Session 2 Flashcards
(90 cards)
1
Q
Why do we need a cardiovascular system?
A
- Getting the oxygens and nutrients close to the cells as the diffusion distance is too big for simple diffusion.
- Removal of waste and carbon dioxide from the blood and into lungs to be removed.
2
Q
What are capillaries?
A
Composed of a single layer of endothelial cells surrounded by basal lamina. Also have gaps between endothelial cells to allow small water soluble molecules to enter.
3
Q
Why does the heart need its own blood supply?
A
- LV is filled with oxygenated blood but it’s too thick for the oxygen to diffuse
- Has a blood supply of coronary arteries.
4
Q
What are the main coronary arteries? (LABEL ON DIAGRAM)
A
- Left anterior descending artery
- Circumflex artery
- Left main artery
- Right coronary artery
- Right marginal artery
5
Q
What are the problems with coronary arteries?
A
- End arteries: do not anastomose so connections are not made
- Prone to atheromas and possibly eventual blockages and therefore MIs.
6
Q
What are the layers of the pericardium?
A
- Endocardium
Protection to valves and heart chambers - Myocardium
Cardiac muscle - Visceral layer
Inner serous layer that secretes small amounts of fluid - Parietal layer
Outer serous layer - Fibrous layer
Anchors heart to the surrounding walls and prevents overfilling
7
Q
What are the pressures in systemic and pulmonary circulations?
A
S: 120/80 (high)
P: 25/10 (low)
8
Q
What is coordinated contraction?
A
Both sides of the heart contract at the same time and pump the same volume of blood to maintain stroke volume.
9
Q
What is systole?
A
Contraction and ejection of blood from ventricles
10
Q
What is diastole?
A
Relaxation and filling of ventricles
11
Q
How much blood does the heart pump per minute at a heart rate of 70 bpm?
A
4.9 L/min (approx. volume of blood in a 70kg average man)
12
Q
What is the heart muscle?
A
- Specialised form of muscle
- Have gap junctions for communications (intercalated discs)
- Contract in response to an action potential triggered by spread of an excitation wave from cell to cell
- Action potential lasts for the whole duration of a whole contraction, aka. 280 ms.
- Figure of 8 arrangement
13
Q
What are the four heart valves?
A
- Mitral valve (right side, blood in)
- Tricuspid valve (left side, blood in)
- Pulmonary valve (right side, blood out)
- Aortic valve (left side, blood out)
14
Q
How do valves work?
A
- Open/close depending on the pressure difference
- Valve cusps open to allow blood to flow in and close to seal and prevent blood back flow
- Cusps of mitral + tricuspid connected to PAPILLARY MUSCLE AND CHORDAE TENDINAE to prevent inversion of valves
15
Q
When are valves open?
A
Mitral + tricuspid open = aortic and pulmonary closed and vice versa
16
Q
What is the cardiac conduction system?
A
- Action potential generated by pacemaker cells in the SAN
- Activity spreads over atria = atrial systole
- Wave reaches AVN and pauses for 120ms to allow atria to finish contraction
- Excitation from AVN spreads down septum
- Spreads to ventricular myocardium from endocardial to epicardial surface
- Ventricular contraction from the apex up
- Blood forced through outflow valves
17
Q
What is the Wiggers diagram?
A
A diagram showing all the changes in volume and pressure during cardiac contraction
18
Q
What is atrial contraction?
A
Phase 1.
- Atrial pressure rises (A wave)
- P wave in ECG - atrial depolarisation
- Atrial contraction = 10% of ventricular filling (90% passive)
- Mitral/tricuspid valves open
- Ventricles reach EDV = 120ml
19
Q
What is isovolumetric contraction?
A
Phase 2.
- Mitral valve closure: IV pressure > Atrial pressure
- Ventricle contracts: rise in pressure
- C wave due to mitral valve closure
- No change in ventricular volume as all valves closed and blood can’t move
- QRS - ventricular depolarisation
- Closure of valves = S1 (FIRST HEART SOUND)
20
Q
What is rapid ejection?
A
Phase 3.
- IV pressure > Aortic pressure: aortic valve opens
- Atrial base pulled downward as ventricle contracts (X-DESCENT)
- Rapid drop in ventricular volume = blood into aorta
- Mitral + tricuspid valves closed
21
Q
What is reduced ejection?
A
Phase 4.
- Decline in ventricular pressure, rate of ejection falls
- Atrial pressure rises due to venous return from lungs (V wave)
- Ventricular depolarisation - T wave
- Aortic/pulmonary valves open
22
Q
What is isovolumetric relaxation?
A
Phase 5.
- Aortic pressure > IV pressure = back flow of blood, makes aortic valve close
- Valve closure = dicrotic notch
- Decline in ventricular pressure but volume constant as all valves closed
- END SYSTOLIC VOLUME (70-80ml)
(EDV - ESV = stroke volume) - Closure of aortic/pulmonary valves - S2 heart sound
23
Q
What is rapid filling?
A
Phase 6.
- Fall in atrial pressure after mitral valve opens = Y descent
- Atrial pressure > IV pressure = mitral valve opening, ventricular filling begins
- Normally silent but sometimes S3 sound present - normal in children, may be pathology in adults
- Mitral/tricuspid valves open
24
Q
What is reduced filling?
A
Phase 7.
- Diastasis: rate of filling slows down
- Ventricle reaches inherent relaxed volume
- More filling due to venous pressure
- 90% full ventricles, extra 10% from atrial contraction
- Mitral/tricuspid valves open
25
What is valve regurgitation?
Valve doesn't close all the way and there is back leakage of blood into ventricle
26
What is valve stenosis?
Valve doesn't open enough and there is obstruction to blood flow
27
What is aortic valve stenosis?
- Less blood gets through = increased LV pressure and LV hypertrophy
- Left sided heart failure; not enough blood around body = angina and syncope
- Stress = microangiopathic haemolytic anaemia as blood cells burst
28
What are causes of aortic valve stenosis?
- Degeneration (senile fibrosis/calcification)
- Congenital (bicuspid when normally tricuspid)
- Chronic rheumatic fever - commissural fusion (autoantibodies attack valve)
29
What kind of murmur does aortic valve stenosis create?
Crescendo-decrescendo systolic murmur
30
What are the causes of aortic valve regurgitation?
- Valvular damage (eg. endocarditis)
| - Aortic root dilation - leaflets pulled apart
31
What is aortic valve regurgitation?
- Blood flows back into LV
- Stroke volume increases
- Systolic pressure increases
- Bounding pulse, head bobs and nails flush with piles
- LV hypertrophy
32
What is mitral valve regurgitation?
- Chordae tendinae & papillary muscles stop preventing prolapse = Prolapse
- Increased preload = LV hypertrophy
33
What kind of murmur does aortic valve regurgitation create?
Diastolic murmur (after S2)
34
What are the causes of mitral valve regurgitation?
- Damage to papillary muscle (MI)
- Left sided heart failure (LV stretch)
- Rheumatic fever (leaflet fibrosis)
35
What kind of murmur does mitral valve regurgitation create?
Holosystolic murmur (after S2, short)
36
What is mitral valve stenosis?
- Commissural fusion of valve leaflets
- Caused by rheumatic fever mostly
- Blood struggles to flow from LA to LV = increased LA pressure
- LA dilation can cause: AF, thrombus formation, oesophagus compression (+ dysphagia)
- Pulmonary oedema + hypertension, RV hypertrophy
37
What kind of murmur does mitral valve stenosis create?
- Snap as valve opens
| = Diastolic rumble
38
What is the afterload?
The load that the heart must eject blood against (equivalent to aortic pressure)
39
What is the preload?
Amount the ventricles are stretched in diastole (EDV/central venous pressure)
40
What is total peripheral resistance?
Resistance to blood flow offered by all the systemic vasculature
(More constricted vessels = higher peripheral resistance)
41
Why do arterioles offer the greatest resistance?*
- More smooth muscle in tunica media
- Narrows lumen
- Reduces pressure before capillaries so capillaries do not burst
42
What happens when the vessels are constricted?*
- Resistance causes a pressure drop
- Will drop on venous side
- Will rise on arterial side
43
What happens if you decrease TPR?* (and CO is unchanged)
- Arterial pressure falls (easier pumping)
| - Venous pressure rises (more blood reaches veins)
44
What happens if you increase TPR?* (and CO is unchanged)
- Arterial pressure increases (higher pressure needed to pump blood through the resistance)
- Venous pressure decreases (less blood getting through)
45
What happens if CO increases and TPR stays the same?*
- Arterial pressure increases (heart pumping out more blood)
- Venous pressure decreases (heart is being emptied more)
46
What happens if CO decreases and TPR stays the same?*
- Arterial pressure decreases (less blood pumped around body)
- Venous pressure increases (heart not emptied as much)
47
Why can heart failure occur with increased venous pressure when CO decreases?
- Blood does not leave the heart quickly enough
- Heart is not emptied as much so SV is increased
PULMONARY/PERIPHERAL OEDEMA
48
What happens when the heart needs more blood?
Arterioles and precapillary sphincters dilate so TPR falls and the heart can pump more blood so that there are no changes in pressure
49
How does the heart respond to changes in central venous pressure and arterial blood pressure?
Extrinsic and intrinsic mechanisms.
50
What is the meaning of afterload?
Load that the heart must eject blood against (eg. aortic pressure; higher pressure = higher load)
51
What is the meaning of preload?
The amount that the ventricles are stretched/filled in diastole (EDV/CVP)
52
What is the meaning of total peripheral resistance?
Resistance to blood flow offered by all systemic vasculature (more constricted vessels = higher peripheral resistance)
53
Why do arterioles offer the greatest resistance?
- Narrow lumen
| - Have more smooth muscle in tunica media
54
What happens when arterioles constrict?*
- Increased resistance
- Pressure in capillaries on venous side falls (constriction causes drop in pressure)
- Pressure on arterial side rises
MORE RESISTANCE = LARGER PRESSURE DROP
55
What happens when TPR falls and CO is unchanged?*
- Arterial pressure falls
| - Lower resistance means increased venous pressure as more blood reaches the veins more readily
56
What happens when TPR is increased and CO is unchanged?*
- Arterial pressure increases as it's harder to pump blood through the constriction
- Venous pressure falls as blood is not getting through as easily
57
What happens when CO increases and TPR stays the same?*
- Arterial pressure increases as heart is pumping out more blood
- Venous pressure reduces as heart is emptied out more
58
What happens when CO decreases and TPR stays the same?*
- Arterial pressure drops as less blood is pumped around body
- Venous pressure rises as heart is not emptied out as much and heart failure can occur, as well as pulmonary and peripheral oedema
59
What happens when tissues need more blood?
- Arterioles and precapillary sphincters dilate
| - Peripheral resistance falls, so heart pumps more blood to prevent drop in arterial blood pressure caused by lower TPR
60
How does the heart respond to changes in certain venous pressure and arterial blood pressure?
- Intrinsic mechanisms: myocardial cells
| - Extrinsic mechanisms: neural/hormonal effects
61
How do you calculate cardiac output?*
Heart rate x stroke volume
62
How do you calculate stroke volume?
End diastolic volume - end systolic volume
63
How can stroke volume be increased?
- Increasing end diastolic volume
| - Decreasing end systolic volume
64
When does ventricular filling occur?
Diastole
65
How does the ventricle fill and how is it dependent on pressure?*
- Ventricle fills until walls stretched enough to produce pressure in ventricles equal to venous pressure
- Higher venous pressure = more filling of heart
- More filling = higher LV pressure
66
What is decreased compliance?
- Stiff heart (less filling)
- Hypertrophy
- Higher pressure
67
What is increased compliance?
- Heart dilated (more filling)
| - Lower pressure
68
What is the Frank-Starling law of the heart?
- INTRINSIC CONTROL MECHANISM
- The more the heart fills, the harder it contracts (up to a limit)
- Harder heart contracts = bigger stroke volume
- Increase in venous pressure fills heart more
69
What influences how much ventricles fill?
Compliance (eg. stiffness/dilation)
70
What is the Starling curve and what does it show?*
- Increased venous return = increased left ventricular end-diastolic pressure and preload
- Increase in SV
71
What is the length-tension curve for cardiac muscle and why is it relevant?*
Shows that the length of the sarcomere matters.
- Too short: filament overlap interferes w/ contraction
- Stretching of muscle causes increase in Ca2+ sensitivity and increases the force of contraction
72
What is the purpose of the Frank-Starling law of the heart?*
- Ensuring that both sides of the heart maintain the same output
- Allows pulmonary and systemic circulation to operate in series
- Same volume of blood pumped to the body and lungs
73
What is contractility?
Force of contraction for a given fibre length (how hard the fibre will contract)
74
What does a change in contractility cause?*
- Change in slope of Starling curve
| - Increase = increased force of contraction
75
What can affect contractility?
```
Increase = sympathetic stimulation, circulating adrenaline
Decrease = reducing sympathetic stimulation
```
76
When does aortic pressure increase?
When peripheral resistance increases, which makes it harder for the heart to pump
77
Why does increased TPR reduce filling of the heart?
Reduces venous pressure
78
What determines cardiac output (how much the ventricle empties)?
- Force of contractions (EDV and contractility)
- How hard it is to eject blood (aortic impedance)
- Cardiac output
79
What controls contractility and heart rate?
Autonomic nervous system
80
What will a decrease in arterial BP cause?
- Reduce parasympathetic NS activity
- Stimulates sympathetic NS activity
= Increases HR and contractility
81
What happens if the body metabolism increases?
- TPR will reduce due to dilating arterioles
- Fall in arterial pressure
- Rise in venous pressure
- Heart responds by pumping more
82
How does the CVS respond to eating a meal?*
- Local vasodilation in gut
| Slide 23! :) Notes!
83
What happens when you stand up?
- Gravity action causes blood to pool in legs
| - Venous pressure decreases, and so does CO and arterial pressure
84
What increases HR and TPR?
- Baroreceptor reflex
| - Autonomic NS
85
What happens if reflexes don't work?
Postural hypotension
86
What happens during exercise?*
- Muscle pumping and venoconstriction return more blood to heart
- TPR decreases - increased venous return
- Increased heart rate and contractility (sympathetic drive)
87
How is a jugular venous pulse measured and what is it?
- Biphasic pulse: two peaks per cardiac cycle, one weak and one small ('beats' twice)
88
Where can the JVP be felt?
Behind the sternocleidomastoid muscle
- Normally 5-8cm H2O
- Can be measured with a central line inserted into internal jugular vein to allow seeing waveform
89
How does height of JVP vary over time?* (DIAGRAM)
- Atrial systole (rise)
- Atrial diastole (fall)
- Tricuspid valve closure (rise)
- Ventricular systole (fall)
- Maximum atrial filling pressure (rise)
90
What causes JVP pressure to rise?
- Right sided heart failure
- Volume overload (IV infusion)
- Impaired filling of heart
- e.g. stab wounds
