2 november 2011 control of cardiac output properties of blood vessels announcements & reminders...

2 November 2011Control of Cardiac Output

Properties of Blood Vessels

Announcements & Reminders

Test 2 on MondayPhoto-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.

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

Figure 12.20

Stroke Volume

Animation

S 2

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

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↑VR→ ↑EDV → ↑SV

Fig. 09.21

Low EDV

High EDV

Length-tension “curve” for Cardiac muscle

Overinflation of ventricles leads to less effective pumping

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Overinflation of ventricles results in reduction in stroke volume

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Treatments?…..diuretics

Contractility

NE from Symp postganglionics & EPI from Adrenal medulla

Note: cardiac myofibers NOT innervated by parasympathetic division

Increase Ejection Fraction

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3 Effects of SympatheticStimulation

1: Increase rate of contraction2: Increase peak tension3: Decrease twitch duration

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Why should the contraction be shorter?

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

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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

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Hypertrophic cardiomyopathy

Figure 12.20

Animation

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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)

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.

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End of material for Test # 2

Begin material for Test # 3

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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

MAP = CO x TPR

Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance

MAP = (HR x SV) x TPR

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