lecture 20 Flashcards
systole
heart is contracting
diastole
heart is relaxing
Atrial systole
- heart is contracting
- last bit of blood out of the atria and pumped into ventricles
ventricular systole
- blood is ejected from the heat into aorta and pulmonary artery
ventricular diastole
- blood is moving through AV and passively filling the ventricles
End diastolic volume
the amount of blood left in the ventricles at the end of ventricular diastole
End systolic volume
amount of blood in the ventricles after ventricular ejection
Stroke volume is
- the amount of blood ejected from the heart during ventricular systole
- EDV-ESV= stroke volume
- average resting SV = 135-60 = 70ml/beat
Mechanical events of 1 cardiac cycle
- Late diastole: both sets of chambers are relaxed and ventricles fill passively through AV
- Atrial systole: atrial contraction forces a small amount of additional blood in ventricles
- Isovolumic ventricular contraction : ventricles start contracting but there’s not enough force to eject blood out
- AV slam shut creating ‘S1 sound’
- SV still have not opened yet - Ventricular ejection: ventricles are contracting, SV open and blood is ejected
- Isovolumic ventricular relaxation: SV slam shut creating S2 sound, AV are closed just momentarily unitil enough blood drains in atria until diastole relaxation is fully complete and AV open
cardiac output is
- volume of blood pumped by one ventricle in a given period of time
- CO= SV x HR
- average resting CO= 5L/min
Autonomic effect in SA node
- it receives sympathetic input and vagus nerve carries parasympathetic info to the SA node
- sympathetic turns up heart rate
- parasympathetic decreases heart rate
- chronotropic effect
Autonomic effect on ventricular myosites
- receives sympathetic input
- turns up contractility (inotropic effect)
- to turn down contractility simply remove sympathetic stimulus
Sympathetic branch on SA node
- speed up HR by spitting out neurotransmitter norepinephrine on B1 adrenergic receptor
- positive chronotrope effect
parasympathetic branch on SA node
- slow down HR by spitting out neurotransmitter acetylcholine onto M2 muscarinic receptor
- negative chronotrophy effect
why is stroke volume proportional to contraction force
the harder the ventricles contracts the more blood it will eject
force of contraction is determine by
- sympathetic input: spit out sympathetic stuff on ventricular myocardium and it will contract more forcefully and heart rate will speed up so time shortens
- sarcomere length: if u stretch the sarcomere the heart will contract more forcefully (not true in skeletal muscle)
the frank-starling curve
- if u stretch the sarcomere (by stuffing blood inside) the heart will contract more forcefully because the heart will pump all blood returned to the heart
- higher EDV= longer sarcomere length
factors that increase EDV
- increased venous return and decreased heart rate (more filling time)
SNS effect on myocyte contractility
- Norepinephrine or epinephrine bind to beta-1 adrenergic receptors which activates GS
- Adenylyl cylase is activated and converts ATP into cAMP which activates pKa
- Resulting in phosphorylation of phospholamban that allows it to go away and removes inhibition off SERCA
- SERCA will remove remove Ca2+
- calcium in sarcoplasm will decrease, speeding up the relaxation cycle which will shorten contraction time
- calcium in SR will increase which will give rise to more calcium released which will cause more troponin moving tropomyosin out of the way and actin binding to myosin resulting in high force cross bridges leading to more forceful contraction
*after step 2 - Phosphorylation voltage gated sodium Ca2+ which increases open time
- More calcium is released from ECF to in which causes a greater release of calcium from SR which causes greater force of contractility
SNS effect on myocyte contractility
- Norepinephrine or epinephrine bind to beta-1 adrenergic receptors which activates GS
- Adenylyl cylase is activated and converts ATP into cAMP which activates pKa
- Resulting in phosphorylation of phospholamban that allows it to go away and removes inhibition off SERCA that is in the SR
- SERCA will remove remove Ca2+
- calcium in sarcoplasm will decrease, speeding up the relaxation of ventricular myocytes
- calcium in SR will increase which will give rise to more calcium released which will cause more troponin moving tropomyosin out of the way and actin binding to myosin resulting in high force cross bridges leading to more forceful contraction
*after step 2 - Phosphorylation voltage gated sodium Ca2+ which increases open time
- More calcium is released from ECF to in which causes a greater release of calcium from SR which causes greater force of contractility