What is the likely diagnosis and immediate management for a patient with sudden severe dyspnea, no chest pain, and coarse crepitations on auscultation?

Acute Cardiogenic Pulmonary Edema

The most likely diagnosis is acute cardiogenic pulmonary edema, and immediate management must include oxygen therapy targeting saturation >94%, intravenous furosemide, and sublingual or intravenous nitrates, with urgent consideration of non-invasive ventilation (CPAP or BiPAP) given the severe respiratory distress. 1

Clinical Diagnosis

The presentation of sudden severe dyspnea with coarse crackles (crepitations) and absence of chest pain is highly characteristic of acute cardiogenic pulmonary edema (ACPE). 2, 3

Key distinguishing features that support this diagnosis:

• Coarse crackles indicate fluid accumulation in alveolar spaces from elevated pulmonary venous pressure 2
• Sudden onset is typical of flash pulmonary edema from acute cardiac decompensation 3, 4
• Absence of chest pain helps differentiate from acute coronary syndrome, though ACS must still be excluded as a precipitating cause 1
• Physical examination in ACPE typically reveals fine to coarse crepitant rales, S3 gallop, jugular venous distention, and signs of low cardiac output 2

Immediate Management Algorithm

First 15 Minutes - Stabilization Phase

Airway and Breathing:

• Administer high-flow oxygen immediately targeting SpO2 >94% 1
• Initiate non-invasive ventilation (CPAP or BiPAP) promptly if respiratory distress is present, as coarse lung sounds and severe dyspnea indicate significant pulmonary congestion 1
• Prepare for endotracheal intubation if the patient develops respiratory failure with hypoxemia, hypercapnia, acidosis, physical exhaustion, or diminished consciousness 1

Pharmacologic Intervention:

• Intravenous furosemide as first-line diuretic for volume overload - this is the cornerstone of ACPE treatment 1, 2
• Sublingual or intravenous nitrates titrated to blood pressure to reduce preload and afterload 1, 2
• Consider morphine for dyspnea relief, though use caution as opiates can depress respiration 1, 3

Hemodynamic Targets

• Maintain systolic blood pressure between 100-120 mmHg 1
• Target heart rate <60 beats/min in absence of neurological complications 1
• If blood pressure control is needed, use intravenous beta-blockers, nitrates, sodium nitroprusside, or calcium channel blockers 1

Essential Diagnostic Workup (Concurrent with Treatment)

Do not delay treatment while awaiting diagnostic confirmation - the clinical presentation warrants immediate intervention. 1

Mandatory investigations:

• Point-of-care troponin testing urgently to assess for concurrent myocardial infarction as precipitant 1
• 12-lead ECG to exclude ST-elevation myocardial infarction or new left bundle branch block 1
• Chest radiograph shows pulmonary edema with sensitivity of 57% and specificity of 89% for acute heart failure 5
• Transthoracic echocardiography is mandatory to assess ventricular function, valve function, and exclude mechanical complications 1
• Natriuretic peptide level (BNP or NT-proBNP) should be measured in all patients with suspected heart failure 5
• Arterial blood gas to assess oxygenation, ventilation, and acid-base status 2

Critical Differential Diagnoses to Exclude

While ACPE is most likely, several life-threatening conditions can mimic this presentation:

Pulmonary embolism must be considered, particularly if there are risk factors such as recent immobilization, surgery, malignancy, or prior DVT/PE 6. However, PE typically presents with pleuritic chest pain (75% of cases) rather than the absence of chest pain described here. 6

Acute aortic regurgitation can cause flash pulmonary edema and must be excluded with careful auscultation for diastolic murmur and echocardiography 4. This is a critical pitfall - a "common" presentation of pulmonary edema may hide rare but treatable causes requiring surgical intervention. 4

Pneumonia typically presents with fever, productive cough, and localized findings rather than bilateral coarse crackles 6. The sudden onset without preceding infectious symptoms makes this less likely. 5

Common Pitfalls and How to Avoid Them

Pitfall #1: Assuming chronic findings without comparison

• Always compare ECG to prior tracings - new left bundle branch block with dyspnea is a STEMI equivalent requiring urgent catheterization 1

Pitfall #2: Delaying treatment for diagnostic certainty

• The combination of sudden severe dyspnea and bilateral coarse crackles warrants immediate diuretics and vasodilators even before imaging confirmation 1

Pitfall #3: Missing mechanical complications

• Echocardiography must be performed urgently to exclude acute valvular dysfunction (especially mitral regurgitation or aortic regurgitation), ventricular septal rupture, or papillary muscle rupture 1, 4

Pitfall #4: Inadequate respiratory support

• Non-invasive ventilation should be initiated early and not delayed until the patient deteriorates further 1, 7

Disposition and Monitoring

• Transfer immediately to intensive cardiac care unit for hemodynamic monitoring and advanced heart failure management 1
• Ensure 24/7 echocardiography availability 1
• Continuous monitoring of oxygen saturation, blood pressure, heart rate, and urine output 2
• If cardiogenic shock develops (systolic BP <90 mmHg, cardiac index <2.2 L/min/m², pulmonary wedge pressure >18 mmHg), this carries high mortality and requires immediate invasive strategy with consideration of mechanical circulatory support 1, 3

Specific Treatment Adjustments Based on Blood Pressure

If hypertensive (SBP >140 mmHg):

• Aggressive vasodilator therapy with nitrates is the priority 2
• Diuretics for volume overload 2

If normotensive (SBP 100-140 mmHg):

• Balanced approach with both vasodilators and diuretics 2

If hypotensive (SBP <90 mmHg) or signs of organ hypoperfusion:

• Inotropic drugs are required 2, 3
• Vasopressors may be necessary 3
• This represents cardiogenic shock requiring intensive monitoring and possible mechanical support 3