Physiology_625_725_Chapters_20_2023_Speed.pptx

Circulation Physiology Chapter 20 - Textbook of Medical Physiology - Guyton&Hall Joshua S. Speed, PhD [email protected] G558, Fifth floor, Guyton Building Office hours-by appointment only Chapter 20: Cardiac output, venous return and their regulation. Cardiac Output (CO, Q) is the quantity of blood...

Circulation Physiology Chapter 20 - Textbook of Medical Physiology - Guyton&Hall Joshua S. Speed, PhD [email protected] G558, Fifth floor, Guyton Building Office hours-by appointment only Chapter 20: Cardiac output, venous return and their regulation. Cardiac Output (CO, Q) is the quantity of blood pumped into aorta each minute Values in healthy, young adults: men - 5.6 L/min; women - 4.9 L/min Venous Return (VR) is the quantity of blood flowing from the veins into the right atrium each minute. VR = CO in equilibrium CO varies widely with level of activity of the body and METABOLIC DEMAND. Basic body metabolism, age, sex, and body size can also affect CO. CO = Arterial pressure TPR Cardiac index: cardiac output/surface area CI used for comparison since CO changes with body size. Normal adult CI peaks around 10 years old (4 L/min/m2), then gradually declines with age. At 80 years, cardiac index is roughly half its peak at age 10. CO is determined by venous return and Frank Starling Mechanism Under most normal conditions, CO is determined by peripheral factors 1. Venous return is the sum of venous flow from all local tissues into the right atrium. Under unstressed conditions, it is the most important determinant of cardiac output. (metabolic demand determines venous return) 2. Cardiac function: The heart automatically pumps out what it receives from venous return (Frank Starling Mechanism) Additionally, stretching of the right atrium stretches the sinus node and triggers the Bainbridge reflex raise heart rate. Bainbridge reflex: neural reflex activated by stretch receptors in the atria increased atrial filling  increased atrial stretch  increase heart rate Stretch of the heart - makes it pump harder CO is determined by venous return and Frank Starling Mechanism Frank - Starling Mechanism Ability of heart to change its force of contraction and stroke volume in response to changes in venous return. Increase Right Atrial Pressure (increase filling) Increase atrial stretch Stretch sinus node Bainbridge reflex increase heart rate sympathetic stimulus Automatic Increase contraction force Increase Stroke Volume (SV) and Cardiac Output Remember: Under most normal conditions, CO is mainly controlled by peripheral factors/venous return. The heart is not the primary controller of CO. CO regulation is the sum of blood flow regulation in all local tissues. Tissue metabolism regulates most local blood flow Under most normal conditions, CO determined by peripheral factors • As output (work) increases, oxygen consumption and CO increase in parallel. Increase in parallel • CO is determined by the sum of all factors that influence local blood flow. • All the local blood flows summate to form the venous return, and the heart automatically pumps the returning blood back into the arteries. VR = CO in equilibrium CO regulation is the sum of blood flow regulation in all local tissues All local blood flow summates to form VR Heart pumps this returning blood back into the arteries Effect of total peripheral resistance (TPR) on long term cardiac output level Change in TPR does not necessarily mean a change in BP. Under most normal conditions, any time the long-term level of TPR changes (but no other function of the circulation changes), the CO will change in the opposite direction (Chronic effect). ↓TPR ↑ CO When no other functions of the circulation change When TPR is normal, CO is normal ↑ TPR ↓ CO CO = Arterial pressure TPR Arterial pressure = TPR X CO Cardiac Function Curve When the heart becomes a limiting factor The heart has limits to how much blood it can pump. The Cardiac Function Curve defines these limits. Cardiac Output Curve MAX PUMPING ABILITY 25L/min CFC shifts up Pumps better than normal 13L/min CFC shifts down Plateau level for a normal heart is around 13 L/min The heart can pump an amount of venous return up to 2.5 the normal before becoming a limiting factor in the control of CO Pumping below normal 2L/min CO = Arterial pressure TPR Changing cardiac function Cardiac function curve defines how much blood heart can pump Hypereffective Heart (cardiac function curve (CFC) shifts up) ↑CFC (1)Sympathetic activation/Parasympathetic inhibition. (2)Cardiac hypertrophy (long term increase in workload such as endurance exercise, increase in heart mass without damage) Cardiac hypertrophy + sympathetic stimulation can increase CO up to 40 L/min Hypoeffective Heart (cardiac function curve shifts down) Coronary artery occlusion/heart attack (AMI) Suppression of sympathetic activity to heart (neural lesion, ganglionic blockade) Cardiac ischemia (angina pectoris) Myocarditis (infection) Any factor that decreases Pericarditis (constrictive) the hearts ability to pump. Valvular disease (congenital) Increased AP (“afterload”) ↓CFC Importance of autonomic nervous system (ANS) in maintaining arterial pressure (AP) when VR/CO increase ANS Intact Metabolic stimulantvasodilator  CO (Sympathetic blockade)  If autonomic nervous system (ANS) is intact DNP will induce a significant peripheral vasodilatation and a decrease in TPR. AP will be unchanged by the ANS and CO will increase.  If ANS is blocked DNP will have the same effects on TPR, but accompanied by a profound fall in AP. Consequently, CO will decrease or not change No change AP CO = Arterial pressure TPR Maintenance of AP by ANS is essential to increase CO when TPR in peripheral tissues decrease (to increase venous return) If TPR , CO and ANS maintains arterial pressure Effects of nervous system to increase AP during exercise CO and exercise What happens to CO during exercise in a normal person?  Exercise increases muscle metabolism  Arterial vasodilatation to increase supply of blood, oxygen and nutrients to sustain adequate muscle contraction  Decrease TPR Exercise   metabolism  vasodilatory products vasodilation resistance Flow What happens to blood pressure?  Would decrease due to vasodilatation and lower TPR, but...  There is a compensatory increase in central autonomic nervous signaling (sympathetic)  Consequently, there is a simultaneous increase in heart rate, heart contractility (pumping) and venous constriction  Thus, arterial pressure increases more muscle blood flow Arterial Pressure Cardiac Output = Total Peripheral Resistance Pathologically high and low cardiac outputs High cardiac output caused by low TPR (increased metabolic demand) A. Beriberi: B1 deficiency, peripheral vasodilation due to insufficient nutrient usage B. Arteriovenous fistula (shunt): opening between major artery and vein, flow diverts C. Hyperthyroidism: basal metabolism increased, O2 consumption increases D. Anemia: reduced viscosity and reduced O2 delivery (vasodilation and metabolic need) Low cardiac output caused by: A. Cardiac factors: coronary artery blockage, valvular disease, myocarditis, cardiac tamponade, cardiac metabolic derangements B. Decreased venous return: decreased blood volume (hemorrhage), venous dilation (SN deactivation), large vein obstruction, decreased tissue mass. Venous Return Curve Plateau at negative pressures is caused by collapse of large veins. When right atrial pressure equals mean systemic pressure, venous return will be 0. VR= __Psf – Pra__ RVR Principal factors that affect venous return 1. Right Atrial Pressure (Pra)- exerts a backward force on veins to impede flow 2. Mean Systemic Filling Pressure (Psf)- Degree of filling of the systemic circulation 3. Venous resistance to blood flow (RVR)- Resistance between peripheral blood vessels and right atrium. Additional but helpful info for upcoming lectures  Pressure gradient for venous return: when is zero, no venous return. If the right atrial pressure rises to equal mean systemic filling pressure, then you will not have a pressure gradient. The greater the difference between them, the greater the venous return and, consequently, the higher the CO.  Blood volume and CO: Acute increases in blood volume increase CO due to a large increase in mean systemic filling pressure and a reduction in vascular resistance (volume-induced distension of vessels). Later on, increase in capillary pressure, filled-up of the venous reservoirs (spleen, liver), and autoregulatory increase in peripheral resistance lead to a compensatory decrease in mean systemic filling pressure and consequently, a gradual decrease in CO (to normal).  Sympathetic stimulation affects heart and systemic circulation. The heart becomes a stronger pump and increases mean systemic filling pressure. Although resistance to venous return increase, right atrial pressure hardly changes. Therefore, CO increases (short periods of time-compensatory mechanisms return CO to normal)  Sympathetic inhibition (spinal anesthesia or lesion, hexamethonium) decrease mean systemic filling pressure and the effectiveness of the heart as a pump. Hence, CO decreases. Methods to measure CO • Measure of CO using Oxygen Fick Principle: It divides the oxygen intake by the difference in oxygen content of arterial blood and mixed venous blood CO (L/Min) = O2 absorbed per min by lungs (ml/min) Arteriovenous O2 difference (ml/L blood) In humans: O2 absorption calculated using an O2meter. To calculate A-V difference, venous and arterial blood can be obtained from peripheral vessels. • Indicator dilution Method: The CO is equal to the amount of indicator (dye) injected, divided by its average concentration in the arterial blood after a single circulation through the heart (dilution of dye in blood through time). • Echocardiography Combination of two dimensional (2D) ultrasound with Doppler measurements to calculate Cardiac Output (2D measurement of aortic diameter and doppler calculations of flow through aortic valves)---determines stroke volume. Stroke volume x Heart rate = CO The major regulator of coronary blood flow is: A. Parasympathetic activation B. Availability of carbohydrates C. Oxygen D. Calcium E. Fatty acids The major regulator of coronary blood flow is: A. Parasympathetic activation B. Availability of carbohydrates ✓C. Oxygen D. Calcium E. Fatty acids Which of the following best describes the hemodynamics of a patient with an arterio-venous (AV) fistula? A. ↓ AP, ↑ TPR, ↓ CO B. ↑ AP, ↓ TPR, Unchanged CO C. Unchanged TPR, ↓ CO D. ↓ TPR, ↑ CO E. ↓ TPR, ↓ CO, ↓ AP Which of the following best describes the hemodynamics of a patient with an arterio-venous (AV) fistula? A. ↓ AP, ↑ TPR, ↓ CO B. ↑ AP, ↓ TPR, Unchanged CO C. Unchanged TPR, ↓ CO ✓D. ↓ TPR, ↑ CO E. ↓ TPR, ↓ CO, ↓ AP