Acute Heart Failure

Causes of Acute Heart Failure

Coronary artery disease

• Acute coronary syndrome (ACS), including myocardial infarction and ischaemia, is a leading cause
• Mechanical complications such as ventricular septal rupture following myocardial infarction

Arrhythmias

• Atrial fibrillation and flutter
• Ventricular arrhythmias, including tachycardia, fibrillation, and ectopy

Valvular heart disease

• Acute mitral or aortic regurgitation due to infective endocarditis, ischaemic papillary muscle rupture, or aortic dissection
• Thrombosis or perforation of prosthetic valves

Hypertension

• Uncontrolled or severe hypertension
• May be associated with bilateral renal artery stenosis

Myocarditis

• Acute inflammation of the myocardium caused by viral or other infections

Cardiomyopathy

• Hypertrophic cardiomyopathy
• Dilated cardiomyopathy, including familial variants
• Takotsubo (stress-induced) cardiomyopathy
• Tachycardia-mediated cardiomyopathy

Structural and mechanical disorders

• Cardiac tamponade, aortic dissection, or ventricular rupture
• Postpartum cardiomyopathy
• Shunt syndromes or congenital structural abnormalities

High-output states

• Conditions such as thyrotoxicosis, severe anaemia, or sepsis that increase cardiac demand

Precipitating Factors

Dietary and lifestyle factors

• Excessive salt or fluid intake
• Alcohol abuse
• Dietary indiscretions

Nonadherence

• Failure to adhere to prescribed medications or dietary restrictions

Infections

• Systemic infections, particularly sepsis or endocarditis

Hemodynamic stress

• Uncontrolled hypertension
• Arrhythmias, including both tachycardia and bradycardia

Drug effects

• Cardiodepressant agents (e.g., beta-blockers or calcium channel blockers when inappropriately used)
• NSAIDs or antiarrhythmic drugs that exacerbate volume retention or depress myocardial function

Other triggers

• Pulmonary embolism
• Severe emotional or physical stress
• Endocrine abnormalities such as hyperthyroidism

Common Comorbidities

• Coronary artery disease
• Diabetes mellitus
• Hypertension
• Atrial fibrillation
• Renal insufficiency

Hemodynamic Changes

Volume overload

• Pulmonary and systemic venous congestion:
  • Pulmonary congestion results in dyspnoea and orthopnoea, often progressing to pulmonary oedema
  • Systemic venous congestion manifests as jugular venous distension, hepatomegaly, and peripheral oedema
• Increased ventricular pressures and reduced output:
  • Elevated left and right ventricular filling pressures impair effective cardiac output
  • Backward pressure transmission contributes to pulmonary and systemic symptoms

Neurohormonal Activation

Sympathetic nervous system (SNS)

• Increased activity triggers tachycardia and enhances myocardial contractility as compensation
• Peripheral vasoconstriction raises systemic vascular resistance but increases afterload and myocardial oxygen demand, worsening ischaemia

Renin-angiotensin-aldosterone system (RAAS)

• Promotes sodium and water retention to increase intravascular volume and maintain perfusion
• Aldosterone contributes to myocardial fibrosis and vascular stiffness, promoting maladaptive remodelling

Vasoconstrictor neurohormones

• Endothelin-1 and vasopressin induce vasoconstriction, fluid retention, and increased systemic vascular resistance
• Elevated endothelin-1 levels are associated with greater disease severity and poorer outcomes

Myocardial Stress and Dysfunction

Impaired relaxation and contraction

• Sustained haemodynamic stress impairs diastolic (lusitropic) and systolic (inotropic) function
• Leads to reduced cardiac filling and ejection efficiency

Cellular damage

• Increased myocardial energy demand results in metabolic dysfunction, oxidative stress, and apoptosis of myocytes
• Loss of viable myocytes contributes to ongoing myocardial dysfunction

Adaptations and Remodeling

Acute adaptations

• The Frank-Starling mechanism enhances stroke volume by increasing myocardial stretch
• This compensatory response temporarily maintains cardiac output in early dysfunction

Chronic maladaptations

• Myocardial hypertrophy and fibrosis:
  • Chronic pressure overload stimulates pathological hypertrophy
  • Fibrotic tissue stiffens the myocardium and disrupts conduction, increasing arrhythmia risk
• Eccentric remodelling:
  • Ventricular dilation increases wall stress and myocardial oxygen demand
  • These structural changes further reduce contractile efficiency

Systemic Effects

Renal perfusion impairment

• Reduced cardiac output decreases renal perfusion, activating RAAS and promoting fluid retention
• Progressive congestion leads to cardiorenal syndrome, with mutual worsening of cardiac and renal function

Endothelial dysfunction

• Elevated vasoconstrictors impair nitric oxide-mediated vasodilation, increasing afterload
• Chronic dysfunction contributes to atherosclerosis and systemic inflammation

Inflammatory mediators

• Cytokines such as tumour necrosis factor-alpha (TNF-α) exacerbate myocardial injury and fibrosis
• Systemic inflammation promotes peripheral resistance and a catabolic state, contributing to fatigue and muscle wasting

Prevalence

• Approximately 900,000 individuals in the UK have heart failure
• Acute presentations account 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 patients with acute heart failure (AHF) is 70 years
• Men account for 61% of AHF cases overall, though women predominate in patients aged ≥85 years
• In both the United States and Europe, AHF leads to approximately 1 million hospitalisations annually
• AHF is the most common cause of hospital admission among older adults

Clinical Presentations

• New-onset AHF accounts for 37% of cases
• Acute decompensation of chronic heart failure accounts for 63%

Common presentation subtypes

• Decompensated heart failure: 65%
• Pulmonary oedema: 16%
• Hypertensive AHF: 11%
• Cardiogenic shock: 4%
• Right-sided heart failure: 3%

Common Risk Factors

Strong risk factors

• Coronary artery disease (CAD): Leading cause of heart failure
• Age ≥70 years: Prevalence ≥10% in this age group
• Previous heart failure: 75% of hospitalised patients have a history of HF
• Diabetes mellitus: Associated with ischaemia and renal dysfunction
• Hypertension: Key modifiable risk factor, especially if poorly controlled
• Family history: Increases risk if there is a history of ischaemic heart disease or cardiomyopathy

Lifestyle factors

• Smoking
• Excessive alcohol intake

Other risk factors

• Arrhythmias: Both tachyarrhythmias and bradyarrhythmias
• Non-adherence to medications
• Drug-related: NSAIDs, corticosteroids, diltiazem, verapamil
• Systemic diseases: Sarcoidosis, haemochromatosis, prior chemotherapy
• High dietary salt intake

Emerging Insights

• The National Heart Failure Audit (2020/21) reported a mean patient age of 77.8 years in England and Wales
• There was an 11% reduction in hospital admissions compared to 2019/20, likely due to the COVID-19 pandemic
• Gender trends show men dominate in younger age groups, while women are more prevalent in older age groups

Symptoms

Breathlessness

• Orthopnoea: Worsening dyspnoea when lying flat, relieved by sitting up
• Paroxysmal nocturnal dyspnoea (PND): Sudden episodes of breathlessness at night, often waking the patient from sleep
• Effort dyspnoea: Progressive shortness of breath with exertion

Fatigue and weakness

• Caused by reduced cardiac output and poor tissue perfusion
• Patients report difficulty with routine activities and prolonged recovery after exertion

Peripheral oedema

• Typically bilateral and pitting, affecting the lower limbs
• Tends to worsen during the day and improve with leg elevation

Nocturnal cough

• May indicate pulmonary congestion
• Frothy sputum suggests alveolar fluid accumulation

Unintentional weight loss (cardiac cachexia)

• Associated with chronic heart failure
• Characterised by muscle wasting, poor appetite, and nutritional deficiencies

Cognitive changes

• Common in older adults with low cardiac output
• May present as confusion, memory impairment, or reduced concentration

Gastrointestinal symptoms

• Right-sided heart failure may cause nausea, bloating, early satiety, and abdominal discomfort
• Often due to hepatic congestion and gastrointestinal oedema

Risk Factors

Cardiovascular risk factors

• History of coronary artery disease, myocardial infarction, or hypertension
• Presence of atrial fibrillation or other arrhythmias

Metabolic conditions

• Diabetes mellitus increases AHF risk due to microvascular disease and diastolic dysfunction

Lifestyle factors

• Smoking and excessive alcohol intake contribute to myocardial damage
• Poor adherence to medication or diet may trigger acute decompensation

Systemic conditions

• Chronic kidney disease
• Sarcoidosis or haemochromatosis as infiltrative or metabolic causes

Medication history

• NSAIDs, corticosteroids, and calcium channel blockers (e.g., diltiazem, verapamil) may worsen fluid retention
• Discontinuation or inappropriate dosing of heart failure medications may precipitate symptoms

Signs of Fluid Overload

Elevated jugular venous pressure (JVP)

• A hallmark of systemic venous congestion
• Best assessed at a 45° angle
• Often difficult to detect but has high specificity (~93%)

Peripheral oedema

• Bilateral, pitting oedema in the lower limbs, usually worse around the ankles
• Tends to reduce with prolonged leg elevation

Pulmonary crepitations

• Fine crackles on auscultation, typically at the lung bases
• Indicate pulmonary congestion and interstitial oedema
• Crackles are "wet" and Velcro-like, distinct from coarse crackles in fibrosis

Pleural effusion

• Dullness to percussion and decreased breath sounds at the lung bases
• More commonly affects the right side

Hepatomegaly

• Palpable, tender liver due to hepatic venous congestion
• May be accompanied by hepatojugular reflux

Ascites

• Abdominal distension resulting from portal hypertension and systemic venous congestion

Signs of Poor Perfusion

Cold extremities

• Caused by peripheral vasoconstriction in response to reduced cardiac output

Narrow pulse pressure

• Small difference between systolic and diastolic pressure suggests low stroke volume

Delayed capillary refill

• Capillary refill time >2 seconds indicates peripheral hypoperfusion

Oliguria

• Reduced urine output due to decreased renal perfusion

Central cyanosis

• Bluish discoloration of the lips and tongue caused by systemic hypoxaemia

Altered mental status

• Confusion or disorientation, especially in elderly patients
• Reflects cerebral hypoperfusion

Cardiac Examination

Displaced apex beat

• Lateral displacement indicates left ventricular dilation

Gallop rhythm (third heart sound – S3)

• Suggests elevated ventricular filling pressures and impaired diastolic function
• A fourth heart sound (S4) may also be heard in some patients

Cardiac murmurs

• Mitral or tricuspid regurgitation murmurs may occur due to ventricular dilation or overload
• Murmurs may soften once haemodynamic compensation is achieved

Other Findings

Tachycardia

• A compensatory mechanism for reduced cardiac output

Tachypnoea

• Rapid breathing caused by pulmonary congestion or hypoxaemia

Pulmonary oedema

• Severe cases present with pink, frothy sputum and respiratory distress

Weight gain

• Rapid increase in weight indicates fluid retention and worsening heart failure

Hepatojugular reflux

• A sustained rise in JVP during abdominal pressure confirms systemic venous congestion

Initial Investigations

Electrocardiogram (ECG)

•  Purpose: Perform a 12-lead ECG to detect arrhythmias, ischaemic changes, conduction blocks, and left ventricular hypertrophy
•  Key findings:
  • Atrial fibrillation or other arrhythmias
  • ST-segment and T-wave abnormalities suggestive of myocardial ischaemia
  • Evidence of left ventricular hypertrophy or prior myocardial infarction

Chest X-ray

•  Purpose: Evaluate for pulmonary and cardiac abnormalities
•  Key findings:
  • Signs of pulmonary congestion, interstitial or alveolar oedema, and pleural effusions
  • Cardiomegaly, although left ventricular dysfunction can occur without it

Natriuretic peptides

•  Purpose: Assess BNP or NT-proBNP levels to support diagnosis and severity assessment
•  Key findings:
  • NT-proBNP >450 ng/L (<50 years), >900 ng/L (50–75 years), >1800 ng/L (>75 years)
  • Lower levels reduce likelihood of heart failure
  • Elevated levels may also reflect renal impairment, sepsis, or pulmonary embolism

Troponins

•  Purpose: Detect myocardial injury or infarction
•  Key findings:
  • Elevated levels are common in acute heart failure and indicate worse prognosis
  • May reflect type 2 myocardial infarction or myocardial strain

Full blood count (FBC)

•  Purpose: Identify anaemia or infection contributing to symptoms
•  Key findings:
  • Anaemia can worsen heart failure
  • Leukocytosis may indicate infection

Renal function tests (urea, creatinine, electrolytes)

•  Purpose: Assess kidney function and guide use of diuretics or RAAS inhibitors
•  Key findings:
  • Renal impairment, hyponatraemia, or hyperkalaemia

Liver function tests

•  Purpose: Detect hepatic congestion or hypoperfusion
•  Key findings:
  • Elevated liver enzymes suggest right heart failure or passive liver congestion

Blood glucose and HbA1c

•  Purpose: Screen for diabetes and assess glycaemic control
•  Key findings:
  • Elevated glucose or HbA1c levels may worsen cardiac function

Thyroid function tests

•  Purpose: Evaluate thyroid dysfunction as a precipitant
•  Key findings:
  • Hyperthyroidism and hypothyroidism both impact cardiac output and rhythm

C-reactive protein (CRP)

•  Purpose: Detect systemic inflammation or infection
•  Key findings:
  • Raised CRP may be associated with worsening heart failure or concurrent infection

Specific Investigations

Echocardiography

•  Purpose: Evaluate cardiac structure and function
•  Key findings:
  • Reduced LVEF (≤40%) confirms HFrEF
  • HFpEF may show diastolic dysfunction or structural changes
  • Identifies valvular disease, wall motion abnormalities, or intracardiac shunts

Arterial blood gas (ABG)

•  Purpose: Assess oxygenation, ventilation, and acid–base status
•  Key findings:
  • Hypoxaemia or hypercapnia in pulmonary oedema
  • Metabolic acidosis with elevated lactate in shock

D-dimer

•  Purpose: Exclude pulmonary embolism in appropriate clinical contexts
•  Key findings:
  • Elevated levels warrant further imaging (e.g. CTPA) for thromboembolic disease

Thoracic ultrasound

•  Purpose: Assess pulmonary congestion or pleural effusion, especially when BNP is unavailable
•  Key findings:
  • B-lines indicating interstitial oedema
  • Pleural effusions suggestive of volume overload

Myocarditis screening

•  Purpose: Consider in younger patients or those with viral prodrome or unexplained heart failure
•  Key findings:
  • Positive viral or autoimmune serologies (e.g. coxsackievirus, parvovirus B19)

Special Considerations

Blood gas analysis

• Indicated in patients with severe respiratory compromise or suspected circulatory shock

Coronary angiography

• Performed when acute coronary syndrome is suspected or to assess for ischaemic aetiology

Swan-Ganz catheterisation (right heart catheterisation)

• Used in refractory cases to guide therapy or clarify haemodynamic status when diagnosis is uncertain

Pulmonary Conditions

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: Visualises thrombus in pulmonary arteries.
  • D-dimer: Elevated levels suggest thrombotic activity.

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: Localised consolidation.
  • Blood cultures: May identify causative pathogens.
  • Elevated white blood cell count.

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.

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.

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

Myocardial Ischaemia or Infarction

• Symptoms: Chest pain, dyspnea, and diaphoresis.
• Investigations:
  • ECG: ST-segment changes or Q waves.
  • Troponins: Elevated levels indicate myocardial injury.

Arrhythmias

• Symptoms: Palpitations, syncope, or sudden onset of breathlessness.
• Investigations:
  • ECG: Atrial fibrillation, ventricular tachycardia, or bradyarrhythmias.

Pulmonary–Cardiac Overlaps

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

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.

Immediate Stabilisation

• 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.

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.

Organise Hospital Transfer

• Ensure rapid hospital transfer for patients presenting in the community with suspected AHF.

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 oedema.

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.

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

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.

Monitoring

• 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.

Patient Education

• Discuss coping strategies for increased urine output due to diuretics.
• Address dietary sodium restriction and medication adherence.

Discharge Planning

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.

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 variability between hospitals in England and Wales (6% to 26%).
• Patients admitted to cardiology wards have lower mortality (6%) compared to those on general medical wards (10.2%).
• Involvement of heart failure specialists reduces inpatient mortality further (7.9% vs 14.9%).

One-Year Mortality

• One-year mortality remains high at approximately 39%.
• This figure remained unchanged during the COVID-19 pandemic (2020/21) compared to previous years.
• Long-term survival remains poor despite therapeutic advancements.

Five-Year Outcomes

• AHF patients have poor five-year survival across all ejection fraction categories.
• The mortality rate is 75.4% following the index admission.
• Cardiovascular events and recurrent hospital admissions are major contributors to mortality.

Predictors of Adverse Outcomes

Demographics and Baseline Characteristics

• Older age and male sex are associated with increased mortality.

Clinical Parameters

• Hypotension, respiratory rate >30 breaths/min on admission, and renal dysfunction predict poor outcomes.

Laboratory Findings

• Hyponatraemia, anaemia, elevated troponin, and high BNP/NT-proBNP levels correlate with worse prognosis.

Comorbidities

• Ischaemic heart failure, history of prior heart failure admissions, and comorbid conditions such as malignancy contribute to higher risk.

Care Delivery

• Admission to cardiology wards and involvement of heart failure specialists improve survival rates.

Prognostic Factors by Setting

• Data from the National Heart Failure Audit show that patients receiving specialist cardiology care have significantly better outcomes than those managed on general medical wards.

Arrhythmias

• Timeframe: Short-term
• Likelihood: High
• 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
• 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: Optimise fluid balance and avoid nephrotoxic medications

Liver Damage

• Timeframe: Variable
• Likelihood: Moderate
• 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
• Fluid accumulation in the alveoli impairs gas exchange, causing dyspnoea and hypoxia
• Symptoms: Severe breathlessness and frothy sputum
• Management: Diuretics, oxygen therapy, and ventilatory support

Stroke

• Timeframe: Variable
• Likelihood: Moderate
• 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
• 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
• 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
• Mitral and aortic regurgitation are common, exacerbating heart failure symptoms
• Management: Surgical or percutaneous interventions for severe cases

Complications of Treatment

Glyceryl Trinitrate (Nitrates)

• Side effects: Headache and hypotension
• Management: Adjust infusion rate and discontinue if hypotension persists

Nesiritide

• Side effects: Hypotension and headache
• Management: Reduce or stop infusion if hypotension occurs

Diuretics

• Risks: Over-diuresis leading to renal dysfunction, hypokalaemia, and activation of neurohormonal systems
• Management: Adjust dosing to avoid excessive fluid removal; monitor renal function

Inotropes (e.g., Dobutamine, Milrinone)

• Risks: Arrhythmias and worsening ischaemia
• Management: Use cautiously; consider concurrent anti-arrhythmic therapy (e.g., amiodarone)

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