Regulation of Cardiac Output & Venous Return PDF
Document Details
Uploaded by SportyBlessing
Tags
Summary
This document provides an overview of cardiac output and venous return, explaining their definitions, factors affecting these processes, and their significance in the cardiovascular system. It details the relation between cardiac output, stroke volume and heart rate, along with important factors such as preload, afterload, and myocardial contractility.
Full Transcript
L21 The Cardiac Output (CO) and Venous Return (VR) and their regulation ILOs At the end of this session, the student will be able to: Define cardiac output, cardiac index, stroke volume, end-diastolic, and endsystolic volumes, and ejection fraction & their normal values. Interpret the relation b...
L21 The Cardiac Output (CO) and Venous Return (VR) and their regulation ILOs At the end of this session, the student will be able to: Define cardiac output, cardiac index, stroke volume, end-diastolic, and endsystolic volumes, and ejection fraction & their normal values. Interpret the relation between the cardiac output, stroke volume, and heart rate. Determine the factors affecting the stroke volume and heart rate. Interpret the preload and the factors determining it. Correlate the factors affecting the venous return (preload) to the stroke volume. Interpret the Frank-Starling law and correlate its importance to the homeostasis of the heart. Correlate the changes of the afterload to the stroke volume. Describe the effect of blood volume changes on the stroke volume. Definitions and normal values: Cardiac output (CO) is the volume of the blood pumped out by each ventricle per minute. It is also called cardiac minute volume. Normal values: the normal CO at rest is 5- 6 liters per minute, and it is equal for both ventricles. The following factors, among others, directly affect cardiac output: (1) the basic level of body metabolism, (2) whether the person is exercising, (3) the person’s age, and (4) the size of the body. In severe exercise, CO may reach 25 L/min in non-athletes & up to 35 L/min in athletes. The cardiac index (CI) is the cardiac output per square meter of body surface area and its normal value in average adults is about 3.2 L/m2/min at rest. The cardiac output = heart rate X stroke volume The stroke volume (SV) is the volume of blood pumped by each ventricle per beat. It is about 70-90 ml in an average size, resting man in the supine position. It equals the difference of the ventricular end-diastolic and end-systolic volumes. The end-diastolic volume (EDV) is the volume of blood present in the ventricles at the end of the diastole. It equals 130 ml. It is affected by the venous return (VR) The end-systolic volume (ESV) is the volume of blood present in the ventricles at the end of systole (i.e. the volume of blood that remains in the ventricle after ejection). It is about 50 ml. It is affected by arterial blood pressure & cardiac contractility e.g. increased arterial blood pressure or decreased cardiac contractility will decrease SV & increase ESV). Thus, the average resting SV = EDV- ESV = 130 -50 = about 80 ml In a resting, supine man, the average CO = 5.5 L/min (80 mL × 70 beats/ min) The ejection fraction (EF): This is the percentage of the end-diastolic blood volume that is ejected per beat. The ejection fraction is a valuable index of ventricular function. It equals the SV/ EDV x 100 and normally at rest, it averages 80 / 130 x 100= 65% (range 60 -75 %) i.e. only about 2/3 of the EDV is normally ejected during each systole. Conditions affecting cardiac output: No change: during sleep and on exposure to moderate changes in temperature. CO increases during exercise, excitement, and anxiety, during eating, in pregnant women, and on exposure to high environmental temperature. CO decreases on standing from lying down and in heart diseases. Factors affecting the cardiac output: The cardiac output = heart rate X stroke volume Changes in heart rate, stroke volume, or both can produce changes in cardiac output. The heart rate has a direct effect on the cardiac output. SV depends on preload, afterload as well as myocardial contractility. The preload is proportionate to the end-diastolic volume, while the afterload is the resistance against which blood is expelled (arterial blood pressure). When the stroke volume is increased, it would increase the cardiac output, provided that the heart rate is unchanged. 1. 2. 3. 4. 5. The Venous Return (Preload) Efficacy of cardiac contractility= Systolic Performance of the Ventricle The Arterial Blood Pressure (Afterload) The Heart Rate Blood Volume & Viscosity (1) THE VENOUS RETURN (VR) = PRELOAD It is not the heart itself that is normally the primary controller of cardiac output. Instead, it is the various factors of the peripheral circulation that affect the flow of blood into the heart from the veins, called venous return (VR), that are the primary controllers. VR is the volume of the blood flowing from the veins into the right atrium/min. The VR is a basic determinant of the SV and CO. It acts by affecting the EDV. The heart acts as a hydraulic pump that permits the pumping of a variable amount of VR. During rest, the VR is 5- 6 liters/min and an equal CO is ejected by the ventricles through their intrinsic auto-regulatory mechanisms. These mechanisms are aided by the sympathetic tone of the heart to increase the CO up to 15-25 liters/min e.g. during muscular exercise (cardiac permissive level). Greater outputs more than the permissive level can still be ejected by: - Neuro-hormonal mechanism (increasing the sympathetic activity and secretion of catecholamines from the adrenal medulla) - Cardiac hypertrophy (which can increase the CO up to 35 liters/minute in well-trained athletes). When the venous return is increased, the cardiac output will increase through the following mechanisms: IThe relation between ventricular stroke volume and end-diastolic volume through the Frank–Starling Law: when an extra amount of blood flows into the ventricles, the cardiac muscle itself is stretched to greater length. This in turn causes the muscle to contract with increased force. Therefore, the stroke volume is increased. II- The stretch of the right atrial wall increases the heart rate by the atrial stretch receptor reflex; this, too, increases the cardiac output. FACTORS THAT AFFECT THE VENOUS RETURN (VR) Various factors assist in returning the deoxygenated venous blood to the right atrium of the heart and determine the degree of cardiac filling during diastole and hence the EDV. 1) Venous pressure gradient: This is the difference between the mean circulatory pressure MCP (or mean systemic filling pressure (MSFP)= the mean pressure in the systemic circulation = 7-10 mmHg) and the right atrial pressure RAP (normally = 2 mmHg during recumbency and 0 mmHg in the standing position) and it is the primarily determinant of the VR (= cardiac input). MSFP depends on: Blood volume (direct relation) Venous compliance (inverse relation) Pressure gradient = MSFP – RAP = 7 – 2 = 5 mmHg The greater the pressure gradients, the more becomes the VR and vice versa. 2) 3) 4) 5) Lying down position → No effect Standing = Effect of gravity > the pressure gradient for V.R. → Tends to pool down ≈ 500 ml blood in veins of lower limbs → ↑ capillary blood P. → escape of fluid to interstitial space → ≈ 15 % ↓ in blood volume in 15 min→ ↓ VR → ↓ COP → Syncope This is normally prevented by other factors mainly contraction of muscles of lower limbs. Skeletal muscle pump: Skeletal muscles act as peripheral hearts. Their contraction compresses the capillaries and venules inside them. This propels blood toward the heart, and the backflow of blood is prevented by the venous valves. This occurs by muscle tone and during exercise. Such effect is also exerted, but to a lesser extent, by arterial pulsations. Valves in the veins are important to prevent backflow of the blood in the veins. (No valves in big, very small, GIT & brain veins). Arteriolar diameter: Arteriolar dilatation e.g. in the skin in hot weather and in the splanchnic area during digestion, decreases the resistance to blood flow and increases the VR, and vice versa. Capillary tone: 90% of the capillaries are partially or totally closed under normal conditions. Severe capillary dilatation as with histamine release in tissue injury leads to the 6) 7) 8) 9) pooling of blood in the capillaries, which decreases the MCP resulting in a marked reduction of the VR, CO and circulatory shock. Respiratory pump: During inspiration, the negativity of the intra-thoracic pressure increases, so the thoracic veins dilate and their resistance to blood flow is decreased. At the same time, the intra-abdominal pressure increases (due to the descent of the diaphragm) which compresses and increases the pressure in the abdominal veins. The resulting increase in pressure gradient between the thoracic and abdominal veins helps VR towards the heart. Sympathetic stimulation: This increases the VR by increasing the venous tone and the cardiac suction forces as well as by producing arteriolar V.D. in skeletal muscles. Venous (venomotor) tone: This is a state of partial constriction of the venules during rest caused by continuous sympathetic discharge to these vessels. It creates an upstream pressure that maintains the VR against gravity. Cardiac suction forces: During ventricular systole, the downward movement of the A-V ring acts as a suction force that draws blood from the veins into the atria. Also, during early ventricular diastole, the rapid ventricular expansion is associated with increased inflow from the filled atria, which decreases the atrial pressure resulting in the suction of blood from the veins. Blood volume: A decrease of the blood volume (e.g. due to hemorrhage) decreases the MCP resulting in a reduction of the VR, and vice versa. Gravity: This antagonizes the VR from the lower limbs. However, this effect is normally antagonized by the thoracic and muscular pumps, the venomotor tone, and the cardiac suction forces. (2) Efficacy of myocardial contractility “Systolic performance of the ventricles”: It is the overall force generated by the ventricular muscle during systole. It is determined by the number of cross-bridges cycling during contraction, which is determined by: I- Preload (Frank- Starling law): It is the load or pre-stretch on ventricular muscle at the end of diastole, i.e. EDV. According to Frank-Starling law: ↑V.R. → ↑EDV → ↑ Force of contraction due to a change in the length of muscle fiber, but with the same Ca2+. II- Level of contractility: A change in the force of contraction at any given preload Myocardial contractility is affected by the following factors: 1) Neural input: When the sympathetic nerves to the heart are stimulated, the force of contraction increases. Circulating catecholamines augment the positive inotropic effect of norepinephrine liberated at the nerve endings. Sympathetic stimulation makes its effect by increasing the amount of Ca2+ entry from the extracellular fluid, thus increasing the intracellular calcium. When the strength of contraction increases without an increase in fiber length, more of the blood that normally remains in the ventricles is expelled; that is the ejection fraction increases. Parasympathetic stimuli have the opposite effect. 2) Changes in cardiac rate (HR): (force-frequency relation = Bowditch effect) A high heart rate produces a small increase in contractility. Because Ca2+ enters the cell more rapidly than it is sequestered by the sarcoplasmic reticulum, intracellular Ca2+ increases. The increased contractility helps compensate for the reduced filling time associated with high heart rates. However, an increased heart rate to the extent that shortens the diastolic time will interfere with cardiac filling and cardiac contraction. 3) Ca2+ availability → ↑contractility 4) Digitalis & other inotropic drugs → ↑contractility 5) Myocardial contractility is depressed in heart failure, hypoxia, and acidosis (3) THE AFTERLOAD (ARTERIAL BLOOD PRESSURE): Increased arterial blood pressure ( o r s ys t e m i c v a s c u l a r r e s i s t a n c e ) will interfere with the force of contraction. This causes an initial decrease in the stroke volume and cardiac output for several beats. Indeed, the end-diastolic volume of the next beat increases leading to increase the force of contraction (Frank-Starling law) thus CO returns to normal. Changes in ABP do not affect CO provided VR is kept constant. (4) EFFECTS OF CHANGES IN THE (HR) ON THE (CO) The heart rate has a direct effect on the cardiac output, if increases, within limits, CO increases. However, if the heart rate increases so much to the extent that it shortens the diastolic time, during which, coronary and heart filling take place, the cardiac output may decrease rather than increase. As the HR decreases below 70 beats/ minute, the SV is increased (because the ventricles have enough time for maximum filling), and the CO remains almost constant. If the HR decreases below 50 beats/minute, the increase in the SV cannot compensate for the slowing of the heart, and the CO is decreased. As the HR increases from 70 to 180-200 beats/ minute, the SV is decreased because of the shortening of the diastolic time. However, the CO remains constant or increases slightly due to heart acceleration. If the HR increases above 180-200 beats/minute, the diastolic time becomes much shorter and decreases the end-diastolic volume, force of contraction, stroke volume, and CO. Here, the decrease in SV is not compensated by heart acceleration. Therefore, both excessive acceleration and slowing of the heart are associated with a decrease in CO. The heart rate is primarily affected by autonomic nerves, with sympathetic stimulation increasing the rate and parasympathetic decreasing it. (5) BLOOD VOLUME AND BLOOD VISCOSITY: Increased blood volume helps the venous return, while hemorrhage decreases the venous return and cardiac output. Increased blood viscosity increases resistance against blood flowing in the circulation and returning to the heart, and in conditions of low blood viscosity such as anemia, the venous return and cardiac output are increased.