Heart failure with reduced ejection fraction (HFrEF)

A 68 year old male with a history of hypertension, type 2 diabetes mellitus, and coronary artery disease presents with progressive shortness of breath over the past 2 weeks. He reports fatigue, orthopnea, paroxysmal nocturnal dyspnea, and bilateral lower extremity swelling, along with recent weight gain. On examination, he appears dyspneic with elevated jugular venous pressure, bilateral pitting edema, and diffuse crackles on lung auscultation. Cardiac examination reveals a displaced apical impulse and an S3 gallop. Chest X-ray shows cardiomegaly, pulmonary congestion, and bilateral pleural effusions. Laboratory evaluation reveals elevated BNP and NT-proBNP, worsening renal function, and hyponatremia. Echocardiography demonstrates a dilated left ventricle, global hypokinesis, and LVEF 35 percent. Diagnosis?

Diagnosis is acute decompensated heart failure with reduced ejection fraction (HFrEF), likely secondary to ischemic cardiomyopathy.

1. Definition

Heart failure with reduced ejection fraction (HFrEF) is a clinical syndrome characterized by:

1. Symptoms and/or signs of heart failure
2. Left ventricular ejection fraction ≤40 percent
3. Often supported by elevated natriuretic peptides or objective evidence of structural heart disease

It results from impaired myocardial contractility, leading to reduced cardiac output, elevated filling pressures, and neurohormonal activation.

2. Etiology

2.1 Ischemic

1. Coronary artery disease
2. Prior myocardial infarction

2.2 Non-ischemic

1. Dilated cardiomyopathy
2. Myocarditis
3. Alcohol or cocaine toxicity
4. Chemotherapy-induced cardiomyopathy
5. Peripartum cardiomyopathy

2.3 Pressure or Volume Overload

1. Chronic hypertension
2. Aortic stenosis
3. Mitral or aortic regurgitation

2.4 Tachycardia-induced

1. Atrial fibrillation
2. Supraventricular tachycardia

2.5 Infiltrative and Metabolic

1. Amyloidosis
2. Hemochromatosis
3. Sarcoidosis

3. Pathophysiology

3.1 Core Mechanism

1. Reduced contractility → decreased stroke volume
2. Decreased cardiac output → hypoperfusion

3.2 Neurohormonal Activation

1. RAAS activation → vasoconstriction and sodium retention
2. Sympathetic activation → increased heart rate and oxygen demand
3. ADH release → water retention and hyponatremia

3.3 Ventricular Remodeling

1. Left ventricular dilation with eccentric hypertrophy
2. Increased wall stress
3. Fibrosis and myocyte loss

3.4 Hemodynamic Consequences

1. Increased LV end-diastolic pressure → pulmonary congestion
2. Increased right-sided pressures → systemic congestion
3. Reduced renal perfusion → worsening renal function

3.5 Vicious Cycle

Low cardiac output → neurohormonal activation → remodeling → further decline in ejection fraction

4. Hemodynamic Profile

1. Decreased cardiac output and cardiac index
2. Increased LV end-diastolic pressure
3. Increased pulmonary capillary wedge pressure (>18 mm Hg)
4. Increased systemic vascular resistance
5. Increased right atrial pressure

5. Classification

5.1 By Ejection Fraction

1. HFrEF ≤40 percent
2. HFmrEF 41–49 percent
3. HFpEF ≥50 percent

5.2 NYHA Functional Classification

1. Class I: No limitation
2. Class II: Mild limitation
3. Class III: Marked limitation
4. Class IV: Symptoms at rest

5.3 ACC/AHA Staging

1. Stage A: At risk
2. Stage B: Structural disease without symptoms
3. Stage C: Symptomatic heart failure
4. Stage D: Refractory heart failure

6. Clinical Features

6.1 Symptoms

1. Dyspnea
2. Orthopnea
3. Paroxysmal nocturnal dyspnea
4. Fatigue
5. Peripheral edema
6. Weight gain
7. Early satiety

6.2 Signs

1. Elevated jugular venous pressure
2. S3 gallop
3. Pulmonary crackles
4. Displaced apical impulse
5. Peripheral edema

6.3 Advanced Features

1. Hypotension
2. Cold extremities
3. Cardiorenal syndrome

7. Diagnosis

7.1 Laboratory

1. Elevated BNP or NT-proBNP
2. Age-adjusted NT-proBNP thresholds may support diagnosis

1.  >450 pg/mL if <50 years

2. >900 pg/mL if 50–75 years

3. >1800 pg/mL if >75 years

3. Hyponatremia indicates severe disease
4. Elevated creatinine indicates renal involvement

7.2 Imaging

1. Chest X-ray shows cardiomegaly, pulmonary edema, and pleural effusions

7.3 ECG

1. Left ventricular hypertrophy
2. Q waves
3. Left bundle branch block
4. Arrhythmias

7.4 Echocardiography

1. LVEF ≤40 percent
2. Dilated left ventricle
3. Hypokinesis
4. Valvular abnormalities

7.5 Advanced Evaluation

1. Cardiac MRI for infiltrative or inflammatory disease
2. Coronary angiography for ischemic evaluation
3. Right heart catheterization for hemodynamic assessment

8. Management

8.1 Guideline-Directed Medical Therapy

1. ARNI preferred or ACE inhibitor or ARB
2. Evidence-based beta blockers (metoprolol succinate, carvedilol, bisoprolol)
3. Mineralocorticoid receptor antagonists
4. SGLT2 inhibitors

8.2 Symptom Relief

1. Loop diuretics for volume overload
2. Add thiazide diuretics if resistant

8.3 Additional Therapies

1. Hydralazine plus isosorbide dinitrate in selected patients
2. Ivabradine if heart rate ≥70 in sinus rhythm
3. Digoxin reduces hospitalization
4. Intravenous iron in iron deficiency
5. Anticoagulation in atrial fibrillation

8.4 Device Therapy

1. ICD indicated if:
• LVEF ≤35 percent
• On optimal medical therapy for ≥3 months
• Life expectancy >1 year
2. CRT indicated if:
• LVEF ≤35 percent
• Sinus rhythm
• LBBB with QRS ≥150 ms
• Persistent symptoms despite GDMT

9. Acute Decompensated Heart Failure

1. Oxygen or noninvasive ventilation if hypoxic
2. Intravenous loop diuretics are first line
3. Vasodilators such as nitroglycerin in hypertensive patients
4. Inotropes for hypoperfusion or cardiogenic shock

10. Prognosis and Monitoring

1. Prognosis is variable and depends on disease severity
2. Poor prognostic factors:
• Low ejection fraction
• Elevated BNP
• Renal dysfunction
• Hyponatremia
3. Monitor renal function and electrolytes regularly
4. Repeat echocardiography after clinical change or therapy optimization

11. Key Clinical Insight

Dyspnea + orthopnea + S3 gallop + LVEF ≤40 percent = HFrEF

Congestion versus hypoperfusion guides management

12. Exam Level Pearls

1. Four pillar therapy reduces mortality and hospitalizations
2. S3 gallop indicates systolic dysfunction
3. BNP supports diagnosis
4. Do not discontinue GDMT even if ejection fraction improves
5. LVEF ≤35 percent indicates need for ICD evaluation
6. LBBB with wide QRS indicates benefit from CRT
7. IV loop diuretics are first line in acute decompensation

Acute Pericarditis

A 30 year old male presents to the emergency department with central chest pain for the past few days. The pain is pleuritic and positional, worsening with inspiration and improving when sitting up and leaning forward. He reports a recent history of fever, myalgia, and sore throat two weeks prior. On examination, a pericardial friction rub is heard over the left parasternal region. Laboratory studies show elevated CRP and ESR with normal or mildly elevated troponin levels. ECG demonstrates diffuse concave ST-segment elevation and PR-segment depression without a territorial pattern or significant reciprocal changes (except aVR). Diagnosis?

Diagnosis is Acute Viral (Idiopathic) Pericarditis.

1. Definition

Acute pericarditis is inflammation of the pericardium, most commonly viral or idiopathic, characterized by pleuritic chest pain, pericardial friction rub, and typical ECG changes.

2. Etiology

1. Viral or idiopathic most common
2. Common viruses include coxsackievirus, echovirus, influenza, and adenovirus
3. Bacterial causes, including tuberculosis
4. Autoimmune diseases such as SLE and rheumatoid arthritis
5. Post-cardiac injury syndromes including Dressler syndrome
6. Malignancy
7. Uremia
8. Drug-induced or radiation-related

3. Pathophysiology

1. Inflammation of visceral and parietal pericardium
2. Leads to friction, causing pleuritic positional chest pain
3. Produces diffuse ST elevation and PR depression
4. May result in pericardial effusion
5. Rapid accumulation of fluid can lead to cardiac tamponade

4. Clinical Features

4.1 Diagnostic Criteria, at least 2 required

1. Pericardial chest pain
2. Pericardial friction rub
3. Diffuse ST elevation or PR depression
4. New or worsening pericardial effusion

4.2 Additional Features

1. Pain radiating to trapezius ridge
2. Dyspnea
3. Low-grade fever
4. Pain relieved by leaning forward

5. Diagnostic Evaluation

5.1 Electrocardiography

1. Diffuse concave ST-segment elevation
2. PR-segment depression
3. Reciprocal PR elevation and ST depression in aVR
4. No territorial pattern

5.2 Laboratory Findings

1. Elevated CRP and ESR
2. Troponin normal or mildly elevated
3. Significant elevation suggests myopericarditis

5.3 Imaging

1. Echocardiography recommended in all patients to assess for pericardial effusion and tamponade
2. Chest X-ray usually normal unless large effusion
3. CT or MRI if diagnosis is uncertain

6. Management

6.1 First-line Therapy

1. NSAIDs such as ibuprofen, indomethacin, or aspirin
2. Colchicine for 3 to 6 months to reduce recurrence
3. Proton pump inhibitor for gastric protection

6.2 Refractory or Specific Cases

1. Corticosteroids reserved for:
• Autoimmune pericarditis
• NSAID or colchicine intolerance
2. Avoid routine use in viral pericarditis due to increased recurrence risk

6.3 Additional Measures

1. Restrict physical activity until symptom resolution
2. Treat underlying cause when identified
3. Hospital admission for high-risk patients, including:
• Fever > 38°C
• Large pericardial effusion
• Cardiac tamponade
• Immunosuppression
• Trauma
• Myopericarditis

7. Complications

1. Pericardial effusion
2. Cardiac tamponade
3. Recurrent pericarditis
4. Myopericarditis
5. Rarely constrictive pericarditis

8. Key Clinical Insight

Pleuritic, positional chest pain with a pericardial friction rub strongly suggests pericarditis

Diffuse ST elevation with PR depression and no territorial pattern differentiates it from myocardial infarction

9. Exam Level Pearls

1. Pericardial friction rub is highly specific
2. Diffuse ST elevation distinguishes from STEMI
3. PR depression is characteristic
4. Troponin may be normal or mildly elevated
5. Colchicine reduces recurrence risk

Deep Venous Thrombosis (DVT)

A 50 year old male presents to the emergency department with right calf pain and swelling on the third postoperative day. He recently underwent open cholecystectomy 3 days ago. He has a history of hypertension treated with amlodipine. On examination, there is calf tenderness on palpation. Vital signs show blood pressure of 120/80 mm Hg, pulse rate of 88 beats per minute, respiratory rate of 18 breaths per minute, oxygen saturation of 92 percent on room air, and temperature of 97.9 F. D dimer is elevated. Duplex ultrasound shows a thrombus with lack of compressibility and filling defects in the right lower extremity. Diagnosis?

Diagnosis is Deep vein thrombosis.

1. Definition

Deep vein thrombosis is the formation of a thrombus in the deep venous system, most commonly in the lower extremities, and is part of the spectrum of venous thromboembolism.

2. Etiology and Risk Factors

1. Virchow triad
• Venous stasis such as postoperative immobility
• Endothelial injury from surgery
• Hypercoagulability
2. Additional risk factors
• Recent surgery and hospitalization
• Malignancy
• Obesity and advanced age
• Pregnancy or estrogen therapy
• Inherited thrombophilia

3. Pathophysiology

1. Thrombus formation occurs in low flow venous sites, often in calf veins
2. Initiated by endothelial injury, stasis, and hypercoagulability
3. Leads to venous obstruction and inflammation
4. Thrombus may propagate proximally, increasing risk of pulmonary embolism

4. Clinical Features

1. Unilateral calf pain and swelling
2. Tenderness and warmth
3. Erythema and dilated superficial veins
4. May be asymptomatic in up to 50 percent of cases

If pulmonary embolism develops:
5. Shortness of breath
6. Pleuritic chest pain
7. Tachycardia and hypoxia

Homans sign is not reliable and is not recommended

5. Diagnosis

5.1 Clinical Probability

1. Wells score
• ≥2 indicates likely DVT
• <2 indicates unlikely DVT

5.2 Laboratory

1. D dimer is highly sensitive but not specific
2. Used to exclude DVT in low probability patients

5.3 Imaging

1. Compression duplex ultrasound is the diagnostic test of choice
2. Findings include
• Non compressible vein
• Intraluminal thrombus
• Filling defects

6. Management

1. Anticoagulation is the cornerstone of treatment
• Direct oral anticoagulants such as apixaban or rivaroxaban are first line
• Alternatives include LMWH followed by warfarin
2. Duration of therapy
• Typically 3 to 6 months
• Longer for unprovoked or recurrent DVT
3. Thrombolysis
• Reserved for selected patients with extensive proximal or iliofemoral DVT and low bleeding risk
4. Inferior vena cava filter
• Only if anticoagulation is contraindicated or ineffective

7. Prevention

1. Pharmacologic prophylaxis
• LMWH or fondaparinux
2. Mechanical methods
• Sequential compression devices
• Graduated compression stockings
3. Early ambulation after surgery

8. Complications

1. Pulmonary embolism
2. Post thrombotic syndrome
3. Recurrent thrombosis
4. Phlegmasia cerulea dolens, a severe limb threatening form

9. Key Clinical Insight

Postoperative patient with unilateral calf pain, swelling, and non compressible vein on ultrasound strongly indicates deep vein thrombosis

10. Exam Level Pearls

1. Most DVTs originate in calf veins and may propagate proximally
2. Proximal DVT has higher risk of pulmonary embolism than distal DVT
3. Clinical signs alone are not sufficient for diagnosis
4. D dimer is useful only in low risk patients
5. Compression ultrasound is the test of choice