRS axis, a qR complex (small q-wave and large R-wave) or R-wave in leads I and aVL, rS complex (small r-wave and large S-wave) in lead III, and absence of other causes of leftward axis. The differential diagnosis of leftward axis includes the following: LAFB, LBBB, inferior myocardial infarction, left ventricular hypertrophy, ventricular ectopy, paced beats, and Wolff-Parkinson-White syndrome.
SR, rate 85, RBBB, left posterior fascicular block (LPFB). The combination of a RBBB plus a fascicular block is also called a “bifascicular block.” LPFB is much less common than LAFB. It usually occurs concurrently with an RBBB rather than in isolation. The T-wave inversions in the inferior leads are commonly found with this type of bifascicular block. LPFB is associated with a rightward QRS axis, a qR complex (small q-wave and large R-wave) in lead III, and absence of other causes of rightward axis. The differential diagnosis of rightward axis includes the following: LPFB, lateral myocardial infarction, right ventricular hypertrophy, acute (for example pulmonary embolism) and chronic (for example emphysema) lung disease, ventricular ectopy, hyperkalemia, overdoses of sodium channel blocking drugs (for example cyclic antidepressants). Normal young or slender adults with a horizontally positioned heart can also demonstrate a rightward QRS axis on the ECG.
AV junctional rhythm, rate 50, acute anterior and high lateral myocardial infarction. P-waves are present with a short PR-interval (<0·12 seconds), suggesting an AV junctional origin of the beats. The rate is typical of an AV junctional origin. ST-segment elevation is present in the mid-precordial leads leading to the diagnosis of an anterior wall myocardial infarction (MI). ST-segment elevation is also present in leads I and aVL, corresponding to the high lateral wall of the left ventricle. Reciprocal ST-segment depression is present in the inferior leads. The presence of reciprocal changes significantly increases the specificity of ST-segment elevation for an acute MI.
SR with second degree AV block type 1 (Mobitz I, Wenckebach), rate 50, left ventricular hypertrophy (LVH), RBBB. Mobitz I is characterized by regular P-waves (the atrial rate here is approximately 65/minute) with progressive prolongation of the PR-interval until a P-wave fails to conduct to the ventricle. Usually there is also progressive shortening of the RR interval until the P-wave is non-conducted. LVH is diagnosed on this ECG based on the R-wave amplitude in lead aVL >11 mm. Leftward axis is due to LVH.
Ventricular tachycardia (VT), rate 140. When the ECG rhythm is a wide-complex regular tachycardia, the differential diagnosis includes sinus tachycardia (ST) with aberrant conduction, supraventricular tachycardia(SVT) with aberrant conduction, and VT. ST is ruled out based on the absence of a regular association between atrial and ventricular complexes. The distinction between SVT with aberrant conduction versus VT is difficult. In this case, the presence of AV dissociation (P-waves are intermittently seen, especially in leads V1 and II) excludes the diagnosis of SVT. In general, wide-complex regular tachydysrhythmias that do not show regular sinus activity should always be treated as VT; inappropriate treatment of VT as an SVT may induce hemodynamic compromise.
SR, rate 87, Wolff-Parkinson-White syndrome (WPW). WPW, the most common ventricular pre-excitation syndrome, is characterized by the triad of:
- short PR-interval <0·12 seconds
- prolongation of the QRS complex >0·10 seconds
- a slurred upstroke of the QRS complex (“delta wave”).
WPW can simulate ventricular hypertrophy, bundle branch block, and previous MI. Leftward axis in this case is attributed to WPW.
ST, rate 155. When the ECG rhythm is a narrow-complex regular tachycardia, the differential diagnosis includes ST, SVT, and atrial flutter. Distinguishing amongst these three entities is based on close evaluation of the atrial activity. In this case, there is a 1:1 relationship between the P-waves and the QRS complexes, thus confirming the diagnosis of ST.
Sinus bradycardia (SB), rate 50, LVH, acute pericarditis. LVH is diagnosed in this case based on the R-wave amplitude in V5 (or V6) + the S-wave amplitude in V1 >35 mm. Diffuse ST-segment elevation is also present. The absence of reciprocal ST-segment changes and the presence of (subtle) PR-segment depression in several leads favors the diagnosis of acute pericarditis rather than acute MI or BER. This patient’s cardiac examination was notable for an audible friction rub.
Atrial flutter with 2:1 AV conduction, rate 150. The ECG rhythm is a narrow-complex regular tachycardia; therefore, the differential diagnosis is ST, SVT, and atrial flutter. Atrial activity (“flutter-waves”) can be found in the inferior leads at a rate of 300/minute. The atrial complexes are inverted and manifest as a “sawtooth” pattern in the inferior leads, typical of atrial flutter. Whenever the ventricular rate is 150 ± 20/minute, atrial flutter should strongly be considered and the ECG should be closely scrutinized for the presence of flutter-waves.
SR, rate 85, T-wave abnormality consistent with anterior and inferior ischemia, rightward axis. The ECG is highly suggestive of acute pulmonary embolism, which this patient had. The ECG demonstrates the classic SI QIII TIII finding (large S-wave in lead I, small Q-wave in lead III, inverted T-wave in lead III), present in 10–15% of cases of pulmonary embolism. T-wave inversions are common in pulmonary embolism, and the combination of T-wave inversions that occur simultaneously in the inferior and anteroseptal leads should strongly prompt consideration of this diagnosis. Rightward axis is often found on ECGs of patients with acute (for example acute pulmonary embolism) or chronic (for example emphysema) pulmonary disease.
Atrial fibrillation with rapid ventricular response, rate 155. When the ECG rhythm is a narrow-complex irregular tachycardia, the differential diagnosis includes atrial fibrillation, atrial flutter with variable AV conduction, and multifocal atrial tachycardia (MAT). Distinguishing between these three entities is based on close evaluation of the atrial activity. Atrial flutter will be associated with regular atrial activity (flutter-waves). MAT will be associated with irregular atrial activity, and the atrial complexes will vary in morphology (there must be at least three different morphologies for the diagnosis to be made). Atrial fibrillation will not be associated with any notable atrial complexes at all.
AV sequential electronic pacemaker, rate 70, 100% capture. Atrial pacing occurs, indicated by an initial pacemaker “spike” (PS). This is followed by an atrial complex, which then is followed by another PS after a preset delay. The second PS is immediately followed by a QRS complex, indicating successful ventricular depolarization. The QRS complexes have an LBBB-type of morphology and ST-segment/T-wave discordance. The most important finding is that each pair of PSs is followed by ventricular “capture,” indicating proper functioning of the electronic pacemaker.
AV junctional tachycardia, rate 110, RBBB. P-waves preceding the QRS complexes are absent, thus excluding an atrial rhythm. In contrast, P-waves can be found following the QRS complexes (best seen in the precordial leads). This “retrograde” atrial activity is typical of AV junctional rhythms. An RBBB morphology of the QRS complexes is also noted. The rhythm converted to SR with RBBB after a single dose of intravenous adenosine.
ST, rate 110, RBBB, right ventricular hypertrophy (RVH), anteroseptal MI. Although many criteria exist for the diagnosis of RVH, the most common are rightward axis, R:S ratio in lead V1 >1 and in V6 <1, and R-wave amplitude in lead V1 >7 mm. In the presence of RBBB, however, the R-wave amplitude in lead V1 must be >15 mm, as is the case here. This patient had developed RVH from severe chronic obstructive pulmonary disease. Q-waves are present in the right precordial leads, indicating an old anteroseptal MI.
Supraventricular tachycardia (SVT), rate 135, RBBB. This wide-complex regular tachycardia without evidence of sinus P-waves should prompt immediate consideration of ventricular tachycardia. However, the treating physician was quickly able to obtain a copy of a previous ECG, (shown in case #7) which demonstrated sinus rhythm with a pre-existing RBBB. Most importantly, the QRS complex morphologies were identical between the two ECGs; therefore, the diagnosis of SVT with RBBB was made. The patient was treated successfully with adenosine.
Accelerated AV junctional rhythm, rate 84, prolonged QT, J-waves suggestive of hypothermia. The artifact noted in the ECG was caused by shivering – this patient’s body temperature was 25·6 degrees Celsius (78·1 degrees Fahrenheit). J-waves (also known as “Osborne waves”) are most notable in the precordial leads. These are positive deflections in the terminal portions of the QRS complex. The exact cause of the J-wave in hypothermic patients is unknown. Although considered highly sensitive and specific for hypothermia, J-waves are not pathognomonic for hypothermia. Hypothermia is also associated with prolongation of the QRS and QT- intervals (QT = 0·540 seconds in this case; QTc = 0·640 seconds). Other causes of prolonged QT-interval include hypokalemia, hypomagnesemia, hypocalcemia, acute myocardial ischemia, elevated intracranial pressure, drugs with sodium channel blocking effects (for example cyclic antidepressants, quinidine, etc.), and congenital prolonged QT syndrome. QT-interval prolongation in hypothermia and hypocalcemia is completely due to ST-segment prolongation; the T-waves remain unchanged. This is not true for other causes of QT prolongation
