During exercise the heart rate is 190 bpm and the stroke volume is 115 ml/beat. What is the cardiac output?

Transcription

1 The Cardiovascular System Part III: Heart Outline of class lecture After studying part I of this chapter you should be able to: 1. Be able to calculate cardiac output (CO) be able to define heart rate and stroke volume 2. Describe the intrinsic regulatory mechanisms of the heart with a detailed description of the Frank-Starling Law. 3. Describe the extrinsic regulatory mechanisms of the heart. 4. What happens during heart failure? 5. Describe how Atrial Natriuretic Peptide (ANP) effect blood volume and pressure. 6. Be able to explain the answers to the clinical applications questions and the normal physiology of the heart is affected. Regulation of Heart Function: Cardiac Output Cardiac output (CO): The volume of blood pumped by Cardiac Output = Heart Rate x Stroke Volume CO = HR x SV Units for cardiac output are ml/min or L/min. Heart rate: Number of times the heart beats (contracts) each minute. Average resting heat rate = Stroke volume: Volume of blood pumped per beat by each ventricle. Average resting stroke volume = ml/beat Cardiac output can increase due to either an increase in stroke volume or heart rate. Cardiac Output Questions What is the cardiac output of someone at rest? Assume a stroke volume of ml and a heart rate of 70 bpm. 1 The average person has about 5 liters of blood in their body. Under resting conditions, how long will it take for the entire blood supply to pass through the heart? During exercise the heart rate is 190 bpm and the stroke volume is 115 ml/beat. What is the cardiac output? Regulation of Heart Function: Intrinsic and Extrinsic Factors Both heart rate and stroke volume are controlled by: Intrinsic mechanisms: By the heart tissue itself. Extrinsic mechanisms: Influence of nerve innervation and hormones. Intrinsic Regulation of the Heart Regulation of Stroke volume Stroke volume is regulated by three intrinsic variables: 1. End-diastolic volume (EDV) or preload 2. Total peripheral resistance or afterload 3. Contractility (strength of contraction)

2 End-diastolic volume (EDV End-diastolic volume or preload: Volume of blood in the ventricles at the end of diastole (just before the ventricles contract). The volume of blood is the workload imposed on the ventricles prior to 2 Stroke volume is directly proportional to the EDV or preload Increased preload causes an increase in ventricular stretch resulting in an increase in contractile force resulting in an increase in stroke volume. This is the basis of the Frank-Starling law of the heart. In other words: If there s more blood (up to a point) in the ventricle, the ventricle will generate more tension and eject the greater volume of blood. If there s less blood, less tension will be generated. Frank-Starling Law of the Heart Frank-Starling Law of the Heart: Strength of ventricular contraction varies with the enddiastolic volume. As the EDV is increased, the Length Tension Relationship: Cardiac Muscle In other words, whatever goes into the heart gets pumped out. So what is the physiology behind such an incredible phenomenon? Myocardial Stretch Explanation of the Frank-Starling Law of the Heart The Frank-Starling Law: Changes in contractile strength and stroke volume are due to variations in the degree that the myocardium is stretched by the end diastolic volume. Explanation: Prior to ventricular filling with blood during diastole, the sarcomere lengths of myocardial cells are short with the actin filaments from each side overlapping in the middle of the sarcomere. The contraction strength is weak in this position. As the ventricles fill with blood, the myocardial cells begin to stretch. The stretching results in a better position of the thick and thin filaments to yield greater contractile forces. Since the overlapping of actin and myosin is produced by stretching of the ventricles, and since the degree of stretching is controlled by the degree of filling (the end-diastolic volume), the strength of contraction is intrinsically adjusted by the end-diastolic volume Thus, a greater amount of blood in a ventricle prior to contraction results in greater stretch of the myocardium and produces a more forceful contraction Note: Lt and Rt ventricle chamber size is the same.

3 Test Your Knowledge! As venous return increases, stroke volume will. As end diastolic volume decreases, stroke volume will As heart rate increases, stroke volume will 3 Frank-Starling law and Total Peripheral Resistance Frank-starling law explains how the heart can adjust to a rise in total peripheral resistance: 1. A rise in peripheral resistance causes a decrease in the stroke volume of the ventricle, so that 2. more blood remains in the ventricle and the EDV is greater for the next cycle, as a result, 3. the ventricle is stretched to a greater degree in the next cycle and contracts more This allows a healthy ventricle to sustain a normal cardiac output. Total Peripheral Resistance (afterload) Total peripheral resistance (afterload): Refers to the pressure against which the ventricles must It is the pressure that must be overcome in order for the semilunar valve to open and blood to be ejected. The afterload for the left ventricle is the blood pressure in the aorta. If aortic BP is high (due to hypertension perhaps), the LV will have to expend a lot of energy to open the aortic valve and expel less blood. If aortic BP is low, the LV will expend less energy opening the aortic valve and expel more blood. So, stroke volume is inversely proportional to peripheral resistance. Greater peripheral resistance, the Question In a healthy heart, how is a rise in peripheral resistance compensated for by the heart? Frank-Starling Law of the heart: 1. A rise in peripheral resistance causes a decrease in the stroke volume of the ventricle, so that 2. more blood remains in the ventricle and the EDV is greater for the next cycle, as a result, 3. the ventricle is stretched to a greater degree in the next cycle and contracts Contractility Contractility refers to how hard the ventricle is squeezing. An increase in contractility will result in an increase in stroke volume. Normally the ventricles eject ~70 ml of blood out of a EDV of 110 to 130 ml, which is ~60% More blood is pumped per beat as the EDV increases, and thus the ejection fraction (~60%) remains relatively constant. Contractility strength is related to the Frank-Starling Law of Extrinsic control mechanisms (nerve innervation, hormones, drugs) will have additional affects and will be discussed shortly.

4 Clinical Considerations: Heart Failure A failing heat gradually enlarges and eventually fails because it is not able to pump all of the blood returned to it. Further stretching of the cardiac muscle fibers in a failing heart does not increase the stroke volume. Right heart failure Failure of the right ventricle causes blood to back up in the veins that 4 Filling the veins with blood causes edema, especially in the legs and feet. Edema is the accumulation of fluid in the tissues (interstitial space) Left heart failure Failure of the left ventricle causes blood to back up in the veins (pulmonary veins) that Filling of these veins causes edema in the lungs, which makes breathing difficult Extrinsic Regulation of the Heart Extrinsic control of heart rate involve factors originating outside the heart and is regulated by the: Cardioacceleratory center Extrinsic Control: Nervous System The autonomic nervous system exerts influence upon the heart rate and force primarily via the cardiac centers of the medulla oblongata. Cardiac Centers consist of the: Cardioacceleratory Center Cardioacceleratory Center: Increase heart rate and Sympathetic center Projects to the SA and AV nodes as well as the ventricular myocardium via cardiac sympathetic nerves. Stimulates sympathetic nerves to release of norepinephrine (NE) onto the SA and AV nodes, and the ventricular myocardium. Results in an increased heart rate and force of contraction. How does epinephrine increase heart rate? Norepinephrine Action Norepinephrine from sympathetic axons and epinephrine stimulate β1 receptors. Acts to increase heart rate by helping to open more Na+ channels (pace maker channels) and keep those channels open longer. This speeds the depolarization to Cardioinhibitor Center Cardioinhibitory Center: Parasympathetic center Projects to the SA and AV nodes via the vagus nerve (cranial nerve X) which carries parasympathetic nerves. Stimulates parasympathetic nerves to release of acetycholine onto the SA and AV nodes, and the ventricular myocardium. Results in a decreased heart rate and force of contraction.

5 How does Acetylcholine decrease heart rate? Acetylcholine Action ACh from parasympthetic axons causes the opening of separate K+ channels. Acts to slow heart rate by slowing the depolarization to threshold. 5 Arrhythmias: Abnormal Heart Rates Bradycardia: Heart rate is slower than normal resting heart rate. Less than Tachycardia: Heart rate is faster than normal resting heart rate. Faster than

6 Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) 6 Atrial Natriuretic Peptide (ANP) is a hormone secreted by the specialized myocardial cells within the atria in response to increased stretch due to a rise in blood volume and pressure. ANP decreases blood volume and blood pressure by: Decreases sodium reabsorption in the kidneys (collecting ducts) which increases Na+ (natriuresis) and water (diuresis) excretion in the urine. Increases glomerular filtration rate (GFR) by Inhibits the release of renin, aldosterone, and antidiuretic hormone (vasopressinz which reinforce the natriuretic-diuretic effect. Increases vasodilation of arterioles by decreasing the sympathetic output from the medulla oblongata. Brain Natriuretic Peptide (BNP) is synthesized by ventricular myocardial cells and certain brain neurons and has similar effects as ANP. BNP is a blood test marker for acute heart failure. Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP)