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Cardiac (Heart) Failure Made Easy (Pathophysiology and Diagnosis)

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DEFINITION OF CARDIAC FAILURE

It is a state in which there is:

a. Forward failure: inability of heart to maintain cardiac output sufficient to meet the metabolic demands of peripheral tissues AND/OR

b. Backward failure: ability to do so with elevated filling pressure

PATHOGENESIS OF CARDIAC FAILURE

1. Myocyte loss and/or dysfunction:

a. Myocyte loss:

b. Myocyte dysfunction (Changes in expression of contractile proteins, ion channels, enzymes, receptors and secondary messengers):

2. Compensatory mechanisms:

a. Increased myocardial contractility:

b. Myocardial hypertrophy:

c. Neurohumoral mechanisms:

d. Sympathetic stimulation:

DELETERIOUS EFFECTS OF PROLONGED COMPENSATORY MECHANISM

1. Continuous sympathetic activation: β-adrenergic downregulation and desensitization (less inotropic response)

2. Increased heart rate: Increased metabolic demands and myocardial cell death

3. Increased circulating volume and preload: Beyond limits of Starling’s law, pressure is transmitted to pulmonary vasculature leading to alveolar exudation and pulmonary congestion

4. Increased total peripheral resistance: Higher afterload leading to decreased stroke volume and cardiac output

5. Continuous neurohumoral activation: Chronically elevated angiotensin-II and aldosterone trigger production of cytokines, which stimulate macrophages and stimulate fibroblasts resulting in myocardial remodelling which leads to loss of contractility.

PRECIPITATING AND AGGRAVATING FACTORS OF CARDIAC FAILURE

1. Increased metabolic demands (like your company is already in loss and your workers ask for more salary):

2. Increased preload (when the Starling’s law is overwhelmed – increased ventricular filling pressure leads to transmission of pressure back to systemic veins from right side leading to systemic venous congestion and to pulmonary vasculature from left side leading to pulmonary congestion):

3. Increased afterload (increased resistance against which the ventricles must pump leading to reduced stroke volume):

4. Impaired contractility (reduces stroke volume and cardiac output):

5. Direct drop in cardiac output:

6. Poor compliance with therapy

Mnemonic: FAILURE

  • F: Forget to take medications
  • A: Arrhythmias, Anemia
  • I: Infection, Ischemia, Infarction
  • L: Lifestyle changes
  • U: Upregulators (thyroid, pregnancy)
  • R: Rheumatic heart disease and other valvular disease
  • E: Embolism

TYPES OF CARDIAC FAILURE

A) Systolic Vs Diastolic Heart Failure:

1. Systolic heart failure: Impaired contraction (LVEF <40%)

2. Diastolic heart failure: Impaired filling (diastolic dysfunction) and normal systolic function (LVEF >40%) e.g.

B) Acute Vs Chronic Heart Failure:

1. Acute heart failure (sudden): Cardiogenic shock and Acute pulmonary edema without peripheral edema e.g. MI, rupture of cardiac valve

2. Chronic heart failure (insidious):

C) Low output vs High output failure:

1. Low output heart failure: Heart fails to generate adequate cardiac output or can do so with high filling pressures e.g. ischemic heart disease, hypertension, cardiomyopathy, valvular disease, pericardial disease

2. High output heart failure: Heart fails to maintain sufficient circulation despite increased cardiac output (>8 L/minute) or increased cardiac index (>3.9 L/minute/sq.m) e.g. hyperthyroidism, anemia, pregnancy, AV fistula, beriberi, etc.

D) Left-sided vs Right-sided heart failure:

1. Left-sided (left ventricular) failure (LVF): Reduction in left ventricular output, increase in left atrial pressure and increase in pulmonary venous pressure. e.g. Aortic stenosis

2. Right-sided (right ventricular) failure (RVF): Reduction in left ventricular output, resulting in systemic venous congestion. e.g. Cor pulmonale, Pulmonary valvular stenosis, Multiple pulmonary emboli

Cor pulmonale: RV dilation +/- RV hypertrophy +/- overt RVF secondary to Pulmonary HTN resulting from:

  • Diseases of lung: COPD, Chronic asthma, Pulmonary TB, ILD, Bronchiectasis, High altitude dwelling, Cystic fibrosis, Pleural fibrosis
  • Diseases of pulmonary circulation: Recurrent pulmonary embolism, Primary pulmonary hypertension, Collagen vascular disease, Chronic liver disease
  • Diseases of thorax: Kyphoscoliosis, Neuromuscular diseases, Sleep apnea syndrome, Pickwickan syndrome (Obesity-hypoventilation syndrome)

Pulmonary hypertension (PH): Mean pulmonary artery pressure >25 mmHg or Resting systolic pulmonary artery pressure >40 mmHg; Dana Point classification –

  • I : Pulmonary artery hypertension (Cor pulmonale)
  • II: Left heart disease
  • III: Lung disease and/or hypoxia (Cor pulmonale)
  • IV: Thromboembolic (Cor pulmonale)
  • V: Unclear multiple mechanisms

3. Biventricular (Congestive) heart failure: Examples –

E) COMMON CAUSES OF HEART FAILURE

1. Pressure overload of ventricle:

2. Volume overload of ventricle:

3. Inflow obstruction of ventricle:

4. Impaired ventricular function:

Common causes of valvular heart diseases:

1. Mitral Stenosis (MS): Normal orifice 4-6 sq.cm; Mild 1.5-2.5 sq.cm; Moderate 1-1.4 sq.com; Severe/Critical/Tight <1 sq.cm

  • Rheumatic fever (almost all cases)
  • CVD: SLE, RA
  • Rare causes (4 “M”s): Mucopolysaccharidosis, Myxoma (atrial), Malignant carcinoid, Methysergide

2. Mitral Regurgitation (MR):

  • Rheumatic Heart Disease
  • Ischemic (Papillary muscle dysfunction and rupture)
  • Degenerative (Mitral valve prolapse)
  • Infective (Endocarditis)
  • Connective tissue disorder (SLE, RA, Marfan’s syndrome, Ehler-Danlos syndrome)
  • LV dilation of any cause
  • Congenital MR

3. Aortic Stenosis (AS): Normal orifice 3-4 sq.cm; Critical stenosis <0.8 sq.cm

  • Valvular: Congenital, RHD, Aortic sclerosis, SLE, Infective endocarditis, Radiation
  • Subvalvular: HOCM, Congenital
  • Supravalvular: Congenital

4. Aortic Regurgitation (AR):

  • Aortic valve disease: RHD, Congenital (bicuspid valve), Infective endocarditis, Trauma (rupture)
  • Aortic disease: Aortitis (Syphilitic, CVD, Autoimmune vasculitis), Hypertension, Aneurysm

5. Tricuspid stenosis (TS):

  • RHD
  • Carcinoid syndrome
  • Congenital

6. Tricuspid regurgitation (TR):

  • Functional: RHD or CHD with severe PAH, Inferior wall MI, Corpulmonale, Cardiomyopathy
  • Organic: RHD, Ebstein’s anomaly, Carcinoid syndrome, Tricuspid valve prolapse, Infective endocarditis, Trauma

6. Pulmonary stenosis (PS):

  • Congenital (may be associated with maternal rubella syndrome)
  • May be isolated or associated with Tetralogy of Fallot

PATHOPHYSIOLOGY AND CLINICAL FEATURES OF CARDIAC FAILURE

Signs and symptoms Underlying mechanism
Left-sided heart failure
Symptoms
Dyspnea Backflow causes interstitial pulmonary edema, leading to:
  • reduced pulmonary compliance
  • increased airway resistance
  • stimulation of juxta-capillary (J) receptros – hyperventilation (Herring-Breuer reflex terminates inspiratory effor before full inspiration leading to rapid shallow breathing)
  • increased ventilatory drive due to V/Q mismatch
Orthopnea (dyspnea on lying supine; relieved by sitting)
  • Increased venous return from lower limbs and abdomen to lungs
  • Elevation of diaphragm
  • Reabsorption of peripheral edema accumulated while ambulant
  • Extra mechanisms for PND:
    • Depression of respiratory center during sleep
    • Reduced adrenergic stimulation of myocardium
Paroxysmal nocturnal dyspnea i.e. PND (awakens patient from sleep; persists even after sitting)
Cough +/- frothy blood-tinged sputum Pulmonary congestion
Rupture of engorged bronchial veins – hemoptysis
Confusion and/or impaired memory or syncope e.g. Complete heart block (Stokes-Adams-Morgagni syndrome) Cerebral hypoperfusion and arterial hypoxemia
Decreased urine output Decreased renal perfusion during daytime leading to pre-renal AKI
Nocturia Redistribution and better perfusion of kidneys at night when supine
Signs
Pulmonary crackles Opening of small airways closed by interstitial edema prior to inspiration; initially at lung bases (hydrostatic forces greatest) and later diffuse
Cardiac “asthma” Wheezing caused by compression of conduction airways by pulmonary congestion – most prominent at night
Accentuated P2 Pulmonary artery hypertension due to backflow of elevated left atrial pressure
Mitral regurgitation murmur Excessive stretching of mitral valve annulus due to left ventricular dilation
Pulsus alternans A sign of advanced ventricular dysfunction
Narrow pulse pressure Reduced systolic BP due to reduced stroke volume
Increased diastolic BP due to generalized vasoconstriction
Right-sided heart failure
Symptoms
Peripheral edema, sacral edema, ascites, effusions and/or anasarca Increased hydrostatic venous pressures (in dependent parts) –
  • Pretibial and ankle region: Ambulant patient
  • Sacral region: Bed-ridden patients

RAAS activation leading to salt and water retention
Congestive Hepatosplenomegaly (+/- RUQ pain) Portal and splenic circulation engorgement
Pain and tenderness is due to the stretching of capsule
Anorexia/weight loss Diminished appetite due to hepatic and intestinal congestion
Increased metabolism due to increased myocardial oxygen consumption and excessive work of breathing
Intestinal fat malabsorption and protein losing enteropathy (rarely)
Signs
Elevated JVP Elevated right sided pressure
Positive abdomino-jugilar reflex suggests inadequate ventricular compliance
Kussmaul sign Paradoxical elevation of JVP with inspiration (as opposed to decrease) reflects increased right atrial pressure
Palpable right ventricular heave Right ventricular hyperthrophy (RVH)
Tricuspid regurgitation murmur Excessive stretching of tricuspid valve annulus due to right ventricular dilation
Right- or left-sided heart failure
Symptoms
Ischemic Chest pain/pressure
a. Angina: retrosternal; exertional/emotional; <20 min; relieved by rest and GTN; radiating to left arm, jaw and backb. Myocardial infarction: similar to angina but >20 min; not relieved by GTN		 Primary myocardial ischemia: CAD

Secondary myocardial ischemia: increased filling pressures, poor cardiac output (with consequent poor coronary diastolic filling) or hypoxemia
Palpitations
a. Extrasystoles: “Heart misses a beat; jumps”
b. SVT/VT: “Heart flutters”
c. AF: “Heart races irregularly”		 Sinus tachycardia due to decompensated heart failure
Atrial/ventricular tachyarrhythmias arising in dilated heart chambers
High cardiac output failure
Chronic fatigue/weakness Chronic state of hypoxemia from inadequate oxygen delivery to peripheral tissues
Generalized decreased muscle strength, decreased endurance and multi-organ system dysfunction
Cardiac Cachexia Anorexia
Gut congestion leading to decreased absoprtion
Increased metabolic demands
Immobility leading to skeletal muscle atrophy
Increased chornic inflammatory markers
Signs
S3 gallop (S1+S2+S3 = Triple rhythm)
Sounds like “-Ken-tuck-y”		 Abnormal filling of dilated ventricle
S4 gallop (S1 S2+S4 = Triple rhythm; S1+S2+S3+S4 = Quadruple rhythm) Forceful contraction of the atria into a stiffened ventricle; common in diastolic dysfunction
Cardiomegaly (Displaced apex beat) Work hypertrophy and Volume dilation

FRAMINGHAM CRITERIA FOR DIAGNOSIS OF CARDIAC FAILURE

Definite diagnosis requires: 2 Major OR 1 Major + 2 Minor criteria

A) Major Criteria:

Mnemonic: 3CDEFGH

  1. Crackles
  2. CVP raised (Neck vein distension)
  3. Cardiomegaly on Chest X-ray
  4. Dyspnea – PND
  5. Edematous lungs (Acute pulmonary edema)
  6. Fall of weight >4.5 kg in 5 days in response to CHF treatment
  7. Gallop rhythm (S3)
  8. Hepatojugular reflux positive

B) Minor Criteria:

Mnemonic: MNOPQRS

  1. Megaly of liver (Hepatomegaly)
  2. Night cough
  3. Oedema – bilateral ankle
  4. Pleural effusion
  5. Quantitative PFT – Vital capacity reduced by 1/3 of maximum
  6. Rapid pulse (tachycardia > 120/min)
  7. SOB on strain (sternous exertion)

AHA and NYHA CLASSIFICATION OF HEART FAILURE

ACC/AHA grade NYHA functional class
A: At risk of heart failure but without structural disease or symptoms None
B: Structural heart disease but without heart failure I: Asymptomatic HF – no limitations of daily activities
C: Structural heart disease with prior or current heart failure symptoms II: Mild HF – symptomatic with moderate exertion
III: Moderate HF – symptomatic with minimal exertion
D: Refractory heart failure requiring specialized interventions IV: Severe HF – symptomatic at rest

COMMON DIAGNOSTIC STUDIES FOR CARDIAC FAILURE

A) Chest X-ray Features of Pulmonary edema:

Mnemonic: ABCDE 1. Alveolar edema (Bat’s wing – increased bronchovascular markings) 2. B (Kerley) lines (Interstitial edema – engorged peripheral lymphatics in base/lower lobe) 3. Cardiomegaly 4. Dilated prominent upper lobe veins 5. Effusion – Pleural (unilateral or bilateral)

B) ECG: Features of –

  1. Ventricular hypertrophy
  2. Atrial abnormality
  3. Arrhythmias
  4. Conduction abnormalities, previous MI and active ischemia

C) Echocardiography: Assessment of –

  1. Ejection fraction (Normal 50-70%)
  2. Valvular functions
  3. Chamber size and shape
  4. Differential systolic and diastolic dysfunction

D) Brain Natriuretic Peptide (BNP):

Origin: BNP is secreted by the cardiac ventricles in response to left ventricular stretching or wall tension. Cardiac myocytes secrete precursor pro-BNP which is secreted into ventrciles, where it is cleaved into biologically active C-terminal portion and biologically inactive N-terminal (NT pro-BNP) portion.

Functions of Natriuretic peptides (ANP and BNP):

  1. Downregulates sympathetic nervous system and RAAS
  2. Facilitates natriuresis and diuresis
  3. Increase smooth muscle relaxation and decrease peripheral resistance

Uses in heart failure:

  1. A negative result rules out disease more effectively than a positive result rules in disease
  2. Predictor of prognosis
  3. Monitoring

BNP levels:

  1. <100 pg/ml: Heart failure unlikely
  2. 100-250 pg/ml: Compensated heart failure
  3. 250-500 pg/ml: Both diastolic and systolic dysfunction
  4. 500-1000 pg/ml: Decompensated heart failure
  5. >1000 pg/ml: Increased risk of substantial heart failure

E) Others: RFT (look for renal dysfunction), CBC (look for anemia), Serum electrolytes (electrolyte imbalances) and TFT (thyroid dysfunction) because these may contribute to HF symptoms and progression.

History and physical examination should focus on distinguishing between ischemic causes of HF (coronary artery disease [CAD]) and nonischemic causes of HF (valvular heart disease, diabetes, hypertension, alcohol abuse, neuromuscular disorders, and cardiomyopathies). The family history should be explored for premature CAD, HF, arrhythmias, and sudden cardiac death.
The baseline ECG should be reviewed for evidence of myocardial infarction, conduction disturbances, and arrhythmias.

MANAGEMENT OF ACUTE DECOMPENSATION (ACUTE CARDIOGENIC PULMONARY EDEMA)

Pathophysiology of Cardiogenic Pulmonary Edema:

It is defined as an episode of acute heart failure accompanied by severe respiratory distress and oxygen saturation <90% on room air before all treatment.

  1. As pulmonary congestion increases, oxygen saturation decreases – decreased myocardial oxygen supply (risk of ischemia and further worsening of cardiac performance)
  2. Hypoxemia and increased fluid content in lungs induces pulmonary vasoconstriction increasing the right ventricular pressure – this compromises left ventricular function through ventricular interdependence mechanism (interventricular septum is common to both the ventricles)
  3. Circulatory insufficiency leads to metabolic acidosis – further impairs cardiac performance

Mnemonic: POD MAN

1. Precipitants: Find and treat it simultaenously

2. Position: Propped-up (raise the head of bed or use 2-4 pillows) or Sitting position

3. Oxygen +/- NIV: 100% Oxygen, preferably under positive airway pressure

4. Diuretics:

Intravenous loop diuretics like:

Mechnism of furosemide benefit:

Avoid in hypertensive pulmonary edema – patient are euvolemic or hypovolemic

5. Morphine: 2-5 mg i.v. slowly

6. Methylxanthines: I.V Aminophylline 250-500 mg reduces bronchoconstriction, increases renal blood flow and sodium excretion (by diuresis) and increases myocardial contractility

7. Adrenergic drugs (Inotropes):

Useful in hypotensive pulmonary edema or cardiogenic shock

  1. With normal or low-normal blood pressure: Dobutamine
  2. With shock: Dopamine
  3. With SVT: Digoxin
  4. Inodilators: Milrinone (risk of life-threatning arrhythmia), Levosimendan (novel calcium sensitizer)

8. Nitrates and Nesiritide (Vasodilators):

Mechanism: Venodilation reduces preload and Arteriolar dilation reduces afterload – both reduces overloading of heart

a. GTN infusion if SBP >110 or 2 Puffs GTN spray if SBP >90

b. Sublingual nitrates: 5-10 mg Isosorbide dinitrate

c. Nitroprusside (when acute afterload reduction needed – hypertensive emergency, acute aortic regurgitation, acute mitral regurgitation, acute VSD): 20-30 mcg/min

d. Nesiritide (recominant BNP): arterial and venous dilator + diuretic effect; i.v. 2 mcg/kg bolus followed by 0.01 mcg/kg/min infusion

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