+ control of cardiac output by manpreet & olivia
TRANSCRIPT
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+
Control Of Cardiac Output By Manpreet & Olivia
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+Introduction
Terminology
Components of stroke volume
Cardiac cycle
Pressure-volume loops
Frank-Starling mechanism
Factors affecting CO
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+TerminologyCardiac 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
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+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
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+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
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+Cardiac Cycle
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+Pressure-Volume Loops
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+
=> ‘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
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+Factors Affecting Cardiac Output
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Factors Decreasing Heart Rate and Force of ContractionFactor EffectCardioinhibitor nerves (vagus) Release of acetylcholineProprioreceptors Decreased 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 system Anticipation of relaxationCatecholamines Decreased epinephrine and norepinephrineThyroid hormones Decreased T3 and T4Calcium Decreased Ca2+Potassium Increased K+Sodium Increased Na+Body temperature Decrease in body temperature
Decreasing HR
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+Increasing HR
Major Factors Increasing Heart Rate and Force of Contraction
Factor EffectCardioaccelerator nerves Release of norepinephrineProprioreceptors Increased 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
Catecholamines Increased epinephrine and norepinephrineThyroid hormones Increased T3 and T4Calcium Increased Ca2+Potassium Decreased K+Sodium Decreased Na+Body temperature Increased body temperatureNicotine and caffeine Stimulants, increasing heart rate
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+Summary Table: Factors Affecting SV
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+
Thank you! Questions?