A 75-year-old man presented to the emergency department (ED) with the complaint of dizziness for the past week. He denied any chest pain, shortness of breath, tinnitus, hearing loss, or syncope. He has a medical history of hypertension, diabetes mellitus, and glaucoma. His medications included aspirin, pravastatin, amlodipine, hydrochlorothiazide, carvedilol, and timolol eye drops. His dose of carvedilol was increased from 6.25 to 12.5 mg last week by his primary physician. He denied any toxic habits. On physical examination in the ED, he was vitally stable with no significant findings. Initial ECG is shown in Figure 2.1.1. All prior ECGs showed normal sinus rhythm. CT of the head showed no abnormality. The patient was transferred to the telemetry floor where carvedilol was kept on hold. How would you manage this patient?
This case describes the importance of medication review in the elderly population. Elderly patients taking excessive atrioventricular (AV) node-blocking agents can have symptoms of dizziness and syncope with remarkable ECG changes. The temporal association of the medication dose increase and careful review of the medication list are key to diagnose the etiology of dizziness and AV block. β-Blockers (oral or topical) and calcium channel blockers can be offending agents for this presentation.
Type II AV block is a disease of the conduction system in which conduction block occurs between the atria and ventricles, leading to 1 or more of the atrial impulses not conducting to the ventricles.
Types of AV block include the following:
Mobitz type I (Wenckebach phenomenon) second-degree AV block: Progressive PR interval prolongation precedes a nonconducted P wave. The first P wave after block conducts to the ventricle with a shorter PR interval compared with the last P wave before block.
Mobitz type II second-degree AV block: Intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening.
High-grade AV block: Two or more consecutive P waves are nonconducted.
Mobitz type I and type II second-degree AV block cannot be differentiated from the ECG when 2:1 AV block is present; 2:1 AV block can be assessed using various maneuverers and pharmacologic testing to categorize the block as Mobitz type I or II. Carotid sinus massage or adenosine slows AV nodal conduction, and with reduction in block from 2:1 to 3:2, Mobitz type I can be revealed. However, atropine and exercise enhance AV nodal conduction and will eliminate Mobitz type I.
Reversible causes include ablation and medications that block AV conduction such as β-blockers, calcium channel blockers, and digoxin. Other causes include myocardial infraction, cardiomyopathy, endocarditis, and myocarditis. A diagnosis is usually made based on history and ECG.
Symptoms include dizziness, syncope, fatigue, chest pain, shortness of breath, and sudden cardiac arrest.
The management of patients with Mobitz type I second-degree AV block depends on the presence or absence of symptoms. If the patient is asymptomatic, then no intervention is needed. If symptoms are present, then potential reversible causes should be identified such as increased vagal tone, hypothyroidism, hyperkalemia, and medications that block AV conduction. If no cause is identified, then the patient will need a pacemaker. Mobitz type II, however, can progress to complete heart block, and thus a pacemaker is indicated. If the patient is hemodynamically unstable, then the patient should be treated with atropine and temporary cardiac pacing on an urgent basis. In the appropriate clinical scenario, infectious or infiltrative disease may be considered (Lyme disease or sarcoidosis).
Key Points
Mobitz type I AV block is a disease of the AV node that, in most cases, is secondary to medications and is reversed once medications are discontinued.
Mobitz type II AV block is the disease of the distal conduction system (His-Purkinje system) and may progress rapidly to complete heart block, leading to sudden cardiac death. The definitive treatment for this form of AV block is an implantable pacemaker.
A 68-year-old man was admitted to the hospital for elective right knee arthroplasty. ECG done postoperatively showed a heart rate of 85 bpm. The ECG is shown in Figure 2.2.1. The intraoperative course was uneventful. He has a medical history of hypertension, hyperlipidemia, coronary artery disease, and right knee osteoarthritis. He denied any chest pain, shortness of breath, dizziness, palpitations, or syncope. He takes aspirin, atorvastatin, metoprolol, losartan, and Tylenol as needed for pain. Based on the ECG findings, the surgeon decided to transfer the patient to the telemetry floor. What further investigation would you do as a result of these ECG findings?
This case describes the management of first-degree atrioventricular (AV) block. The ECG findings are incidental, and because the patient is asymptomatic, no further intervention is required. First-degree AV block is a misnomer and is not associated with any pathology. No further treatment is required in this case.
First-degree AV block is a conduction delay from the atria to the ventricles. It is almost always asymptomatic and is usually diagnosed on ECG (PR interval >200 milliseconds). Physiologically, it could be due to increased vagal tone. Other causes include a structural abnormality of the AV node or medications that slow AV conduction such as β-blockers, digoxin, and calcium channel blocker. It can also be associated with myocardial infarction, Lyme disease, or infiltrative disease (sarcoidosis).
Patients are usually asymptomatic. If symptoms are present, then signs of bradycardia may be seen.
Asymptomatic patients with first-degree AV block do not require any specific therapy. In rare circumstances, a pacemaker is required when symptoms are consistent with the loss of AV synchrony. In such cases, the indication for a pacemaker device is symptomatic bradycardia instead first-degree AV block. It is also associated with increased risk of atrial fibrillation and increased long-term mortality.
Key Points
First-degree AV block is benign, often an incidental finding, and rarely symptomatic.
Asymptomatic patients do not require any therapy.
A 50-year-old man was brought to the emergency department by emergency medical services (EMSs) as an ST-segment elevation myocardial infarction (STEMI) notification. He woke up around 5:00 a.m. with substernal chest pain associated with diaphoresis and dyspnea. EMS was called, and the ECG showed ST elevation in V1, V2, V3, and V4 (shown in Figure 2.3.1). The patient received aspirin, Plavix (clopidogrel), and sublingual nitroglycerin and was taken to the cardiac catheterization lab where he was found to have a culprit lesion in the left anterior descending artery, for which a drug-eluting stent was placed. He was then transferred to the telemetry floor, where he remained free of chest pain. During the same night, he was noticed to have wide-complex tachycardia on the telemetry monitor that persisted for 30 seconds and then resolved. The patient remained asymptomatic during the event. How will you manage the case?
This patient had a STEMI leading to ventricular tachycardia. Ventricular arrhythmias, ranging from isolated ventricular premature beats to ventricular fibrillation, are common in the immediate post–myocardial infarction (MI) period. Ventricular arrhythmias in the setting of acute MI result from injured myocardium (capable of developing reentrant circuits), arrhythmia triggers (spontaneous ventricular premature beats), and modulating factors (electrolytes imbalance).
Ventricular tachycardia consists of wide-complex tachycardia that lasts >30 seconds. It can be further classified as monomorphic or polymorphic ventricular tachycardia. Most common causes include MI and electrolyte imbalances. Diagnosis is usually made with ECG and telemetry monitoring. Ventricular tachycardia is identified as sustained or nonsustained based on a duration cutoff of 30 seconds.
Symptoms include sudden cardiac death, palpitations, syncope, dizziness, nausea, and shortness of breath.
Reperfusion arrhythmia within 48 hours of an MI should be observed with conservative management of ischemia and electrolyte abnormalities. Sustained ventricular tachycardia after 48 hours of revascularization should be evaluated for automated implantable cardioverter-defibrillator placement. β-Blocker therapy can be used, and no further treatment is needed if the patient remains asymptomatic.
For ventricular fibrillation and pulseless ventricular tachycardia, immediate cardiopulmonary resuscitation while attaching an automated external defibrillator should be performed. Biphasic defibrillation uses 120 to 200 J of energy, whereas monophasic defibrillators use 360 J.
For monomorphic ventricular tachycardia in unstable patients, synchronized cardioversion with 100 J is performed. For stable patients, procainamide, amiodarone, or sotalol can be used. If drug therapy fails, elective cardioversion is an option.
Polymorphic ventricular tachycardia should be treated like ventricular fibrillation. Polymorphic ventricular tachycardia with a prolonged QT interval can be treated with magnesium, discontinuation of offending medications, and in refractory cases, overdrive pacing.
Electrolyte imbalances should be corrected and monitored closely.
Key Points
Arrhythmias of ventricular origin are common after reperfusion in STEMI.
Management of ischemia and electrolytes and observation for 48 hours are required.
A 70-year-old man presented to the emergency department (ED) with complaint of progressive shortness of breath for the past few months. It was associated with dizziness and fatigue. He denied chest pain, palpitations, cough, fever, or chills. He has a medical history of hypertension, diabetes mellitus, and hyperlipidemia. His home medications included aspirin, pravastatin, sitagliptin, hydrochlorothiazide, and omeprazole. In the ED, the patient was vitally stable, except that his heart rate was 45 bpm. Chest x-ray showed no abnormalities. Laboratory data revealed normal electrolytes, pro-B-type natriuretic peptide, and thyroid panel. His 12-lead ECG showed sinus bradycardia with exit block (shown in Figure 2.4.1). The patient was transferred to the telemetry floor, where it was noted that his heart rate was decreasing to 30 bpm with abrupt increase to 80 bpm and frequent pauses of 3 seconds in between. How would you manage this patient?
The clinical presentation and ECG findings are suggestive of sick sinus syndrome (SSS). Most patients with SSS present with nonspecific symptoms such as fatigue, lightheadedness, palpitations, and dyspnea. The medication history, electrolytes, and thyroid studies should be evaluated. Definitive treatment in this case is placement of a permanent pacemaker.
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