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Chapter IV Cardiovascular Physiology (2)
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ChapterIV Cardiovascular Physiology.2(2012)

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Page 1: ChapterIV Cardiovascular Physiology.2(2012)

Chapter IV

Cardiovascular Physiology (2)

Page 2: ChapterIV Cardiovascular Physiology.2(2012)

Section B

Pump function of the heart

Page 3: ChapterIV Cardiovascular Physiology.2(2012)

1. Concept : The cardiac events that occur from the

beginning of one heartbeat to the beginning of the next are called the

cardiac cycle. 60 (s/min) Duration (s/beat) = ——————— HR (beats/min)

Normal range of HR: 60-100 bpm (75bpm)

I. Cardiac Cycle

Page 4: ChapterIV Cardiovascular Physiology.2(2012)

2. The Cardiac Cycle

• If the heart rate is 75 bpm, each

cardiac cycle takes for 0.8s.

• The cardiac cycle is composed of d

iastole and systole.

Page 5: ChapterIV Cardiovascular Physiology.2(2012)

2. The Cardiac Cycle

0.1s

0.3s

0.5s

0.7s

Page 6: ChapterIV Cardiovascular Physiology.2(2012)

3.Mechanical events in cardiac cycle

a. Atrial systoleb. Isovolumic ventricular contractionc. Rapid ejection d. Reduced ejection e. Isovolumic ventricular relaxationf. Rapid filling g. Reduced filling

Ventricular ejection

Ventricular filling

Page 7: ChapterIV Cardiovascular Physiology.2(2012)

pressure volume valves blood flow

What happen in the heart during each cardiac cycle

Page 8: ChapterIV Cardiovascular Physiology.2(2012)

i. Before atrial systole , A-V valves are open and blood flows into the ventricles (about 75% of the blood).

ii. Atrial contraction causes an additional 25% of filling of the ventricles, so the atria simply function as primer pumps.

iii. During atrial systole, A-V valves open and semilunar valves close.

iv. The ventricular pressure is lower than pressures in the atrium and the aorta.

v. 0.1s

a. Atrial systole

Page 9: ChapterIV Cardiovascular Physiology.2(2012)
Page 10: ChapterIV Cardiovascular Physiology.2(2012)

b. Isovolumic (isovolumetric) ventricular contraction

Interval between the start of ventricular systole and the opening of the semilunar valves is called isovolumic ventricular contraction. i. The ventricular pressure is higher than atrial press

ure and lower than aortic pressure. ii. A-V valves are closed and semilunar valves are n

ot open. iii.The ventricular pressure rises rapidly but does no

t reach the peak. iv.The ventricular volume has no change. v. 0.05s

Page 11: ChapterIV Cardiovascular Physiology.2(2012)
Page 12: ChapterIV Cardiovascular Physiology.2(2012)

c. Rapid ejection phasei. The ventricular pressure is higher than aorti

c pressure and much higher than atrial pressure , and reaches the peak at the end

of rapid ejection.ii. A-V valves are closed and semilunar valves are open. iii. The blood is rapidly ejected from ventricle to aorta. iv. The volume of ventricle decreases rapidly .

Page 13: ChapterIV Cardiovascular Physiology.2(2012)
Page 14: ChapterIV Cardiovascular Physiology.2(2012)

d. Reduced ejection phase During the next two thirds of ejection

phase, about 30% of emptying occurs. This period is called reduced

ejection phase. Although the ventricular pressure is

slightly lower than the aortic pressure during this phase, the blood is still leaving the ventricles. Momentum keeps

the blood moving forward.

Page 15: ChapterIV Cardiovascular Physiology.2(2012)
Page 16: ChapterIV Cardiovascular Physiology.2(2012)

e. Isovolumic (isovolumetric) ventricular relaxation The period between closure of the semil

unar valves and opening of the A-V valves is called isovolumic ventricular

relaxation.

i. Ventricular pressure falls back to the diastolic pressure level at the end of reduced ejection phase, but it is till higher than atrial pressure.

ii.Seminlunar valves are closed and A- V valves are not yet open. iii. Blood remains in the atria. iv.A sharp fall in ventricular pressure without a change in ventricular volume. v. 0.06-0.08s

Page 17: ChapterIV Cardiovascular Physiology.2(2012)
Page 18: ChapterIV Cardiovascular Physiology.2(2012)

f. Rapid filling (inflow) phase

i. When ventricular pressure is lower than atrial pressure , A-V valves are open and blood flow rapidly into the

ventricle. ii. The ventricular volume increases rapidly, the ventricular pressure decreases .

Page 19: ChapterIV Cardiovascular Physiology.2(2012)
Page 20: ChapterIV Cardiovascular Physiology.2(2012)

g. Reduced filling (inflow) phase

• During the last 2/3 of filling

phase, only a small amount of blood

flows into the ventricles at a much

slower rate.

Page 21: ChapterIV Cardiovascular Physiology.2(2012)
Page 22: ChapterIV Cardiovascular Physiology.2(2012)

Ventricular state

Atrial pressure

Ventricular pressure

Aortic pressure

A-V valves

Semilunar valves

Ventricular volume

Blood flow

Duration

Atrial systole

Isovolumic contraction

Rapid ejection

Reduced ejection

Isovolumic relaxation

Rapid filling

Reduced filling

Begin to contract

Continue to

contract

Continue to

contract

Begin to relax

Continue to relax

Continue to relax

Relax ﹥ ﹤↑

﹤ ↑Sharply﹤﹤↑↑peak ﹥﹤ ↓ ﹤﹤↓Sharply ﹤﹥ ﹤﹥ ↓ ﹤

Open Close

CloseClose

Close

Close Open

CloseClose

Open Close

Open Close

-↓Sharply

-↑Sharply

-V→Aorta

(rapidly)

V→Aorta (slowly)

-Atrium→V (rapidly)

Atrium→V (slowly)

Atrium→V

0.1s

0.05s

0.1s

0.15s

0.06-0.08s

0.11s

0.22s

Open

↓↓

Page 23: ChapterIV Cardiovascular Physiology.2(2012)

4. Function of valves

To ensure a uni

directional flow o

f the blood.

Page 24: ChapterIV Cardiovascular Physiology.2(2012)

5. Heart sound

Concept: The sounds produced

by the heart during a cardiac cycle

are called heart sounds. Cause: closure of valves turbulence of blood vibration of ventricles and large vessels.

Page 25: ChapterIV Cardiovascular Physiology.2(2012)

A.First Heart sounda. Its tone is lower and duration is longer.

b. Its intensity reflects the contractility of the myocardia. The stronger the cardiac muscle contraction, the louder the first sound.

c. It marks the beginning of ventricular systole.

d. It is mainly caused by the closure of mitral and tricuspid valves just after the start of ventricular systole.

Page 26: ChapterIV Cardiovascular Physiology.2(2012)

B.Second heart sounda. Its tone is higher and duration is shorter.

b. Its intensity reflects the aortic or pulmonary pressure. The higher the arterial blood pressure, the louder the second sound.

c. It indicates the beginning of ventricular diastole.

d. It is mainly caused by the closure of aortic and pulmonary valves just after the end of ventricular systole.

Page 27: ChapterIV Cardiovascular Physiology.2(2012)

C. Third heart sound Third heart sound coincides with the period of rapid ventricular filling and is probably due to vibrations set up by inrush of blood.

D. Fourth heart sound (atrial heart sound)

Fourth heart sound may be due to ventricular filling and is rarely heard in normal adults.

Page 28: ChapterIV Cardiovascular Physiology.2(2012)

II. Cardiac Output

Page 29: ChapterIV Cardiovascular Physiology.2(2012)

• End-diastolic pressure (EDP) is the pressure in the ventricle at the

end of ventricular diastole. (5mmHg)

• End-diastolic volume (EDV) is the volume of blood in the ventricle that reaches a maximum at the end

of ventricular diastole. (135ml)

Page 30: ChapterIV Cardiovascular Physiology.2(2012)

65 130 195 220 275Period of filling Left ventricular volume (ml)

EDPEDV

Page 31: ChapterIV Cardiovascular Physiology.2(2012)

• End-systolic pressure (ESP) is the pressure in the ventricle at the end

of the ejection phase.

• End-systolic volume (ESV) is the volume of blood that remains in the ventricle at the end of the ejection

phase. (65ml)

Page 32: ChapterIV Cardiovascular Physiology.2(2012)

65 130 195 220 275Period of filling Left ventricular volume (ml)

ESPESV

Page 33: ChapterIV Cardiovascular Physiology.2(2012)

II. Cardiac Output1. Stroke volume and ejection fraction A. Stroke volume(SV) i. Concept : The volume of blood pumped out of

each ventricle each beat is called stroke volume. SV=EDV-ESV

ii. Normal range: 60-80ml(70ml)

Page 34: ChapterIV Cardiovascular Physiology.2(2012)

B. Ejection fraction(EF)

i. Concept : The ratio of SV to end–diastolic volume is called theejection fraction.

EF=(SV/EDV) ×100% ii. Normal range: 55%-65%

Page 35: ChapterIV Cardiovascular Physiology.2(2012)

2. Cardiac output and cardiac index

A. Cardiac output (CO) i. Concept : The quantity of blood pumped by

each ventricle per minute is called cardiac output. CO=SV×HR ii. Normal range: 4.5-6L/min

(5.0L/min)

Page 36: ChapterIV Cardiovascular Physiology.2(2012)

B. Cardiac index

Page 37: ChapterIV Cardiovascular Physiology.2(2012)

B. Cardiac index

i. Concept : Cardiac index is the cardiac output per square meter of

body surface area.

ii. Resting cardiac index Normal range: 3.0-3.5L/min/m2

iii. 10 years: 4 L/min/m2 80 years: 2.4 L/min/m2

Page 38: ChapterIV Cardiovascular Physiology.2(2012)

3. Cardiac Reserve

A. Concept: The ability of heart to increase

its cardiac output from the resting cardiac output is called cardiac reserve.

Page 39: ChapterIV Cardiovascular Physiology.2(2012)

B.Heart can increase output by different ways

① By increasing HR (60 ~ 180 beats /min) ② By increasing SV

a. By decreasing ESV b. By increasing EDV

Page 40: ChapterIV Cardiovascular Physiology.2(2012)

4.Regulation of Cardiac Output(Factors affecting cardiac output) A. Control of Heart Rate

40 ~ 180 beats/min HR↑→CO↑

> 180 beats/min cardiac cycle↓→ relaxation period↓↓ →

amount of ventricular filling(EDV)↓→ preload ↓ → SV↓→CO↓ < 40 beats/min cardiac cycle↑→ relaxation period↑→ a

mount of ventricular filling reaches its maximum, and HR is too low→CO↓

Page 41: ChapterIV Cardiovascular Physiology.2(2012)

c

The factors that affect the heart rate

Page 42: ChapterIV Cardiovascular Physiology.2(2012)

①Sympathetic nerve, Adr, NA, Ca2+, increased body temperature → HR↑

②Parasympathetic nerve, Ach, ischemia, toxin → HR ↓

The factors that affect the heart rate

Page 43: ChapterIV Cardiovascular Physiology.2(2012)

B. Control of stroke volume

★ Preload ★ Afterload

★ Contractility

i. Effects of preload

The preload of the ventricle is the ventricular

end-diastolic pressure (EDP).

The initial length of the ventricle is the

ventricular end-diastolic volume (EDV).

Page 44: ChapterIV Cardiovascular Physiology.2(2012)

Intrinsic regulation of heart pumping ——the Frank –Starling mechanism Within physiologic limit, the more the

heart fills with blood during diastole, the greater the force of contraction during systole and the greater the quantity of

blood pumped into the aorta.

Page 45: ChapterIV Cardiovascular Physiology.2(2012)

Stroke Volume

Preload (EDV)

Preload↑( EDV ↑ ) ↓

Initial length of myocardium↑

↓ Force of contraction↑

↓SV↑

↓ CO↑

It is also called heterometric autoregulation. Significance: to adjust the stroke volume subtly.

Page 46: ChapterIV Cardiovascular Physiology.2(2012)

Factors determining EDV

(1) Duration of ventricular diastole (2) Venous return

Page 47: ChapterIV Cardiovascular Physiology.2(2012)

ii. Changes in myocardial contractility (homometric autoregulation)

Definition: myocardium’s intrinsic ability to efficiently contract and empty the ventricle independent of preload & afterload

Significance: to adjust SV dramatically.

Page 48: ChapterIV Cardiovascular Physiology.2(2012)

Low

Stroke Volume

Preload (End-Diastolic Volume)

Increase inCardiacContractility

At a given EDV, SV increases With cardiac contractility

Normal

High

Page 49: ChapterIV Cardiovascular Physiology.2(2012)

Positive inotropic agents: sympathetic nerve, Adr, NA, and digitalis drug

Negative inotropic agents: vagus nerve, anoxia, acidosis, and Ach

Page 50: ChapterIV Cardiovascular Physiology.2(2012)

iii. Effects of afterload • The arterial pressure is the afterload.• Resistance to ventricular ejection

Page 51: ChapterIV Cardiovascular Physiology.2(2012)

Stroke volum↓

Ejection period↓ + ejection speed↓

Isovolumic contraction phase↑ + contraction speed↓

Afterload(arterial pressure)↑

Residual blood(ESV)↑

Preload(EDV)↑

Heterometric and homometric autoregulation

Restore the SV

Page 52: ChapterIV Cardiovascular Physiology.2(2012)
Page 53: ChapterIV Cardiovascular Physiology.2(2012)