Heart Failure

Lets rapidly overview the topic of heart failure with the two video sessions, then go through the text material, and again come back to the videos to revise:

Heart Failure is inability of the heart to pump effectively.

Due to heart failure, the tissues do not get sufficient blood supply (Ischemia). For example: Kidneys. Kidneys start secreting renin, and the Renin Angiotensin Aldoterone System (RAAS) gets activated. This leads to vasoconstriction and increased peripheral resistance, which further increases the work load of the heart. Due to Aldosterone, sodium and water are retained; on causing increase in blood volume. Thus the work load on the heart goes on increasing in a vicious manner. Further the renal function may go on diminishing.
Other  organs also suffer the lack of blood supply, and the patient gets weakness, fatigue, and loss of appetite.
In general, due to left sided heart failure and failure of emptying of the left side of the heart, the back pressure goes towards the lungs, hence the patient is likely to get breathlessness (dyspnea), cough, expectoration, orthopnea (breathlessness on lying down, feeling better  for some time on sitting up/standing up), and paroxysmal nocturnal dyspnea (Events of intermittent breathlessness during the night – forcing the patient to sit up to feel better for some time.
Right sided heart failure involves incomplete emptying of the right side of the heart, leading to increased back pressure behind in the venous system leading to systemic venous congestion, peripheral edema over legs, face, and other sites, raised jugular venous pressure (JVP), venous congestion in the liver, spleen leading to hepatomegaly and splenomegaly, and accumulation of edema fluid in extravascular spaces leading to conditions like ascites and pleural effusion.

SAQ/LAQ/Viva

Mention mechanism of action of digoxin (digitalis).

Digoxin is a positive ionotropic agent. It increases the force of contraction and cardiac output.  Its mechanism of action follows the steps shown below:

(A) Increased Sodium and Calcium

  1. Inhibits the Na+K+ATPase pump (enzyme)
  2. Increases the entry of Sodium (Na+)
  3. Increases the intracellular Sodium
  4. Calcium entry is facilitated by affecting the Na-Ca Exchanger. (Digoxin inhibits the ability of Na-Ca Exchanger, to throw out Calcium; hence Calcium increases inside)
  5. Increased force of contraction
  6. Increased cardiac output

(B) Digoxin decreases AV conduction and decreases the heart rate


SAQ/LAQ/Viva

Mention the manifestations of digitalis toxicity, and its management.

Digoxin is a drug with low therapeutic index, so the increase in dose can produce serious adverse effects.

  1. Gastro-Intestinal Toxicity or GI Intolerance: Most common  toxicity of digoxin. It is usually first symptom of toxicity to appear.  The symptoms include – sense of nausea, anorexia, vomiting, diarrhea.
  2. Cardiotoxicity:  – Bradycardia is usually the first sign of digitialis toxicity. Digoxin produces sinus bradycardia. Digoxin decreases AV condution. So it may lead to AV Block and AV dissociation. It can also sometimes lead to other arrythmias such as ventricular tachycardia.
  3. CNS Toxicity: Headache, fatigue, malaise, confusion, neuralgia
  4. Visual toxicity: Blurring of vision, xanthopsia/chromatopsia (red/green colour vision disturbances)
  5. Hearing defects
  6. Gynecomastia, skin rash

Management of Digoxin Toxicity: Principles of treatment

  1. Stop Digoxin
  2. Monitor Serum Potassium levels
  3. Start Potassium Chloride (KCl)
  4. If not started, start a potassium sparing diuretic/Aldosterone antagonist e.g. Spironolactone
  5. Monitor Blood levels of Digoxin
  6. Monitor ECG
  7. Most specific treatment: Digoxin-specific immune antibody fragment [Fractionated antibody of Digoxin] – Digibind – 40 mg Intravenous is equivalent to 0.5 mg of Digoxin
  8. For managing Sinus bradycardia – Atropine
  9. For managing AV block/AV dissociation – Atropine
  10. For managing supraventricular tachycardia/atrial arrthythmias – Beta blockers or Adenosine or Calcium channel blockers
  11. For management of ventricular  extrasystoles / ventricular tachycardia – Lidocaine / Phenytoin / Procainamide

 

SAQ/LAQ/Viva

Explain how digoxin reverses the manifestations of heart failure.

1. Digoxin increases sodium and calcium entry/concentration in the myocardium, and increases the force of contraction of the heart – so there is more complete emptying of the heart – leading to increased cardiac output –

   (a) So the tissue perfusion improves, and the tissue gets enough blood supply. [Improved blood supply to various organs – Decrease in Fatigue, weakness] 

(b) Renal perfusion improves – less activation of RAAS (Renin Angiotensin Aldosterone System). [Kidney function improves] [Increased excretion of fluids, diuresis, decrease in edema]

 (c) These changes lead to decrease in sympathetic activity, retained vagal tone — [Heart rate and oxygen demand decreases]

     (d) Due to improved flow of the blood in circulation, the fluid  that was accumulating in the extravascular comparment starts entering the circulation. – so – venous congestion is relieved – [Decrease in edema, breathlessness, orthopnea JVP, hepatomegaly, splenomegaly, and other symptoms]

2. Digoxin decreases AV condution – decreases the heart rate — decreases the oxygen consumption. [Also controls abnormal impulses coming from atrium to ventricle]

3. Digoxin abbreviates (shortens) the systole — Less fiber tension developed — [Decreased oxygen consumption]

4. Diastole is prolonged — so the heart gets enough time to completely fill. [As the heart remains in diastole for comparatively more time period, it itself gets more blood supply. So cardiac function improves]

5. Thus due to digoxin, the available energy for the cardiac function is utilized in a better way – The heart can do more work at same energy consumption or can do more work at same energy consumption [Better energy utilization]


 

4 Replies to “Heart Failure”

  1. Sir , in the mechanism of digoxin : Na+ K+ ATPase pump is inhibited which eventually inhibits NCX pump (Na+ Ca2+ exchanger) ! So there should be no increase in Na+ !
    How sodium is increased ?

    1. Na+K+ATPase pump is supposed to throw out sodium. When this pump is inhibited, sodium is concentrated inside.
      There is also a Na Ca Exchanger Pump which normally is supposed to throw out calcium.
      Due to action of digoxin, the capacity of this pump to throw out calcium is diminished. Hence Calcium increases inside the cell.

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