Deck 1 Flashcards
21-year-old female with a history of “seizure” disorder. She is on no medications and her electrolytes are normal. This ECG is most consistent with which ONE of the following? * * Difficulty rating
a) Wolff-Parkinson-White (WPW) pre-excitation
b) Long QT syndrome
c) Hypokalemia
d) Tricyclic overdose
e) Hypothyroidism
b) Long QT syndrome
Answer: Dx: Congenital (hereditary) long QT syndrome. The ECG demonstrates sinus rhythm with a very prolonged QT interval of 0.6 second. Note the broad T waves with notching (or possibly U waves) in the precordial leads. This characteristic may identify patients with long QT syndrome at increased risk for torsade de pointes and syncope and sudden death. Patients at high risk of recurrent syncope or sudden death are usually considered for implantable cardioverter defibrillator therapy along with beta-blockade. Over a dozen different “channelopathies” have been identified in the pathogenesis of congenital long QT syndrome. (Lehnart SE et al..Inherited arrhythmias: a National Heart, Lung, and Blood Institute and Office of Rare Diseases workshop consensus report about the diagnosis, phenotyping, molecular mechanisms, and therapeutic approaches for primary cardiomyopathies of gene mutations affecting ion channel function Circulation. 2007; 116:2325-45. T wave morphology can be helpful in determining the type of congenital LQTS (Moss AJ et al. ECG T-wave patterns in genetically distinct forms of the hereditary long QT syndrome. Circulation 1995; 92: 2929-34). Multiple medications can cause acquired LQTS also increasing the risk of torsade de pointes and sudden death. The measurement of the QT poses a number of challenges and controversies.
Visually, one should use the longest QT (often best seen in chest leads), and not restrict measurement to lead II or any single other lead. A number of rate-correction algorithms have been proposed; none has emerged as a consensus method. A variety of automated methods have also been devised–but computer generated QT measures (and indeed, all computer assessments) should always be visually validated. Low amplitude, but prolonged T waves may lead to underestimation by eye or computer.
18-year-old pre-op ECG for knee surgery. What does this ECG show? * * Difficulty rating
a) Limb lead reversal
b) Ectopic atrial rhythm (EAR)
c) Dextrocardia
d) Coronary sinus rhythm
e) Multifocal atrial rhythm (MAT)
Limb lead reversal. The left and right arm leads are reversed. The clue is inversion of the P wave and QRS complex in lead I. Whenever you see a negative P wave and QRS complex in lead I the likely diagnosis is limb lead reversal.
Dextrocardia is another possibility, but in dextrocardia there is loss of R wave progression in the left chest leads which is not seen in this tracing. Another clue is the dissimilarity of the morphology of the QRS complexes in lead I and V6. No evidence of multiple P wave morphologies are present ruling out MAT.
(The variability in heart rate here is due to respiratory sinus arrhythmia, a physiologic finding that is most apparent in younger healthy subjects.) Also, note the slight J point/ST elevations in leads with a positive QRS, consistent with normal variant (benign) early repolarization pattern.
Question: History: 36-year-old male with hypertension and hypercholesterolemia presents to the emergency room with 3 hrs of chest pain and the following ECG. How would you manage this patient based on this ECG? * * * Difficulty rating
a) Thrombolytic therapy
b) Urgent cardiac angiography and stand-by angioplasty
c) Conservative management with nonsteroidal analgesia
d) Work-up for pulmonary embolism
e) Urgent trans-esophageal echocardiogram
This patient’s ECG is consistent with acute pericarditis. Always consider myocardial infarction first when you see ST elevations, but don’t forget the differential diagnosis of ST elevations not only includes 1) ischemic heart disease (MI, Prinzmetal angina, ventricular aneurysm) but also 2) pericarditis, 3) left bundle branch block (LBBB) (in V1-V3) and 4) normal (“early repolarization”) variant (J point elevation). In this ECG two features point to pericarditis: First, the diffuseness of the ST elevations (I, II, III, aVF, V3-V6). In myocardial infarction the ST elevations tend to be localized (inferior, anterior, posterior, lateral), often, but not always with reciprocal ST depressions. Second, the PR segment displacement which has been attributed to subepicardial atrial injury. PR elevation can be seen in aVR and PR depression is best seen in II, aVF, V4-V6. Obviously troponin and CK-MB blood tests and possible transthoracic echocadiogram (for effusion and possible evidence of diffuse myocarditis) will be helpful, following a careful history and physical exam. Reference: Spodick DH. Diagnostic electrocardiographic sequences in acute pericarditis: significance of PR segment and PR vector changes. Circulation 1973; 48:575.
Question: Elderly female admitted with obtundation. What electrolyte abnormality is strongly suggested? * * * Difficulty rating
a) Hyponatremia
b) Hypernatremia
c) Hyperkalemia
d) Hypokalemia
e) Hypercalcemia
Hyperkalemia (K+ = 8.7 mEq/L) secondary to acute renal failure. The ECG shows symmetrically peaked (“tented”) T waves associated with potassium levels in excess of 6 mEq/L. The tracing also shows broad and flattened sinus P waves that may precede frank sino-ventricular conduction seen with severe hyperkalemia (i.e., conduction from the sinus node to the ventricles through specialized inter-nodal tissue without atrial depolarization). This conduction pattern may simulate a junctional rhythm. The narrow QRS complex in this tracing is somewhat atypical for severe hyperkalemia. Milder degrees of hyperkalemia may actually facilitate AV conduction. Note that T wave peaking with hyperkalemia is a relative finding: the absolute magnitude of the T waves cannot be used to rule in or rule out hyperkalemia. Indeed, in some cases of hyperkalemia with left ventricular hypertrophy, the T wave peaking may affect inverted T waves or cause relative normalization. The presence of relatively low voltage and sinus bradycardia in this clinical setting should also raise consideration of hypothyroidism/myxedema, which by itself usually also causes T wave flattening. Note is made that even relatively high levels of potassium may not produce classic changes on the ECG depending on a number of factors, including the rate that the K+ goes up. Thus specific levels of serum potassium cannot be linked to unique ECG patternsl
85-year-old male without symptoms and on no pertinent cardiac medications. What is the rhythm here? * * * Difficulty rating
a) Atrial tachycardia with AV block
b) Sinus bradycardia (marked) conistent with sick sinus syndrome
c) Sinus rhythm with 2:1 AV block
d) Sinus rhythm with complete (third degree) AV block
e) Sinus rhythm with 3:2 AV Wenckebach
The ECG shows a very slow ventricular rate (about 32/min) with non-conducted sinus P waves alternating with normally conducted P waves. The sinus (P) wave rate is about 64. The conducted PR intervals are constant at about 200ms. It is not possible to identify with certainty the location of block (nodal vs. infranodal) from this single ECG showing 2:1 AV conduction. The site of block could be proximal (in the AV node) or more distal, in the His-Purkinje system, especially intra-Hisian in this case given the narrow QRS. In general, with 2:1 block, involvement of the AV node is favored by a narrow QRS complex and a prolonged PR interval, or by the presence of intermittent AV Wenckebach. Block that is infranodal (in the His-Purkinje system) would be favored by a concomitant bundle branch block and/or a PR interval of 160 ms or less. Possibly useful bedside diagnostic tests for locating the site of chronic 2:1 block (in the absence of active ischemia) would include autonomic interventions. Sympathetic stimulation (e.g. by mild exercise) should increase heart rate and improve conduction with a nodal location of block, but worsen conduction in infra-nodal block. Carotid sinus massage (if not contraindicated) would decrease heart rate and worsen AV conduction in the case of nodal block but might improve AV conduction in infra-nodal block. Pacemaker placement is indicated for symptomatic 2:1 block at any site without a reversible cause (e.g., drug effect, Lyme disease) and for asymptomatic 2:1 block due to infranodal disease. Intracardiac His bundle electrograms would definitively locate the site of block. This patient had intermittent 3:2 AV Wenckebach at other times, and then resumed 1:1 conduction on subsequent ECGs, consistent with AV node disease. The ECG also shows left atrial abnormality, borderline left axis deviation and LVH by voltage, along with non-specific ST-T changes. The LVH could be from systemic hypertension, but always raises concern about aortic stenosis.
Question: 71-year-old female with mitral stenosis and a history of atrial fibrillation. What is the rhythm now? * * * * Difficulty rating
a) Atrial flutter with variable AV block
b) Multifocal atrial tachycardia with variable AV block
c) Sinus rhythm with variable AV block
d) Ectopic atrial rhythm with variable AV block
e) Accerated idioventricular rhythm
Rhythm: Ectopic atrial (non-sinus) rhythm (borderline for atrial tachycardia – atrial rate around 95/min) with 2:1 block and 3:2 AV Wenckebach (beats 4 and 5), accounting for the bradycardic QRS rate (about 48/min). Note the negative P waves in lead II indicating a non-sinus pacemaker. Other important abnormalities: right bundle branch block, left anterior fascicular block and a markedly prolonged QT(U) interval. This patient was on digoxin and quinidine. The evidence for quinidine excess (assuming the serum potassium is normal and no other factors prolonging ventricular repolarization are identifiable) is the very long QT(U) interval best seen in V2-V5. This finding predisposes to torsade de pointes and may occur with “therapeutic” or “subtherapeutic” levels of quinidine or other class 1A antiarrhythmic drugs. Atrial rhythm/ tachycardia with Mobitz I block also strongly raises the question of digitalis toxicity in patients on that class of medication. (However, atrial tachycardias with AV block in the general population are usually not due to digitalis excess.) With pure 2:1 AV block, it may be impossible from the surface ECG to tell if the non-conducted beats are due to nodal or infranodal block. The clue here centers on beats 4 and 5 where 3:2 Wenckebach is evident, indicating block in the AV node. The atrial rate of close to 100 cycles/min is faster than the usual ectopic atrial escape rhythm, so this ECG can be read as accelerated ectopic atrial rhythm or “slow/borderline atrial tachycardia” with AV block.
49-year-old woman with a “rapid heart beat” has the following ECG. What is the rhythm? * * * * Difficulty rating
a) Sinus tachycardia
b) AV nodal reentrant tachycardia
c) Atrial flutter with 2:1 AV block
d) Atrial fibrillation
e) Atrial tachycardia
The ECG shows classic AV nodal reentrant tachycardia (AVNRT). This tracing demonstrates a regular, narrow complex tachycardia at a rate of 150 bpm. The differential diagnosis of a regular narrow tachycardia in general includes 5 major mechanisms: sinus tachycardia, AVNRT, atrial tachycardia, orthodromic atrio-ventricular reentrant tachycardia (AVRT) involving retrograde conduction over a “concealed” bypass tract, or atrial flutter with 2:1 block. If P waves can be located it can be helpful in determining the mechanism of the tachycardia.
In this tracing, P waves can be located at the end of the QRS in lead II (best seen on the rhythm strip). In the beginning of the tracing, P waves are buried in the end of QRS complex, but then gradually come further out behind it. By the end of the tracing inverted P waves can be clearly seen in the rhythm strip. This finding rules out the diagnosis of AV re-entry due to a concealed bypass tract (in which case the R-P interval is fixed and cannot be as short as in the beginning of this tracing since the ventricles and atria are activated sequentially). There is clearly a 1:1 AV relationship here with no extra atrial waves in between ruling out atrial flutter with 2:1 AV conduction. That leaves 2 diagnoses: AVNRT and atrial tachycardia. Often it is impossible to tell the difference between the two unless initiation or termination of arrhythmias is recorded. However, in this case there are subtle but important diagnostic clues allowing one to infer the exact diagnosis. Note that not only the R-P relationship is changing, but ventricular rate is becoming faster. At the same time, the P-R interval gets shorter. Usually, if ectopic P waves are conducted over the AV node, the PR interval increases with increased heart rate consistent with decremental properties of the AV node. In this case PR interval gets shorter suggesting that P waves are unrelated to the subsequent QRS. This strongly supports the diagnosis of AVNRT. The gradual increase in the R-P interval (slowing of conduction over the ~fast~ AV nodal pathway can often be seen in typical AVNRT prior to spontaneous termination (that typically occurs in the ~fast~ pathway). Slowing of fast pathway conduction results in more delayed engagement of the ~slow~ pathway giving it more time to recover, hence the apparent shortening of PR the interval.
Absence of visible P waves or the presence of a “pseudo S” pattern in II, III, or aVF, or a “pseudo R prime” pattern in V1 is characteristic of AVNRT due to near simultaneous activation of the atrium and the ventricle from the AV node. If the diagnosis is still in doubt, adenosine (if not contraindicated) may be useful in slowing conduction in the AV node. Reentrant rhythms (AVNRT or AVRT) may “break” abruptly, converting to sinus; the ventricular response of either atrial tachycardia or atrial flutter will sometimes slow abruptly often revealing underlying atrial activity. (Note: the final “wide complex” waveform appears to be an artifact superimposed on an AVNRT beat.)
The ECG is from a 56-year-old male with known severe mitral regurgitation and history of adenocarcinoma who presented to the emergency ward in shock and died after aggressive attempts at resuscitation. He did not have a pericardial effusion. All of the following statements about this ECG are correct EXCEPT for which ONE of the following? * * * * Difficulty rating
a) The rhythm is atrial fibrillation
b) Right axis deviation is present
c) The ECG is absolutely diagnostic of an underlying anterior wall MI
d) The ECG is consistent with a non-ischemic cardiomyopathy
e) Low limb lead voltage is present
Answer: The surprising diagnosis was cardiomyopathy associated with a widely disseminated adenocarcinoma of unknown primary origin. The ECG shows atrial fibrillation with markedly decreased voltage in the limb leads, a rightward axis, and loss of R wave progression V1-V3. A transthoracic echocardiogram showed no significant pericardial effusion. The differential diagnosis also includes anterior myocardial infarction, myocarditis, severe chronic obstructive pulmonary disease, and an infiltrative process such as amyloidosis or more rarely, tumor resulting in a “pseudo-infarction” pattern of this type. However, as illustrated here, loss of R wave progression, sometimes with frank Q waves, is not pathognomonic of anterior MI.
This is the admitting ECG of a previously healthy 49-year-old man who presented with progressive muscle weakness and constipation. He had no chest pain or dyspnea. The ECG is most consistent with which ONE of the following diagnoses? * * * Difficulty rating
a) Hypokalemia
b) Hyperkalemia
c) Hypocalcemia
d) Hypercalcemia
e) Hypothyroidism
The ECG shows sinus rhythm with the following key abnormality: a very short ST segment with a consequently short QT interval (about 300 msec here). The differential diagnosis of a short QT (lower limits are not well-defined) is much narrower than that of prolonged QT. The two chief causes of a short QT are hypercalcemia and digoxin therapy (associated with characteristic “scooping” of the ST-T complex). A third and relatively rare cause is hereditary short QT (“channelopathy”-related) that may be associated with ventricular arrhythmia and sudden cardiac arrest. (see Gussak I, eta. Idiopathic short QT interval: a new clinical syndrome? Cardiology 2000;94:99–102). Cardiac arrhythmias, however, are unusual with hypercalcemia; but AV block, sinus arrest, sino-atrial block, ventricular tachycardia, and cardiac arrest have been reported, usually in patients receiving rapid IV injections of calcium. This patient’s serum calcium was 16 mg/dl. He was found to have hyperparathyroidism; at surgery, he had successful resection of a parathyroid carcinoma, an unusual cause of hypercalcemia.
The patient is an elderly man who presented to the emergency ward with dizziness and new renal failure. What is the cause of the very wide QRS?
Dx: Hyperkalemia (7.6 mEq/L), secondary to the renal failure. The ECG demonstrates findings consistent with severe hyperkalemia – most importantly marked widening of the QRS complex. The QRS complex here shows an intraventricular conduction delay (IVCD) with a left bundle branch block (LBBB) morphology and left axis deviation. However, the QRS duration (about 240 ms) is much wider than that seen with an “uncomplicated” LBBB (or with left anterior fascicular block) due to intrinsic conduction disease. There is also peaking of the T waves with prolongation of the PR interval and flattening of the P waves. If the hyperkalemia is left untreated, the ECG will progress to a sinusoidal pattern and eventually asystole with subsequent hemodynamic collapse and death.
51-year-old male with bicuspid aortic valve, aortic insufficiency and hypertension had an episode of chest pain 2 days prior to this tracing. Without clinical information, this type of pattern of T wave inversions is LEAST likely attributable to which ONE of the following? * * * * Difficulty rating
a) Non-Q wave MI with Wellens’ syndrome (T wave inversions due to left anterior descending; LAD) ischemia
b) Takotsubo syndrome
c) Evolving pericarditis
d) Central nervous system pathology (especially intracranial bleed)
e) Apical hypertrophic cardiomyopathy
Answer: This ECG shows sinus rhythm at about 65 beats/min with diffuse, prominent anterior T wave inversions consistent with probable ischemia/non-Q wave myocardial infarction (MI). Sometimes this pattern is referred to as ~Wellens’~ T waves~ (de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J. 1989;117:657~ 665 or “LAD-T wave” pattern. The ECG also shows findings consistent with left atrial abnormality and left ventricular hypertrophy, along with non-specific mild PR prolongation (220 msec), QT prolongation for rate (480 msec), and borderline left axis deviation. Ischemia/infarction should be on the top of your differential diagnosis list in this patient with a recent history of chest pain. A tracing during the episode of chest pain revealed 1-2 mm ST elevation in leads I, aVL, V3-V6. Cardiac catheterization revealed noncritical coronary artery disease and global left ventricular dysfunction. A subsequent echocardiogram taken on the day of this tracing revealed normal left ventricular function. Most likely the patient had a transient thrombus or spasm in the proximal LAD, with severe myocardial “stunning.” Enzymes were only slightly elevated. Other specific diagnoses to consider in a patient with diffuse deeply inverted T waves include 1) CNS disease–not clinically present here (intracranial hemorrhage, head injury, tumor); 2) apical hypertrophic cardiomyopathy (usually most marked in the mid-lateral precordial leads; 3) intermittent right ventricular pacing or intermittent LBBB (“memory T waves”; however this syndrome is usually associated with with upright T waves in I and aVL (Shvilkin A, Ho KKL, Rosen MR, Josephson ME. T vector direction differentiates post-pacing from ischemic T wave inversion in the precordial leads. Circulation 2005; 111:969-974); 4) takotsubo (stress) cardiomyopathy (left ventricular apical “ballooning” pattern on angiogram), and 5) idiopathic global T wave inversions (a diagnosis of exclusion). Pericarditis may be associated with diffuse T wave inversions, but they are relatively low amplitude (usually <5mm),
The patient is an elderly female with a known history of left bundle branch block who presented to the emergency ward with shortness of breath. What is your diagnosis? * * * Difficulty rating
Answer: Dx: Sinus bradycardia, left bundle branch block (LBBB ) with primary ST-T wave changes. The ECG demonstrates an LBBB morphology with primary biphasic and inverted T waves in leads 2, 3 and F. Uncomplicated bundle branch blocks should only have “secondary” T wave changes. That is the ST-T waves should be opposite in direction to the major vector of the QRS. For example, if this ECG with LBBB was uncomplicated, the ST-T waves in the inferior leads would be upright. This patient has inverted T waves suggesting that a “primary” or ischemic process is evolving in the inferior distribution. However, the absence of primary ST-T changes does not exclude ischemia/MI. The patient did in fact rule in for a myocardial infarction, with positive cardiac biomarkers. This example illustrates that ischemic ECG changes can sometimes be read despite the presence of a left bundle branch block.
Question: A middle-aged woman with a history of a “heart murmur” since childhood presents with worsening dyspnea. The ECG is most consistent with which ONE of the following major diagnoses? * * * Difficulty rating
a) Mitral regurgitation
b) Mitral stenosis
c) Aortic regurgitation
d) Aortic stenosis
e) Pulmonic stenosis
The ECG reveals sinus rhythm with the following abnormalities: left atrial abnormality (LAA) in concert with a relatively tall R wave (increased Rs ratio) in lead V1 and an inverted T wave in that lead, along with right axis deviation (RAD). The combination of a predominant R wave (even with overall low amplitude QRS voltage) and rightward axis deviation with a normal QRS duration suggests right ventricular hypertrophy. This pattern along with left atrial abnormality should make one strongly consider mitral stenosis. An important finding on this ECG is the relatively tall R wave in V1. The differential diagnosis of this finding includes: normal, childhood ECG, posterior myocardial infarction (usually with Q&39;s inferiorly), RVH (usually with right axis and T wave inversions in V1-V2), rightward displacement of the heart (e.g. left pneumothorax), Wolff-Parkinson-White pattern due to posterior or lateral wall pre-excitation, hypertrophic cardiomyopathy with large septal forces (usually see large lateral Q waves as well), RBBB. In this case, the presence of RAD and anterior T wave strain suggests RVH as the cause for the tall R in V1, and the concomitant presence of LAA strongly suggests the diagnosis of mitral stenosis. The patient in fact had severe mitral stenosis, which was treated surgically.
Note: The S1Q3T3 pattern ( rS complex in lead I, qR and T wave inversion in lead III) noted here is sometimes attributable to RV overload due to pulmonary embolism (see Case 146). However, this pattern is non-specific and may be seen with a variety of causes of RV overload, acute and chronic, as well as in other settings. The presence of marked left atrial abnormality and the absence of sinus tachycardia are both against a unifying diagnosis of acute pulmonary embolism in this case. Also of note is the absence of the anticipated right precordial T inversions often associated with RV overload syndromes (formerly called an RV “strain” pattern).
Note that evidence for LAA here is best seen at higher gain. The P waves are broad (>120ms in duration) in multiple leads and there is a biphasic P wave in lead V1 with a broad (>40ms) terminal portion. The late P wave forces also go toward lead aVL.
36-yr-old male with the development of chest pain at rest, transferred for cardiac evaluation after a presumed myocardial infarction. (However, serial cardiac enzymes were negative). This ECG is most consistent with which ONE of the following? * * * * Difficulty rating
a) Normal variant/athlete’s heart
b) Apical hypertrophic cardiomyopathy/Yamaguchi’s syndrome
c) Dilated cardiomyopathy
d) Anterior wall ischemia (left anterior descending distribution)
e) Critical valvular aortic stenosis
Hypertrophic cardiomyopathy, apical variant (Yamaguchi’s syndrome). The ECG shows sinus bradycardia at about 58/min with marked left ventricular hypertrophy (LVH) and unusual, very deep (“giant”) T wave inversions in the precordial and limb leads. ST depressions are seen in the lateral chest leads. Yamaguchi’s cardiomyopathy is characterized by isolated apical hypertrophy. The surface ECG shows LVH and T wave inversions predominantly in V3-V5 but often present in other leads. Apical hypertrophic cardiomyopathy as well as more common forms of hypertrophic cardiomyopathy are important causes of pseudo-infarct patterns. The initial report of Yamaguchi’s syndrome can be found in Am J Cardiol 44:401,1979.
59-year-old female with sudden palpitations and lightheadedness. What is the rhythm? * * * * Difficulty rating
a) Atrial fibrillation with WPW (Wolff-Parkinson-White) pre-excitation
b) Ventricular tachycardia (monomorphic)
c) Ventricular tachycardia (torsades de pointes)
d) Atrial fibrillation with right bundle branch block aberrancy
e) Tremor artifact with Parkinson’s disease
Answer: The ECG shows a dramatic example of atrial fibrillation with the Wolff-Parkinson-White (WPW) syndrome, with conduction down the bypass tract. This rhythm is for the most part a wide complex tachycardia with a rate of about 230 beats/min. The differential diagnosis includes 1) ventricular tachycardia, 2) supraventricular tachycardia with aberrancy, and 3) WPW with conduction down the bypass tract. The major clues include the “irregularly irregular” rhythm and the extremely rapid rate. Ventricular tachycardia may be mildy irregular but this degree of irregularity would be unusual at this very fast rate. The short refractory period of certain bypass tracts can allow extremely rapid heart rates, especially during atrial fibrillation. A correct diagnosis is very important because drugs that slow AV conduction (verapamil, beta blockers, digoxin, adenosine) are not useful. Verapamil by vasodilation and reflex neuroautonomic changes may increase conduction down the bypass tract. The effects of digoxin are still controversial and this drug may shorten the refractory period of the bypass tract. Call cardiac EP experts stat! A drug of choice is IV procainamide and if this is unsuccessful, DC cardioversion should be performed promptly, if not otherwise contraindicated.
Question: 60-yr-old female with a history of anti-phospholipid syndrome who presented with anterior chest discomfort. * * * Difficulty rating
Sinus rhythm is present (note the positive P waves in lead II) with AV Wenckebach causing 4:3 conduction in the setting of an acute/evolving ST elevation/Q wave inferior wall infarction. The ECG demonstrates pathologic Q waves and prominent ST elevations in leads 2, 3, and aVF. There are also ST segment depressions in leads 1 and aVL, consistent with reciprocal changes; slight ST depressions in V2-3 are also noted. In this context these ST depressions are likely reciprocal to posterior–lateral ST elevations (not seen on the standard 12-lead). The rhythm, as described, is sinus with AV Wenckebach showing progressive prolongation of the PR intervals, shortening of the R-R intervals (not always seen) and block of every fourth P wave. Note that the PR of the conducted P wave after the non-conducted (“dropped”) one is shorter than the PR before the last conducted PR in each cycle. This is the key marker of AV Wenckebach. The presence of “group” beating is an important clue and characteristic of second degree blocks. Group beating may also be seen with pauses after atrial (conducted or blocked) or ventricular premature beats. AV Wenckebach in the context of an acute inferior MI is attributed to high vagal tone and/or nodal ischemia. The block proximal, i.e., at the level of the AV node and transient. The findings are consistent with occlusion of a dominant right coronary that also supplies the AV node and the posterior and possibly lateral wall. Of further note, is the subtle finding that the 4th P wave in each Wenckebach cycle comes somewhat earlier than anticipated. This pattern is most consistent with a ventriculo-phasic sinus arrhythmia, and not to a blocked PAC. The term ventriculo-phasic response (VR) refers to transient shortening of the sinoatrial cycle interval when a QRS complex occurs between two sinus P waves during second or third degree AV block. The actual mechanism is not fully ascertained; it may be related to mechano-electrical interactions.
