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Heart Failure Treatment Using Entresto – UTS Physiological Systems 91703 2018 – Ryan Machado

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UTS Physiological Systems 91703 2018 – Assessment Task Five : Oral Communication Skills – by Ryan Machado

Hello and welcome to physiological developments my name is ryan machado and today we’ll be discussing the drug entresto and its ability to treat heart failure to fully understand the effect of this medical breakthrough and was first discussed the normal physiology the heart the beating mechanism of the heart begins in the sinoatrial node inside of which an

Electrical stimulus known as an action potential is generated this action potential passes through the myocardial cells of the atria causing contractions as it passes through the heart muscle the action potential then reaches the atrioventricular node at which point conduction slows was the blood that is in the atria is emptied into the ventricles the atria and

The ventricles are connected by two branches covering the left and right side of the heart which stem off from the atrioventricular node called the atrioventricular bundle of his from here through these bundles the action potential travels rapidly through to the apex of the heart eventually breaking off to smaller branches known as purkinje fibers which are large

Diameter fibers that conduct electrical signals quickly spreading the action potential upwards through the ventricular heart muscle causing it to contract so what happens in heart failure upon myocardial infarction which many of you recognized as a heart attack the muscle cells literally die due to lack of oxygen and in this the uninjured portion undergoes what

Is known as concentric hypertrophy to compensate for the impaired functioning of the damaged area in which new protein users arrange themselves in parallel thickening the heart wall that in turn results in excessive pressure during systole or the squeezing of the heart this is then followed by eccentric hypertrophy in the in the injured portion where the heart

Muscle stretches and thins enlarging the size of the ventricular chamber due to the arrangement of the new protein units in series changing the heart shape form was originally an elliptical shape to a more spherical configuration this increases the blood volume overload during diastole ii of the relaxation of the heart the wear and tear of the heart muscle as a

Result of the ventricular remodeling impairs the normal contraction and relaxation mechanisms in heart function resulting in reduction in cardiac output of an increased amount of time due to which the hogs unable to function properly to meet the metabolic demands of the body the resultant decrease in blood flow stimulates the production of an enzyme called renin

In the kidneys which forms angiotensin one when released into the bloodstream this angiotensin one is converted by the angiotensin converting enzyme ace to form the peptide angiotensin ii which increases blood pressure by constricting the blood vessels and reabsorbing sodium in the kidney tubules causing water retention and pressure overload during systole which

Not only introduces cardiac function but causes congestion in the heart hence the name congestive heart failure resulting in difficulty breathing reduced hood hot capacity during exercise and rest and eventually death the remodeling of the ventricle also stimulates the release of neutral endopeptidase naturalism which is essentially a counter regulatory system for

The renin-angiotensin-aldosterone system this increases sodium excretion dilate dilating blood vessels – and decreasing blood pressure which increases blood volume excessively during diastole these two systems must be effectively managed in cockpit in the heart failure patients and this is critical so this is where entresto comes in so in 2016 the pharmaceutical

Giant novartis entire international developed the drug entrusted to treat patients with chronic systolic heart failure now remember that systole refers to the pumping ability of the heart the drug entresto whose chemical name is often decca saudi mexicans contains a salt complex of the anionic forms of sakaguchi which is an f inhibitor and far-sighted which in which

Is an angiotensin receptor blocker the drugs simultaneously inhibits the release of naturalism by via second ritual and locks the angiotensin type 281 receptor via velocity the inhibition of nettleson induces enhances the peptide hormones that are usually degraded by it allowing the heart to regulate blood entry rate into the ventricles reducing overall stress

Or degradation of the cardiac chamber wall during diastole e of relaxation the inhibition of angiotensin ii prevents sustained activation of the renin-angiotensin-aldosterone system creating decreasing vasoconstriction sodium reabsorption and cardio myocyte growth which is a result of the malla dot a maladaptive response of two ventricular remodeling regulating

Blood pressure load during systole which also reduces the fluid retention that causes heart congestion now let’s compare these effects of interest o2 other treatments so other treatments include the usage of ace inhibitors and ab medications which are angiotensin receptor blockers ace inhibitors and arbs or arms are used in conjunction with diuretics to reduce the

Expression of angiotensin 2 in the nevada’s clinical trials it was shown that interests are had significant superiority to ace inhibitors reducing the risk of cardiovascular death or heart failure related hospitalization by 20% many other comparative studies have also supported this finding showing that interest her overall reduces heart failure mortality and heart

Failure related hospitalization by 4 to 5 percent more than what ace inhibitors and ab many medications do and overall what impact does this have this allows heart patients to have a better chance of a prolonged life with less chance of heart fairly related a hospitalization or cardiovascular death and this overall increases the cardiac death holly would despite

Having congestive heart failure thank you very much

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Heart Failure Treatment Using Entresto – UTS Physiological Systems 91703 2018 – Ryan Machado By Ryan Machado