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Heart Failure (Ref. Hari. 18th ed., Pg-1901)

Basic Concepts

Cardiac output and BP are inadequate for the body's requirement.

Pump failure due to:

  1. Heart muscle disease: IHD; cardiomyopathy.
  2. Restricted filling: Constrictive pericarditis, tamponade, restrictive cardiomyopathy. This may be the mechanism of action of fluid overload: an expanding right heart impinges on the LV, so filling is restricted by the ungiving pericardium
  3. Inadequate heart rate: B-blockers, heart block, post MI. Negatively inotropic drugs: eg most antiarrhythmic agents.
  4. Excessive preload: eg mitral regurgitation or fluid overload (eg NSAID cause in fluid retention). Fluid overload may
    Cause LVF in a normal heart if renal excretion is impaired or big volumes are involved and common with beta blockers if there is simultaneous compromise of cardiac function, and in the elderly.
  5. Chronic excessive after load: eg aortic stenosis, hypertension. 

Types of heart failure

  1. Systolic / diastolic failure –
    1. Systolic failure –  
      1. Dilated cardiomyopathy
      2. MI
    2. Diastolic failure
      1. Constrictive pericarditis
      2. Restrictive cardiomyopathy
      3. HOCM
      4. acute MI.
      5. Cardiac Tamponade
  2. High output/ low output failure –
    1. High output failure – Thyrotoxicosis, anemia, pregnancy, Paget’s disease, Beri – Beri. Q
    2. Low output failure
      1. Ischemic heat disease
      2. Hypertension
      3. Pericarditis
      4. Cardiomyopathy.
  3. Right sided / left sided failure –
    1. Right sided failure – due to MS pulmonary hypertension, congenital PS.
    2. Left sided failure Mainly due to aortic stenosis, MI, HT
Extra Edge:

Heart failure does not occur in TOF (PGI Dec 2007)



  1. Dyspnea,        
  2. Orthopnea,                  
  3. Paroxysmal nocturnal dyspnea (PND),
  4. Pink frothy sputum in pulmonary oedema,               
  5. Wheeze (cardiac 'asthma'),
  6. Nocturia,        
  7. Cool peripheries,        
  8. Weight loss (Cardiac cachexia) (Ref. Hari.  18th ed.,  Pg- 1905)
  9. Muscle wasting.


  1. Peripheral oedema,
  2. Abdominal distension (ascites) 
  3. Jaundice.

Signs of LVF Cool peripheries, peripheral cyanosis.



  1. Resting tachycardia (Earliest feature) Q,
  2. Pulsus alternans Q

Auscultation: S3 gallop (Most important) Q , murmurs of mitral or aortic valve disease.



  1. Tachypnea,
  2. Bibasal end- inspiratory crackles,
  3. Wheeze ('cardiac asthma'),
  4. Pleural effusions.

Signs of RVF:  

  1. Raised JVP,
  2. Edema,
  3. Ascites,
  4. Hepatomegaly.

Framingham criteria for diagnosis of CHF – (AIIMS Nov. 2008)


(At least one major and two minor or two major criteria are required. Q)

Major criteria –

  1. Paroxysmal nocturnal dyspnea
  2. Raised JVP
  3. Crepitations
  4. Cardiomegaly
  5. Acute pulmonary edema
  6. S3
  7. Increased venous pressure (> 16cm H2O)
  8. Positive hepatojugular reflux

Minor criteria –

  1. Extremity edema
  2. Orthopnea (night cough)
  3. Dyspnea on exertion
  4. Hepatomegaly
  5. Pleural effusion
  6. Vital capacity reduced by 1/3 from normal.
  7. Tachycardia ( 120/m)

Compensatory mechanism in heart failure.

  1. Heart failure is associated with Hyponatremia
    1. Increased ADH and Aldosterone results which causes retention of water and sodium.
    2. Secondary water gain exceeds primary sodium gain resulting in hyponatremia.
  2. Elevated serum urea levels may be seen.
    1. Cardiac failure is associated with prerenal azotemia. ​
  3. Right atrial mean pressure is increased congestive heart failure.
  4. In patients will heart failure the levels of circulating norepinephrine may be markedly elevated reflecting the increased activity of the adrenergic nervous system. (Increase peripheral vasoconstriction).
  5. Increase epinephrine leads to tachycardia.


  1. Left atrial filling pressure closely approximates­ Pulmonary capillary wedge pressure (PCWP)
  2. PCWP is increase in cardiac pulmonary edema but it is normal in non cardiogenic pulmonary edema 

Causes of non-cardiogenic pulmonary edema

  1. High altitude
  2. Narcotic over dose
  3. Burns
  4. Smoke inhalation
  5. Septicemia
  6. Post cardiopulmonary bypass
  7. P. falciparum
  8. Chest trauma

Investigations If ECG and BNP (Brain natriuretic peptide, are normal, heart failure is unlikely, and an alternative diagnosis should be considered; if either abnormal then echocardiography is required.


Recent Advances: Biomarkers of heart failure (HF) (Ref. Hari. 18th ed., Pg- 1906)

  1. Circulating levels of natriuretic peptides are useful adjunctive tools in the diagnosis of patients with HF.
  2. Both B-type natriuretic peptide (BNP) and N-terminal pro-BNP, which are released from the failing heart, are relatively sensitive markers for the presence of HF with depressed EF.
  3. They also are elevated in HF patients with a preserved EF, albeit to a lesser degree.


  1. Cardiomegaly
  2. Prominent upper lobe veins
  3. Classical perihilar 'bat's wing' shadowing Q
  4. Pleural effusions
  5. Kerley B lines Q

ECG may indicate the cause.


Echocardiography is the key investigation may Q indicate the cause (MI, valvular heart disease) and can confirm the presence or absence of LV dysfunction. Ejection fraction (EF) is the best parameter to asses LVF. Normal EF is about 65% to 72% (LQ 2012). In CHF EF is reduced.


Recent Advances: Heart failure – Management (Ref. Hari. 18th ed., Pg – 1906)  


Treatment: Heart Failure HF should be viewed as a continuum that is composed of four interrelated stages.

Stage A  includes patients who are at high risk for developing HF but do not have structural heart disease or symptoms of HF (e.g., patients with diabetes mellitus or hypertension).
Stage B  includes patients who have structural heart disease but do not have symptoms of HF (e.g., patients with a previous MI and asymptomatic LV dysfunction).
Stage C includes patients who have structural heart disease and have developed symptoms of HF (e.g., patients with a previous MI with dyspnea and fatigue).
Stage D includes patients with refractory HF requiring special interventions (e.g., patients with refractory HF who are awaiting cardiac transplantation).

Basic principle of drug therapy in CHF

  1. Drugs to reduce preload = NO3, diuretic
  2. Drug to in cause pumping of myocardium = digoxin
  3. Drug to reduce after load = ACEI.

Drugs: the following drugs are used:

  1. Diuretics: Loop diuretics routinely used to relieve symptoms eg furosemide. 
    SE: Hypokalemia,  add K+ sparing diuretic (eg spironolactone) if K+ <3.2mmol/ predisposition to arrhythmias, concurrent digoxin therapy (Low K+ increases risk of digoxin toxicity), 
    If refractory oedema, add a thiazide e.g. metolazone
  2. ACE-inhibitor: Consider in all patients with left ventricular systolic dysfunction; improves symptoms and prolongs life
  3. Digoxin improves symptoms even in those with sinus rhythm
  4. Vasodilators: Nitrate
  5. Inotropic drugs – Milrinone, dopamine.   
  6. Beta-blockers (eg carvedilol) â-blocker reduce mortality in heart failure Q 

Doses of Dopamine:


Dose (μ gm/kg/min):  Receptor Effect
1 – 2 Dopaminergic Increase renal blood flow
2 – 5 Beta Increase heart rate
>5 Alpha Increase peripheral resistance

of using beta blockers in CHF (AIIMS May 2011, AIPG 2012)

  1. Control tachycardia and effect of high catecholamine level
  2. Three beta blockers are recommended for CHF: Bisoprolol, carvedilol and metoprolol
  3. Start with the lowest dose and long term use with gradual dose increment may prolong survival
  4. Beneficial effect on remodeling
  5. Decreasing risk of sudden cardiac death 

Recent Advances:


New drugs in the management of CHF

  1. Eplerenone (Aldosterone receptor blocker)
  2. Nesiritide (Vasodilation) (BNP analogue)
  3. Levosimendan used for the treatment of acute and decompensated CHF, exerts potent positive inotropic action and peripheral vasodilatory effects. (Ref. Hari. 18th ed., pg- 1912).
  4. Coenzyme Q is a universal antioxidant drug, improves diastolic volume and ejection fraction in CHF patients. (Ref. Hari. 18th ed.,  pg- 1912).
  5. Arjuna terminalis (AIIMS May 2012)
  6. Hydralazine + isosorbide dinitrate (Ref. Hari. 18th ed., pg- 1908)
  7. Istaroxine

Extra Edge:  Nesiritide:  (Ref. Hari. 18th ed., Pg-2237)

  1. The newest vasodilator, is a recombinant form of brain-type natriuretic peptide, which is an endogenous peptide secreted primarily from the LV in response to an increase in wall stress.
  2. Nesiritide effectively lowers LV filling pressures and improves symptoms during the treatment of acute HF.

Recent Advances


Positive Inotropic Drugs Used in Heart Failure

  1. Levosimendan
    It is a drug that sensitizes the troponin system to calcium, also appears to inhibit phosphodiesterase and to cause some vasodilation in addition to its inotropic effects.
  2. Istaroxime
    1. It increases contractility by inhibiting Na+,K+ ATPase (like cardiac glycosides) but in addition, facilitates sequestration of Ca2+ by the SR.
    2. Although they have positive inotropic effects, most of their benefits appear to derive from vasodilation.
    3. It is used for treatment of acute decompensated heart failure. 
  3. Icatibant
    It is a selective and specific antagonist of bradykinin B2 receptors. Bradykinin is a mediator for angioedema.
    Icatibant is used in the treatment of acute attacks of hereditary angioedema (HAE) in adults (with C1-esterase-inhibitor deficiency). Angioedema is a dangerous side effect of ACEI therapy.

Device Therapy:

  1. Cardiac Resynchronization
    1. Approximately one-third of patients with a depressed Ejection Fraction (less than 35%) and symptomatic HF (NYHA class III–IV) manifest a QRS duration >120 ms.  
    2. This ECG finding of abnormal inter- or intraventricular conduction has been used to identify patients with dyssynchronous ventricular contraction.
    3. The mechanical consequences of ventricular dyssynchrony include suboptimal ventricular filling, a reduction in LV contractility, prolonged duration (and therefore greater severity) of mitral regurgitation, and paradoxical septal wall motion.
    4. Biventricular pacing, also termed cardiac resynchronization therapy (CRT), stimulates both ventricles nearly simultaneously, thereby improving the coordination of ventricular contraction and reducing the severity of mitral regurgitation. (Ref. Hari. 18th ed., pg – 1911)
  2. Implantable Cardiac Defibrillators (ICD) (Ref. Hari. 18th ed., pg -1912) 
    1. The prophylactic implantation of ICDs in patients with mild to moderate HF (NYHA class II–III) has been shown to reduce the incidence of sudden cardiac death in patients with ischemic or nonischemic cardiomyopathy.
    2. In case of ICD collapse the imaging modality of choice is chest x-ray. (AIIMS Nov 2012) 

Treatment of acute pulmonary edema

  1. Strict bed rest. (Raised head end of the bed)
  2. Sublingual nitroglycerin (0.4 mg x 3 every 5 min) is first-line therapy for acute cardiogenic pulmonary edema. (Ref. Hari. 18th ed.,  pg -2237)
  3. Metolazone and IV frusemide
  4. IV morphine  ( dose = 2 to 3 mg iv.) and nitrates may relieve symptoms
  5. DVT prophylaxis: eg heparin 5000u/8h sc.
  6. Inotrope may be needed.
  7. Finally, a heart transplant  

Unusual Types of Pulmonary Edema: (Ref. Hari. 18th ed., Pg - 2238)

  1. Reexpansion pulmonary edema
    1. It can develop after removal of air or fluid that has been in the pleural space for some time.
    2. These patients may develop hypotension or oliguria resulting from rapid fluid shifts into the lung.
    3. Diuretics and preload reduction are contraindicated,
    4. Intravascular volume repletion often is needed while supporting oxygenation and gas exchange.
  2. High-altitude pulmonary edema
    1. It often can be prevented by use of dexamethasone, calcium channel-blocking drugs, or long-acting inhaled 2-adrenergic agonists.
    2. Treatment includes descent from altitude, bed rest, oxygen, and, if feasible, inhaled nitric oxide; nifedipine may also be effective.
  3. Pulmonary edema resulting from upper airway obstruction,
    1. It recognition of the obstructing cause is key
    2. Treatment is to relieve or bypass the obstruction.

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