1. CHAPTER 4
THE CARDIOVASCULAR SYSTEM

2. The busy and hard working heart!
Weight of the heart 300g
Work: 75/min, beats /day
35 million beats /year, 2.5 billion beats/life
70ml/beat, 7200 l/day
The work of the heart in one life is equivalent to lifting 30 tons to the Mount Everest
The busy and hard working heart!

3. MAIN FUNCTIONS OF THE CIRCULATORY SYSTEM
Transport and distribute essential substances to the tissues.
Remove metabolic byproducts.
Adjustment of oxygen and nutrient supply in different physiologic states.
Regulation of body temperature.
Humoral communication.

4. Systemic and Pulmonary Circulation

5. A. Heart location in the chest

6. B. Heart Chambers

7. B. Heart Chambers 1. Right Heart 2. Left Heart
a. receives venous blood from systemic circulation via superior and inferior vena cava into right atrium
b. pumps blood to pulmonary circulation and left ventricle from right ventricle
2. Left Heart
a. receives oxygenated blood from pulmonary circulation
b. pumps blood into systemic circulation

8. 1. Atrioventricular a. tricuspid--between RA and RV; three leaflets b
1. Atrioventricular a. tricuspid--between RA and RV; three leaflets b. mitral--between LA and LV; two leaflets
C. Heart Valves
2. Semilunar
a. pulmonic--three leaflets
b. aortic--three leaflets

10. Heart Valves Prevent backward regurgitation
Provide low resistance to forward flow

11. Cardiac Cycle
Diastole
Systole

12. Section 1 The Heart as a Pump
I. The Cardiac Cycle
Concept:
The period from the end of one heart contraction to the end of the next
Properties:
1) Diastole is longer than systole
2) The sequence of systole and diastole

14. 2 The Phases of the Cardiac Cycle
Period of isometric (isovolumetric
or isovolumic) contraction
Events: ventricular contraction
ventricular pressure rise 
atrioventricular valve close 
the ventricular pressure increase sharply
Period: 0.05 sec
Importance: enable the ventricular pressure to rise from 0 to the level of aortic pressure (after-load)

15. (2) Period of ejection
Events: ventricular contraction continuously
the ventricular pressure rise above the arterial pressure
semilumar valves open
 blood pours out of the ventricles

16. Rapid ejection period (0.10s, 60% of the stroke volume)
Reduced ejection period (0.15s, 40% of the stroke volume)

17. (3) Period of isometric (isovolumic) relaxation
Events:
ventricular muscle relax
the ventricular pressure fall
lower than the aortic pressure
aortic valve close
the ventricular pressure fall sharply

18. Period: s
Importance: Enable the ventricular pressure fall to the level near the atrial pressure

19. (4) Period of filling of the ventricles
Events: Ventricular muscle relax continuously
 the ventricular pressure is equal or lower than the atrial pressure
 atrioventricular valve open
 blood accumulated in the atria rushes into the ventricular chambers quickly from the atrium to the ventricle.

20. Period of rapid filling. (0.11s, amount of filling, 2/3)
Period of reduced filling (0.22s, little blood fills into the ventricle)

21. (5) Atrial systole
Significance, 30% of the filling
During high output states or in the failing heart,
the amount added by atrial contraction may be of major importance
in determining the final cardiac output.

23. LEFT VENTRICULAR PRESSURE/VOLUME P/V LOOP
120 F E D 80
LEFT VENTRICULAR PRESSURE (mmHg) 40 B A C 50
100
150
LEFT VENTRICULAR VOLUME (ml)

25. 2） Pressure changes in the atria, the a, c, and v waves.
a wave, the atrial contraction
c wave, bulging of the A-V valves when the ventricles begin to contract

26. v wave, at the end of ventricle contraction, caused by the accumulated blood in the atria while the A-V valves are closed

27. Heart Sounds
The sounds heard over the cardiac region produced by the functioning of the heart.

28. Heart Sounds S1- first sound
Atrioventricular valves and surrounding fluid vibrations as valves close at beginning of ventricular systole

29. S2- second sound Results from closure of aortic and pulmonary semilunar valves at beginning of ventricular diastole
S3- third sound is produced by vibrations of the ventricular walls when suddenly distended by the rush of blood from the atria

30. :>O :>D S1 CARDIAC CYCLE S2 Aortic opens Aortic closes Mitral
Atrial Systole
Rapid Ejection
Reduced Ejection
Isovolumic Relax.
Rapid Ventricular
Filling
Reduced Ventricular
Filling
Isovolumic contract.
Atrial Systole
Aortic
opens
:>O
Aortic
closes
Mitral
opens
Mitral
Closes S1
CARDIAC CYCLE
:>D S2

31. II Cardiac Output
Stroke Volume – The volume pumped by the heart with each beat,
= end diastole volume – end systole volume, about 70 ml
2. Ejection Fraction – Stroke volume accounts for the percentage of the end diastolic volume,
= stroke volume / end diastole volume X 100%, normal range, 55-65%

32. 3. Minute Volume, or Cardiac Output – the volume of the blood pumped by one ventricle,
= stroke volume X heart rate.
It varies with sex, age, and exercise
4. Cardiac Index, the cardiac output per square meter of body surface area.
the normalized data for different size individuals,
the normal range is about 3.0 – 3.5 L/min/m2

33. Determinants of Cardiac Output (CO)
Contractility
Stroke Volume
Preload
Afterload
Cardiac output is a function of the interplay of multiple physiologic parameters.
Stroke volume is influenced in a predictable order:
1. Preload first influences contractility.
2. The combined effect of preload and contractility then influences the afterload response.
3. Only after the stroke volume is established does the heart rate respond to adjust the final cardiac output.
Heart Rate
Cardiac Output

34. Definitions
Preload
amount of stretch on the ventricular myocardium prior to contraction
Afterload
the arterial pressure (or some other measure of the force) that a ventricle must overcome while it contracts during ejection
impedance to ventricular ejection
Preload can be simply stated as the volume stretching the ventricular muscle prior to ejection. Afterload is the resistance to flow from the circulatory system.

35. Definitions Contractility
myocardium’s intrinsic ability to efficiently contract and empty the ventricle
(independent of preload & afterload)
Contractility has historically been the most difficult parameter to measure in the clinical setting. It clearly is the most important parameter that is affected by cardiac pathology and cardioactive medications.

36. Determinants of Cardiac Output
1. Preload

37. Determinants of Cardiac Output- Preload
Preload = ventricular filling or volume

38. Determinants of Cardiac Output - Preload
Preload approximated by measuring:
1. Central venous pressure (CVP) = right atrial pressure.
2. Pulmonary capillary diastolic wedge pressure (PCWP) = LVEDP
Parameters:
1. CVP 3mm Hg (normal range 1 - 5)
2. PCWP 9mm Hg (normal range )

39. the Frank - Starling mechanism
Left ventricle (LV) function curve, or Frank - Starling curve (1914):
Normal range of the LVEDP, 5-6 mmHg
Optimal initial preload, mmHg (Sarcomere, 2.0 – 2.2 µm
When the LVEDP > 20 mmHg, LV work is maintained at almost the same level, does not change with the increase of LVEDP
Mechanism
Concept of heterometric regulation

40. Factors determining the preload (LVEDP)
Period of the ventricle diastole (filling) – heart rate
Speed of the venous return (difference between the venous pressure and atrial pressure)
Importance of the heterometeric regulation
In general, heterometric regulation plays only a short-time role, such as during the body posture change, artery pressure increase, and unbalance of ventricular outputs.
In other conditions, such as exercise, cardiac output is mainly regulated by homometric regulation.

41. Determinants of Cardiac Output - Afterload

42. Short time change of the arterial pressure
Transit arterial pressure rise
isovolumetric contraction phase become longer
period of ejection shorter
stroke volume less
more blood left in the ventricle left
LVEDP increase
through heterometeric regulation
stroke volume return to normal in next beat.

43. Long time high arterial pressure
through neural and humoral regulation
the stroke volume is maintained at normal level
pathogenesis of the cardiovascular system

44. Determinants of Cardiac Output - Contractility
Contractility (neural and humoral regulation)
Sympathetic nerve (norepinephrine) or the epinephrine and norepinephrine (adrenal gland) enhance the strength and the velocity of the cardiac contraction.
The change of myocardial property is independent of the preload.
We call it the contractility.
Importance: exert a long – time influence on the cardiac output.

45. Action of Sympathetic Stimulation
Sympathetic nerve stimulation increases cardiac contractility.
At rest the heart is under sympathetic tone.
Noradrenaline enhances calcium entry into cardiac cells.
Parasympathetic stimulation has little affect on contractility due to the innervation pattern of the heart.

46. PRESSURE/VOLUME RELATIONSHIPS UNDER DIFFERENT CONDITIONS
PRELOAD
AFTERLOAD
CONTRACTILITY

47. Determinants of Cardiac Output - The heart rate
Normal range of the heart rate 60 – 100 beats/min
Within physiological limit?, the higher the heart rate, the more blood that the heart pump.

48. 1, at rest (without any regulation)
2, during exercise (with humoral and neural regulation)

49. IV Cardiac Output Reserve
The maximal cardiac output subtracts the normal value.
It reflects the ability of the heart to adapt the change of environment (internal or external)

50. Normal range
End diastole volume 145ml – end systole volume 75ml = stroke volume 70 ml
Heart rate 75 beats/min
Normal cardiac output = 70 X 75 = 5.25 L /min
Maximal level
Maximal diastole volume 160 ml (reserve 15ml);
Maximal systole residual volume 20 ml (reserve 55ml)
Maximal heart rate (without the stroke volume decrease )180 beats/min (reserve 105 beats/min)
Maximal cardiac output (160 – 20) X 180 = 25.2 L/min