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Notes de cours

Cardiovascular System - 73 pages

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Complete set of notes for this element in the Bristol A100 Pre-clinical course. This is everything you need to know to achieve 90% marks. It is presented in a simple question, simple answer layout. If you have any questions or if anything doesn’t make sense, email me at mh14782@my.bristol.ac.uk. Special thanks to all my lecturers who made many of the diagrams.

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Publié le
18 mai 2016
Nombre de pages
73
Écrit en
2014/2015
Type
Notes de cours
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Table of Contents
Cardiovascular Physiology ................................................................................................. 1
Lecture 2 – Components & Haemodynamics ................................................................................ 1
Lecture 3 – Control of Heart Rate & Electrocardiogram ................................................................ 4
Lecture 4 – Arrhythmia 1 ............................................................................................................... 9
Lecture 5 – Arrhythmias 2 ........................................................................................................... 10
Lecture 6: Pump Function ............................................................................................................ 12
Lecture 7: Tissue Blood Flow ....................................................................................................... 17
Lecture 8: Antianginal Drugs ....................................................................................................... 20
Lecture 9: Nitric Oxide ................................................................................................................. 23
Lecture 10: Tissue Fluid and Oedema .......................................................................................... 25
Lectures 11 & 12: Cardiac Embryology ........................................................................................ 29
Lecture 13: Regulation of Arterial Pressure ................................................................................. 35
Lecture 14 – Hypertension .......................................................................................................... 38
Lecture 15: Antihypertensive Drugs ............................................................................................ 42
Lecture 16: Angina ....................................................................................................................... 43
Lectures 17 & 27 - Antiarrhythmics 1&2 ..................................................................................... 45
Lecture 18: Blood Clotting (Haemostasis) ................................................................................... 49
Lecture 19: Thrombosis ............................................................................................................... 54
Lecture 20: Anticoagulants 1 ....................................................................................................... 56
Lectures 21 & 23: Atheroma ........................................................................................................ 57
Lecture 22: Anticoagulants 2 ....................................................................................................... 59
Lectures 24 & 25: Lipoproteins and the Cell Biology of Atherosclerosis ..................................... 61
Lecture 26: Integrated Responses ............................................................................................... 63
Lecture 28: Heart Failure ............................................................................................................. 67
Lecture 29: Drugs for Heart Failure ............................................................................................. 70




Cardiovascular Physiology
Lecture 2 – Components & Haemodynamics

• What are the functions of the cardiovascular system?
1. Transport of nutrients
2. Removal of waste products
3. Distribution of oxygen, electrolytes and nutrients
4. Tissue fluid production
5. Provides the infrastructure for the immune system
6. Temperature regulation (red when hot, pale when cold)
7. Male reproduction à erections
• Why is the top of the heart called the base? Because it’s widest here
• What are the 3 layers of the heart? Endocardium, myocardium,
epicardium
• How else can we call the atrioventricular valves? Parachute valves, due
to their appearance
• What is the annulus fibrosis? A fibrous ring around the heart that electrically insulates the atria
from the ventricles (See later)

,• What is the % of oxygen in the blood of the right atrium? 70%
• What is the % of oxygen in the blood of the left atrium? 99%
• What is the function of the atria? To pump venous blood from circulation to the ventricles
• If the atrial volume is less than the ventricular volume, how do the ventricles get filled completely
before they contract? During atrial systole, the ventricles are still relaxing and filling. The ventricles
are filled by:
o The atria contracting and pushing blood into the ventricles (active 30%)
o The relaxing of the ventricles which ‘sucks’ blood into it before it contracts (passive 70%)
• Why does the right ventricle produce a lower pressure? Because higher pressure would damage
the lungs
• What are the heart valves anchored into? The annulus fibrosis
• What do the valves do? Prevent backflow
• What is valve regurgitation? When the valves don’t close properly and so blood flows back
• What are the ‘lub dub’ sounds called and what are they caused by?
1. Lub = first heart sound, S1 = closure of the atrioventricular valves
2. Dub = second heart sound, S2 = closure of the semi-lunar valves
• What sorts of other noises can you hear in the S1? Murmurs,
gallop rhythms, rubs and click
• What sorts of other noises can you hear in the S2? During
inspiration, the S2 sound can split into 2 distinct sounds
• Where on the chest do you auscultate for the sounds of each
valve? See diagram
• What is endocarditis? A bacterial valve infection
• What are the risk factors for developing endocarditis?
1. Poor dental hygiene
2. Dental procedures
3. Valve defects and prosthetic valves
4. Intravenous drug use
• What is the stroke volume? Volume of blood ejected per
beat
• What is the cardiac output? The volume ejected by the
heart per minute
• What is heart rate? The number of beats per minute
• How are the three above related? CO = SV x HR
• Describe the different layers in blood vessels, saying what
is found in each layer
o Tunica intima = endothelium and elastic lamina
o Tunica media = smooth muscle and elastic lamina
o Tunica adventitia = connective tissue
• What percentage of total blood volume is found in the following regions of the CV system?




• Describe the relative pressures and resistances of the systemic and pulmonary circulation.
Systemic Circulation Pulmonary Circulation
Pressure Higher Lower

, Resistance Higher Lower
• What equation can be used to explain the above differences? The modified Ohm’s law in physics
can be applied to haemodynamics. V = IR can be modified to ΔP = QR, where ΔP is the pressure, Q is
the blood flow and R is the resistance. In the circulation, Q has to stay constant (unless patient is
bleeding), so if the pressure in the pulmonary circulation is lower (to not damage the lungs), then
the resistance must be lower too!
• Describe the different types of vessels in the body?
Vessel Description Example
Large elastic artery - Large amount of elastin and collagen in the tunica Aorta and
media pulmonary
- uses the Windkessel effect to maintain blood arteries
pressure during diastole (see below)
Muscular artery - Distributing arteries because it distributes blood to Brachial,
various parts of the body radial,
- has a lot of smooth muscle in the tunica intima to femoral
prevent kinking of the vessel at joints arteries
Arterioles - Resistance vessels -
- Has smooth muscle in tunica intima that can cause
vasoconstriction when contracts (mainly under
sympathetic control from α2 receptors)
Capillaries - Consists of an endothelium on a basal lamina (so its -
one cell thick)
- exchange vessels
- filtration through gaps in capillary walls forms tissue
fluid
Venules - Drains blood from capillary network -
Veins - Capacitance vessels (as 70% of blood is in here) -
- Has valves to prevent backflow
- Has smooth muscle that can contract, causing
venoconstriction, which raises CVP (See below)
• What is the Windkessel effect? It’s the effect where elastic arteries stretch to a larger diameter
during systole and then recoil and eject the ‘extra’ blood during diastole. It keeps the systemic blood
pressure up during diastole.




• What is compliance? The ability of a hollow organ
such as a vessel to distend and increase volume, which increases the pressure on the walls.
• What is central venous pressure, CVP? It’s the pressure of the blood returning to the heart and is
hence also called the filling pressure/preload
• What is mean arterial pressure? It’s the mean pressure in the arteries of the body
• What’s total peripheral resistance? It’s the total resistance that the heart has to work against when
it’s pumping blood. It’s largely made up of the resistance brought about by the arterioles.
• How is cardiac output related to mean arterial pressure and total peripheral resistance? If you
related the equation ΔP = QR to the entire system, ΔP can be thought of as MAP, Q can be thought
of as cardiac output and R can be though of as TPR, which leads to the equation MAP = TPR x CO,
which is more commonly written as CO = MAP/TPR

, • What is the main factor in arterioles that determines resistance? The diameter of the vessel
• What equation describes how resistance varies with radius? Poiseulle’s law, which states that R =
8vL/πr4, where L is the length of the vessel, v is the viscosity of the fluid and R is the resistance. We
need to know that R α 1/r4. So if the radius shrinks by half, then the resistance will increase by (24 =
16) a factor of 16!
• How can blood flow to one organ be altered without much effect on flow in another organ?
Because flow through a particular bed depends on the individual resistances, which can be altered
independently.
• What is the equation to calculate the total peripheral resistances given the resistances in all the
particular individual resistances of the beds? Because in real life the blood flows in parallel, not in
series, the equation is:
• What does this equation mean in terms
of how the total peripheral resistance compares to any individual resistance (RT compared to R1 or
R2 etc.)? It means that the TPR is less than any of the
individual resistances.
• What are the two types of flow patterns through
vessels? Turbulent and laminar
• How does pressure and velocity of the blood
compare to the total cross-sectional area of the type of
vessel?
o As cross sectional area
increases (arteries à
capillaries), the pressure drops, as does
the flow rate
o As it increases again (capillaries à
veins), the flow rate increase again
but the pressure stays low

Lecture 3 – Control of Heart Rate &
Electrocardiogram

• How does holding your breath affect your heart rate?
Decreases it
• What is the Valsalva maneuver? When you try to exhale through
your nose whilst holding your nose/not letting air out (i.e.
straining)
• How does the Valsalva maneuver affect your heart rate? At first it
decreases it because your aortic pressure spikes as you strain and increase intrathoracic pressure.
Towards the end of the maneuver your heart rate increases to compensate for the drop in aortic
pressure
• What cells in the heart generate the action potentials? The cells in the SAN and AVN. They are
modified myocytes with few contractile filaments, and so do not contract.
• What cells in the heart conduct the action potentials? Again, modified myocytes that run down the
septum and up the ventricles.
• What do we mean by ‘the annulus fibrosis electrically insulates the atria from the ventricles’? It
stops conduction getting down the bundle branches in the septum without the AVN firing.
• What 2 structures in the heart are capable of generating their own action potentials? SAN and
AVN, because they have ‘excitable’ cells
• What is the physiological pacemaker? SAN
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