Download Summary of Factors that Regulate Cardiac Output

2 November 2011
Control of Cardiac Output
Properties of Blood Vessels
Announcements & Reminders
Test 2 on Monday
Photo-shoot Friday 1pm Biology Suite
1QQs & Moodle
1QQ # 24 for 8:30
1. What is the difference between a heart
sound and a heart murmur?
2. What type of cell has “funny” Na+
channels and what is unusual about
these channels?
3. In what situation might an ectopic
pacemaker actually be beneficial?
1QQ # 24 for 9:30
1. How would heart rate be affected by an
antagonist of beta adrenergic receptors?
Explain your answer.
2. What type of cell has T-type Ca++
channels and what is the purpose of
these channels in those cells?
3. Suppose your sinoatrial node pacemaker
cells ceased working. Would your heart
continue to beat, and if so, would it beat
faster or slower than before? Explain.
S1
So far, we’ve dealt with the factors that
control Cardiac Output by changing
heart rate.
3
CO = HR x SV
2
+ sympathetic
- parasympathetic
1
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat
S2
Figure 12.20
Stroke Volume
Animation
S3
Frank-Starling Law of the Heart
Does not depend on hormones or nerves
Assures that the heart adjusts its output based on VENOUS RETURN
Ventricular Function Curve
Ways to enhance
Venous Return:
1) muscle contractions
2) “respiratory pump”
3) venoconstriction
FS LoH = SV is proportional to EDV
↑VR→ ↑EDV → ↑SV
S4
Length-tension “curve” for Cardiac muscle
Fig. 09.21
High EDV
Low EDV
Overinflation of
ventricles leads to less
effective pumping
S5
Overinflation of
ventricles results in
reduction in stroke
volume
Treatments?
…..diuretics
S6
NE from Symp
postganglionics
& EPI from
Adrenal medulla
Contractility
Increase Ejection Fraction
Note: cardiac myofibers
NOT innervated by
parasympathetic division
S7
3 Effects of
Sympathetic
Stimulation
1: Increase rate of contraction
2: Increase peak tension
3: Decrease twitch duration
Why should the
contraction be shorter?
S8
Summary: Control of Stroke Volume
FS LoH
• End diastolic volume (preload)
• Contractility (strength of ventricular
contraction due to adrenergic stimulation)
• Pressure in arteries that must be
overcome = Afterload
Afterload is analogous to trying to pump more air into a tire that is already fully inflated
(heart contracting to overcome diastolic pressure.)
S9
High blood pressure increases the workload of the heart….. Cardiac
hypertrophy….increase chance of irregular conduction of AP through heart
Hypertrophic cardiomyopathy
S 10
Figure 12.20
Animation
S 11
Factors that control Cardiac Output by
changing heart rate and stroke volume.
Afterload (MAP)
CO = HR x SV
EDV (FSLoH)
+ sympathetic
- parasympathetic
contractility
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat
Summary of Factors that Regulate Cardiac Output
S 12
Fig. 12.28
Even persons with heart
transplants can adjust CO
in the absence of
innervation of heart.
Notice: No Parasymp
innervation of Cardiac
Myofibers, Parasymp
to Conducting Cells
only.
End of material for Test # 2
Begin material for Test # 3
S 13
Heart is pump that generates
pressure gradient.
Blood flows through vessels,
which have resistance.
Arterioles have greatest
resistance and create
“backpressure” in the arteries
and aorta.
Mean Arterial Pressure = diastolic +1/3(systolic – diastolic)
= 70 + 1/3(120-70)
= 70 + 17
= 87 mm Hg
S 14
Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance
MAP = CO x TPR
MAP = (HR x SV) x TPR