BISC 307L 1st Edition Lecture 26 Current Lecture Pressure Volume Changes in Left Ventricle o o o o o Summary of everything Focuses on the left ventricle Plot of the pressure in the left ventricle and the volume A the left ventricle has completed its relaxation and has not yet begun to refill pressure at a minimum And volume at a minimum because after ejection phase o B the ventricles start to fill increase volume flat part due to the fact that the blood is trickling No change in pressure At the end the pressure does go up a little due to the atrium contracting for the final bit of filling End diastolic volume o C Volume is the same but the pressure increases This is when the ventricle is contracting and the AV closes so pressure goes up The valve going out to the artery is still closed so this pressure goes up Isovolumic ventricular contraction phase phase 3 Then the pressure exceeds the pressure in the artery so the valve opens and the ventricle ejects blood into the aorta o D At the end of contraction end systolic volume when the blood is ejected out of the ventricle this is also called the stroke volume at the end Now start of relaxation of the left ventricle and the pressure falls and the semilunar valve closes and there is a vertical drop this is isovolumic because the AV valve is still closed so there is no change in volume Wiggers Diagram o o correlates mechanical and electrical events during the cardiac cycle o go through it on your own besides the very top o can understand everything below the ECG Cardiac Output Regulation of Heart Rate o o Cardiac output is the bottom line how much blood the heart pumps out per unit time both parts of the heart o Regulation of cardiac output accomplished by the heart rate or stroke volume or both o Regulation of heart rate Function of the autonomic nerves In general an effect on the heart that regulates the heart rate is called a chronotropic effect can speed up or slow down positive or negative Parasympathetic negative effect Sympathetic positive chronotropic effect and inotropic effect Inotropic contractibility of heart 1 Atropine increases heart rate by masking the parasympathetic activity ongoing parasympathetic activity and ongoing sympathetic activity if you block either the other one will show up more active They are usually both active simultaneously If you remove all external neural influences on the heart then you get the intrinsic heart rate 100 min Cardiac Output Regulation of Stroke Volume o o inotropic effects the regulation of the force of contraction o stroke volume is going to be directly related to the force of contraction and the force of contraction is directly related to the initial length of fibers and the contractibility of the heart inherently o stroke volume as a function of end diastolic volume o regulation y axis can be thought of as force of contraction and EDV is the maximum filling of the heart initial length of the fibers o Stroke volume increases as EDV increases but then levels off like the force vs length curve of the skeletal muscle o This is linear if you look at the normal values that is the dot but that is only one point in this linear relationship o Conclusion from beat to beat the blood returning to the heart may not be the same every time o With less venous return to the heart there is a decrease in EDV and when it fills less this makes the stroke volume go down o But if suddenly you hang upside down there is more venous return and EDV is more and this increases stroke volume o Over quite a range as the initial stretch of the ventricle increases the force generated by the ventricle increases and vice versa The result is that the heart will automatically pump out all of the blood that is returned to it o This is an inherent property of the heart muscle o This is called the FRANK STARLING curve and the FRANK STARLING law of the heart o The two sides of the heart are the same so over time the cardiac output of the two sides are the same o EDV depends on 1 Venous return to the heart due to skeletal muscle pump respiratory pump sympathetic vasoconstriction by the time you get to the veins the pressure is very low so there are skeletal muscle pumps leg muscle pumps squeeze leg veins respiratory pump action of the diaphragm lowers the thoracic pressure and raises the abdominal pressure which is a pump because most of the vena cava goes through the diaphragm so the pressure pushes the blood out of the abdominal cavity into the thoracic sympathetic nerves innervate smooth muscle in the leg veins and this will squeeze the blood out of the veins Positive Inotropic Effect of Norepinephrine o with sympathetic stimulation of the heart the curve shifts upward o ongoing positive ionotropic effect of sympathetic activity can increase and decrease this curve Heart Failure Insufficient Cardiac Pumping o o heart is unable to pump sufficient blood o a heart attack or myocardial infarction or clot blocking coronary arteries damage to heart muscle heart weakened on one side o damage could affect conducting system such as bundle of hist o depend on what side weakening is on usually both sides o left sided heart failure weakening of left ventricle receiving blood from lungs via right out to body so when weakened left ventricle will have difficulty pumping out blood as fast as receiving blood from right ventricle raising P in lungs pushing more blood into left side of heart pushing back into balance excessively high pulmonary BP o pulmonary hypertension as one problem cause excess fluid leakage out of capillaries where congestion comes from lung congestion fluid intereferes with gas exchange poor oxygenation of blood o left ventricle has a hard time emptying blood from right ventricle and high pulm BP it is enlarged cardiomegaly overstretching of cardiac muscle further weakens heart o systemic BP is low so kidney senses this and increases fluid retention in body to fill up BP again wrong thing to do build up of blood v raises BP more which stretches more and weakens further so in attempt to compensate neg feedback systems are triggered and eventually ends in death o evol dumb design occur in elderly people never lived this long before mechanisms prevent young people from dying by hemorrhage and dehydration preserve life in reproductive periods o evol fitness to these traits o treatments o diuretics lower fluid content and heart V o ACE inhibitors lower BP o Angiotensin 2 Receptor Antagonists lower BP o Vasodilators