ACUTE HEART FAILURE

Muhammad Khairulanwar Bin Muhamad Kamal

012012050-144Emergency Medicine [Y5]

Overview

■ Introduction■ Pathophysiology■ Classification■ Aetiology■ Diagnosis■ Management in Emergency (ED)■ Disposition decision

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

PathophysiologyInefficient pump

Responsive adaptations

Maladaptation

Long term disease progressionsAcute

exacerbation

■ “Inefficient pump” decrease cardiac output (CO)– Myocardial injury– Stress

■ “Responsive adaptations” Neurohormonal mediated cascades activation– Renin angiotensin aldosterone system (RAAS)– Sympathetic nervous system (SNS)

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

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

Assays for BNP in ED use

N-t pre-pro-BNP

Classification*

Classification

■ Acute vs Chronic■ Systolic vs Diastolic dysfunction■ Right sided vs Left sided■ High output vs Low output

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 )

Current categorization

■ Heart failure with a reduced ejection fraction (HFrEF) [SYSTOLIC]

■ Heart failure with preserved ejection fraction (HFpEF) [DIASTOLIC]

Common causes of heart failure

Diagnosis

■ History■ Clinical examination■ Fisk factors■ Precipitating factor■ Investigations

History – cardinal symptoms

■ Dyspnoea on exertion■ Orthopnoea■ Paroxysmal nocturnal dyspnoea■ Edema■ Fatigue

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

Dyspnoea

■ Differential for dyspnoea– Exacerbation of asthma or COPD– Pulmonary embolus– Pneumonia– Acute coronary syndrome– Anaphylaxis

Risk factors

■ Male■ Old ages■ Hypertension■ Diabetes mellitus■ Valvular heart disease■ obesity

Precipitating factors

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

Vitals

■ Sinus tachycardia■ Pulse pressure: ↓■ SBP: ↓■ Cold extremities■ ↑ JVP

– Giant v waves

Examination of Jugular Veins

CVS Examination

■ Palpation: Cardiomegaly with hyperdynamic point of maximum impulse

■ Auscultation– S₃– PSM

RS Examination

■ Crepitations / Rales■ Signs of pleural effusion

PA Examination & extremities

■ Hepatomegaly: Tender, pulsatile■ Ascites

■ Peripheral edema

Investigations

1. Chest X-ray2. Electrocardiogram3. Biomarkers4. Ultrasonography5. Routine lab tests: CBC, RFT, LFT, TSH, electrolytes

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

■ 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

Electrocardiogram

■ Not useful for diagnosis– Early recognition of arrhythmias – atrial fibrillation– Signs of ischaemia or injury

■ Irregularly irregular rhythm.■ No P waves.■ Absence of an isoelectric baseline.■ Variable ventricular rate.■ QRS complexes usually  < 120 ms

Routine

■ Complete blood count to evaluate anaemia■ Basic metabolic panel

– Electrolytes– Renal status

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

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

Signs of pulmonary congestion

■ Sonographic B-lines– Dx – >2 B-lines

in any sonographic windows along the anterior and posterior chest

Signs of volume overload

■ IVC >2 cm diameter■ Collapsibility index <50%

– Indicates raised in central venous pressure

Management in ED

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

■ High risk features admission to ward■ Patient required invasive monitoring / procedure ICU■ Lower risk features observation unit (12-24h)

References

■ Tintinalli’s Emergency Medicine, 8th edition■ Rosen’s Emergency Medicine, 8th edition■ Harrison’s Principle of Internal Medicine, 19th edition

Thank you!