Cardiac glycosides

Effect of heart failure and digoxin on the Frank-Starling relationship.

The normal set point required to maintain adequate tissue perfusion is a cardiac output of 5 L/min.

During heart failure the relationship between cardiac output and venous pressure becomes shifted down and to the right (patient moves from point A to B).

Sympathetic activation and increased fluid retention result in an increased venous pressure (preload) which acts to increase cardiac output by increasing the stretch of cardiac fibers (patient moves from B to C).

If cardiac output remains below 5 L/min, the kidney continues to retain fluid, and venous pressure continues to rise, until either a 5 L/min cardiac output is achieved, or the patient “drowns in their own fluids” (e.g. due to pulmonary congestion).

Digoxin can shift the curve upwards and to the left by a mechanism different from sympathetic stimulation (increased contractility - so that the patient ideally moves from point C to D).

The resulting increase in blood flow to the kidney results in a diuresis (patient moves from D to E) with an associated reduction in venous pressure due to reduced venous volume.

(Just a little extract from my vet Physiology assignment. Still needs a lot of editing so there are probably some errors)

Cardiac Glycosides

To understand the act of cardiac glycosides on the heart you need to understand how the myocardial muscle contracts and relaxes. An action potential initiates contraction by opening voltage gated calcium channels on the outer membrane 14. Calcium rushes into the cell releasing the sarcoplasmic reticulum calcium stores. The calcium is key in binding to protein called troponin in the muscle fibre structure to initiate contraction 14.

It is then in the relaxation of the muscle that the cardiac glycoside disrupts the normal physiological process. During normal relaxation calcium would dissociate from triponin and be taken back up into the SR and the rest would be moved out with a Na+/Ca2+ exchange transporter protein in the cell membrane 14. To keep the sodium levels down in the cell to allow this pump to work it interacts with the Na+/K+ ATPase pump which takes the excess sodium out in exchange for potassium into the cell 14.

When the cardiac glycoside binds extracellularly to the Na+/K+ pump it inhibits the pump 3,4,7. Due to this pump’s key role in the Na+ balance the inhibition also effects the Na+/Ca2+ pump causing a build up of extra Ca2+ in the cell 3. This means the next time the heart contracts there will be more Ca2+ in the cells and this will cause call depolarisation and stronger heart contraction contraction. This is why cardiac glycoside poising initially slows the heart rate but increases the hearts contraction forces 3,7.

Digitalis purpurea (Foxglove) in my grandmothers garden on the island Fyn, Denmark.

This biennial plant is quite toxic and contains the cardiac glycoside ‘Digitoxin’ and Digoxin. In the right doses, these chemicals can help the heart beat more strongly (increase cardiac output) and the plant is therefor used to extract this kind of heart medicine.

It feels a bit ‘witch-y’ to have such potent medicinal plants in your garden.

Mechanism of Cardiac Glycosides
But do you know their Uses and Adverse Effect? Please write for me the main one!
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