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Goldberg - Elettrocardiografia Clinica
Un Approccio Semplificato
Quiz Master: Autovalutazione delle Capacità di Interpretazione Clinica di un ECG
This online section, designed for additional skill mastery, includes 50 ECG cases, grouped thematically. They are of varying levels of difficulty, ranging from entry level to much more challenging. Good luck! This part is self-scored. Working in small groups may be helpful.
Life-Savers: Stat ECG Diagnoses
The following five patients all have different life-threatening problems that you can diagnose from their electrocardiograms ECGs without any further history.
Case 1 A 60-year-old man
Case 2 A 50-year-old man
Case 3 A 68-year-old man
Case 4 A 75-year-old woman
Case 5 A 52-year-old man
Two patients arrive in your clinic office at the same time. Both complain of severe chest discomfort. Only one ambulance and one taxicab are available for transporting them to the nearest hospital, which is 15 miles away. Who gets the taxi, and who gets the ambulance?
Case 6 A 50-year-old man with chest pain
Case 7 A 50-year-old man with chest pain
Four Cases of Mistaken Identity
The following ECGs are incorrectly identified as shown. For each mistakenly interpreted ECG, what is your correct diagnosis?
Case 8 “Left bundle branch block or left ventricular hypertrophy with inferior myocardial infarction”
Case 9 “Complete heart block”
Case 10 “Sinus (or ectopic atrial) tachycardia”
Case 11 “Right axis deviation resulting from lateral wall infarction”
Both of these patients are complaining of palpitations, characterized as an “irregular heartbeat sensation.” What are the diagnoses?
Incomplete Diagnoses of Complete Right Bundle Branch Block
Right bundle branch block was correctly diagnosed in these two patients with chest pain. That finding is only part of the story, however. What else is going on?
Morphing P Waves
What subtle arrhythmia is present in this ECG?
Why is this healthy female crying? (Clue: Consider the QRS duration.)
An ECG is obtained in this 45-year-old man before he undergoes appendectomy. He complains of lower left quadrant pain. The ECG is unchanged from a previous one, at which time the work-up revealed normal cardiac function. What is the diagnosis?
Heart Failure (with Reduced Ejection Fraction) after Myocardial Infarction
Two months after having a myocardial infarction, this 75-year-old man presents with bibasilar rales on chest auscultation, distended neck veins while sitting, and an S3 gallop. His ECG is unchanged from a month ago and serum cardiac enzymes are negative. What does the ECG show?
These older adult women both have chronic heart failure and both complain of nausea. What are the two arrhythmias? What is the probable common underlying problem?
Case 20 (Clue: Previous ECGs showed atrial fibrillation with a rapid rate.)
Case 21 (Clue: Look very carefully at leads II and V1.)
This ECG (from a patient with normal serum electrolytes) is most consistent with therapy using which one of the following drugs?
f. None of the above
Narrowed-Down Differential Diagnoses
The following patients both have severely stenotic (narrowed) heart valves. One has mitral stenosis, and the other has pulmonary (pulmonic) valve stenosis. Can you tell which ECG is from which patient?
Pause for Thought
A 72-year-old woman has intermittent lightheadedness near-syncope. What does this single ECG monitor lead show that may be a clue to her symptoms?
The following patients both complain of a fast heartbeat. One has atrial flutter with 2 : 1 block. The other has paroxysmal supraventricular tachycardia (PSVT) due to atrioventricular nodal reentrant tachycardia (AVNRT). Which is which?
A 75-year-old man has an ECG before undergoing cataract surgery. He denies a history of previous cardiovascular problems. However, what does his ECG show?
Three Patients with Recurrent Syncope
The following three patients (Cases 29–31) report recurrent episodes of fainting, confirmed by family members. Can you diagnose the cause in each case?
Case 29 A 21-year-old woman on no medications with normal serum electrolyte values
Case 30 A 37-year-old man
Case 31 A 75-year-old woman
This 52-year-old man has a history of recent “indigestion,” nausea, and an irregular pulse. What is the rhythm? What is the major underlying problem?
Hidden P Wave “ST-ories”
Can you diagnose these two arrhythmias?
Myocardial Infarction Simulator
This 46-year-old man has chest discomfort and profound dyspnea. Initially he was thought to have had a myocardial infarction. What alternative life-threatening diagnosis would account for all these findings?
The following highly irregular rhythms are often confused. What is the arrhythmia in each case?
These two recordings show underlying sinus rhythm with abrupt changes in cardiac electrical activity and intermittently wide duration QRS complexes. What are the diagnoses?
A middle-aged cardiologist left her bifocals at home and nearly overlooked the following diagnosis. (Clue: See arrow.)
Long and Short of It
Both these patients have mental status changes. Can you diagnose the cause from the ECG alone? (Clue: The key to their treatable diagnoses relates to the beginning of the ST segment.)
Case 41 A 30-year-old woman
Case 42 A 65-year-old man
This 78-year-old man has a pacemaker (functioning in VVI mode) for complete heart block. He comes into your office with shortness of breath and evidence of pulmonary edema. In addition to the pacemaker pattern, what does his ECG show?
ECG/Coronary Arteriogram Matchup
Assign the ECG (A to D) that matches up best with the history given immediately below (Cases 44–47) for these four middle-aged men.
Case 44 This man has had chest pain for the past 4 hours. He has a markedly elevated troponin level. He has severe three-vessel coronary disease with 80% to 90% proximal stenoses of the epicardial major coronary arteries, along with an anterior wall motion abnormality.
Case 45 This man had chest discomfort 3 days ago. His serial troponin levels are normal. He is found to have an occluded large left circumflex coronary artery and a severe inferoposterolateral wall motion abnormality.
Case 46 This man had chest pain 1 month ago. His serum troponin level is now normal. Currently, he is complaining of dyspnea. His coronary angiogram reveals an occluded proximal left anterior descending coronary artery, with an anterior wall aneurysm noted on cardiac echocardiography.
Case 47 This man has had pleuritic chest pain for 12 hours with a normal troponin level on evaluation. His left ventricular wall motion and coronary arteries appear normal, based on echocardiography and coronary arteriography.
Calculation Leads to Diagnosis
A 40-year-old woman complains about feeling weak. She is not taking any medication. A previous ECG was within normal limits. Based on the present ECG, what laboratory values do you want to check as a priority?
Interest-Piquing T Waves
What underlying, life-threatening condition explains all findings? (Additive clues: QRS voltage, P waves, and QTc interval.)
Severe hyperkalemia. Note the markedly prolonged PR interval, peaked T waves, and widened QRS complex.
Anterior wall ST segment elevation myocardial infarction (STEMI). Note the marked ST elevations (and hyperacute T waves) in leads V1 through V6, I, and aVL, with reciprocal ST depressions in leads III and aVF. Q waves are present in leads V3 through V6. Also, note the left axis deviation, with possible prior inferior wall infarction.
Sustained monomorphic ventricular tachycardia. Note the wide complex tachycardia (QRS duration up to 200 msec) with a wide R wave in lead V1, a QS wave in lead V6, and extreme axis deviation.
Sinus rhythm with complete (third-degree) heart block. Note the idioventricular (or very slow junctional) escape rhythm at about 33 beats/min.
Sinus tachycardia with electrical alternans. This combination is highly specific for pericardial effusion with tamponade.
Acute pericarditis. Note the diffuse ST segment elevations (leads I, II, III, aVF, and V3 to V6) with PR segment deviations (up in lead aVR, down in leads V4 to V6). This patient gets the taxi.
Acute ST segment elevation anterior myocardial infarction. ST elevations are localized to leads V1 to V3, I, and aVL, with slow R wave progression in leads V1 to V3. In addition, note the ST depressions in leads II, III, and aVF, consistent with reciprocal changes. This patient needs an ambulance stat.
Wolff–Parkinson–White (WPW) pattern. Note the classic triad: short PR intervals, wide QRS complexes, and delta waves (i.e., slurring of the early part of the QRS complexes in leads I, aVL, V1, V2, and other leads). The polarity of the delta waves (slightly positive in V1 and V2 and positive in the lateral chest leads) and the overall QRS axis (horizontal) are most consistent with a right-sided bypass tract.
Sinus rhythm with isorhythmic AV dissociation (but not complete heart block!). This patient does not require a pacemaker.
Atrial flutter with 2:1 AV conduction.
Left–right arm lead (electrode) reversal, which accounts for the negative P waves and negative QRS complexes in lead I.
Sinus rhythm with Wenckebach type (Mobitz I) AV block.
Atrial tachycardia at 150 beats/min with variable AV block.
Right bundle branch block with acute anterior ST segment elevation/Q wave myocardial infarction. Note the prominent Q waves in leads V1 to V3, with ST elevations in leads V1 to V5 and lead aVL.
Right bundle branch block with anterior subendocardial ischemia. Note the ST segment depressions in leads V2, V3, and V4; also left axis deviation.
Wandering atrial pacemaker (WAP). Do not confuse this slow rhythm (a relative of sinus bradycardia) with multifocal atrial tachycardia (MAT). WAP, per se, may be seen normally with increased vagal tone or, nonspecifically, in the context of sinus bradycardia due to multiple causes.
Healthy (and hungry) neonate. Note the very narrow QRS complex (about 60 msec) with a rightward axis, tall R wave in lead V1, and high sinus rate (125 beats/min). All of these findings are appropriate for the patient’s age.
Dextrocardia with situs inversus. Note the apparently reversed limb and chest leads. This patient has a normal heart (right side of chest) with an inflamed appendix (left side of lower abdomen!).
Sinus rhythm with a prolonged PR interval (“first-degree” AV block). The ECG also shows left atrial abnormality, left ventricular hypertrophy, and right bundle branch block. Q waves and ST segment elevations are seen in leads V1 through V5, I, and aVL. The findings are consistent with a left ventricular aneurysm, which was confirmed with echocardiography.
Atrial fibrillation with a slow and at times regularized ventricular response should make you suspect digitalis toxicity. The ST-T changes are nonspecific but consistent with digitalis effect (and/or with ischemia or hypertrophy).
Atrial tachycardia (unifocal) with 2 :1 AV block. (A very subtle “extra” P wave in the ST segment is best seen in leads V1 and V2.) An important, but increasingly rare cause of this arrhythmia is digitalis toxicity. The ECG shows low voltage in the extremity (limb) leads. Based on the very slow (“poor”) precordial lead R wave progression, this patient may have had a previous anterior myocardial infarction. Based on the prominent precordial voltage, left ventricular hypertrophy (LVH) is likely present. The abnormal ST-T changes are nonspecific, and consistent with digitalis toxicity, ischemia, and LVH, singly or in combination.
The theme common to Case 20 and 21, therefore, is digitalis (digoxin) toxicity.
c. Amiodarone effect. Note the prominently prolonged QT(U) interval.
Pulmonary (pulmonic) valve stenosis. The ECG shows signs of right ventricular hypertrophy (relatively tall R waves in lead V1 with right axis deviation) and right atrial abnormality.
Mitral valve stenosis. The ECG shows signs of right ventricular hypertrophy (i.e., relatively tall R waves in lead V1 with right axis deviation) along with prominent left atrial abnormality.
2 :1 sinoatrial (SA) block causes an entire P–QRS–T cycle to be “dropped.” This patient had symptomatic sick sinus syndrome and required a permanent dual-chamber pacemaker.
AV nodal reentrant (reentry) tachycardia (AVNRT), a type of PSVT. In some of the beats small retrograde P waves (negative in lead II, positive in lead aVR) are visible immediately after the QRS complex, at the very beginning of the ST segment (so-called pseudo-S and pseudo-R waves, respectively).
Atrial flutter with 2 :1 AV conduction. Note the flutter waves at a rate of 300 beats/min (e.g., leads aVR, aVL, and V1. The presentation is consistent with typical atrial flutter, with a counterclockwise motion of the macroreentrant flutter wave around the right atrium (isthmus-dependent).
Inferoposterolateral myocardial infarction. Note the Q waves in leads II, III, aVF, V5, and V6, and the tall R waves in leads V1 and V2.
Sinus rhythm with a markedly prolonged QT(U) interval (about 600 msec). This patient has a hereditary (congenital) type of long QT syndrome, associated with a “channelopathy.” Syncope was caused by recurrent episodes of torsades de pointes type of ventricular tachycardia. Work-up and therapy in this context usually involve genetic testing, implantable cardioverter–defibrillator (ICD) implantation and beta blockade, as well as family member evaluation, under the care of cardiac electrophysiology and cardiac genetics teams.
Atrial fibrillation with the Wolff–Parkinson–White (WPW) syndrome. The clues to this diagnosis are the extremely rapid wide-complex tachycardia (about 300 beats/min at times) with a very irregular rate. This rhythm constitutes a medical emergency since it may spontaneously degenerate into ventricular fibrillation.
Sinus rhythm at 100 beats/min with advanced second-degree AV block (3:1 conduction pattern). The QRS complexes show a bifascicular block pattern (right bundle branch block and left anterior fascicular block). Evidence for left atrial abnormality/left ventricular hypertrophy is also present. Note that one of the P waves is partly hidden in the T waves (see V1). The patient required a permanent pacemaker.
Sinus rhythm at 95 beats/min with a 4:3 Wenckebach AV block. Note the group beating pattern associated with this type I AV block. Of major note, this arrhythmia was due to an acute/evolving ST elevation/Q wave inferior myocardial infarction.
Junctional rhythm at 60 beats/min. Note the negative (retrograde) P waves partly “hidden” at the end of the ST segments.
Atrial tachycardia with 2:1 AV block. Note the “hidden” P wave in the ST segments. The atrial rate is 160 beats/min with a ventricular rate of 80 beats/min.
Acute right ventricular overload (cor pulmonale), in this case due to massive pulmonary embolism. Note the sinus tachycardia, SIQIIITIII pattern, slow R wave progression, and prominent anterior T wave inversions. The latter are consistent here by right ventricular overload (sometimes called a right ventricular “strain” pattern).
Multifocal atrial tachycardia (MAT).
Atrial fibrillation (AF).
Sinus rhythm with intermittent left bundle branch block (LBBB). The first three sinus beats are conducted with a left bundle branch block pattern; the next three sinus beats occur with a normal QRS complex. Careful inspection reveals that the disappearance of the LBBB is associated with rate slowing of the sinus rate. Therefore, the LBBB here is likely related to an increase in the rate, a finding referred to as acceleration- or tachycardia-dependent bundle branch block.
Sinus rhythm with transient accelerated idioventricular rhythm (AIVR). This rhythm may occur without apparent cause as an escape mechanism with slowing of the sinus rate or in “competition” with the sinus rate. In this instance, the AIVR episode is initiated by a premature ventricular complex (PVC). Note the underlying AV dissociation. A classic setting of AIVR is after coronary artery occlusion and reperfusion, occurring either spontaneously, or after a percutaneous coronary (angioplasty) intervention or with thrombolysis therapy.
Sinus rhythm with atrial bigeminy marked by blocked (nonconducted) atrial premature atrial complexes (blocked PACs). The arrow points to a subtle P wave from an atrial premature atrial complex (beat). Note that each premature P wave comes so early in the cardiac cycle that it fails to conduct through the AV node, which is still refractory following the previous sinus beat. Note also that the effective ventricular rate here is about 50 beats/min, mimicking a sinus bradycardia. This arrhythmia must also be distinguished from sinus rhythm with 2:1 AV block, in which sinus P waves come “on time” but fail to conduct through the AV junction due to second-degree AV heart block.
Hypercalcemia. Note the relatively short QT interval due to an abbreviated ST segment such that the T wave appears to take off right from the end of the QRS complex.
Systemic hypothermia. Note the characteristic J (Osborn) waves, best seen in leads V3 to V5. These “humped” waves appear as convex “out-pouchings” at J point, the locus that defines the junction between the end of the QRS and beginning of the ST segment.
Acute inferolateral ST elevation myocardial infarction (STEMI) superimposed on a ventricular pacemaker pattern. Note the ST elevations in leads II, III, aVF, V5, and V6, and the reciprocal ST depressions in leads V1 to V3.
B. Diffuse, marked ST depressions (except, importantly, in lead aVR), most apparent in the anterior leads. These findings are consistent with non-ST segment myocardial infarction. This constellation of findings usually indicates severe three vessel coronary disease, and sometimes left main coronary disease.
A. Q waves and ST-T changes consistent with evolving ST segment elevation inferoposterolateral myocardial infarction.
C. Q waves and persistent ST elevations consistent with anterior wall infarction and ventricular aneurysm.
D. Diffuse concave ST elevations and characteristic PR segment deviations (up in aVR and down in the inferolateral leads), virtually diagnostic of acute pericarditis.
This patient had hypocalcemia. Calculate the QTc, with QT = 0.48 sec (480 msec) and RR = 0.85 sec (850 msec).
Using the square root formula:
Using an alternative linear (Hodges’) formula (see Chapter 3) one gets:
Therefore the QTc is clearly prolonged here by both rate correction methods. Further inspection shows that the prolonged QTc appears to be due to a long (“stretched-out”) ST segment, rather than a broad T wave. Thus the most likely diagnosis is hypocalcemia. In contrast, hypokalemia generally flattens the T wave and prolongs the QT(U) interval. The ECG indicates the importance of checking serum calcium, albumin and phosphate, as well as magnesium and potassium levels, in addition to other relevant laboratory tests in this case.
Note the combination of the tall, peaked T waves from hyperkalemia with the voltage criteria for left ventricular hypertrophy (LVH). Left atrial abnormality is also present. Patients with chronic renal failure typically have hypertension, leading to LVH. QT prolongation may also be present in this context from concomitant hypocalcemia (associated with increased phosphate levels and abnormal vitamin D metabolism). Therefore, the ECG triad of peaked T waves (consistent with hyperkalemia), QT (ST phase) prolongation (consistent with hypocalcemia), and LVH (consistent with hypertension) should strongly suggest chronic renal failure.
Cardiac arrest! The rhythm strip shows sinus rhythm with ST segment depressions that are consistent with ischemia, followed by the abrupt onset of ventricular flutter (very rapid, “sinusoidal” ventricular tachycardia such that the QRS and T cannot be distinguished) degenerating quickly into ventricular fibrillation. Emergency institution of the CPR protocol is required, with defibrillation as soon as possible.