lecture 20

Question 1

systole

Answer 1

heart is contracting

Question 2

diastole

Answer 2

heart is relaxing

Question 3

Atrial systole

Answer 3

• heart is contracting
• last bit of blood out of the atria and pumped into ventricles

Question 4

ventricular systole

Answer 4

• blood is ejected from the heat into aorta and pulmonary artery

Question 5

ventricular diastole

Answer 5

• blood is moving through AV and passively filling the ventricles

Question 6

End diastolic volume

Answer 6

the amount of blood left in the ventricles at the end of ventricular diastole

Question 7

End systolic volume

Answer 7

amount of blood in the ventricles after ventricular ejection

Question 8

Stroke volume is

Answer 8

• the amount of blood ejected from the heart during ventricular systole
• EDV-ESV= stroke volume
• average resting SV = 135-60 = 70ml/beat

Question 9

Mechanical events of 1 cardiac cycle

Answer 9

1. Late diastole: both sets of chambers are relaxed and ventricles fill passively through AV
2. Atrial systole: atrial contraction forces a small amount of additional blood in ventricles
3. 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
4. Ventricular ejection: ventricles are contracting, SV open and blood is ejected
5. 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

Question 10

cardiac output is

Answer 10

• volume of blood pumped by one ventricle in a given period of time
• CO= SV x HR
• average resting CO= 5L/min

Question 11

Autonomic effect in SA node

Answer 11

• 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

Question 12

Autonomic effect on ventricular myosites

Answer 12

• receives sympathetic input
• turns up contractility (inotropic effect)
• to turn down contractility simply remove sympathetic stimulus

Question 13

Sympathetic branch on SA node

Answer 13

• speed up HR by spitting out neurotransmitter norepinephrine on B1 adrenergic receptor
• positive chronotrope effect

Question 14

parasympathetic branch on SA node

Answer 14

• slow down HR by spitting out neurotransmitter acetylcholine onto M2 muscarinic receptor
• negative chronotrophy effect

Question 15

why is stroke volume proportional to contraction force

Answer 15

the harder the ventricles contracts the more blood it will eject

Question 16

force of contraction is determine by

Answer 16

• 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)

Question 17

the frank-starling curve

Answer 17

• 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

Question 18

factors that increase EDV

Answer 18

• increased venous return and decreased heart rate (more filling time)

Question 19

SNS effect on myocyte contractility

Answer 19

1. Norepinephrine or epinephrine bind to beta-1 adrenergic receptors which activates GS
2. Adenylyl cylase is activated and converts ATP into cAMP which activates pKa
3. Resulting in phosphorylation of phospholamban that allows it to go away and removes inhibition off SERCA
4. 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
5. Phosphorylation voltage gated sodium Ca2+ which increases open time
6. More calcium is released from ECF to in which causes a greater release of calcium from SR which causes greater force of contractility

Question 20

SNS effect on myocyte contractility

Answer 20

1. Norepinephrine or epinephrine bind to beta-1 adrenergic receptors which activates GS
2. Adenylyl cylase is activated and converts ATP into cAMP which activates pKa
3. Resulting in phosphorylation of phospholamban that allows it to go away and removes inhibition off SERCA that is in the SR
4. 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
5. Phosphorylation voltage gated sodium Ca2+ which increases open time
6. More calcium is released from ECF to in which causes a greater release of calcium from SR which causes greater force of contractility