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Acute Left Ventricular Failure (ALVF)

Acute Left Ventricular Failure (ALVF) is a sudden inability of the left ventricle (LV) to pump blood effectively to meet the body's metabolic needs.


  • Leads to:

    • Pulmonary congestion (fluid in lungs)

    • Systemic hypoperfusion (poor blood supply to organs)

    • Potential progression to acute heart failure syndromes or cardiogenic shock


  • Pathophysiology:

    • ↓ Myocardial contractility (weakened heart muscle)

    • Impaired diastolic filling (stiff ventricle)

    • Acute hemodynamic shifts due to:

      • Ischaemia

      • Arrhythmias

      • Hypertensive crisis

      • Valvular emergencies


Key Causes of Acute Left Ventricular Failure (ALVF)


Cause Mechanism / Impact
Acute Myocardial Infarction (AMI) Myocardial necrosis → ↓ Contractility → Cardiogenic shock
Coronary Artery Disease (CAD) Chronic ischaemia → Progressive LV dysfunction
Hypertensive Crisis Acute ↑ Afterload → LV strain & decompensation
Valvular Heart Disease Acute MR/AR → Volume overload → LV failure
Arrhythmias (AF, VT) Rapid/irregular rhythms → ↓ Cardiac Output (CO), dyssynchrony
Stress Cardiomyopathy (Takotsubo) Catecholamine surge → Transient LV dysfunction
Myocarditis Inflammation → Direct myocardial injury → ↓ Pump function
Decompensated Chronic Heart Failure Worsening of stable CHF due to triggers (e.g., infection, arrhythmia)
Pulmonary Embolism (Massive) Severe hypoxia + RV strain → ↓ LV preload
Sepsis / Severe Infections Systemic inflammatory response → ↓ Myocardial contractility
Toxins / Drugs Alcohol, cocaine, chemotherapy agents → Direct cardiac toxicity
Volume Overload Rapid fluid or sodium excess → ↑ Preload → LV overload
Thyrotoxicosis ↑ Metabolic demand → High-output state → LV decompensation


Additional Mechanism Ventricular Interdependence: RV failure / Pulmonary Hypertension → ↓ LV preload due to septal shift (Harjola et al., 2016).


The right ventricle (RV) and left ventricle (LV) share a common wall — the interventricular septum — and are both enclosed within the pericardium (heart's outer layer).


If the RV fails (e.g., due to pulmonary hypertension = ↑ pressure in lungs), this can:

  1. Dilate the RV: The RV enlarges as it struggles to pump against high lung pressures.

  2. Shift the septum towards the LV: This physically compresses the LV chamber.

  3. ↓ LV filling (preload): The LV gets less blood during diastole (relaxation phase), reducing stroke volume.

  4. ↓ Cardiac Output: Less blood pumped out to the body → worsened systemic hypoperfusion.


🚩 Clinical Example

  • In massive pulmonary embolism: sudden RV strain → septal shift → acute LV underfilling → shock & hypotension.

👉 This is why right heart problems can rapidly worsen left heart function, even if the LV itself isn't initially diseased.


Clinical Features of Acute Left Ventricular Failure (ALVF)


Symptom Pathophysiology Explanation
Sudden-onset dyspnoea (breathlessness) LV failure → ↑ left atrial & pulmonary capillary pressure → pulmonary interstitial & alveolar oedema → impaired gas exchange & hypoxia.
Orthopnoea Worsens when lying flat due to redistribution of blood to the lungs, increasing pulmonary venous return and congestion.
Paroxysmal nocturnal dyspnoea (PND) Recumbency during sleep → gradual pulmonary fluid accumulation → awakens patient gasping for air.
Fatigue, weakness, confusion Systemic hypoperfusion → ↓ oxygen delivery to muscles & brain → fatigue, weakness, altered mentation.
Cough with frothy, pink-tinged sputum Severe pulmonary oedema → leakage of fluid + RBCs into alveoli → pink, frothy sputum.


Signs & Explanations


Sign Mechanism
Tachypnoea Compensatory response to hypoxia & acidosis from impaired gas exchange.
Tachycardia Sympathetic activation to maintain cardiac output in response to ↓ stroke volume.
Bilateral basal crackles Pulmonary oedema causes fluid accumulation in alveoli, most evident at lung bases.
Hypotension Occurs if cardiac output severely compromised (e.g., cardiogenic shock).
Hypertension Seen in hypertensive crisis-induced ALVF due to excessive afterload.
Cold, clammy skin Peripheral vasoconstriction as a compensatory mechanism to preserve central circulation during hypoperfusion.
Raised JVP (jugular venous pressure) If right heart strain or RV failure coexists (ventricular interdependence), venous return backs up.
S3 Gallop Rhythm Indicates rapid ventricular filling against a stiff or failing LV, heard as an extra diastolic heart sound.


Diagnosis of Acute Left Ventricular Failure (ALVF) in Primary Care

📋 History

  • Risk Factors: Previous heart failure (HF), myocardial infarction (MI), hypertension, valvular disease.

  • Triggers: Recent infections, non-compliance with HF meds, fluid overload, or new medications (e.g., NSAIDs).

  • Symptoms:

    • Sudden-onset breathlessness

    • Orthopnoea, paroxysmal nocturnal dyspnoea

    • Fatigue, confusion


🩺 Examination

  • Vital Signs:

    • BP: Hypotension or hypertension

    • Pulse: Tachycardia

    • RR: Tachypnoea

    • SpO2: Hypoxia if <92%

  • Signs of Pulmonary Oedema:

    • Bilateral crackles, wheeze

  • Signs of Systemic Congestion:

    • Peripheral oedema

    • Raised JVP

    • Hepatomegaly (if right heart failure)


Investigations

  • Pulse Oximetry: Detect hypoxia early.

  • ECG:

    • Arrhythmias (e.g., AF, VT)

    • Ischaemia

    • LV hypertrophy


  • Blood Tests:

    • BNP / NT-proBNP: Elevated = heart failure likely.

    • Electrolytes & renal function: Assess for precipitating factors & safety of medications.

    • Troponin: If MI suspected.


  • Chest X-ray (if available):

    • Pulmonary oedema (Bat's wing appearance)

    • Cardiomegaly

    • Pleural effusions


  • Point-of-Care Ultrasound (POCUS):

    • Detect lung congestion

    • Evaluate LV function

    • Useful if trained personnel available.


👉 Early recognition and referral to secondary care is essential if ALVF is suspected, especially if there are signs of hypoxia, hypotension, or shock.


Key Differentials to consider


Differential Diagnosis Distinguishing Features
Acute Coronary Syndrome (ACS) Chest pain, ECG changes (ST elevation, Q waves), ↑ Troponin, chest pain dominant
Pulmonary Embolism (PE) Sudden dyspnea, pleuritic chest pain, hypoxia, clear lungs, Wells score risk assessment
Pneumonia Fever, productive cough, unilateral crackles, consolidation on X-ray, ↑ CRP/WCC
COPD Exacerbation Wheeze, prolonged expiration, smoking history, no pulmonary edema, normal BNP
Acute Asthma Exacerbation Wheeze, ↓ Peak flow, younger patients, reversible with bronchodilators, normal BNP
Pneumothorax Sudden dyspnea, unilateral reduced breath sounds, hyper-resonance, asymmetrical chest findings
Pericardial Effusion / Tamponade Hypotension, raised JVP, muffled heart sounds, pulsus paradoxus, ECG: low voltage
Anxiety / Panic Attack Dyspnea without hypoxia, normal ECG, no crackles, psychological stress, younger age
ARDS Severe hypoxia, bilateral crackles, rapid onset post-infection/trauma, normal BNP
Aortic Dissection Sudden severe chest/back pain, unequal pulses/BP, widened mediastinum on X-ray, high-risk profile
Acute Kidney Injury / Fluid Overload Oliguria, recent nephrotoxin use, metabolic derangements, volume overload signs
Cirrhosis / Nephrotic Syndrome Ascites, peripheral edema, stigmata of liver disease, proteinuria



The management of acute left ventricular failure (ALVF) in primary care settings necessitates a multifaceted approach that addresses the underlying causes, alleviates symptoms, and stabilizes the patient. The initial management should focus on prompt diagnosis and implementation of early therapeutic strategies to reduce morbidity and mortality associated with this condition.


Management Table for Acute LVF


Category Key Actions
1. Immediate Stabilisation - Sit patient upright (45–90°) - Oxygen therapy: if SpO2 <92% (aim 94–98%) - IV Diuretics: Furosemide 40 mg IV - Nitrates: GTN (if systolic BP >90 mmHg) - Avoid: Beta-blockers, NSAIDs, IV fluids
2. Initial Pharmacological Treatment - Loop diuretics: Ongoing use for symptom relief - Nitrates: Further doses as needed for preload reduction - Analgesia/Anxiolytics: E.g., low-dose morphine (rare, for severe distress only)
3. Referral & Specialist Care - Urgent hospital admission: especially if SpO2 <90%, hypotension, or chest pain. - Advanced care: Inotropes, vasodilators, ventilatory support, specialist review for further diagnostics & management

👉 Beta-blockers, ACE inhibitors, and ARBs are introduced in stable patients post-admission under specialist guidance.


🔍 Why IV Diuretics Are Preferred in Acute LVF

  • Faster onset of action: IV furosemide works within 5–15 mins, essential for rapid decongestion.

  • More reliable absorption: Acute LVF may impair gut perfusion, reducing oral drug absorption.

  • Potent diuresis: Immediate and more controlled fluid removal to relieve pulmonary oedema.


❌ Oral Diuretics: Limited Role

  • Too slow: Oral furosemide onset is 60–120 mins, inadequate for acute distress.


  • Unpredictable effect: Variable absorption in acute illness.

✅ When to Use Oral Diuretics

  • Once patient is stable post-admission, oral diuretics may be prescribed to:

    • Maintain fluid balance

    • Prevent re-accumulation of fluid

    • Transition from IV to oral therapy before discharge


Primary Care Note

  • If IV access is unavailable, and the patient is mildly symptomatic, a high-dose oral diuretic might be cautiously used while arranging urgent hospital admission.

  • But in true acute pulmonary oedema or severe ALVF, immediate hospital transfer for IV therapy is critical.


Ongoing and Supportive Care After Acute LVF Stabilisation

Key Post-Discharge Measures


  • Patient Education:

    • Salt restriction: 

    • Avoid universal low-salt diets in acute LVF. Assess baseline salt intake (e.g., processed food consumption) before advising changes.
    • When to Advise Salt Reduction:
      • Patients with high habitual salt intake (e.g., frequent takeaways, salty snacks).
      • Those with persistent congestion (e.g., pulmonary edema, peripheral edema).
      • Caution with Hyponatremia: Prioritize fluid restriction over salt reduction; consult specialists for hyponatremia management.
    • Guideline Targets:
      • Salt: ≤5 g/day (~2,000–3,000 mg sodium), equivalent to a no-added-salt diet.
      • Fluid: Restrict to 1.5–2 L/day in hyponatremia or severe fluid overload, guided by specialist advice.
    • Alignment: This approach aligns with NICE (NG106), ESC (2021), and recent evidence (e.g., SODIUM-HF), balancing symptom control with avoiding harm from excessive restriction.




    • Fluid restriction: Typically 1.5–2L/day (adjust based on clinical advice)

    • Smoking cessation & alcohol moderation

    • Daily weight monitoring: Early detection of fluid retention

    • Symptom awareness: Prompt reporting of dyspnoea, swelling, weight gain


  • Vaccination:

    • Annual influenza vaccine

    • One-off pneumococcal vaccine


Optimising Medical Therapy

  • Start/Up-titrate:

    • ACE inhibitors (or ARBs if intolerant) → ↓ afterload, improve survival

    • Beta-blockers: Once stable, reduce risk of future decompensation

    • Mineralocorticoid Receptor Antagonists: E.g., spironolactone if LVEF ↓ and symptoms persist (specialist guidance)


    • Consider SGLT2 inhibitors in line with latest heart failure guidelines (if applicable)


Follow-Up & Monitoring

  • Specialist HF clinic review: Tailored medication titration, echocardiography monitoring

  • Renal function & electrolytes: Regular monitoring, especially on diuretics or MRAs

  • Rehabilitation: Heart failure rehab programmes to improve exercise tolerance and quality of life


✅ Key Points for Primary Care

  • Acute LVF requires rapid stabilisation and urgent referral.

  • Primary care supports long-term management: education, prevention, and medication adherence.

  • Follow national guidelines for ongoing care to reduce readmissions and improve outcomes.



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  25. Local Guidelines and Resources: