Differentials for pulmonary thromboembolism

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Differential Diagnosis of Pulmonary Thromboembolism (PTE)

PE is a great mimic. The clinical features - acute dyspnea, pleuritic or anginal chest pain, hypoxia, tachycardia, and hemodynamic instability - overlap with many conditions. Below is a category-based breakdown.

1. Cardiovascular

Condition	Key distinguishing features
Acute coronary syndrome (ACS)	ECG ST changes in coronary distribution, troponin rise, responds to nitrates; PE may also elevate troponin (RV strain), so CTPA/angiography often needed
Aortic dissection	Tearing pain radiating to back, widened mediastinum on CXR, BP differential between arms, D-dimer strongly elevated but CT aortography confirms
Decompensated heart failure	Orthopnea, PND, bilateral crackles, raised JVP with bilateral edema; BNP helps, but RV failure from massive PE can mimic this
Pericarditis / pericardial effusion	Positional chest pain relieved by leaning forward, pericardial rub, diffuse saddle-shaped ST elevation on ECG, PR depression
Acute myocarditis	Often younger patients post-viral illness, global ST changes, elevated troponin, wall motion abnormalities on echo
Pulmonary hypertension (primary or secondary)	Gradual onset dyspnea, RV hypertrophy on ECG/echo; may coexist with or result from chronic PE

2. Pulmonary

Condition	Key distinguishing features
Pneumonia	Productive cough, fever, consolidation on CXR, lobar infiltrate; can coexist with PE
Pneumothorax	Sudden pleuritic pain + absent breath sounds unilaterally, hyperresonance, visible on CXR
Acute bronchitis / COPD exacerbation	Wheezing, increased sputum, prior COPD history; ECG signs of RV strain may appear in COPD too
Asthma exacerbation	Diffuse expiratory wheeze, response to bronchodilators, known history
Pleuritis / Pleurisy	Secondary to connective tissue disease (SLE, RA), viral illness; localized rub without embolic features
Pulmonary infarction (from PE itself)	Note: PE with infarction causes chest wall tenderness, mimicking musculoskeletal disease - a trap
Intrathoracic malignancy	Lung cancer may present with hemoptysis/dyspnea; also a risk factor for PE, so can coexist

3. Musculoskeletal

Condition	Key distinguishing features
Costochondritis / Musculoskeletal chest pain	Reproducible on palpation, no hypoxia, no tachycardia; most common diagnosis confused with PE
Rib fracture	Trauma history, point tenderness, visible on X-ray or CT

4. Neuropsychiatric

Condition	Key distinguishing features
Anxiety / Panic disorder	Hyperventilation, low CO2 on ABG, normal SpO2, normal ECG; diagnosis of exclusion
Syncope	Massive PE can present with syncope - must exclude structural cardiac, vasovagal, arrhythmic causes

5. Abdominal / Other

Condition	Key distinguishing features
Hepatobiliary / splenic pathology	Right-sided or subdiaphragmatic processes (e.g., cholecystitis, splenic infarct) can cause referred pleuritic pain
Esophageal perforation	Boerhaave syndrome - retrosternal chest pain after vomiting, surgical emergency; chest X-ray may show mediastinal air

Clinically Critical Distinguishing Points

ECG: The S1Q3T3 pattern and T-wave inversions in V1-V4 suggest RV strain from PE, but also appear in COPD, asthma, and idiopathic pulmonary hypertension. Sinus tachycardia is the most common ECG finding in PE and is non-specific.
CXR: A near-normal CXR in severe respiratory compromise is highly suggestive of PE. Westermark sign (focal oligemia) and Hampton hump (peripheral wedge density) are classical but uncommon.
D-dimer: Sensitive but not specific - elevated in dissection, malignancy, infection, post-surgery. A negative high-sensitivity D-dimer effectively rules out PE in low/intermediate probability patients.
Wells score: Central to narrowing the differential. The criterion "alternative diagnosis less likely than PE" directly scores the probability relative to these differentials.

Summary Table (from Braunwald's Heart Disease)

The official differential list from Braunwald's Table 87.5:

Acute coronary syndromes, COPD exacerbation, Aortic dissection, Pneumonia, Acute bronchitis, Decompensated heart failure, Pulmonary hypertension, Pericardial disease, Intrathoracic malignancy, Musculoskeletal pain, Pneumothorax, Anxiety, Hepatobiliary or splenic pathology

Sources:

Braunwald's Heart Disease, 15th ed., Table 87.5
Fuster & Hurst's The Heart, 15th ed., p. 1768
Goldman-Cecil Medicine, Chapter 68
Rosen's Emergency Medicine, 9th ed.

Treatment of hypertensive emergency according to harrisons medicine

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Treatment of Hypertensive Emergency - Harrison's Principles of Internal Medicine (22nd Ed., 2025)

Definition & Classification

Harrison's defines hypertensive urgency vs emergency by the presence or absence of active end-organ damage, not solely by the BP number:

Hypertensive urgency: SBP/DBP ≥180/100 mmHg, asymptomatic - treat with oral agents as an outpatient
Hypertensive emergency: Same BP threshold plus evidence of active, ongoing end-organ damage

End-organ damage that defines a hypertensive emergency:

Hypertensive encephalopathy (headache, vision defects, nausea, vomiting, seizures)
Acute left ventricular failure
Acute kidney failure
Aortic dissection
Eclampsia / severe preeclampsia
Pheochromocytoma crisis

General Principles of Treatment

Admit to ICU with hemodynamic monitoring
Use intravenous antihypertensive agents - oral therapy is insufficient
Goal: gradual, controlled BP reduction - not immediate normalization. Overshoot risks ischemia (coronary, renal, cerebral)
Once BP is controlled, transition to oral agents
Investigate secondary causes - especially renovascular disease, which is relatively common in hypertensive emergencies

IV Agents Named by Harrison's

Drug	Class	Key Points
Sodium nitroprusside	Potent vasodilator	"Long history of success"; monitor carefully to avoid overshooting and causing hypotension
Nicardipine (IV)	Dihydropyridine CCB	"Perhaps the most commonly utilized agent in contemporary practice"; no dose adjustment in elderly; contraindicated in severe aortic stenosis
Labetalol (IV)	Alpha + Beta blocker	Effective; contraindicated in obstructive airway disease, COPD, bradycardia, 2nd/3rd-degree heart block

Special Situations Requiring Particularly Rapid Treatment

Harrison's explicitly flags three conditions that demand the fastest intervention:

1. Acute Aortic Dissection

Immediate ICU admission
Goal: reduce heart rate to 60-80 bpm AND SBP to ≤120 mmHg
First-line: IV beta-blockers (propranolol, metoprolol, or short-acting esmolol) + IV sodium nitroprusside if needed
Alternative: Labetalol IV (has both alpha and beta blocking properties)
If beta-blockers and nitroprusside cannot be used: IV verapamil or diltiazem; or add parenteral enalaprilat (ACE inhibitor) to a beta-blocker
Contraindicated: isolated direct vasodilators like hydralazine - these increase hydraulic shear and heart rate and can propagate the dissection

2. Eclampsia / Severe Preeclampsia

Safe agents in pregnancy: labetalol (IV), nifedipine (CCB, oral/sublingual), hydralazine (direct vasodilator)
Avoid: ACEIs and ARBs (teratogenic)
Methyldopa is an alternative (centrally acting alpha-2 agonist)

3. Pheochromocytoma Crisis

Agents: phentolamine (alpha-blocker), nicardipine, nitroprusside, nitroglycerin, IV magnesium sulfate
Avoid beta-blockers without prior alpha-blockade - risk of unopposed alpha-adrenergic stimulation causing paradoxical worsening of hypertension

Key Cautions from Harrison's

Do not normalize BP immediately - a controlled reduction is the goal; rapid normalization risks ischemic complications in organs adapted to high perfusion pressures
Nitroprusside requires careful monitoring to avoid hypotension
After acute management, always investigate for secondary causes of hypertension (especially renovascular disease)

Source: Harrison's Principles of Internal Medicine, 22nd Edition (2025, McGraw-Hill Medical) - Chapter on Hypertension and Pharmacologic Therapy, and Chapter on Aortic Diseases

Make a clinical decision-making flowchart for urgency vs emergency

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