BISC 307L 2nd Edition Lecture 27 Current Lecture Pressure Volume Changes in the Left Ventricle Y axis pressure in L ventricle X axis volume of L ventricle Start at point A the left ventricle has completed its relaxation and has not yet begun to fill Its pressure is at a minimum Its volume is also at a minimum because the ejection phase just ended The ventricles start to fill with blood and increase in volume from 65 to 135 between A and B The volume of the L ventricle is increasing as it is filling but over most of this time the pressure in the left ventricle isn t changing At the tail end of this process when the L atrium contracts the boost in pressure and volume results in the additional filling of the LV so you get to point B Point B which is the maximum volume the heart has is called the end diastolic volume Then the ventricle begins contracting As soon as it starts contracting the atrioventricular valve closes Between B until C the pressure is building up to 80mmHg but there is no change in volume This is called the isovolumic ventricular contraction phase B C is like phase 3 in the last figure in the last set of notes From B C the pressure builds due to the contraction and from C D there is ventricular ejection which is phase 4 in the previous diagram in the last set of notes Volume goes down from 135 65 At the end of systole you have the ESV end systolic volume at point D The difference between the ESV and EDV is the stroke volume which is how much blood is ejected per cycle So in D we start the relaxation of the left ventricle and the pressure starts to fall The valve to the aorta closes and as the heart relaxes the pressure in the ventricles go down and there is an isovolumic change in pressure D A Until ventricular pressure falls below 4 or 5 mmHg down here the AV valve to the left atrium is also closed This is an isovolumic ventricular relaxation no change in volume just pressure going down which is phase 5 in the previous diagram in the last set of notes And then the cycle repeats There is a slide called the Wigger s Diagram in this set of powerpoints Herrera told us to study it ourselves and that it is a useful diagram that correlates to mechanical and electrical events during the cardiac cycle but didn t mention anything about it beyond that Cardiac Output Cardiac output is one of the most important parameters in measuring heart health it is the measure of how much blood is pumped out by either side of the heart per unit of time It is equal to the heart rate x stroke volume and is usually 5L minute CO regulation is important and accomplished by varying the heart rate stroke volume or both Regulation of Heart Rate Regulation of Heart Rate is a function of autonomic nerves In general an effect on the heart that regulates the heart rate is called a chronotropic effect and can be positive or negative Sympathetic stimulation has positive chronotropic effect Parasympathetic stimulation has a negative effect Effects on the contractility of the heart are called inotropic effects and can also be positive or negative effects Sympathetic has a positive inotropic effect PS doesn t have any kind of inotropic effect Semi intact Dog Experiment The normal HR of the dog was 60 min Different drugs were tested on it to see their effects 1 Propranolol it is still used today also known as Inderal It is a nonspecific Beta blocker it blocks the positive chronotropic effect of symp nerves and causes the heart to slow down to 40 beats per minute This reveals an ongoing parasympathetic effect known as the maximum parasympathetic effect it is what the PS does to the heart in the absence of any other factors 2 Atropine blocks action of acetylcholine on mACHR s and causes the heart to speed up If you eliminate PS action the heart speeds up to 120 min which is the maximum sympathetic effect 3 So we can see that normal HR is due to a balance between ongoing parasymp and symp activity resulting in an intrinsic heart rate of 100 min If you add both propranolol and atropine to remove all the external neural influences on the heart you do indeed end up with an intrinsic heart rate of approximately 100 min Cardiac Output Regulation of Stroke Volume Stroke volume is directly related to the force of contraction which is going to be most strongly affected by the initial length of fibers and is due to the inherent contractility of the heart This graph shows stroke volume as a function of EDV There is force on the y axis and length on the x axis chart Over range force increases as you increase the amount of overlap but if you stretch it too far it plateaus and there is less overlap Stroke volume is proportional to the force of contraction So you can think of the Y axis as a measure of the force of contraction And EDV is the maximum filling of the heart before it starts to contract The more filled it is the more stretched so it is proportional to the initial length of fibers So technically you are looking at how force of contraction is dependent on initial length of fibers Stroke volume goes up as EDV goes up and then it levels out This curve is the same as the force vs length curve seen when testing skeletal muscles The curve starts off kind of linearly Typically the heart is filling up to 135 and then expels 70 leaving 65 It fills back up to 135 expels 70 and repeats This is normal and linear and leads to an important conclusion from beat to beat cycle to cycle the stroke volume may not always be the same For example if you are laying down blood pools With less venous return to the heart there will be a decrease in EDV such that it fills less and as a result the stroke volume goes down On the other hand if the heart overfills the EDV is higher and the stroke volume pumps out more The conclusion is over quite a range as the initial stretch of the ventricle increases the force generated by the ventricle goes up And as the stretch decreases the force of contraction and stroke volume both go down The result of this is that the heart will automatically pump out all the blood that is returned to it This is an inherent property of the heart muscle Starling discovered this relationship in an isolated heart In the absence of any neural influences the heart will pump out all of the blood in it This is called the Frank Starling Law of the Heart Curve This finding is important because it helps guarantee that the input and output of the two systems of the heart is equal and in …
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