Cardiac Output 2023 PDF

Cardiac output Dr K Thaxter Nesbeth Physiology Section Department of Basic Medical Sciences  OBJECTIVES We will: Discuss cardiac output and myocardial performance Discuss factors influencing cardiac output such as – Heart rate – Stroke volume...

Cardiac output Dr K Thaxter Nesbeth Physiology Section Department of Basic Medical Sciences  OBJECTIVES We will: Discuss cardiac output and myocardial performance Discuss factors influencing cardiac output such as – Heart rate – Stroke volume – Contractility – Preload – Afterload Explain the Frank-Starling law of the heart  Myocardial Performance The ability of the heart to meet the demands of the body adequate supply of blood, moving appropriately meeting the metabolic needs on a moment to moment basis. Maintained by careful management of multiple parameters: cardiac output, stroke volume, peripheral resistance, venous return, heart rate, cardiac contractility  Cardiac Output (CO) CO is the amount of blood pumped by each ventricle in one minute Indicator of the function of the heart Increased or decreased according to needs of body CO is the product of heart rate (HR) and stroke volume (SV) CO = HR x SV (ml/min) = (beats/min) x ml/beat = 75 x 70 = 5250ml/min HR is the number of heart beats per minute SV is the amount of blood pumped out by a ventricle with each beat  Measurement of CO Fick principle states Total uptake or release of a substance by an organ is the product of the blood flow through that organ and the arteriovenous concentration difference of the substance. Oxygen Fick method: CO = (Rate of O2 absorbed by lungs) [O2]la - [O2]rv Cardiac output = Q dot  Fick principle Involves calculating the oxygen consumed over a given period of time from measurement of the oxygen concentration of the venous blood and the arterial blood.  Heart Rate Physiological variation with age – infants have HR of 160 bpm or more – young adult: 60- 85 bpm – HR rises again in the elderly Tachycardia: resting adult HR above 100 – stress, anxiety, drugs, heart disease or ↑ body temp. Bradycardia: resting adult HR < 60 – in sleep and endurance trained athletes – Pulse = surge of pressure in artery  Extrinsic Innervation of the Heart Vital centers of medulla 1. Cardiac Center – Cardioaccelerator center Activates sympathetic neurons that increase HR – Cardioinhibitory center Activates parasympathetic neurons that decrease HR Cardiac center receives input from higher centers (hypotha-lamus), monitoring blood pressure and dissolved gas concentrations Effects of Autonomic Stimulation (reminder) Stroke volume = End diastolic volume – End systolic volume  THE FRANK-STARLING LAW OF THE HEART: Control of Stroke volume The force of contraction is related to the degree of stretch of the myocardial fibres. Intrinsic regulatory system of heart muscle = length-tension relationship Initially the stretch increases the contractility but beyond a certain limit: will decrease the contractility. More stretch in diastole causes more contractile force in systole!  Strength of ventricular contraction varies directly with EDV – Is an intrinsic property of myocardium – As EDV increases, myocardium is stretched more, causing greater contraction & SV Preload = End diastolic volume  Preload (End Diastolic Volume) Critical factor controlling stroke volume – ↑preload → ↑stretch of muscle → ↑force of contraction → ↑SV – ↑EDV leads to ↑stretch of myocardium. Factors Influencing Frank Starling Law / Stroke volume Afterload = End Systolic Pressure Pressure against which ventricles contract Wall tension in ventricles during systole Presha in arteries against which ventricles pump Determined by peripheral resistance Affected by – Pleural Pressure – Vascular compliance – Vascular resistance Regulation of Cardiac Output  https://www.youtube.com/watch?v=vFRkS B46bl8 Factors affecting Cardiac Output  Sympathetic Stimulation Increases contractility of the heart, increases (SV), therefore decreases End systolic volume Increases HR (positive chronotropic effect) – MOST IMPORTANT in CO adjustment – Can go to triple resting HR – Reduced filling time (diastole) at high rates 2. Parasympathetic stimulation: Heart primarily under influence of PNS at rest – reduced HR PNS returns HR to baseline after fright / exercise Mechanical factors: strength of ventricular contraction varies directly with myocardial stretch: Frank-Starling Law  Contractility Any increase in the force of contraction (Work) that CANNOT be attributed to the Frank–Starling mechanism of the heart The vigor of contraction The change in developed force at a given resting fiber length Factors Affecting Stroke Volume Mechanical factors affecting Cardiac Output (Summary)  Mechanical Factors affecting Cardiac Output Increased Venous Return – Cardiac muscle fibers are stretched by increased blood volume returning to the heart – (increased venous return and EDV). Increased stretch results in greater force of contraction, Increases stroke volume: Frank-Starling Law of the heart  Mechanical factors affecting CO Bainbridge effect in hospital medicine What goes into the (healthy) heart comes out! Bainbridge effect/reflex Effect of intravenous infusion Increase in end-diastolic volume increases heart rate Atrial stretch receptors stimulated by increased right atrial pressure Direct effect on sinoatrial node  Factors affecting Cardiac Output Exercise – activates the sympathetic nervous system increases heart rate Increases contractility Increases stroke volume Squeezing action of skeletal muscles on veins increase venous return, contributing to increased stroke volume.  Cardiac reserve: – the difference between cardiac output at rest & the maximum volume of blood the heart is capable of pumping per minute – i.e. the difference between resting and maximal CO – permits cardiac output to increase dramatically during periods of physical activity  Factors affecting Cardiac Output Sudden Drop in Blood Pressure – results in low venous return decreases stroke volume **heart rate increased due to sympathetic activity, and normal cardiac output is maintained. Rising Blood Pressure – reduces sympathetic activity, decreasing heart rate. increases arterial pressure ventricles must overcome arterial pressure before semilunar valves open, increasing ESV and decreasing stroke volume. Reduced cardiac output helps bring blood pressure down to normal levels.  Factors affecting Cardiac Output Sudden Drop in Blood Volume - (eg. due to severe blood loss) low venous return and therefore decreased stroke volume. Sympathetic activity increases heart rate Maintains cardiac output. Excess Calcium – Increases stroke volume by enhancing contractility.  https://www.johnwiley.net.au/highered/inter actions/media/Distribution/content/Distributi on/cardio3a/bot.htm http://wps.pearsoned.it/fisiologia_umana5/1 65/42312/10831895.cw/justcontent/index.ht ml full question bank interactive https://www.youtube.com/watch?v=P4xbJch9 Jm0 definition of terms https://www.youtube.com/watch?v=vFRkSB4 6bl8 cardiac output animation