Regulation of Stroke Volume & Heart Rate Flashcards

1
Q

<p>What is the control mechanism of heart rate?</p>

A

<p>Neural</p>

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2
Q

<p>What is the regulation mechanism for stroke volume?</p>

A

<p>Preload</p>

<p>Afterload</p>

<p>Neural</p>

<p>Pathological</p>

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3
Q

<p>How does the sympathetic nervous system regulate heart rate?</p>

A

<p>Releases noradrenaline from nerves and adrenal medulla.</p>

<p>Act on Beta 1 receptors on sinoatrial node</p>

<p>This increases the slope of the pace maker potential between heart beats</p>

<p>Increases heart rate</p>

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4
Q

<p>What is the effect of the parasympathetic nervous system on heart rate?</p>

A

<p>Vagus nerve releases acetycholine</p>

<p>Acts on muscarinic receptors on the sinoatrial node</p>

<p>Hyperpolarises cells and decreases the slope of the pacemaker potential</p>

<p>Decreases heart rate = bradycardia</p>

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5
Q

<p>What does starlings law state?</p>

A

<p>Starling’s Law states - the energy of contraction is proportional to the initial length of the cardiac muscle fibre</p>

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6
Q

<p>Why is the slope decreasing to the left side of the peak tension?</p>

A

<p>Actin filaments start to interfere with each other</p>

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7
Q

<p>What is the length of the cardiac muscle fibres proportional to?</p>

A

<p>End diastolic volume</p>

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8
Q

<p>What is the stroke volume related to?</p>

A

<p>Tension</p>

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9
Q

<p>What is preload affected by?</p>

A

<p>End diastolic volume</p>

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10
Q

<p>What ensures self regulation of stroke volume of left and right ventricles?</p>

A

<p>The proportional relationship between the volume of venous return and the stroke volume</p>

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11
Q

<p>What is the afterload?</p>

A

<p>The load against which the muscle tries to contract</p>

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12
Q

<p>What is the aortic pressure affected by?</p>

A

<p>How much blood is pushed into the aorta (cardia output)</p>

<p></p>

<p>How easy it is for the blood to get out of the aorta (total peripheral resistance)</p>

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13
Q

<p>Why does an increase in TPR result in a reduction in stroke volume?</p>

A

<p>Aortic pressure will increase, the ventricle will have to work harder to push open the aortic valve, and it will have less energy left to do the useful bit of ejecting blood.</p>

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14
Q

<p>What is responsible for the variable portion of the total peripheral resistance?</p>

A

<p>The arterioles</p>

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15
Q

<p>What is the total peripheral resistance set by?</p>

A

<p>The arterial pressure - what sets the afterload</p>

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16
Q

<p>What affects preload?</p>

A

<p>Venules/veins and capacitance vessels</p>

<p></p>

<p>These all affect the venous return</p>

17
Q

<p>What affects afterload?</p>

A

<p>Arterioles and resistance vessels</p>

18
Q

<p>What does a bigger end diastolic volume mean?</p>

A

<p>Bigger pre-load and therefore more tension and more strength of contraction</p>

19
Q

<p>How does the sympathetic nervous system affect stroke volume?</p>

A

<p>Noradrenaline from nerves and the adrenal medulla act on beta 1 receptors of the myocytes - which increases contractility - stronger but shorter contraction</p>

20
Q

<p>What does ionotropic refer to?</p>

A

<p>The strength of contraction</p>

21
Q

<p>What is the effect of the parasympathetic nervous system on the contractility of the heart?</p>

A

<p>Little effect - vagus nerve does not innervate the ventricular muscle</p>

22
Q

<p>What is the effect of hypercalcaemia, hypocalcaemia and ischaemia on stroke volume?</p>

A

<p>•Hypercalcemia</p>

<p>–shifts curve up and left – more strength of contraction, more X bridges, more extracellular and therefore more intracellular calcium when the action potential reaches the muscle</p>

<p>•Hypocalcemia</p>

<p>–shifts curve down and right</p>

<p>•Ischaemia</p>

<p>–shifts curve down and right</p>

23
Q

<p>How does the heart compensate for a reduced pumping ability?</p>

A

<p>Works around a bigger end diastolic volume - lower ejection fraction and reduced excersize capacity.</p>

24
Q

<p>What is the effect of barbituates on stroke volume?</p>

A

<p>–shifts curve down and right</p>

25
Q

<p>Why does stroke volume decrease with an increased heart rate?</p>

A

<p>Shortened cardiac cycle cuts into rapid filling stage - smaller EDV (small length of muscle), less tension and therefore less stroke volume</p>

26
Q

<p>What are the combined mechanisms that increase heart rate?</p>

A

<p>Via decreased vagal tone and increased sympathetic tone</p>

27
Q

<p>What shortens systole?</p>

A

<p>Effect of increased sympathetic tone on the contractility - alters ionotropic state</p>

28
Q

<p>How does venous return increase?</p>

A

<p>Via venoconstriction</p>

<p>And skeletal / respiratory pumps</p>

<p>Maintains preload when we expect it to fall with a reduced EDV brought on with a fast heart rate</p>

29
Q

<p>Why does total peripheral resistance fall with a fast heart rate?</p>

A

<p>Arteriolar dilation in muscle, skin & heart</p>

<p>Reduced afterload - makes it easier for heart to pump out blood</p>

30
Q

<p>What are the 4 ways CO increases when workload increases?</p>

A

<p>HR increases</p>

<p>Contractility increases</p>

<p>Venous return increases</p>

<p>Total peripheral resistance falls</p>