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NURBN 2023 - Cardiac

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NURBN 2023 - Cardiac

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  • June 22, 2024
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NURBN 2023 - Cardiac
Define heart failure - ANS-The inability of the ventricles to pump enough blood to meet
the body's metabolic demands. Loss of contraction leads to heart failure.

systolic heart failure - ANS-inability of the heart to generate an adequate cardiac output
to perfuse vital tissues

diastolic heart failure - ANS-ventricles can't relax and fill

cause of heart failure - ANS-Atherosclerosis. Hypertension. High cholesterol. Smoking.

Clinical symptoms of hear failure - ANS-Hypertension. Shortness of breath/congested
lungs. Fluid retention/oedema . Chest pain. Tachycardia.

Pathophysiology of heart failure - ANS-Dysfunctional ventricle that is unable to eject
enough blood (systolic dysfunction)
Inability of ventricles to fill with enough blood (diastolic dysfunction)

Ischemic heart disease & HTN are the most common underlying causes
- HTN: excess mechanical stress on ventricles -> structural change of hypertrophy &
eventual left ventricular dysfunction

Differences between left and right heart failure - ANS-Left: fluid build up in the lungs and
Right: fluid retention in peripheral organs and tissue.

Causes of CHF (Right-sided) - ANS-Congestion of peripheral tissues

Causes of CHF (Left-Sided) - ANS-Decreased cardiac output & pulmonary congestion

Clinical symptoms of right-sided HF - ANS-Peripheral & visceral congestion. Fatigue.
Ascites. Enlarged liver & spleen. Bloating. Anorexia. Distended neck. Nausea.

Clinical symptoms of left-sided HF - ANS-Fatigue. Othopnea. Restlessness. Confusion.
Extreme weakness, cyanosis. Dyspnea.

Pathophysiological steps in HF patients - ANS-- Myocardial injury --> *fall in LV*
performance (lower cardiac output)

, - *Kidneys* sense decreased perfusion, *secrete renin to vasoconstrict + retain Na+ and
H20* via aldosterone; also stimulates sympathetic
- Heart *works against increased filling pressure*; more myocardial injury +
hypoperfusion + downregulate B-receptors
- Main point is that it is a *vicious cycle* caused by *compensatory mechanisms*

How does the RAAS system lead to raised blood pressure? - ANS-Angiotensinogen
converted to angiotensin 1 (by renin from kidneys)
AT-1 to AT-2 via ACE (from pulmonary and renal epithelium) - angiotensin 2 leads to
vasoconstriction and raised ADH from posterior pituitary gland
Aldosterone (ADH) increases water absorption - BP increases

Define arrhythmia - ANS-Any variation from the normal electrical rate and/or sequence
of cardiac activity.

bradyarrhythmia - ANS-slow, irregular heartbeat

tachyarrhythmia - ANS-a fast, irregular heart rate, usually over 150 bpm

Hypertension, High cholesterol & Diabetes. Smoking and weight control. -
ANS-Modifiable hypertensive risk factors

C-reactive protein. Insulin resistance. Oxidative stress. Periodontal disease. Age. -
ANS-Non-modifiable hypertension risk factors

List lifestyle factors which reduce hypertension - ANS-Maintain healthy body weight.
Reduce fatty foods. Be physically active.

Hypertension - ANS-abnormally high blood pressure

Pathophysiology of hypertension - ANS-- Excessive blood volume (Puts high pressure
on vessel walls)
- Excessive constriction of arteries (Smooth muscle cells around arteries contracted)
...Or combination of both

Hypertension and what RAAS has to do with it - ANS-RAAS is the signalling pathway to
regulate blood pressure.

Define the RAAS System: - ANS-Renin is released if there is a drop in BP. Which then
splits into Angiotensin 1, then converted by the angiotensin enzyme into Angiotensin 2 =

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