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In this lecture we re gonna cover the pharmacology heart failure is simply defined as a chronic, is unable to pump enough blood to meet the body’s needs. ventricles squeeze and relax in turn to move blood through the body. first, the oxygen-poor blood that has already the right atrium, which in turn pumps it over to the right ventricle. thirdly, the pulmonary vein empties
Oxygen-rich and finally the left ventricle pumps oxygenated how the heart is able to move blood through specifically, this law states that increased contraction force and thus a rise in the cardiac output. point where heart muscle contraction becomes less efficient. in systolic heart failure the heart muscle in the amount of blood pumped out of the ventricle, dysfunction
Is typically associated with an ejection fraction of less than 40%. on the other hand, in diastolic heart failure and cannot adequately relax to allow for normal ventricular filling. although stroke volume and cardiac output are reduced. now, in the presence of heart failure, in cardiac output and thus reduced perfusion the first one involves the increase in sympathetic
Nervous system activity. arch and carotid sinus will sense changes norepinephrine that in turn stimulates beta-1 stimulation of these receptors increases heart because heart rate and stroke volume are components the product of the two, when they both increase, adequate blood pressure and thereby perfusion to vital organs. receptors located on juxtaglomerular cells for
Regulation of blood pressure and volume called renin. and this brings us to the second major compensatory so, in addition to sympathetic nerves directly the release of renin from the juxtaglomerular mechanisms which are; the renal vascular baroreceptors to low renal perfusion pressure, and the macula renin secretion in response to fall in sodium chloride concentration.
Supplied by the liver called angiotensinogen to produce angiotensin i. ii by another enzyme, which is abundant in now, circulating angiotensin ii exerts its the body with most of its effects being mediated these include stimulation of at1 receptors which leads to vasoconstriction; stimulation causes the pituitary to release antidiuretic to specific vasopressin ii receptors
In the reabsorption of water back into the circulation; angiotensin receptors in the adrenal cortex called aldosterone, which in turn binds to the cells of the distal tubule and the collecting that encode epithelial sodium channels and promoting sodium and water reabsorption and furthermore, vasoconstriction and fluid retention pressures, forcing additional fluid out of
The increased peripheral resistance and greater the heart and accelerate the process of damage at this point, in the final attempt to maintain try to counterbalance overstimulation of the and sympathetic nervous system by activating specifically, in response to increased myocardial secrete a-type natriuretic peptide (anp) and peptide (bnp), and in response to increased
From cardiac injury, vascular endothelial now the main role of these natriuretic peptides and adrenergic activation by stimulating sodium relaxation, inhibiting cardiac hypertrophy however, in the end, even this counter response as heart failure advances, further activation and the sympathetic nervous system ultimately and this brings us to the second part of this now the
Pharmacological management of patients so now let s discuss these one by one starting with beta-blockers. the action of norepinephrine thereby reducing as a side note here, keep in mind that decreased now, similarly via blockade of the ?1 receptors beta-blockers may also reduce renin secretion, ii-induced vasoconstriction as well as aldosterone-induced volume expansion.
Mortality in heart failure patients; these out of these three, carvedilol has a unique blocks beta-1 receptors in the heart but also by preventing norepinephrine from activating to dilate thereby reducing total peripheral resistance. drugs for heart failure that is angiotensin-converting reduces angiotensin ii production and its in addition to this, inhibition of ace,
Increases unlike angiotensin ii, which is a vasoconstrictor, so when ace inhibition occurs, while angiotensin as a result the blood vessels become dilated, blood pressure is lowered thereby reducing another related class of drugs called angiotensin however instead of blocking the enzyme that by binding to at1 receptors located on vascular as heart directly blocking the
Actions of angiotensin ii. less adh and aldosterone secretion, which also because arbs do not inhibit ace, they this makes arbs a good alternative to ace to the vasodilation but also contributes to drugs in this class include candesartan, losartan, telmisartan, and valsartan. failure patients continue to suffer from cardiovascular events. interest as a therapeutic
Approach in the of a new class of drugs called angiotensin receptor-neprilysin inhibitor. including anp, bnp, and cnp and thus terminates their positive actions. and neprilysin inhibitor to simultaneously neprilysin enzyme thereby preventing it from breaking down natriuretic peptides. peptides as well as enhancement of their beneficial the example of drug that belongs
To this class is sacubitril/valsartan. in some cases they don t suppress the excessive therefore, select patients with moderate to another class of drugs called aldosterone antagonists. mineralocorticoid receptor thereby decreasing as decreasing the excretion of potassium leading to cardioprotective effects. the examples of drugs that belong to this now, although
Aldosterone antagonists have some diuretic effect, in order to alleviate so the primary use of loop diuretics is to loop diuretics achieve this by inhibiting the luminal sodium-potassium-chloride cotransporter as a result, in contrast to other diuretic this sodium is then excreted, along with the decrease in plasma volume, cardiac workload drugs that belong to this class
Include bumetanide, furosemide and torsemide. receptor blockers (arbs), usually because pressure can be controlled with another class there are two drugs in this class that are the first one is isosorbide dinitrate, which smooth muscle cell that subsequently activates the formation of cyclic guanosine monophosphate increased intracellular cgmp in turn activates and because
Calcium drives the contraction now, in contrast to isosorbide, the second effects on the vascular smooth muscle, which from the vascular endothelium stimulating cgmp production and decreasing calcium concentration, of calcium release from the sarcoplasmic reticulum, finally, before we end, i wanted to briefly management of heart failure particularly in patients intolerant
To ace inhibitors or beta-blockers now the mechanism of action of digoxin is in that it is used to increase cells’ contractility, digoxin accomplishes that by inhibiting the cells, which is responsible for moving sodium as a result of this inhibition, when sodium another electrolyte mover known as sodium-calcium this in turn causes an increase in the intracellular calcium,
Which is then available to the contractile the end result is increased force of contraction and with that i wanted to thank you for watching stay tuned for more.
Transcribed from video
Pharmacology – HEART FAILURE (MADE EASY) By Speed Pharmacology