+ Control Of Cardiac Output By Manpreet & Olivia

+ Introduction Terminology Components of stroke volume Cardiac cycle Pressure-volume loops Frank-Starling mechanism Factors affecting CO

+ Terminology Cardiac Output => ‘volume of blood pumped by each ventricle per minute’ Measured - litres per minute. CO = SV X HR Stroke volume =>” The volume of blood ejected from each ventricle during each ventricle contraction” SV = End diastolic volume – End systolic volume Affected by: contractility, afterload & preload [SV CAP] E.g SV increases when: increase contractility, increased preload, decreased afterload. SV increases in anxiety, exercise and pregnancy Heart failure has decreased SV

+ Preload & Afterload Preload Preload approximated by ventricular EDV Dependent on venous tone and circulating blood volume VEnodilators (e.g nitroglycerin) decrease preEload Afterload Afterload approximated by MAP Affected by Wall tension Increased afterload -> LV compensates by thickening (hypertrophy) Chronic hypertension (increased MAP) -> LV hypertrophy VAsodilators decrease Afterload (Atrial) ACEi + ARBs decrease both preload and afterload

+ Contractility  ‘Force of contraction of myocardium’ Directly controls SV and impacts ESV Greater contractility -> greater SV (smaller ESV) Positive inotropic agents = increase contractility Negative inotropic agents = decrease contractility. Contractility (& SV) increased with: Catecholamines – which increase activity of Ca2+ pump in sarcoplasmic reticulum. Increased intracellular Ca2+ Decreased extracellular Na+ Contractility (& SV) decreased with Beta blockers, calcium channel blockers Heart failure Acidosis Hypoxia/hypercapnea

+ Cardiac Cycle

+ Pressure-Volume Loops

+ => ‘ability of the heart to change its force of contraction and therefore SV in response to changes in venous return’ As blood returns to the heart in diastole, ventricle fills so volume increases and intra-ventricular pressure also progressively rise Frank-Starling Mechanism Myocardial fibres in the ventricular wall are stretched and put under tension (preload) Cardiac muscle responds to increased stretch with a more forceful contraction

+ Factors Affecting Cardiac Output

+ Factors Decreasing Heart Rate and Force of Contraction FactorEffect Cardioinhibitor nerves (vagus)Release of acetylcholine ProprioreceptorsDecreased rates of firing following exercise Chemoreceptors Increased levels of O2; decreased levels of H+ and CO2 Baroreceptors Increased rates of firing, indicating higher blood volume/pressure Limbic systemAnticipation of relaxation CatecholaminesDecreased epinephrine and norepinephrine Thyroid hormonesDecreased T3 and T4 CalciumDecreased Ca2+ PotassiumIncreased K+ SodiumIncreased Na+ Body temperatureDecrease in body temperature Decreasing HR

+ Increasing HR Major Factors Increasing Heart Rate and Force of Contraction FactorEffect Cardioaccelerator nervesRelease of norepinephrine ProprioreceptorsIncreased rates of firing during exercise Chemoreceptors Decreased levels of O2; increased levels of H+, CO2, and lactic acid Baroreceptors Decreased rates of firing, indicating falling blood volume/pressure Limbic system Anticipation of physical exercise or strong emotions CatecholaminesIncreased epinephrine and norepinephrine Thyroid hormonesIncreased T3 and T4 CalciumIncreased Ca2+ PotassiumDecreased K+ SodiumDecreased Na+ Body temperatureIncreased body temperature Nicotine and caffeineStimulants, increasing heart rate

+ Summary Table: Factors Affecting SV

+ Thank you! Questions?