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Human Phys
Circulatory and Heart pt.2
| Question | Answer |
|---|---|
| Cardiac output | Cardiac output is the volume of blood the heart pumps through the circulatory system per minute (∼ 5 L/min at rest) Cardiac output (CO) = heart rate (HR) × stroke volume (SV) |
| Autonomic control during the cardiac cycle | - parasympathetic and sympathetic inputs to SA and AV node - sympathetic inputs to ventricular myocardium |
| Autonomic control of heart rate | - sympathetic stimulation increases heart rate - parasympathetic stimulation decreases heart rate |
| Autonomic input | - parasympathetic: from vagus nerve to the atria, muscarinic ACh receptors bind acetylcholine - sympathetic: foracic spinal nerves to the ventricles, beta 1 adrenergic receptors bind adrenaline and noradrenaline |
| cAMP | - noradrenaline and adrenaline increase cAMP - acetylcholine decreases cAMP (increases the movement of K+ ions out of the cell) |
| Activation of beta1 adrenergic receptors | Gs protein-coupled) by epinephrine and norepinephrine → ↑ activity of adenylyl cyclase → ↑ intracellular cAMP concentration in SA node cardiomyocytes |
| Step 1 | - increases sodium and L-type calcium channels, causing depolarisation and influx of cations, increasing heart rate |
| Step 2 | - activates protein kinase A (PKA) which: 1) phosphorylates L-type Ca2+ channels causing contraction and conduction 2) phosphorylation of phospholamban causing faster relaxation |
| Parasympathetic stimulation | exerts action on the heart through parasympathetic muscarinic ACh receptors (subtype M2) on SA and AV node cardiomyocytes |
| Step 1 | reduces conduction at sodium channels, decreasing cAMP |
| Step 2 | increases conductance of the slow potassium channels - vagal fibres innervate the AV node: slows cardiac action potential |
| Stroke volume (SV) | Volume of blood pumped by the left or right ventricle in a single heartbeat Cardiac output (CO) = heart rate (HR) × stroke volume (SV) |
| Mechanical events of the cardiac cycle | 1) systole (heart beat) 2) blood ejected from chamber 3) blood pressure increases 4) blood pressure decreases 5) heart chambers fill with blood 6) diastole dilation (relaxation between beats) |
| Pressure volume loops | - end-systolic volume is the amount of blood remaining in the ventricle at the end of systole, after the heart has contracted - end-diastolic volume is the amount of blood that is in the ventricles before the heart contracts |
| Cardiac output regulation: contractility | 1. L-type Ca2+ channels - increases their open probability 2. Ryanodine receptors – increases their open probability 3. Speeds up dissociation of Ca2+ from troponin 4. Increases SERCA activity and Ca2+ re-uptake into SR |
| Cardiac output regulation: 1) preload and 2) afterload | 1) extent of force by which heart muscle fibres are stretched by blood before systole, changing according to venous constriction and blood volume circulation 2) afterload: the force against which the ventricle contracts to eject blood during systole |
| MAP (mean arterial pressure) | MAP = cardiac output (CO) × total peripheral resistance (TPR) - driving force of blood flow |
| Arteries during diastole | Ventricular contraction: 1) contraction, semilunar valve opens, blood flows into arteries, aorta and arteries expand Ventricular relaxation: 1) semilunar valve shuts, preventing backflow, arteries pump blood from elastic recoil |
| Arterioles | Arteriolar smooth muscle regulates lumen diameter to control blood flow to organs Depending on the metabolic requirement blood can be diverted to different tissues |
| Control of arteriolar blood flow to organs 1) | - intrinsic control (tissues regulate own blood supply) - myogenic autoregulation: stretching of arteriole walls causes contraction - active hyperemia – increase in blood flow linked to increased metabolism |
| 2) | - reactive hyperemia – increase in blood flow after flow has been interrupted (ie. pins and needles) - flow autoregulation – response to change in blood supply (pressure) to the organ - response to injury |
| Extrinsic controls | - mediated by CNS, Influence Peripheral Resistance and MAP - Sympathetic/parasympathetic nerves - Hormones in the blood |
| Local controls: hyperemia | - active hyperemia: matches blood flow to metabolic demand |
| Factors controlling arteriole blood flow | neural, hormonal and local - nerves/neurons - epinephrine/adrenaline - internal blood pressure/low oxygen |
Created by:
reub8n
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