Clinical Manifestation - Normal Heart - Myocardium - Myocardial Disease - Case Study - Assessment Answer

Clinical Manifestation - Normal Heart - Myocardium - Myocardial Disease - Case Study - Assessment Answer 

Assessment Task:

Question 1

• Pathogenesis causing clinical manifestation with which mrs brown presented
• Relate pathophysiology back to case study
• Cause-pathogenic processes-structural functional changes-clinical manifestation

Draft

Systolic heart failure is the inability of heart to pump the blood throughout the body according to need. The stoke volume of the heart is 70ml but in above mentioned case stroke volume decreases that is below 70ml. In the normal heart, end diastolic volume is 120ml out of which 70ml is pumped out in each beat which is decreased in systolic heart failure patient. As the patient Mrs Brown had been diagnosed with heart.

Since the patient was previously diagnosed by heart failure 2 years ago, atrial fibrillation must be common because of fibrosis of the layers of heart that is pericardium, myocardium and endocardium.

The other cause might be

1. Ischemic heart disease which means decrease in blood supply to the heart by coronary artries.
2. Hypertension-  hypertension means increase blood pressure which will ultimately increase the afterload in which there will be insufficient blood flow in the body.
3. Aortic and mitranvalvular disease:
4. Myocardial disease

Question1

Systolic heart failure is the incompetence of heart to produce sufficient cardiac output and tissue perfusion (). Different underlying diseases lead to chronic systolic heart failure whose course lasts for long period of time. In the given case study, since Mrs. Brown had been diagnosed from heart failure before, it may have resulted in sudden worsening symptoms of chronic systolic heart failure.  Also, the acute exacerbation of chronic systolic heart failure may be triggered by accumulation of fluids in lungs, since bilateral basal crackles were heard upon auscultation and atrial fibrillation must be common in this case because of fibrosis of layers of heart that is pericardium, myocardium and endocardium.

Further, reduced cardiac output tends to decrease systematic blood pressure and renal blood flow. Here, decrease in blood pressure is detected by baroreceptors that stimulate vasomotor stimulatory centers in medulla and then activate sympathetic nervous system, which as a result release adrenaline and noradrenaline. On the other hand decrease perfusion to kidneys activates Renin-Angiotensin-Aldosterone system. Renin converts angiotensinogen produced in liver to angiotensin I which is then converted to angiotensin II by the enzyme in lungs. Thus, produced adrenaline, noradrenaline and angiotensin II hormone leads to peripheral vasoconstriction. urther leading to increase cardiac output. Hence, increases the afterload, blood pressure and heart rate. Similarly, the most likely cause of mrs browns high blood pressure and

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