Download CV III Cardiac cycle

Cardiac cycle
CV III
Today – cardiovascular continued
Friday – 11am-noon CV IV
– noon -1pm Tutorial on membrane
potentials
Each phase is further subdivided to:
1. Systole
a) Isovolumetric ventricular contraction
b) Ventricle ejection
The rhythmic contraction & relaxation of the
heart
Cycle divided into 2 phases with respect to
ventricle action
1. Systole – ventricle contraction and blood
ejection
2. Diastole – ventricle relaxation and blood
filling
• Note
– Atria contract at the end of diastole, but most
blood (~80%) moves from the atria to the
ventricle prior to atrial contraction.
2. Diastole
a) Isovolumetric relaxation
b) Ventricle filling
1
Heart Valves
Permit blood flow in only one direction
When right atrial
pressure > right
ventricle pressure,
blood fills ventricle
If right ventricle
pressure>right atrial
pressure, AV valve
closes – no flow back
into atria
• For blood ejection
– Pressure in ventricles must > pressure in
aorta and pulmonary artery
• Pressure & volume changes during
cardiac cycle
• After contraction, as ventricles relax,
backpressure from the vessels closes the
aortic and pulmonary valves
2
ECG
Pressure and volume changes
110
in the left heart during a
contraction cycle.
Aortic
Pressure
mm Hg
Left Ventricle
Left Atria
End diastolic volume
0
130
End systolic volume
Volume
(ml)
AV valves open
65
D
S
D
Aortic & pulmonary
valves open
Pressure changes in the right heart during a contraction cycle.
Isovolumetric ventricle contraction
Isovolumetric ventricle relaxation
Pressure-volume curve
120
Left Ventricle Preesure (mm Hg)
E
D
C
Left Ventricle Volume (ml)
Diastolic filling
isovolumetric contraction
aortic valve opens
rapid ejection
slow ejection
aortic valve closes
isovolumic relaxation
Cardiac Output = Heart Rate X Stroke Volume
At rest:
CO = 72 beats / min X 0.07 L/beat =5.0 L/min
Stroke Volume = EDV – ESV
= 135 ml – 65 ml = 70 ml
B
A
0
A–B
B–C
C
C–D
D–E
E
E–A
Cardiac Output
200
i.e about ½ the volume remains in the left ventricle
3
Control of Heart Rate by Autonomic
Nervous system
Understanding cardiac output (CO)
• What controls HR?
• What controls SV?
• SNS ↑ HR via β adrenergic receptors
• PNS ↓ HR via muscarinic Ach receptors
• Normal rhythm of the SA node is 100
beats/min
• But, resting heart rate ~70 beats/min
¾PNS activity dominant at rest
Effect of epinephrine on pacemaker
potential
Effect of Ach on Pacemaker
potential
250 ms
Epi
Control
0
cont
-50
Ach 0.01 μm
4
Evidence for involvement of cAMP
• Conclusion
Probability of
Na+ channel
being open
– “funny” Na+ channel opening is regulated by
the level of cAMP (in addition to
hyperpolarization)
open probability
Increase this much with
cAMP
Membrane voltage
At this voltage
SA node cell
Na+
β
mAch
Adeylate
cyclase
Gs
Gi
“funny” Na+ channel
• Therefore, HR controlled by autonomic
regulation of “funny” Na+ channel
• As channel opening ↑, slope of pacemaker
potential ↑
ATP
cAMP
↑cAMP ↑ channel opening
↓cAMP ↓ channel opening
5
Other factors that can influence HR
1. Arterial pressure receptors
(Baroreceptors)
2. Atrial pressure receptors
• What controls Stroke Volume?
• SV = End Diastolic Volume – End Systolic Volume
EDV
Blood flowing back to heart
(venous return)
ESV
Effectiveness of heart pump
We’ll come back to these later in blood pressure regulation
EDV & SV:
Frank-Starling Mechansim
Stroke Volume (ml)
• Thus, any factor that ↑ venous return will
increase cardiac output
200
100
0
100
200
300
400
Ventricular end diastolic volume (ml)
6
Length-tension relationship of muscle
1
• Ventricle contracts more forcefully when it
is filled to a larger volume
2
3
– Length-tension relationship of cardiac muscle
4
Relative tension
• Why?
1.0
2
3
4
0.5
1
5
1.25
5
1.65
2
2.25
3.65
Sarcomere length (μm)
Contractility
• Therefore, filling ventricles with more
blood stretches the sarcomeres
– They produce more force
• Sympathetic nervous system control
– ↑ SNS activity → ↑ force production at any EDV
↑ SNS activity
Stroke Volume (ml)
• At rest, cardiac muscle sarcomere length
is less than optimal (about position 4 on
previous graph)
200
rest
100
0
100
200
300
400
Ventricular end diastolic volume (ml)
7
• How does SNS affect muscle contractility?
In myocytes cAMP/Protein kinase A:
L-type Ca++
Channel
(dihdryopyride receptor)
β
Adeylate
cyclase
Gs
1. Increase L-type Ca++ channel opening
2. Increase RyR opening
Both serve to increase cytoplasmic Ca++ and
increase contraction
Protein kinase A
3. Increase Ca++ pump activity
Serves to increase Ca++ clearance and
increase relaxation
cAMP
ATP
Ca++
Ca++ pump
SR
Ryanodine receptor
baroreceptors
End Diastolic Volume
(Frank-Starling Mech)
↑ Sympathetic activity
↑ Blood Epinephrine
↓ Parasympathetic activity
Heart Rate
Stroke volume
Relative Contributions of SNS and
PNS to Heart Function
PNS primarily to SA node, AV
node and Atria
→ Mainly effect HR, smaller
effect on atrial contractility
SNS to all areas of heart
→ effects HR and contractility
Cardiac Output
8