acute heart failure [mbbs]
TRANSCRIPT
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ACUTE HEART FAILURE
Muhammad Khairulanwar Bin Muhamad Kamal
012012050-144Emergency Medicine [Y5]
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Overview
■ Introduction■ Pathophysiology■ Classification■ Aetiology■ Diagnosis■ Management in Emergency (ED)■ Disposition decision
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Introduction
■ A complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood
■ Heart fails to act as a pump■ Manifested by cardinal symptoms
– Dyspnoea & fatigue exercise intolerance– Fluid retention pulmonary oedema, splanchnic oedema,
peripheral oedema
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PathophysiologyInefficient pump
Responsive adaptations
Maladaptation
Long term disease progressionsAcute
exacerbation
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■ “Inefficient pump” decrease cardiac output (CO)– Myocardial injury– Stress
■ “Responsive adaptations” Neurohormonal mediated cascades activation– Renin angiotensin aldosterone system (RAAS)– Sympathetic nervous system (SNS)
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Neurohormonal mediated cascadeRAAS & Sympathetic activation
Na+ and water retention,increased systemic vascular resistance
Maintain blood pressure and perfusion*At the cost of increasing myocardial workload, wall tension and myocardial oxygen demand
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Counter regulatory response
■ Atrial natriuretic peptides (Atria)■ B-type natriuretic peptide (Ventricle)■ C-type natriuretic peptide (Localized in endothelium)
■ Effects: Vasodilation, natriuresis, decreased levels of endothelin, and inhibition of RAAS and SNS
■ Importance: (Assays)– Elevated levels portend a worse prognosis– Attenuation provides the basis for most chronic therapies proven to
delay morbidity and mortality
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Assays for BNP in ED use
N-t pre-pro-BNP
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Classification*
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Classification
■ Acute vs Chronic■ Systolic vs Diastolic dysfunction■ Right sided vs Left sided■ High output vs Low output
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Systolic vs diastolic
Systolic DiastolicAge All ages Frequently elderlySex Often male Frequently femaleLV EF Decrease ( <50 ) Normal ( Preserved )LV cavity size Dilate ( increase
intracardiac volume )Normal ( often with LVH )
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Current categorization
■ Heart failure with a reduced ejection fraction (HFrEF) [SYSTOLIC]
■ Heart failure with preserved ejection fraction (HFpEF) [DIASTOLIC]
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Common causes of heart failure
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Diagnosis
■ History■ Clinical examination■ Fisk factors■ Precipitating factor■ Investigations
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History – cardinal symptoms
■ Dyspnoea on exertion■ Orthopnoea■ Paroxysmal nocturnal dyspnoea■ Edema■ Fatigue
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History – other symptoms
■ Cough with expectoration■ CNS : Altered sensorium, confusion, impairment of
memory, headache, insomnia■ GI : Anorexia, nausea, vomiting, pain abdomen, abdominal
fullness■ GU: Nocturia
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Dyspnoea
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■ Differential for dyspnoea– Exacerbation of asthma or COPD– Pulmonary embolus– Pneumonia– Acute coronary syndrome– Anaphylaxis
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Risk factors
■ Male■ Old ages■ Hypertension■ Diabetes mellitus■ Valvular heart disease■ obesity
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Precipitating factors
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General Physical Examination
■ Mild to moderate HF : No distress except when lying flat for more than a few minutes
■ Severe HF: Must sit upright, labored breathing, unable to finish a sentence – Cardiac cachexia– Cyanosis– Edema– Jaundice
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Vitals
■ Sinus tachycardia■ Pulse pressure: ↓■ SBP: ↓■ Cold extremities■ ↑ JVP
– Giant v waves
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Examination of Jugular Veins
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CVS Examination
■ Palpation: Cardiomegaly with hyperdynamic point of maximum impulse
■ Auscultation– S₃– PSM
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RS Examination
■ Crepitations / Rales■ Signs of pleural effusion
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PA Examination & extremities
■ Hepatomegaly: Tender, pulsatile■ Ascites
■ Peripheral edema
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Investigations
1. Chest X-ray2. Electrocardiogram3. Biomarkers4. Ultrasonography5. Routine lab tests: CBC, RFT, LFT, TSH, electrolytes
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Chest x-ray (upright)
– Pulmonary venous congestion– Cardiomegaly (80%) or normal (20%)– Interstitial edema
■ Most specific for a final diagnosis of acute heart failure but the absence of these does not rule it out
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■ Cardiomegaly CTR = 18/30 (>50%)■ Upper zone vessel enlargement (1) – a
sign of pulmonary venous hypertension■ Septal (Kerley B) lines (2) – a sign of
interstitial oedema – see next picture■ Airspace shadowing (3) – due to
alveolar oedema – acutely in a peri-hilar (bat's wing) distribution
■ Blunt costophrenic angles (4) – due to pleural effusions
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Electrocardiogram
■ Not useful for diagnosis– Early recognition of arrhythmias – atrial fibrillation– Signs of ischaemia or injury
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■ Irregularly irregular rhythm.■ No P waves.■ Absence of an isoelectric baseline.■ Variable ventricular rate.■ QRS complexes usually < 120 ms
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Routine
■ Complete blood count to evaluate anaemia■ Basic metabolic panel
– Electrolytes– Renal status
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Cardiac biomarkers
■ It is done when cause of dyspnoea is still unclear after standard evaluation
■ This test will detect ongoing myocyte injury, which may be clinically silent
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Bedside ultrasound
1. Determine cause of dyspnoea e.g. tamponade2. Determine LV function and volume status3. RWMA4. Valvular abnormality
Focused on1. Signs of pulmonary congestion
2. Sign of volume overload3. LV ejection fraction
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Signs of pulmonary congestion
■ Sonographic B-lines– Dx – >2 B-lines
in any sonographic windows along the anterior and posterior chest
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Signs of volume overload
■ IVC >2 cm diameter■ Collapsibility index <50%
– Indicates raised in central venous pressure
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Management in ED
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Disposition decision
■ Lack of ED-based-risk stratification tool■ Mainly based on
– Physician judgement– Physiologic risk assessment– Assessments of barrier to successful outpatient
High risk physiological marker1. Renal dysfunction 3. Low serum sodium2. Low BP 4. Increase natriuretic peptide / cardiac troponin
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■ High risk features admission to ward■ Patient required invasive monitoring / procedure ICU■ Lower risk features observation unit (12-24h)
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References
■ Tintinalli’s Emergency Medicine, 8th edition■ Rosen’s Emergency Medicine, 8th edition■ Harrison’s Principle of Internal Medicine, 19th edition
Thank you!