Cardio-vascular system

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

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

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

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

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

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)?

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

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

The heart: review Figure 13.1

Blood flow in the heart Figure 13.6

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

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

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

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

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

Other properties of the conduction system S/A node: 60-100 beats/min (sinus rhythm = normal rhythm) If S/A node is non functional: the A/V node takes over  40-60 beats/min If both S/A and A/V nodes are shot, ventricular electrical activity takes over  > 40 beats/min

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

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

Cardiac cycle Figure 13.18

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

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

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

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

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

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

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

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?

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

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

Control of heart rate (HR) S/A node fires automatically 60-100/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)

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)

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?

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?