Lecture 12 - Control of Cardiac Output PDF

Body Systems The Cardiovascular System BIOL10811 Stroke Heart Rate X Volume Lecture 12: Control of Cardiac Output...

Body Systems The Cardiovascular System BIOL10811 Stroke Heart Rate X Volume Lecture 12: Control of Cardiac Output Cardiac Output Dr Nick Stafford Division of Diabetes, Endocrinology & Gastroenterology School of Medical Sciences Faculty of Biology, Medicine and Health [email protected] November 2024  Objectives A successful student should be able to Describe how cardiac output is quantified, typical values, and how it is regulated by the CVS Describe the innervation of the heart, and how this regulates heart rate Explain how heart rate and the determinants of stroke volume affect cardiac output  Content 1) Definition of Cardiac Output 2) Heart Rate and Cardiac Output Innervation of the Heart Control of Pacemaker Cells 3) Stroke Volume and Cardiac Output End Diastolic & End Systolic Volume Preload Contractility Afterload What is cardiac output?  1) Definition of Cardiac Output Cardiac Output Heart Rate Stroke Volume (CO) = (HR) X (SV) Volume of blood Volume of blood Number of heart ejected by each ejected by each beats per minute ventricle per minute ventricle per beat  Some typical values for CO CO = HR x SV At rest CO (L/min) ~5 HR (bpm) 70 SV 70 (ml)  How does cardiac output increase when we exercise?  Some typical values for CO CO = HR x SV During At rest exercise CO (L/min) ~5 ~20 HR (bpm) 70 190 SV (ml) 70 105  How would HR and SV in endurance athletes compare to general population at rest?  Some typical values for CO CO = HR x SV During Keely Keely At rest exercise at rest winning CO (L/min) ~5 ~20 ~5.5 ~40 HR (bpm) 70 190 40 190 SV (ml) 70 105 140 210 Physiological Left Heart Ventricular Weight 300 500 Hypertrophy (g)  Control of Cardiac Output – an Overview Factors Affecting HR Factors Affecting SV Heart Rate (HR) X Stroke Volume (SV) Cardiac Output (CO)  Content 1) Definition of Cardiac Output 2) Heart Rate and Cardiac Output Innervation of the Heart Control of Pacemaker Cells  2) Heart Rate and Cardiac Output Factors Affecting HR Chronotropic Effects Autonomic Hormones Innervation Heart Rate (HR) Cardiac Output (CO)  Neural and Hormonal Regulation of Heart Rate CO2, pH 13 ure Chemoreceptors ct Internal Le Carotid 13 ure Artery ct Le Carotid Body Baroreceptors Pressure Aorta Medulla Oblongata Acetylcholine Cardioregulatory SA Node Centre Noradrenaline Sympathetic Ganglia (T1-T4) Cardioinhibitory Centre Cardioacceleratory Centre ↓HR Circulation ↑HR Adrenal Medulla Autonomic Effects on Heart Rate and Cardiac Output Parasympathetic Sympathetic Neurotransmitter/ Acetylcholine (ACh) Noradrenaline (NA) Hormone Adrenaline Chronotropic Effect Negative Positive Effect on HR Lowers HR Increases HR Effect on CO Reduces CO Increases CO Bradycardia Tachycardia Pathologically low HR Pathologically fast HR Autonomic Effects on Ionic control at the SA Node Depolarization Repolarization Na+ Ca2+ K+ K+ Potassium Potassium Calcium HCN KACh Kr Figure 20–22 Autonomic Regulation of Pacemaker Cell Function Autonomic Effects on Ionic control at the SA Node Parasympathetic Depolarization Repolarization Na+ Ca2+ K K+ + K+ Potassium Potassium Calcium HCN KACh Kr Figure 20–22 Autonomic Regulation of Pacemaker Cell Function  Autonomic Effects on Ionic control at the SA Node Sympathetic Depolarization Repolarization Na Na + + Ca2+ K+ K+ Potassium Potassium Calcium HCN KACh Kr Figure 20–22 Autonomic Regulation of Pacemaker Cell Function  Slowing the intrinsic pace: Vagal Tone The SA Node has an inherent rate of >100 bpm  Normal adult resting HR 60-100 bpm…..Why??? At Rest Endurance Athlete At Rest Vagal Tone ↑ Vagal Tone Reduces HR to HR ↓ to 30-60 bpm 60-100 bpm Little/no Little/no sympathe sympathetic tic activity activity + altered ion channel remodelling  Venous Return, Atrial Reflex and HR Factors Affecting HR Venous Return to Atria Atrial Venous Reflex Return 1 Stretches pacemaker cells in SAN Autonomic Hormones Innervation 2 Heart Rate (HR) HR Cardiac Output (CO)  Content 1) Definition of Cardiac Output 2) Heart Rate and Cardiac Output Innervation of the Heart Control of Pacemaker Cells 3) Stroke Volume and Cardiac Output What factors affect stroke volume? 3) Stroke Volume and Cardiac Output Factors Affecting SV Volume of blood ejected by each ventricle per beat EDV End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume ESV Stroke Volume (SV) Cardiac Output (CO) 3) Stroke Volume and Cardiac Output Factors Affecting SV Increased EDV = Increased SV End Diastolic - End Systolic Volume EDV Volume (EDV) (ESV) Stroke Volume ESV Stroke Volume (SV) Cardiac Output (CO) 3) Stroke Volume and Cardiac Output Factors Affecting SV Decreased ESV = Increased SV End Diastolic - End Systolic Volume (ESV) EDV Volume (EDV) Stroke Volume ESV Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV Factors Affecting SV Preload The degree to which ventricular muscle cells are stretched at the end of diastole Preload End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV Factors Affecting SV Contractility The force produced by ventricular muscle cells during systole at a given preload Contractility End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV Factors Affecting SV Afterload The force the ventricle needs to overcome to open the semilunar valve and eject blood Afterload End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV Preload Contractility Afterload The amount the The force produced The resistance which balloon is stretched by the elastic recoil slows down the once you’ve filled it of the balloon release of air from the with air which helps “eject” balloon if you constrict air the outflow Determinants of EDV & ESV: Preload Factors Affecting SV Venous Filling Return Time Preload End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV: Preload Preload is directly proportional to EDV, and dependent on: The rate of venous return The available ventricular filling time (ie ventricular diastole) ↑ Rate/Time of filling = ↑ EDV = ↑ SV Why?? Frank-Starling Law The force developed in a muscle fibre is dependent on the extent it is stretched  Preload and Venous Return Factors affecting venous return #1 Posture – Blood pools in leg veins whilst standing due to gravity  ↓ Venous return  Preload and Venous Return Factors affecting venous return #1 Posture – Blood pools in leg veins whilst standing due to gravity  ↓ Venous return #2 Skeletal Muscle Pump – Movement of skeletal muscles constricts veins aiding venous return. Valves prevent backflow  ↑ Venous return  Preload and Venous Return Factors affecting venous return #1 Posture – Blood pools in leg veins whilst standing due to gravity  ↓ Venous return #2 Skeletal Muscle Pump – Movement of skeletal muscles constricts veins aiding venous return. Valves prevent backflow  ↑ Venous return #3 Respiratory Pump – Inspiration reduces intrathoracic pressure whilst increasing intraabdominal pressure  ↑ Venous return #4 Venous Capacitance – SNS activity reduces compliance and increases central venous pressure  ↑ Venous return Determinants of EDV & ESV: Preload Factors Affecting SV Venous Filling Return Time Preload End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO) Determinants of EDV & ESV: Contractility Factors Affecting SV Autonomic Hormones Innervation Contractility End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV: Contractility Chronotropic Effects Contractility The force produced by ventricular muscle cells during systole at a given preload Inotropic Effects More force = More blood ejected = Increased SV +ve Inotropic Effects -ve Inotropic Effects Hormones NA, Adrenaline, Thyroid, Glucagon  SNS Effects on Contractility Tension in cardiac muscle With SNS activity Force At rest Time SNS increases force of contraction and velocity of conduction  Maximises diastolic time → increased filling  Determinants of EDV & ESV: Contractility Factors Affecting SV Autonomic Hormones Innervation -ve Inotropic +ve Inotropic Effects Effects Contractility (PNS) (SNS) End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO) Determinants of EDV & ESV: Afterload Factors Affecting SV Vascular Tone Afterload End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Determinants of EDV & ESV: Afterload Stiff valves increase Vascular Tone - Arterioles afterload Aortic 13 e e sur Valve ct res Le d P ur Vasodilation oo Vaso- Bl constriction Pulmonary Valve Reduces Increases Afterload The pressure opposing ejection Major impact upon CO Increased Afterload Reduces SV & CO Shortened Ejection Increased Afterload Normal Ejection Prolonged increases in afterload Normal Afterload damage the myocardium and lead to heart failure Longer Isovolumic Contraction Normal Isovolumic Contraction Increased ESV SV Normal ESV Determinants of EDV & ESV: Afterload Factors Affecting SV Vascular Tone Vasoconstriction Afterload Vasodilation End Diastolic Volume (EDV) - End Systolic Volume (ESV) Stroke Volume (SV) Cardiac Output (CO)  Control of Cardiac Output – an Overview Factors Affecting HR Factors Affecting SV Atrial Venous Filling Autonomic Vascular Hormones Reflex Return Time Innervation Tone Chronotropic Inotropic Effects Effects Preload Contractility Afterload Autonomic Innervation Hormones End Diastolic Volume (EDV) - End Systolic Volume (ESV) Heart Rate (HR) X Stroke Volume (SV) Cardiac Output (CO)  Objectives A successful student should be able to  Describe how cardiac output is quantified, typical values, and how it is regulated by the CVS  Describe the innervation of the heart, and how this regulates heart rate  Explain how heart rate and the determinants of stroke volume affect cardiac output