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Control Of Cardiac Output By Manpreet & Olivia

+Introduction

Terminology

Components of stroke volume

Cardiac cycle

Pressure-volume loops

Frank-Starling mechanism

Factors affecting CO

+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

+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

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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

+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

+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

+Summary Table: Factors Affecting SV

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Thank you! Questions?