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Lecture

Lecture V - Regulation of Cardiac Output.docx

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Department
Biological Sciences
Course
BIOC33H3
Professor
Stephen Reid
Semester
Winter

Description
Thiruvarangan Regulation of Cardiac Output (Stroke Volume) **complex** Stroke Volume Regulation 1. Force of Ventricular Contraction 2. End-Diastolic Volume 3. Afterload (Blood Pressure) Stroke Volume Regulation: Ventricular Contractility The sympathetic nerve innervates a cardiac myocyte (muscle cell) by releasing noradrenaline by binding to β receptors. This leads to the production of adenylyl cyclase which leads to the production of cAMP. cAMP activates PKA which opens up Ca 2+ channels. This influx acts on the SR and triggers further release of Ca from the SR. An 2+ increase in Ca triggers contraction.  Force generation  Increase in cytosolic calcium leads to increase in the force of contraction  Circulating hormonal adrenaline has the same effect Increase in intracellular [Ca ] in cardiac muscle cells 2+ 1. Increased binding of Ca to troponin: more cross-bridge formation between the thick and thin filaments 2+ 2. Incr2+se in Ca permeability of the sarcoplasmic reticulum (Ca - induced calcium release). Therefore, ventricular contractility is regulated simply by sympathetic input enhancing calcium influx into the cardiac myocytes which enhance contraction End-Diastolic Volume – it is the ventricular volume (of blood) at the end of diastole available to be pumped when the heart contracts Starling law/curve – Greater amounts of blood entering the heart during diastole lead to greater amounts of blood leaving the heart during systole.  ↑ EDV  ↑ Force of ventricular contractio ↑ SV  ↑ CO  Prevents an increase in heart volume with increased venous return The starling effect is mediated by the position of the thick and thin filaments within the contractile cardiac muscle cells.  Cardiac muscle fibers are shorter than their optimal length (unlike skeletal muscles). **See Slide 15 if necessary** Thiruvarangan o At normal resting length, there is only a limited amount of space for the filaments to slide over each other (smaller contraction force). o Stretching (due to ↑ EDV) increases the potential for cross-bridge formation. The stretching allows the filaments to slide to a greater degree.  A stretched muscle can generate a greater force of contraction  Note: if the muscle stretches too much, it loses its muscle contractility (as in high b.p. – cardiac hypertrophy)  Starling Curves and Sympathetic Activity o Stroke volume can be regulated by altering EDV and/or sympathetic activity. (see slide 17 if necessary) o In order to get a normal stroke volume from a weaker heart, for example, we have to increase the EDV or increase sympathetic input Effects of Pre-Load on End Diastolic Volume Pre-load is the amount of blood within the ventricles just before contraction.  If the end-diastolic pressure (EDP: pre-load) increases then end-diastolic volume will increas SV  CO o Ways to increase pressure can be an increase in blood volume, posture, muscular activity, and venous return  Pre-load can be influenced by ventricular compliance o Compliance is a measure of how easily the ventricle expands o Compliance = Δ Volume / Δ Pressure o Stiffness = Δ Pressure / Δ Volume o compliance and stiffness can be measured from a single curve  A steep slope means are reduced compliance or a high stiffness  Compare Points 1, 2, and 3 (see slide 19) o Normal Curve Figure 1: this graph is a measure of stiffness (slopes) o As EDP↑, EDV ↑  Compare Points 1, 4, and 5 o Normal and Abnormal Curves o As compliance ↓, EDV ↓ at any given EDP Muscular Pump – The Skeletal Muscle Pump: moves bl
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