Pathophysiology of Heart Failure


Heart failure (HF) is a syndrome of ventricular dysfunction

Left ventricular failure causes shortness of breath and fatigue, and right ventricular failure causes peripheral and abdominal fluid accumulation; the ventricles can be involved together or separately.


LV failure characteristically develops in ischemic heart disease, hypertension, mitral or aortic valvular regurgitation, aortic stenosis(abnormal narrowing of the aortic valve.), most forms of cardiomyopathy, and congenital heart disorders (eg, ventricular septal defect, patent ductus arteriosus with large shunts).

RV failure is most commonly caused by previous LV failure (which increases pulmonary venous pressure and leads to pulmonary arterial hypertension, thus overloading the RV) or by a severe lung disorder.

Other causes are multiple pulmonary emboli (a blood clot, air bubble, piece of fatty deposit, or other object that has been carried in the bloodstream to lodge in a vessel and cause an embolism), RV infarction, primary pulmonary hypertension. Some conditions mimic RV failure, except cardiac function may be normal; they include volume overload and increased systemic venous pressure in polycythemia or overtransfusion, acute kidney injury with retention of Na and water, obstruction of either vena cava, and hypoproteinemia due to any cause resulting in low plasma oncotic pressure ( is a form of osmotic pressure exerted by proteins in a blood vessel’s plasma that usually tends to pull water into the circulatory system. It is the opposing force to hydrostatic pressure) and peripheral edema.

Biventricular failure results from disorders that affect the whole myocardium (eg, viral myocarditis, amyloidosis) or long-standing LV failure causing RV failure.

Prescribed drugs:

Furosemide is used most often, usually starting at 40 mg oral once daily, increased up to about 60 mg twice daily(bid)  if needed based on response and renal function. Bumetanide is an alternative. In refractory cases, furosemide 40 to 160 mg IV, ethacrynic acid 50 to 100 mg IV, bumetanide 0.5 to 2 mg orally or 0.5 to 1.0 mg IV, or metolazone 2.5 to 10 mg oral may have an additive effect. IV infusion of furosemide (5 to 10 mg/h) may be helpful in selected patients with severe edema. The dose of diuretic required acutely can usually be gradually reduced; the target is the lowest dose that maintains stable weight and controls symptoms. When HF improves, the diuretic may be stopped if other drugs improve heart function and relieve HF symptoms. Using larger than required doses of diuretics lowers CO, impairs renal function, causes hypokalemia, and increases mortality. Serum electrolytes and renal function are monitored, initially daily (when diuretics are given IV) and subsequently as needed, particularly after a dose increase.

Prescription contains

Diuretics, nitrates, or digoxin

ACE inhibitors, β-blockers, aldosterone antagonists, or angiotensin II receptor blockers (ARBs)

Check for symptoms

Condition of the patient based on the symptoms



Ordinary physical activity causes fatigue, dyspnea, palpitations, or angina.




Comfortable at rest; less than ordinary physical activity causes fatigue, dyspnea, palpitations, or angina.




Symptoms occur at rest; any physical activity increases discomfort.



  • Diuretics are given to all patients with symptomatic systolic dysfunction and current or previous volume overload; dose is adjusted to the lowest dose that stabilizes weight and relieves symptoms. Loop diuretics are typically preferred
  • Digoxin  is most effective in patients with large LV end-diastolic volumes and an S3. Acute withdrawal of digoxin may increase the hospitalization rate and worsen symptoms. In patients with normal renal function, digoxin, 0.125 to 0.375 mg oral once/day depending on age, sex, and body size, achieves full digitalization in about 1 wk (5 half-lives) digoxin level of 0.8 to 2 ng/mL is acceptable.
  • Ventricular arrhythmias are treated with lidocaine or phenytoin
  • Atrioventricular block with a slow ventricular rate may require a temporary transvenous pacemaker.
  • Isoproterenol is contraindicated because it increases risk of ventricular arrhythmia.
  • A K-sparing diuretic, either spironolactone  or eplerenone (which are aldosterone antagonists), can be added to offset the K-losing effects of higher-dose loop diuretics. Hyperkalemia may result, especially when ACE inhibitors or ARBs are also taken, so electrolytes must still be monitored, especially during a dehydrating illness that could cause renal dysfunction. These drugs may have particular benefit in chronic RV failure, in which hepatic congestion results in elevated aldosterone levels as its metabolism is reduced.Thiazide diuretics are not normally used as a single agent unless hypertension is present but may be added to a loop diuretic for added diuresis.


Disease management:

General measures, especially patient and caregiver education and diet and lifestyle modifications, are important for all HF patients.

  • Education

  • Na restriction

  • Appropriate weight and fitness levels

  • Correction of underlying conditions                                        

  • Diet and lifestyle changes

  • Treatment of cause

  • Drugs (numerous classes)

  • Sometimes device therapy (eg, implantable cardioverter-defibrillator, biventricular pacing)

  • Multidisciplinary care

  • Patients with atherosclerosis or diabetes should strictly follow a diet appropriate for their disorder. Obesity may cause and always aggravates the symptoms of HF; patients should attain a body mass index (BMI) of 21 to 25.

  • Regular light activity (eg, walking), tailored to symptoms, is generally encouraged.

  • Patients should have annual influenza vaccination because influenza can precipitate HF, particularly in the elderly.

Counselling on side effects:

ACE Inhibitors:

Hypotension,If the effect (more marked in patients with hyponatremia or volume depletion) is troublesome, it can often be minimized by separating administration of other BP-lowering drugs, reducing the dose of concomitant diuretics, using a longer acting ACE inhibitor (eg, perindopril), or giving the dose at bedtime.

ACE inhibitors often cause mild to moderate reversible serum creatinine elevation due to vasodilation of the efferent glomerular arteriole. An initial 20 to 30% increase in creatinine is no reason to stop the drug but does require closer monitoring, slower increases in dose, reduction in diuretic dose, or avoidance of NSAIDs. Because aldosterone’s effect is reduced, K retention may result, especially in patients receiving K supplements.

Cough occurs in 5 to 15% of patients, probably because bradykinin accumulates, but other causes of cough should also be considered.

Occasionally, rash or dysgeusia occurs.

Angioedema is rare but can be life threatening and is a contraindication to this class of drugs. Alternatively, ARBs can be used, although rarely cross-reactivity is reported. Both are contraindicated in pregnancy.

Serum electrolytes and renal function should be measured before an ACE inhibitor is started, at 1 month, and after each significant increase in dose or change in clinical condition. If dehydration or poor renal function due to acute illness develops, the ACE inhibitor dose may need to be reduced or the drug may be temporarily stopped.


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