Acute Heart Failure

Causes of Acute Heart Failure

1. Coronary Artery Disease
   • Acute coronary syndrome (ACS), including myocardial infarction and ischemia, is a leading cause.
   • Mechanical complications such as ventricular septal rupture following myocardial infarction.
2. Arrhythmias
   • Atrial fibrillation and flutter.
   • Ventricular arrhythmias, including tachycardia, fibrillation, and ectopy.
3. Valvular Heart Disease
   • Acute mitral or aortic regurgitation due to infective endocarditis, ischemic papillary muscle rupture, or aortic dissection.
   • Thrombosis or perforation of prosthetic valves.
4. Hypertension
   • Uncontrolled or severe hypertension, sometimes associated with bilateral renal artery stenosis.
5. Myocarditis
   • Acute inflammation of the myocardium caused by viral or other infections.
6. Cardiomyopathy
   • Hypertrophic cardiomyopathy.
   • Dilated cardiomyopathy, including familial variants.
   • Takotsubo (stress-induced) cardiomyopathy.
   • Tachycardia-mediated cardiomyopathy.
7. Structural and Mechanical Disorders
   • Cardiac tamponade, aortic dissection, or ventricular rupture.
   • Postpartum cardiomyopathy.
   • Shunt syndromes or structural abnormalities.
8. High-Output States
   • Conditions like thyrotoxicosis, severe anemia, or sepsis that increase cardiac demand.
     
     

Precipitating Factors

• Dietary and Lifestyle Factors
  • Excessive salt or fluid intake, alcohol abuse, or dietary indiscretions.
• Nonadherence
  • Failure to adhere to prescribed medications or dietary restrictions.
• Infections
  • Systemic infections, particularly sepsis or endocarditis.
• Hemodynamic Stress
  • Uncontrolled hypertension or arrhythmias (both tachycardia and bradycardia).
• Drug Effects
  • Cardiodepressant agents (e.g., beta-blockers or calcium channel blockers inappropriately used).
  • NSAIDs or antiarrhythmic drugs exacerbating volume retention or myocardial depression.
• Other Triggers
  • Pulmonary embolism, severe emotional or physical stress, and endocrine abnormalities like hyperthyroidism.
    
    

Common Comorbidities

• Coronary artery disease, diabetes mellitus, hypertension, atrial fibrillation, and renal insufficiency are frequently observed in patients with ADHF.
  
  

Hemodynamic Changes

• Pulmonary and Systemic Venous Congestion:
  • Pulmonary congestion results in symptoms like dyspnea and orthopnea, often progressing to pulmonary edema.
  • Systemic venous congestion manifests as jugular venous distension, hepatomegaly, and peripheral edema.
• Increased Ventricular Pressures and Reduced Output:
  • Elevated left and right ventricular filling pressures impair effective cardiac output and lead to backward pressure transmission.
    
    

1. Sympathetic Nervous System (SNS):
   • Increased activity triggers tachycardia and enhances myocardial contractility as a compensatory mechanism.
   • Peripheral vasoconstriction improves systemic vascular resistance but increases afterload and myocardial oxygen demand, exacerbating ischemia.
2. Renin-Angiotensin-Aldosterone System (RAAS):
   • Activation of RAAS promotes sodium and water retention to increase intravascular volume and maintain perfusion, resulting in elevated preload.
   • Aldosterone contributes to myocardial fibrosis and vascular stiffness, perpetuating maladaptive remodeling.
3. Vasoconstrictor Neurohormones:
   • Endothelin-1 and vasopressin potentiate vasoconstriction, fluid retention, and further increase systemic vascular resistance.
   • Elevated endothelin-1 levels correlate with disease severity and adverse outcomes.
     
     

Myocardial Stress and Dysfunction

• Impaired Relaxation and Contraction:
  • Sustained stress compromises diastolic (lusitropy) and systolic (inotropy) functions, leading to inefficient cardiac filling and ejection.
• Cellular Damage:
  • Increased myocardial energy demands cause metabolic derangements, oxidative stress, and apoptosis of cardiac myocytes.
  • Loss of functional myocytes contributes to progressive myocardial dysfunction.
    
    

Adaptations and Remodeling

• The Frank-Starling mechanism temporarily enhances stroke volume by increasing myocardial stretch, optimising contractility.
• These compensatory efforts are critical in maintaining cardiac output in the early stages of dysfunction.
  
  

• Myocardial Hypertrophy and Fibrosis:
  • Chronic pressure overload stimulates pathological hypertrophy, leading to stiff, fibrotic myocardial tissue.
  • Fibrosis disrupts electrical conduction, predisposing to arrhythmias.
• Eccentric Remodeling:
  • Structural changes, such as ventricular dilation, elevate wall stress and myocardial oxygen consumption.
  • These changes impair contractile efficiency and perpetuate the cycle of heart failure.
    
    

Systemic Effects

• Reduced cardiac output compromises renal perfusion, activating RAAS and promoting fluid retention.
• Worsened congestion leads to the cardiorenal syndrome, with bidirectional deterioration of cardiac and renal functions.
  
  

• Elevated vasoconstrictor levels impair nitric oxide-mediated vasodilation, increasing afterload.
• Chronic endothelial dysfunction promotes atherosclerosis and systemic inflammation.
  
  

• Cytokines like tumor necrosis factor-alpha (TNF-α) amplify myocardial injury and fibrosis.
• Systemic inflammation exacerbates peripheral vascular resistance and catabolic states, contributing to muscle wasting and fatigue.
  
  

Prevalence

• Approximately 900,000 individuals in the UK have heart failure, with acute presentations accounting for 5% of all adult emergency hospital admissions.
• Prevalence varies globally:
  • China: 1.3%
  • Malaysia: 6.7%
  • Japan: 1%
  • Singapore: 4.5%
  • India: 0.12%-0.44%
  • South America: 1%
  • Australia: 1%-2%
    
    

Demographics

• In Europe, the average age of AHF patients is 70 years, with men comprising 61% of cases. However, among those aged ≥85 years, women form the majority.
• In the United States and Europe, around 1 million hospitalisations annually are due to AHF, making it the leading cause of hospital admissions in older adults.
  
  

Clinical Presentations

• New-onset AHF accounts for 37% of cases, while 63% occur as acute decompensation of chronic heart failure.
• Presentations vary:
  • Decompensated heart failure: 65%
  • Pulmonary edema: 16%
  • Hypertensive AHF: 11%
  • Cardiogenic shock: 4%
  • Right-sided heart failure: 3%
    
    

Common Risk Factors

1. Strong Risk Factors
   • Coronary artery disease (CAD): Leading cause of heart failure.
   • Age: Prevalence rises sharply in individuals ≥70 years (≥10% in this age group).
   • Previous heart failure episodes: 75% of hospitalized patients have prior heart failure history.
   • Diabetes mellitus: Related to ischemia and renal dysfunction.
   • Hypertension: A critical modifiable risk factor; poorly controlled hypertension frequently leads to heart failure.
   • Family history: Ischemic heart disease or cardiomyopathy increases risk.
   • Lifestyle Factors:
     • Smoking.
     • Excessive alcohol intake.
2. Other Risk Factors
   • Arrhythmias: Both tachyarrhythmia and bradyarrhythmia.
   • Non-adherence to medication: Often leads to exacerbations.
   • Medications: NSAIDs, steroids, diltiazem, and verapamil may exacerbate heart failure.
   • Systemic conditions: Sarcoidosis, haemochromatosis, and prior chemotherapy.
   • High salt intake: Contributes to volume overload.
     
     

Emerging Insights

• The National Heart Failure Audit (2020/21) in England and Wales highlighted:
  • A mean patient age of 77.8 years.
  • A decline in admissions (11%) compared to 2019/20, likely influenced by the COVID-19 pandemic.
  • Gender distribution shifts, with men dominating younger cohorts and women predominating at older ages.
    
    

1. Breathlessness
   • Orthopnea: Worsening dyspnea when lying flat, relieved by sitting up.
   • Paroxysmal Nocturnal Dyspnea (PND): Sudden nighttime attacks of breathlessness.
   • Effort Dyspnea: Progressive shortness of breath on exertion.
2. Fatigue and Weakness
   • Caused by reduced cardiac output leading to poor tissue perfusion.
   • Patients report difficulty in performing routine activities and prolonged recovery after exertion.
3. Peripheral Oedema
   • Swelling of the lower limbs, often pitting and bilateral.
   • Worsens throughout the day and improves with leg elevation.
4. Nocturnal Cough
   • Can be a sign of pulmonary congestion.
   • Frothy sputum suggests alveolar involvement.
5. Unintentional Weight Loss (Cardiac Cachexia)
   • Chronic heart failure can lead to muscle wasting and poor appetite.
6. Cognitive Changes
   • Older patients may present with confusion or memory impairment due to hypoperfusion.
7. Gastrointestinal Symptoms
   • Right heart failure can lead to nausea, bloating, and abdominal discomfort due to hepatic congestion.

Risk Factors

1. Cardiovascular Risk Factors
   • History of coronary artery disease, myocardial infarction, or hypertension.
   • Atrial fibrillation and other arrhythmias.
2. Metabolic Conditions
   • Diabetes mellitus increases the risk of AHF due to microvascular complications.
3. Lifestyle Factors
   • Smoking and excessive alcohol intake contribute to myocardial dysfunction.
   • Poor adherence to medications can precipitate decompensation.
4. Systemic Conditions
   • Chronic kidney disease, sarcoidosis, or hemochromatosis as underlying contributors.
5. Medication History
   • NSAIDs, steroids, calcium channel blockers (e.g., diltiazem, verapamil), or discontinuation of heart failure medications can precipitate worsening symptoms.

Signs of Fluid Overload

1. Elevated Jugular Venous Pressure (JVP):
   • A hallmark of systemic venous congestion.
   • Best assessed at a 45° angle; often difficult to detect but highly specific (specificity ~93%).
2. Peripheral Edema:
   • Bilateral, pitting edema in the lower extremities, often worse at the ankles.
   • Edema reduces after prolonged leg elevation.
3. Pulmonary Crepitations:
   • Fine crackles on auscultation, typically at the lung bases.
   • Reflects pulmonary congestion and interstitial edema.
   • Crackles sound "wet" and Velcro-like, differentiating them from coarser sounds in pulmonary fibrosis.
4. Pleural Effusion:
   • Dullness to percussion and reduced air entry, especially at the lung bases.
   • Often more pronounced on the right side.
5. Hepatomegaly:
   • Palpable, tender liver indicating congestion from increased central venous pressure.
   • Hepatojugular reflux may also be present.
6. Ascites:
   • Abdominal distention due to portal hypertension and systemic venous congestion.
     
     

Signs of Poor Perfusion

1. Cold Extremities:
   • Peripheral vasoconstriction as a compensatory response to reduced cardiac output.
2. Narrow Pulse Pressure:
   • A small difference between systolic and diastolic blood pressure suggests low stroke volume.
3. Delayed Capillary Refill:
   • Capillary refill time >2 seconds is a reliable indicator of poor perfusion.
4. Oliguria:
   • Decreased urine output as a sign of renal hypoperfusion.
5. Central Cyanosis:
   • Bluish discoloration of the lips and tongue due to hypoxemia.
6. Altered Mental Status:
   • Confusion or disorientation, particularly in older adults, may reflect hypoperfusion of the brain.
     
     

Cardiac Examination

1. Displaced Apex Beat:
   • A laterally displaced apex beat suggests left ventricular dilation.
2. Gallop Rhythm (Third Heart Sound - S3):
   • Indicates increased ventricular filling pressure and poor diastolic function.
   • A fourth heart sound (S4) may also be present in some cases.
3. Cardiac Murmurs:
   • Mitral or tricuspid regurgitation murmurs due to ventricular dilation or pressure overload.
   • These murmurs may diminish with compensation.
     
     

Other Findings

1. Tachycardia:
   • A compensatory response to low cardiac output and reduced perfusion.
2. Tachypnea:
   • Rapid breathing due to hypoxia or pulmonary congestion.
3. Pulmonary Edema:
   • Severe cases present with pink, frothy sputum and significant respiratory distress.
4. Weight Gain:
   • Rapid weight gain indicates fluid retention and worsening congestion.
5. Hepatojugular Reflux:
   • Sustained rise in JVP with abdominal pressure confirms systemic venous congestion.
     
     

Initial Investigations

1. Electrocardiogram (ECG)
   • Purpose: Perform a 12-lead ECG to detect arrhythmias, ischemic changes, conduction blocks, and evidence of left ventricular hypertrophy.
   • Key Findings:
     • Atrial fibrillation or other arrhythmias.
     • ST-segment and T-wave abnormalities indicative of myocardial ischemia.
     • Left ventricular hypertrophy or signs of prior myocardial infarction.
2. Chest X-Ray
   • Purpose: Assess for pulmonary and cardiac abnormalities.
   • Key Findings:
     • Signs of pulmonary congestion, interstitial or alveolar edema, and pleural effusions.
     • Cardiomegaly, although left ventricular dysfunction can be present without this feature.
3. Natriuretic Peptides
   • Purpose: Evaluate levels of BNP or NT-proBNP to support diagnosis and assess heart failure severity.
   • Key Findings:
     • Elevated NT-proBNP:
       • 450 ng/L for patients under 50 years.
       • 900 ng/L for ages 50–75 years.
       • 1800 ng/L for those over 75 years.
     • Lower levels argue against heart failure, but elevated levels may also occur in other conditions such as renal impairment or sepsis.
4. Troponins
   • Purpose: Detect myocardial injury or infarction.
   • Key Findings:
     • Elevated levels are common in AHF and correlate with worse prognosis.
     • Interpret cautiously, as elevation may occur due to myocardial strain or type 2 myocardial infarction.
5. Full Blood Count (FBC)
   • Purpose: Rule out anemia or infection as contributing factors.
   • Key Findings:
     • Anemia exacerbates heart failure symptoms.
     • Leukocytosis may indicate underlying infection.
6. Renal Function Tests (Urea, Creatinine, Electrolytes)
   • Purpose: Assess kidney function and guide therapy involving diuretics or renin-angiotensin inhibitors.
   • Key Findings:
     • Renal dysfunction or electrolyte imbalances, including hyponatremia or hyperkalemia.
7. Liver Function Tests
   • Purpose: Evaluate for hepatic congestion and impaired perfusion.
   • Key Findings:
     • Elevated liver enzymes often indicate venous congestion.
8. Blood Glucose and HbA1c
   • Purpose: Screen for undiagnosed diabetes or assess glycemic control.
   • Key Findings:
     • Elevated glucose or HbA1c levels may exacerbate heart failure.
9. Thyroid Function Tests
   • Purpose: Identify thyroid dysfunction as a precipitant of AHF.
   • Key Findings:
     • Hyperthyroidism or hypothyroidism affecting cardiac performance.
10. C-Reactive Protein (CRP)
    • Purpose: Detect systemic inflammation or infection.
    • Key Findings:
      • Elevated CRP levels are associated with heart failure progression.
        
        

Specific Investigations

1. Echocardiography
   • Purpose: Essential for evaluating cardiac structure and function.
   • Key Findings:
     • Reduced left ventricular ejection fraction (LVEF ≤40%) confirms HFrEF.
     • Preserved ejection fraction (HFpEF) with diastolic dysfunction or structural abnormalities.
     • Detects valvular dysfunction, intracardiac shunts, or regional wall motion abnormalities.
2. Arterial Blood Gas (ABG)
   • Purpose: Assess oxygenation, ventilation, and acid-base balance in suspected respiratory or metabolic compromise.
   • Key Findings:
     • Hypoxemia, hypercapnia, or metabolic acidosis with raised lactate levels.
3. D-Dimer
   • Purpose: Rule out pulmonary embolism in patients with suggestive symptoms.
   • Key Findings:
     • Elevated levels require further investigation for thrombotic events.
4. Thoracic Ultrasound
   • Purpose: Identify pulmonary congestion or pleural effusion when BNP/NT-proBNP testing is unavailable.
   • Key Findings:
     • B-lines indicating interstitial edema.
     • Pleural effusions associated with volume overload.
5. Myocarditis Screening
   • Purpose: Investigate viral or autoimmune causes when myocarditis is suspected.
   • Key Findings:
     • Positive serologies for infectious agents such as coxsackievirus or parvovirus B19.
       
       

Special Considerations

1. Blood Gas Analysis
   • Used in patients with severe respiratory distress or suspected shock.
2. Coronary Angiography
   • Performed when acute coronary syndrome is suspected or ischemia needs confirmation.
3. Swan-Ganz Catheterisation
   • Reserved for cases of uncertain diagnosis or when guiding therapy for severe refractory heart failure.
     
     

 Pulmonary Conditions

1. Pulmonary Embolism (PE)
   • Symptoms: Sudden onset of dyspnea, pleuritic chest pain, cough, and sometimes hemoptysis.
   • Risk Factors: Personal or family history of thromboembolism, prolonged immobilisation, trauma, or use of hormonal contraceptives.
   • Investigations:
     • CT pulmonary angiography: Visualizes thrombus in pulmonary arteries.
     • D-dimer: Elevated levels suggest thrombotic activity.
2. Pneumonia
   • Symptoms: Acute dyspnea with fever, productive cough, and pleuritic chest pain.
   • Signs: Focal consolidation, bronchial breath sounds, and increased vocal fremitus.
   • Investigations:
     • Chest X-ray: Localized consolidation.
     • Blood cultures: May identify causative pathogens.
     • Elevated white blood cell count.
3. Asthma
   • Symptoms: Acute wheezing, cough, and shortness of breath, often triggered by allergens or irritants.
   • Signs: Diffuse wheezing on auscultation.
   • Investigations:
     • Spirometry: Obstructive pattern reversible with beta-agonists.
     • Reduced peak expiratory flow rate.
4. Noncardiogenic Pulmonary Edema (NCPE)
   • Symptoms: Acute dyspnea often secondary to conditions like sepsis, pancreatitis, or trauma.
   • Signs: Warm, vasodilated periphery; less pronounced cardiac findings compared to cardiogenic pulmonary oedema (CPE).
   • Investigations:
     • Chest X-ray: Diffuse infiltrates without cardiomegaly.
     • ECG: Usually normal unless associated metabolic disturbances.
5. Acute Respiratory Distress Syndrome (ARDS)
   • Symptoms: Severe hypoxemia, rapid respiratory rate, and diffuse fine crepitations.
   • Investigations:
     • Chest X-ray: Bilateral diffuse infiltrates.
     • Pulmonary artery wedge pressure: <18 mmHg differentiates ARDS from CPE.
       
       

Other Cardiac Mimics

1. Myocardial Ischemia or Infarction
   • Symptoms: Chest pain, dyspnea, and diaphoresis.
   • Investigations:
     • ECG: ST-segment changes or Q waves.
     • Troponins: Elevated levels indicate myocardial injury.
2. Arrhythmias
   • Symptoms: Palpitations, syncope, or sudden onset of breathlessness.
   • Investigations:
     • ECG: Atrial fibrillation, ventricular tachycardia, or bradyarrhythmias.
       
       

Pulmonary-Cardiac Overlaps

1. Interstitial Lung Disease
   • Symptoms: Gradually progressive dyspnea and exertional oxygen desaturation.
   • Signs: Fine bibasilar crepitations without peripheral edema.
   • Investigations:
     • Chest X-ray: Reticular infiltrates in later stages.
     • High-resolution CT: Ground-glass opacities and honeycombing.
     • Spirometry: Restrictive pattern.
       
       

Urgent Actions

1. Identify High-Risk Patients
   • Request urgent cardiology or critical care support for patients with:
     • Respiratory distress or failure.
     • Use of accessory muscles, respiratory rate >25/min, or SpO2 <90% despite oxygen.
     • Hemodynamic instability, shock, or systolic blood pressure <90 mmHg.
     • Severe arrhythmias (e.g., heart rate <40 bpm or >130 bpm).
     • Reduced consciousness or hypoperfusion.
2. Immediate Stabilization
   • Administer oxygen only if SpO2 <90% or PaO2 <8 kPa (<60 mmHg).
   • Use non-invasive positive pressure ventilation (e.g., CPAP or BiPAP) in patients with respiratory distress unresponsive to oxygen alone.
   • Initiate invasive ventilation for refractory respiratory failure, hypercapnia, or acidosis.
3. Address Precipitating Causes
   • Rapidly investigate and treat conditions such as:
     • Acute coronary syndrome (ACS).
     • Hypertensive crisis.
     • Pulmonary embolism.
     • Myocarditis or infections.
     • Cardiac tamponade or valvular rupture.
4. Organise Hospital Transfer
   • Ensure rapid hospital transfer for patients presenting in the community with suspected AHF.
     
     

Pharmacological Treatment

1. Initial Drug Therapy
   • Diuretics:
     • Administer intravenous loop diuretics for congestion.
     • Adjust dose based on symptoms, weight, and urine output.
     • Consider adding a thiazide or aldosterone antagonist for resistant edema.
   • Vasodilators:
     • Use in hypertensive patients or those with severe congestion.
     • Monitor blood pressure closely to maintain systolic BP >90 mmHg.
   • Inotropes and Vasopressors:
     • Reserved for cardiogenic shock or refractory low-output states.
     • Administer only in specialist units with hemodynamic monitoring.
2. Long-Term Medications
   • For Reduced Ejection Fraction (HFrEF, LVEF ≤40%):
     • Initiate an ACE inhibitor or angiotensin receptor blocker (ARB).
     • Start beta-blockers after stabilisation (e.g., when no longer requiring IV diuretics).
     • Add aldosterone antagonists and consider sacubitril/valsartan for persistent symptoms.
     • Sodium-glucose co-transporter 2 (SGLT2) inhibitors (e.g., dapagliflozin) are recommended regardless of diabetes status.
   • For Preserved Ejection Fraction (HFpEF, LVEF ≥50%):
     • Focus on symptom relief with diuretics and management of comorbidities.
   • For Mildly Reduced Ejection Fraction (HFmrEF, LVEF 41-49%):
     • Consider therapies used in HFrEF, including SGLT2 inhibitors.
       
       

Non-Pharmacological Measures

1. Specialist Involvement
   • Ensure review by a heart failure specialist team within 24 hours of hospital admission.
   • Consider advanced therapies like cardiac resynchronisation, implantable defibrillators, or transplantation in appropriate candidates.
2. Monitoring
   • Closely monitor:
     • Renal function, electrolytes, and blood pressure during diuretic and vasodilator therapy.
     • Symptoms of hypoperfusion or fluid overload.
   • Aim for controlled diuresis (0.75-1.0 kg/day weight reduction) while avoiding over-diuresis.
3. Patient Education
   • Discuss coping strategies for increased urine output due to diuretics.
   • Address dietary sodium restriction and medication adherence.
     
     

1. Criteria for Discharge
   • Achieve euvolemia and symptom stabilisation.
   • Initiate guideline-directed medical therapy.
   • Ensure follow-up with the multidisciplinary team within two weeks of discharge.
2. Rehabilitation and Follow-Up
   • Offer cardiac rehabilitation programs focusing on exercise, psychological support, and education.
   • Monitor and titrate medications post-discharge to maximise outcomes.
     
     

Inpatient Mortality

• Overall in-hospital mortality for AHF is approximately 11%, with significant variability between hospitals in England and Wales (ranging from 6% to 26%).
• Patients admitted to cardiology wards have lower mortality (6%) compared to general medical wards (10.2%).
• Involvement of heart failure specialists further reduces inpatient mortality (7.9% versus 14.9%).
  
  

One-Year Mortality

• One-year mortality remains high at approximately 39%, unchanged during the COVID-19 pandemic (2020/21) compared to prior years.
• Despite advancements in therapy, long-term survival for hospitalised AHF patients remains limited.
  
  

Five-Year Outcomes

• AHF patients have a similarly poor five-year survival rate across all ejection fraction categories, with a high mortality rate of 75.4% following the index admission.
• Cardiovascular events and recurrent heart failure admissions are primary contributors to this poor long-term prognosis.
  
  

Predictors of Adverse Outcomes

1. Demographics and Baseline Characteristics
   • Older age and male sex are associated with worse outcomes.
2. Clinical Parameters
   • Hypotension, respiratory rate >30 breaths per minute on admission, and renal dysfunction.
3. Laboratory Findings
   • Hyponatremia, anemia, elevated troponin, and elevated B-type natriuretic peptide levels.
4. Comorbidities
   • Ischemic heart failure, prior heart failure history, and concurrent conditions such as cancer.
5. Care Delivery
   • Admission to specialised cardiology care or involvement of heart failure specialists improves survival.
     
     

Prognostic Factors by Setting

• Data from the National Heart Failure Audit highlights that specialised cardiology care is associated with significantly improved outcomes compared to general medical wards.
  
  

Arrhythmias

• Timeframe: Short-term.
• Likelihood: High.
• Details:
  • Common arrhythmias include atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
  • Symptoms: Palpitations, fainting, or sudden cardiac death.
  • Management: Anti-arrhythmic therapy (e.g., amiodarone), beta-blockers, or cardioversion.
    
    

Kidney Damage or Failure

• Timeframe: Short- to long-term.
• Likelihood: High in severe cases.
• Details:
  • Reduced renal perfusion due to low cardiac output can lead to acute kidney injury or chronic renal failure.
  • Symptoms: Fatigue, poor appetite, and lethargy.
  • Management: Optimize fluid balance and avoid nephrotoxic medications.
    
    

Liver Damage

• Timeframe: Variable.
• Likelihood: Moderate.
• Details:
  • Congestive hepatopathy results from fluid overload causing hepatic congestion and, eventually, fibrosis.
  • Symptoms: Right upper quadrant discomfort, jaundice, or ascites.
  • Management: Address volume overload and optimise heart function.
    
    

Pulmonary Oedema

• Timeframe: Short-term.
• Likelihood: High.
• Details:
  • Fluid accumulation in the alveoli impairs gas exchange, causing dyspnea and hypoxia.
  • Symptoms: Severe breathlessness and frothy sputum.
  • Management: Diuretics, oxygen therapy, and ventilatory support.
    
    

Stroke

• Timeframe: Variable.
• Likelihood: Moderate.
• Details:
  • Formation of intracardiac thrombi, particularly in atrial fibrillation, increases embolic stroke risk.
  • Symptoms: Sudden neurological deficits.
  • Management: Anticoagulation therapy in appropriate patients.
    
    

Muscle Wasting (Cardiac Cachexia)

• Timeframe: Long-term.
• Likelihood: Moderate.
• Details:
  • Chronic inflammation and poor perfusion lead to muscle loss.
  • Symptoms: Weakness, unintentional weight loss.
  • Management: Nutritional support and exercise therapy.
    
    

Anaemia

• Timeframe: Chronic complication.
• Likelihood: Moderate.
• Details:
  • Contributing factors include chronic inflammation and renal dysfunction.
  • Symptoms: Fatigue, pallor, and reduced exercise tolerance.
  • Management: Treat underlying causes; consider erythropoietin-stimulating agents if indicated.
    
    

Valvular Dysfunction

• Timeframe: Chronic complication.
• Likelihood: High in patients with structural heart disease.
• Details:
  • Mitral and aortic regurgitation are common, exacerbating heart failure symptoms.
  • Management: Surgical or percutaneous interventions for severe cases.
    
    

Complications of Treatment

1. Glyceryl Trinitrate (Nitrates):
   • Side Effects: Headache and hypotension.
   • Management: Adjust infusion rate and discontinue if hypotension persists.
2. Nesiritide:
   • Side Effects: Hypotension and headache.
   • Management: Reduce or stop infusion if hypotension occurs.
3. Diuretics:
   • Risks: Over-diuresis leading to renal dysfunction, hypokalemia, and activation of neurohormonal systems.
   • Management: Adjust dosing to avoid excessive fluid removal; monitor renal function.
4. Inotropes (e.g., Dobutamine, Milrinone):
   • Risks: Arrhythmias and worsening ischemia.
     
     
   • Management: Use cautiously, consider concurrent anti-arrhythmic therapy (e.g., amiodarone).
     
     

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