what is systole
- rhythmic contraction of the heart chambers
- during atrial systole blood is pumped from Atria into ventricles
- during ventricular systole blood is pumped from ventricles into aorta and pulmonary artery
What is diastole
- rhythmic relaxation of the heart chambers
- during the diastole the chambers are filling with blood
what are the mechanical events of 1 cardiac cycle
- late diastole - both sets of chambers are relaxed and ventricles fill passively
- atrial systole, atrial contraction forces a small amount of additional blood into ventricles (through AV node)
- isovolumic ventricular contraction - First phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
- ventricular ejection - as ventricular pressure rises and exceeds pressure in the arteries the semilunar valves open and blood is ejected
- isovolumic ventricular relaxation - as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed
what are the events of the wiggers diagram
- summary of the electrical and mechanical events of the cardiac cycle
1. mitral (bicuspid) valve closes - atrial systole (low pressure)
2. aortic valve opens - isovolumic ventricular contraction (90mm Hg)
3. end diastolic volume - the volume of blood in the ventricle at the end of ventricular diastole
4. aortic valve closes - end of ventricular systole
5. mitral valve opens - early ventricular diastole
6. end systolic volume - early ventricular diastole (volume of blood in the ventricle at the end of ventricular ejection)
link the mechanical phases of the Heart to the ECG
- atrial systole P to R
- isovolumic ventricular contraction R to S
- ventricular systole S to T
- ventricular diastole T to P
explain left ventricular pressure and volume relationship during the cardiac cycle
- atrial systole activity contributes 20% of ventricular filling
-> the rest is due to passive flow - isovolumnic contraction = buildup of ventricular pressure without change in volume (no blood ejection) = high volume EDV
- isovolumnic relaxation = ventricles are empty and relaxation results in decrease in pressure that eventually closes aortic valve and then opens mitral valve (Early ventricular diastole) = low volume ESV
describe the pressure and volume changes of the left ventricle during the cardiac cycle
A -> A’ (low pressure, volume increase) - Mitral valve open
A’ -> B (EDV) - pressure increase slightly, volume increase slightly - mitral valve closes
B -> C (pressure increases, volume stays the same) - Aortic valve opens
C -> D (pressure increases, volume decreases) - aortic valve closes - ESV
explain pressure differences and heart sounds
- valve opening and closing due to pressure differences
- Mitral valve closes in systole when increasing ventricular pressure exceeds atrial pressure
- Aortic valve opens in systole when increasing ventricular pressure exceeds aortic pressure
- Aortic valve closes as ventricle relaxes in diastole and pressure drops below aortic pressure
- Mitral valve opens as ventricular pressure drops below atrial pressure
- heart sounds = lub dub
-> associated with valve closure
What is Stroke Volume
- amount of blood pumped by one ventricle during a contraction
SV = end diastolic volume - end systolic volume - average resting SV = 70mL/beat (135-65mL)
what is cardiac output
- volume of blood pumped by one ventricle in a given period of time
- CO = HR(beats/min) x SV (mL/beat)
- average resting CO = 5L/minute
what is the autonomic effect on the SA Node
- modulation of heart rate (a chronotropic effect)
- parasympathetic (signal sent from medulla) or sympathetic
what is the autonomic effect on the ventricular myocytes
- modulation of contractility (an inotropic effect)
- only sympathetic
what is a negative and positive chronotropic effect
- negative chronotropic effect = stimulation by parasympathetic nerves decreases heart rate
-> parasympathetic neuron Acetylcholine on M2 receptor (ACh = pacemaker channels open slower)
-> Gi = decrease cAMP - positive chronotropic effect = stimulation by sympathetic nerves increases heart rate
-> sympathetic neuron, NE on beta 1 receptor (NE = pacemaker channels open faster)
-> Gs = increase cAMP
modulation of stroke volume
- stroke volume is directly proportional to contraction force
- contraction force is determined by
1. sarcomere length (EDV)
2. contractility of muscle
explain the Frank Starling curve (the length tension relationship in the heart)
what causes increase in EDV
- an increase in EDV….
- … causes stroke volume to increase
-> EDV is directly proportional to length of sarcomere
- factors that increase EDV - increased venous return
- decreased heart rate (more filling time)
what is the effect of SNS on ventricular contractility
contractility = the ability of a muscle fiber to contract at any given length
-> depends on intracellular calcium and its interaction with contractile machinery
- SNS activity of ventricular myocytes -> increased contractility -> increased stroke volume
- increased sympathetic activity Increases stroke volume (inotropic)
what is the SNS effect on Myocyte contractility
- increased activity of the L type calcium channels
- Increased SERCA activity
1+2 = increased Ca2+ storage in SR, increased calcium induced calcium release via ryanodine receptors, increased calcium signal with each heartbeat
- increased contractility and shorter duration of contraction
What is phospholamban
- regulatory protein that alters sarcoplasmic reticulum Ca2+- ATPase activity (increases activity)
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