The Cardiac Cycle Flashcards
Effect of sympathetic on heart rate
Increases heart rate by making pacemaker potential reach threshold sooner
- therefore next heartbeat occurs closer
- cardiac interval goes down and heart rate goes up
Mechanisms of sympathetic acting on heart rate
Releases noradrenaline (as well as circulating adrenaline from adrenal medulla) - both act on beta1-receptors on sinoatrial node
Effect of parasympathetic on heart rate
Slows down heart rate by hyper-polarising pacemaker cells - slowing down rate of depolarisation so reaches threshold later
Mechanism of parasympathetic on heart rate
Vagus nerve releases acetylcholine
- acts on muscarinic receptors on sinoatrial node
- hyperpolarises the cells
- decreasing heart rate
What is starlings law of preload?
Energy of contraction is proportional to the initial length of the cardiac muscle fibre
What is the preload?
The initial length of muscle before stimulated to contract
How is the preload increased
Put more blood into the heart —> greater end diastolic volume = greater stretch of the muscle around the ventricle
Greater end diastolic volum = greater tension = greater stretch volume
What is the afterload?
Load against which the muscle tries to contract
= the aortic pressure at the other side of the aortic valve that’s closing the valve
How is the aortic pressure affected?
By how much blood is pushed into the artery
How easy its for the blood to get away from there
As the blood flows away from the heart it reaches resistance in the arterioles = total peripheral resistance (TPR)
What is the total peripheral resistance (TPR)
Measure of how constricted or dilated the arterioles are
- if constricted will have higher arterial pressure
- therefore heart needs to work harder to build up enough pressure to open aortic valve and push blood out
- therefore less energy left to able to eject the blood (stroke volume will decrease)
Impact of sympathetic nervous system on end diastolic volume and stroke volume
Increases contractility
Shortens systolic phase leaving more time for diastole
Mechanism works on top of preload effect
End diastolic volume increases
Stroke volume increases
Impact of parasympathetic nervous system on end diastolic volume and stroke volume
Little effect - the vagus nerve doesnt innervate the ventricular muscle (therefore acetylcholine not released here so doesnt impact strength of contraction)
What is the preload
How full the ventricle is before it starts contracting (end diastolic volume)
Affected by the state of contractions of venules/veins
What is contractility?
How strong a contraction is produced for any given preload or afterload
Affected by the sympathetic system
What is afterload?
How difficult it is for the heart to pump out the blood (the total peripheral resistance)
Affected by the state of contraction of arterioles
Formula for cardiac output
Heart rate x stroke volume
What happens to stroke volume and cardiac output if heart rate is increased?
Increase in cardiac output
Decrease in stroke volume:
- shortened cardiac interval cuts into the rapid filling phase
- reduced end diastolic volume reduces the preload
What happens to cardiac output during exercise? What are the mechanisms for this?
Cardiac output increases 4-6x HR increases: decreased vagal tone increased sympathetic tone Contractility increases: increased sympathetic tone inotropic state altered and systole shortened Venous return increases: venoconstriction skeletal/respiratory pumps (maintains preload) Total peripheral resistance falls: arteriolar dilation in muscle, skin and heart reduces afterload
Define:
Systolic pressure
Diastolic pressure
Pulse pressure
Systolic pressure = peak pressure in aorta
Diastolic pressure = minimum pressure in aorta
Pulse pressure = systolic - diastolic
What is normal arterial pressure?
120/80mmHg