1. Cardio-vascular system

2. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

3. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

4. Overview Roles: - Pumps blood throughout the body vasculature
- Endocrine function
Components
- Heart
- Blood vessels
- Blood

5. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

6. Circulation Parallel flow of blood to various organs 
-- allows for fully oxygenated blood to reach each organ
-- allows for independent regulation
Exception: portal circulation (1 capillary bed to another)
-- hypothalamus-pituitary gland portal system
-- hepatic portal system
Figure 13.3

7. Applications
What is the consequence of the blood clot (a thrombus) located in the right saphenous vein becoming loose ( an embolus)?
What is the consequence of the blood clot (a thrombus) located in the right atrium becoming loose ( an embolus)?
What is the consequence of the blood clot (a thrombus) located in the left atrium becoming loose ( an embolus)?
What is the consequence of the blood clot (a thrombus) located in the left saphenous vein becoming loose ( an embolus)?
What is the consequence of the blood clot (a thrombus) located in the right femoral artery becoming loose ( an embolus)?

8. The heart Located in mediastinum Surrounded by the pericardium
- outer fibrous pericardium
- inner serous pericardium:
- parietal pericardium
- visceral pericardium
- in between: pericardial
cavity  small amount of pericardial fluid (prevent friction)
Application: cardiac tamponade

9. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

10. The heart: review
Figure 13.1

11. Blood flow in the heart
Figure 13.6

12. Coronary circulation What is angina? What is a myocardial infarction?
Figure 13.4

13. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

14. Conduction system of the heart
Two types of fibers:
- contractile fibers (cardiac muscle fibers)
- self-depolarizing fibers in the sino-atrial (S/A) node (pace-maker fibers  autorhythmicity)
Figure 13.10

15. Electrocardiogram
Recording of the electrical activity of the heart by electrodes applied on the skin
ECG wave patterns vary with the location of the electrodes

16. ECG P wave: S/A node is firing
P-Q interval: time it takes for the electrical impulse to travel from the S/A node to the atrio/ventricular (A/V) node
QRS wave: the electrical impulses spread through the bundle of His, bundle branches and Purkinje fibers in the ventricles
T wave: ventricular repolarization
Q-T interval: corresponds to ventricular contraction (=systole)
T-Q interval: ventricular diastole
R-R interval: time between heartbeats

17. Other properties of the conduction system
S/A node: beats/min (sinus rhythm = normal rhythm)
If S/A node is non functional: the A/V node takes over  beats/min
If both S/A and A/V nodes are shot, ventricular electrical activity takes over  > 40 beats/min

18. Applications What is atrial fibrillation?
“ “ ventricular fibrillation?
What is the difference between tetanus and fibrillation?
Atrial and ventricular fibrillations: consequences from each type of abnormal rhythms

19. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

20. Cardiac cycle
Figure 13.18

21. Cardiac cycle
Systole: contraction of heart chambers but mostly ventricles
Diastole: ventricular relaxation (atria have a minimal effects)
Ventricular filling: during diastole, P wave
Ventricular contraction: at first, semi-lunar valves are closed  blood cannot flow out and pressure increase in ventricle  isovolumetric contraction
Ventricular ejection: The pressure against the valves is strong enough to open them  the blood flows out
When the ventricles stop contracting, the pressure falls  isovolumetric relaxation  pressure falls even more semi-lunar valves close and A/V valves open

22. Cardiac cycle
End-diastolic volume = EDV = volume of blood present at the end of diastole in the ventricles
End-systolic volume = ESV = volume of blood present at the end of systole
Stroke volume = SV: amount of blood ejected by the ventricles = EDV-ESV
Ejection fraction = EF = SV/EDV
Note: EF gives a measure of cardiac muscle efficiency

23. What can cause a low ejection fraction?
What are the consequences of a low ejection fraction?

24. Outline 1- Overview 2- Path of blood through the heart and vasculature
3- Anatomy of the heart
4- Electrical activity of the heart
5- The cardiac cycle
6- Cardiac output and its control

25. Cardiac output = CO Cardiac output = volume of blood pumped out by the
heart per minute
CO = SV x HR (CO must adapt to body needs)
Control of CO:
** control of SV:
- Intrinsic control
- Extrinsic control
** control of HR:
-- Autonomic input
-- Hormonal control

26. Control of the stroke volume
SV: a function of
1. Ventricular contractility: a function ventricular health and stretch
2. EDV: ventricular refill is a function of the blood pressure in the central veins (central venous pressure)  end- diastolic pressure = preload
3. ESV: a function of afterload = pressure against blood flow out of the heart – determined by aortic blood pressure

27. Cardiac output = CO Cardiac output = volume of blood pumped out by the
heart per minute
CO = SV x HR (CO must adapt to body needs)
Control of CO:
** control of SV:
- Intrinsic control
- Extrinsic control
** control of HR:
-- Autonomic input
-- Hormonal control

28. Control of the stroke volume
Intrinsic control
- Starling law of the heart: The heart automatically adjust its output to match its input
- Property of the cardiac muscle: the more it is stretched, the stronger it contracts (up to a limit)
(in other word, what ever comes in, goes out)
What would happen if this law is not respected?

29. Control of the stroke volume
Extrinsic control
Neural control:
-- the sympathetic NS has axonal extension over the entire ventricles  β receptors binding to NE  stronger contraction
-- no parasympathetic axonal extension  no direct action on ventricular wall
Hormonal control
-- Epinephrine from adrenal medulla has the same effect as NE from sympathetic nerve endings  increased force of contraction

30. Cardiac output = CO Cardiac output = volume of blood pumped out by the
heart per minute
CO = SV x HR (CO must adapt to body needs)
Control of CO:
** control of SV:
- Intrinsic control
- Extrinsic control
** control of HR:
-- Autonomic input
-- Hormonal control

31. Control of heart rate (HR)
S/A node fires automatically /times per minute. Its activity is modulated by the following factors:
Extrinsic control only
-- Autonomic NS
* action on the S/A node mainly
* NE increases HR
* Ach decreases HR
-- Hormonal control
* Epinephrine from the adrenal gland increases HR
-- drugs and ions (K+, Ca++, digoxin and others)

32. Factors influencing HR
The cardiac center in the medulla oblongata controls the HR (or S/A node).
It receives information from the body through various receptors
Aortic and carotid bodies monitor blood O2 and send the info. to the cardiac center (↓O2↑HR)
CO2 and pH receptors in the hypothalamus also send info. to the cardiac center (under normal conditions, they have more influence on HR then O2 receptors (↑CO2 or ↓pH ↑HR)
Body temperature (↑Temp ↑HR)

33. Applications
Jimmy has an abnormal HR at 144b/min. He has been admitted and is on medication so his HR reverts to a sinus rhythm (when the S/A node is in control). The next day, his HR is unchanged.
Roger also has an abnormal HR at 131b/min. He has been admitted and is on medication so his HR reverts to a sinus rhythm (when the S/A node is in control). The next day, his HR is unchanged.
Marian has been admitted during the night. She has a sinus rhythm (driven by S/A node) at 125 b/min.
Carlie has an abnormal HR at 55 b/min. He has been admitted and is on medication so his HR reverts to a sinus rhythm (when the S/A node is in control). The next day, his HR is unchanged.
Which of these 4 patients would you go see first? Why?
Hint: how is the HR regulated?

34. Applications
Jimmy has been on medication for an abnormal HR at 144 b/min. On a cardiac monitor, you see his heart rate jumping to 190 b/min. Which consequences do you expect?