BMS291 Lecture Notes - Lecture 5: Angiotensin Ii Receptor Blocker, Coronary Artery Disease, Pulmonary Edema
Document Summary
The amount of blood entering the ventricle is a factor of how much time there is between beats. A syndrome that includes different types of dysfunction resulting in inadequate tissue perfusion. Underlying structural abnormality or cardiac dysfunction that results in failure to fill (decreased. Lv preload) or failure to pump blood for the lv particularly during exercise. Compensatory mechanisms triggered by hf create a cycle of worsening failure and symptoms. Stroke volume is dependent on contractility, preload & afterload. Cycle of decreasing contractility, increasing preload and increasing afterload. Is affected by any pathology that disrupts myocyte function. Results in hypertrophy and dilation & progressive contractile dysfunction over time. Decrease contractility decrease sv, but increased edv (preload) further dilation increased preload. Increase preload can improve contractility until myocardium stretching damages sarcomeres. Lv must work harder to overcome resistance to emptying hypertrophy. Oxygen demand by myocardium increases as a result of thickening of muscle relative ischaemia ventricular remodelling.
