2 november 2011 control of cardiac output properties of blood vessels announcements & reminders...
TRANSCRIPT
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2 November 2011Control of Cardiac Output
Properties of Blood Vessels
Announcements & Reminders
Test 2 on MondayPhoto-shoot Friday 1pm Biology Suite
1QQs & Moodle
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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?
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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.
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CO = HR x SV
5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat
S 1
So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate.
+ sympathetic- parasympathetic
2
1
3
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Frank-Starling Law of the Heart
FS LoH = SV is proportional to EDV
Ventricular Function Curve
Does not depend on hormones or nerves
Assures that the heart adjusts its output based on VENOUS RETURN
Ways to enhance Venous Return:1) muscle contractions2) “respiratory pump”3) venoconstriction
S 3
↑VR→ ↑EDV → ↑SV
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Fig. 09.21
Low EDV
High EDV
Length-tension “curve” for Cardiac muscle
Overinflation of ventricles leads to less effective pumping
S 4
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Overinflation of ventricles results in reduction in stroke volume
S 5
Treatments?…..diuretics
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Contractility
NE from Symp postganglionics & EPI from Adrenal medulla
Note: cardiac myofibers NOT innervated by parasympathetic division
Increase Ejection Fraction
S 6
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3 Effects of SympatheticStimulation
1: Increase rate of contraction2: Increase peak tension3: Decrease twitch duration
S 7
Why should the contraction be shorter?
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Summary: Control of Stroke Volume
• End diastolic volume (preload)
• Contractility (strength of ventricular contraction due to adrenergic stimulation)
• Pressure in arteries that must be overcome = Afterload
FS LoH
S 8
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Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.)
High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart
S 9
Hypertrophic cardiomyopathy
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CO = HR x SV
5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat
S 11 Factors that control Cardiac Output by changing heart rate and stroke volume.
+ sympathetic- parasympathetic
EDV (FSLoH)
contractility
Afterload (MAP)
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Fig. 12.28Even persons with heart transplants can adjust CO in the absence of innervation of heart.
Summary of Factors that Regulate Cardiac Output
Notice: No Parasymp innervation of Cardiac Myofibers, Parasymp to Conducting Cells only.
S 12
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End of material for Test # 2
Begin material for Test # 3
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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
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MAP = CO x TPR
Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance
MAP = (HR x SV) x TPR
S 14