Third degree atrioventricular block

A 60 year old male presents with fatigue, dizziness, lightheadedness, and near syncope over several days. He also reports chest pain and shortness of breath on exertion. On examination, the jugular venous pulse shows cannon a waves. Vital signs reveal severe bradycardia (35/min) with a regular pulse and blood pressure 110/70 mmHg. Electrocardiography demonstrates complete dissociation between P waves and QRS complexes, with constant P–P and R–R intervals. The P waves march through independently. The QRS complexes are wide, indicating a ventricular escape rhythm. Diagnosis?

Diagnosis is Third degree (complete) atrioventricular block.

1. Definition

Third degree AV block is characterized by complete atrioventricular dissociation, in which no atrial impulses are conducted to the ventricles, resulting in independent atrial and ventricular rhythms.

2. Etiology

1. Degenerative fibrosis of the conduction system (most common in chronic cases)
2. Ischemic heart disease (especially acute myocardial infarction)
3. AV nodal blocking drugs
• Beta blockers
• Non dihydropyridine calcium channel blockers
• Digoxin
• Amiodarone
4. Electrolyte abnormalities
• Hyperkalemia
5. Inflammatory conditions
• Myocarditis
• Lyme disease
6. Infiltrative diseases
• Sarcoidosis
• Amyloidosis
• Hemochromatosis
7. Autoimmune disorders
8. Congenital AV block

3. Pathophysiology

1. Complete interruption of AV conduction
2. Atria depolarize under SA node control
3. Ventricles are driven by escape rhythms:
• Junctional escape → narrow QRS, rate 40 to 60
• Ventricular escape → wide QRS, rate 20 to 40
4. More distal block → slower rate and worse prognosis
5. Leads to reduced cardiac output and symptoms

4. Clinical Features

4.1 Core Features

1. Severe bradycardia
2. AV dissociation
3. Cannon a waves

4.2 Additional Features

1. Fatigue
2. Dizziness
3. Syncope or near syncope
4. Chest pain
5. Dyspnea

5. Diagnosis

5.1 Electrocardiography

1. No relationship between P waves and QRS complexes
2. P waves march through independently
3. Constant P–P and R–R intervals
4. QRS width depends on escape rhythm
• Wide QRS → infranodal block (more dangerous)

5.2 Additional Evaluation

1. Cardiac biomarkers to assess for ischemia
2. Electrolytes to identify reversible causes

6. Management

6.1 Initial Step

1. Assess hemodynamic stability

6.2 Acute Management

1. Immediate transcutaneous pacing if unstable
2. Atropine may be attempted but often ineffective in infranodal block
3. Epinephrine or dopamine infusion if needed

6.3 Definitive Management

1. Transvenous pacing
2. Permanent pacemaker implantation

6.4 Additional Measures

1. Treat reversible causes
2. Discontinue offending drugs

7. Key Clinical Insight

Severe bradycardia + cannon a waves + AV dissociation on ECG = Third degree AV block

8. Exam Level Pearls

1. Wide QRS suggests infranodal block and worse prognosis
2. Mobitz type II can progress to complete heart block
3. Inferior MI → AV nodal block (better prognosis)
4. Anterior MI → infranodal block (worse prognosis)
5. Third degree AV block is a medical emergency requiring pacing

Cardiac Tamponade

A 38 year old male with stage 5 chronic kidney disease on dialysis presents with progressive shortness of breath, chest discomfort, and fatigue over several days. Vital signs show hypotension (90/60 mmHg), tachycardia (120/min), and oxygen saturation 92% on room air. Peripheral pulses are weak and become fainter during inspiration, consistent with pulsus paradoxus. Examination reveals jugular venous distension and muffled heart sounds. ECG shows low voltage QRS complexes and electrical alternans. Echocardiography demonstrates pericardial effusion with right ventricular diastolic collapse. Diagnosis?

Diagnosis is Cardiac tamponade.

1. Definition

Cardiac tamponade is a life threatening obstructive shock caused by accumulation of fluid in the pericardial space, leading to impaired ventricular filling and reduced cardiac output.

2. Etiology

1. Uremia in end stage renal disease
2. Malignancy (lung, breast, lymphoma)
3. Trauma (penetrating more than blunt)
4. Pericarditis (infectious or autoimmune)
5. Post myocardial infarction
• Free wall rupture
• Dressler syndrome
6. Iatrogenic causes (procedures, cardiac surgery)

3. Pathophysiology

1. Accumulation of pericardial fluid increases intrapericardial pressure
2. Leads to impaired ventricular filling
3. Causes decreased preload and stroke volume
4. Results in reduced cardiac output and obstructive shock

4. Clinical Features

4.1 Beck triad

1. Hypotension
2. Jugular venous distension
3. Muffled heart sounds

4.2 Other Findings

1. Tachycardia
2. Cool extremities
3. Tachypnea (lungs usually clear)
4. Pulsus paradoxus
• Decrease in systolic blood pressure greater than 10 mmHg during inspiration
5. Narrow pulse pressure

5. Diagnosis

5.1 Electrocardiography

1. Low voltage QRS complexes
2. Electrical alternans

5.2 Chest X ray

1. Enlarged cardiac silhouette in large effusions

5.3 Echocardiography (best initial test)

1. Pericardial effusion
2. Right atrial systolic collapse (earliest sign)
3. Right ventricular diastolic collapse (more specific)
4. Plethoric inferior vena cava with reduced inspiratory collapse

5.4 Hemodynamics

1. Equalization of diastolic pressures in all chambers
2. Elevated jugular venous pressure with absent y descent
3. Kussmaul sign typically absent

6. Management

1. Immediate pericardiocentesis is definitive and life saving
2. Intravenous fluids as a temporary measure to maintain preload
3. Avoid positive pressure ventilation as it reduces venous return and may worsen tamponade

7. Key Clinical Insight

Hypotension + JVD + muffled heart sounds + pulsus paradoxus + echo showing RV collapse = Cardiac tamponade

8. Exam Level Pearls

1. Beck triad may be incomplete in many patients
2. Pulsus paradoxus is a key diagnostic clue
3. Electrical alternans suggests large pericardial effusion
4. Echocardiography is the diagnostic test of choice
5. Uremia is a common cause in dialysis patients
6. Tamponade is a form of obstructive shock
7. Right atrial collapse occurs in systole and is the earliest echocardiographic sign

Prinzmetal angina

A 20 year old female presents with recurrent episodes of central chest pain that are non exertional, sudden in onset, and last 5 to 15 minutes. The pain is substernal, severe, and radiates to the left arm, jaw, and neck, and is associated with nausea and diaphoresis. She has a history of Raynaud disease. Vital signs are normal. Electrocardiography shows transient ST segment elevation during an ergonovine provocation test. Coronary angiography demonstrates coronary vasospasm without significant atherosclerosis. Diagnosis?

Diagnosis is Prinzmetal angina (variant angina).

1. Definition

Prinzmetal angina is a form of vasospastic angina caused by transient coronary artery vasospasm, leading to myocardial ischemia in the absence of significant atherosclerotic obstruction.

2. Etiology

1. Coronary artery vasospasm due to:
• Endothelial dysfunction
• Hyperreactivity of vascular smooth muscle
2. Associated conditions:
• Raynaud disease
• Other vasospastic disorders
3. Triggers include:
• Smoking
• Cocaine
• Cold exposure
• Emotional stress
• Ergonovine or acetylcholine

3. Pathophysiology

1. Transient vasospasm of coronary arteries
2. Leads to reduced myocardial blood flow
3. Causes transmural ischemia resulting in transient ST segment elevation

4. Clinical Features

4.1 Core Features

1. Chest pain at rest, often severe
2. Episodes typically occur at night or early morning
3. Not related to exertion
4. Rapid relief with nitrates

4.2 Associated Features

1. Diaphoresis, nausea
2. Association with vasospastic disorders such as Raynaud disease

5. Diagnosis

5.1 Electrocardiography

1. Transient ST segment elevation during episodes
2. ECG normal between episodes

5.2 Cardiac Biomarkers

1. Usually normal
2. May be mildly elevated if ischemia is prolonged

5.3 Coronary Angiography

1. Normal or near normal coronary arteries
2. Demonstrates reversible vasospasm

5.4 Provocation Testing

1. Ergonovine or acetylcholine induces vasospasm
2. Used when diagnosis is uncertain

6. Management

1. Calcium channel blockers are first line therapy
• Diltiazem, verapamil, amlodipine
2. Nitrates for acute relief and prevention
3. Avoid triggers such as:
• Smoking
• Cocaine
• Cold exposure
4. Avoid beta blockers, especially nonselective agents, as they may worsen vasospasm

7. Complications

1. Arrhythmias
2. Myocardial infarction
3. Sudden cardiac death

8. Key Clinical Insight

Rest angina + transient ST elevation + normal coronary arteries + vasospastic history = Prinzmetal angina

9. Exam Level Pearls

1. Occurs at rest, not with exertion
2. ST elevation resolves completely between episodes
3. Smoking is the strongest modifiable risk factor
4. Calcium channel blockers are first line treatment
5. Beta blockers can worsen vasospasm
6. Associated with Raynaud disease and other vasospastic conditions
7. May cause transient arrhythmias or AV block during episodes