The Cardiovascular System Flashcards
(117 cards)
1
Q
What are the structures involved in excitation-contraction coupling of cardiac cells?
A
NOTION 2.1
2
Q
Can cardiac muscle exhibit tetanus?
A
No, cardiac muscle has a long action potential (around 250 ms vs 2ms in skeletal muscle). The long refractory period, therefore means, it cannot exhibit tetanic contraction.
3
Q
How does cardiac muscle form a functional syncytium?
A
Cardiac muscle forms a functional syncytium:
- Electrically connected via gap junctions
- Physically connected by desmosomes
- These form the intercalated discs
4
Q
What can regulate the contraction of cardiac muscle cells?
A
Ca2+ entry from outside cell can regulate contraction (Ca2+ release does not saturate the troponin, so regulation of Ca2+ release can be used to vary the strength of contraction).
5
Q
Some cardiac cells have unstable resting membrane potential, and therefore act as?
A
Pacemakers
6
Q
Non-pacemaker vs pacemaker action potentials
A
NOTION 2.2
7
Q
What ion channels open/close throughout a non pacemaker action potential?
A
- Na+/K+ channels are open
- While Na+ channels close, K+ channels remain open
- K+ channels close, while Ca2+ channels open (L-type)
- Ca2+ channels close (L-type), while K+ channels open
- K+ channels remain open
(NOTION 2.3)
8
Q
Some characteristics of non pacemaker action potentials include:
1. Low resting membrane potential
2. Initial Depolarisation
3. Plateau
4. Repolarisation
What ions are responsible for each of these?
A
- High resting PK+
- Increase in PNa+
- Increase in PCa2+ & decrease in PK+
- Decrease in PCa2+ & increase in PK+
9
Q
What ion channels open/close throughout a pacemaker action potential?
A
- If channels open
- Some Ca2+ channels open (T-type), If channels close
- Lots of Ca2+ channels open (L-type)
- Ca2+ channels close (L-type), K+ channels open
- K+ channels close, If channels open
(NOTION 2.4)
10
Q
What explains autorhythmicity?
A
Pacemaker explains autorhythmicity
11
Q
Some characteristics of pacemaker action potentials include:
1. Pacemaker potential
2. Action Potential
What ions are responsible for each of these?
A
- Gradual decrease in PK+
Early increase in PNa+
Late increase in PCa2+ (T-type) - Increase in PCa2+ (L-type)
12
Q
What are some structures involved in the special conducting system of the heart?
A
- Sinoatrial node (l.e Pacemaker, 0.5 m/s)
- Annulus fibrosus (non conducting)
- Atrioventricular node (Delay box, 0.05 m/s)
- Bundle of His & Purkinje fibres (Rapid conduction system, 5m/s)
(NOTION 2.5)
13
Q
What are the stages of contraction of the heart?
A
- Atrial excitation
- Ventricular excitation
- Ventricular relaxation
(NOTION 2.6)
14
Q
What is the normal shape of an ECG?
A
NOTION 2.7
15
Q
What does a normal ECG trace look like?
What does a 1st degree heart block ECG trace look like?
What does a 2nd degree heart block ECG look like?
What does a 3rd degree heart block ECG look like?
A
NOTION 2.8
16
Q
What is a 1st degree heart block?
A
- The PR interval is prolonged : more than 200msec
- This means conduction through the AV node is slowed.
- This is a benign entity and may not need any treatment.
17
Q
What is 2nd degree heart block?
A
- The PR interval is prolonged progressively over several beats, until the beat is missed.
- ie. A P wave occurs which is not followed by a QRS
- This means conduction through the AV node is slowed.
- This is a benign entity and may not need any treatment.
18
Q
What is a 3rd degree heart block?
A
- There is no relationship between the Pwaves and the QRS complexes.
- This is called “AV dissociation”. The AV node is not conducting anything.
- Atropine will not accomplish anything here.
- It requires a dual-chamber pacemaker.
19
Q
What does an ECG trace look like for:
- Normal (sinus rhythm)
- Atrial flutter
- Atrial fibrillation
- Ventricular fibrillation
A
NOTION 2.9
20
Q
What is the main function of the CVS?
A
Bulk flow system:
- O2 and CO2
- Nutrients
- Metabolites
- Hormones
- Heat
21
Q
What makes the CVS reliable?
A
It beats over 2.5 billion times in 70 years
22
Q
What makes the CVS flexible?
A
- Pump can vary output
- Vessels can redirect blood
- Vessels can store blood
23
Q
Are the pumps of the CVS in series or in parallel?
Are most vascular beds in series or in parallel?
A
Pumps are in series, therefore:
- Output must be equal
Most vascular beds are in parallel, therefore:
- All tissues get oxygenated blood
- Allows regional redirection of blood
NOTION 1.1
24
Q
What is the i) flow at rest ii) cardiac output & iii) oxygen consumption of:
- The brain
- The heart
- The skeletal muscle
- The skin
- The kidney
- The abdominal organs
- Other organs/ tissue
A
NOTION 1.2
25
What is the equation for flow?
Flow = (/\ Pressure)/(resistance)
/\Pressure = Mean Arterial Pressure - Central Venous Pressure (affects all tissues)
Resistance = controlled by radius^4 (selectively redirects flow)
26
What vessel is involved in controlling resistance to each vascular bed?
The arterioles
27
What are venules and veins known as?
Venules & veins are capacitance vessels and control the fractional distribution of blood
28
What is the structure and function of the aorta?
Aorta:
- Elastic arteries
- Wide lumen
- Thick elastic wall
- Damp pressure variations
29
What is the structure and function of the arteries?
Arteries:
- Muscular arteries
- Wide lumen
- Strong, thick, non elastic wall
- Low resistance conduit
30
What is the structure and function of the arterioles?
Arterioles:
- Resistance vessels
- Narrow lumen
- Thick contractile wall
- Control resistance and therefore flow
- Allow regional redirection of blood
31
What is the structure and function of the capillaries?
Capillaries:
- Exchange vessels
- Narrow lumen
- Thin wall
32
What is the structure and function of the venules?
Venules:
- Capacitance vessels
- Wide lumen
- Thin, distensible wall
- Low resistance conduit and reservoir
- Allows fractional distribution of blood between veins and rest of circulation
33
What are some key structures of the heart?
Septum - Myocardium - Atrium - Ventricle - Aorta - Vena cava - Pulmonary trunk - Pulmonary veins - Aortic valve - Pulmonary valve - Mitral valve - Tricuspid valve - Chordae tendinae - Papillary muscle
NOTION 1.3
34
What is the main function of the chordae tendinae & papillary muscles?
They prevent valves inverting backwards, therefore preventing back-flow (the papillary muscles put tension on the chordae tendinae, which prevent the inversion).
35
Cross section of the valves of the heart
NOTION 1.4
36
What are the 5 stages of the cardiac cycle?
1. Late diastole - both sets of chambers are relaxed and ventricles fill passively
2. Atrial systole - Atrial contraction forces a small amount of additional blood into ventricles
3. Isovolumic ventricular contraction - First phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. Maximum blood volume in ventricles = End diastolic volume (EDV)
4. Ventricular ejection - As ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
5. Isovolumic ventricular relaxation - As ventricles relax, pressure in ventricles falls. Blood flows back into cusps of semilunar valve and snaps them closed. Minimum blood volume in ventricles = End Systolic Volume (ESV)
NOTION 3.1
37
Graph displaying:
- Blood pressure in the ventricles, atrium & aorta
- Volume of blood (in ventricles) during systole, and then diastole
- Heart sounds throughout a heart beat
- ECG trace of a heart beat
NOTION 3.2
38
Further detail regarding the pressure and volumes of blood in the chambers of the heart
NOTION 3.3
39
Typical ejection fraction
Between 50-70%
40
Equation for ejection fraction
Ejection fraction = SV / EDV
41
How do you calculate pulse pressure?
Systolic pressure - Diastolic pressure
42
How do you calculate stroke volume?
End diastolic volume (EDV) - End systolic volume (ESV)
43
Why do heart sounds occur?
What events cause the 4 typical heart sounds?
Heart sounds occur due to turbulence in blood flow.
These are caused by:
1st = Closure of the AV (mitral & tricuspid) valves
2nd = Closure of the semi lunar (aortic & pulmonary) valves
3rd = Rapid passive filling phase
4th = Active filling phase
44
What are murmurs?
Additional heart sounds are called murmurs (physiological or pathological).
45
Effects of a systolic murmur on a phonocardiogram
What causes a systolic murmur?
A systolic murmur is displayed on NOTION 3.4.
Systolic murmurs may be caused by:
- Stenosis of aortic/ pulmonary valves or
- Regurgitation through mitral/ tricuspid
46
Effects of a diastolic murmur on a phonocardiogram
What causes a diastolic murmur?
A diastolic murmur is displayed on NOTION 3.5.
Diastolic murmurs may be caused by:
- Stenosis of mitral/ tricuspid valves or
- Regurgitation through aortic/ pulmonary valves
47
What causes a continuous murmur?
Continuous murmur could be due to patent ductus arteriosus. NOTION 3.6 explains this further.
48
How does the sympathetic nervous system regulate HR:
- What hormones are released?
- What receptors do they act on?
- Effect on pacemaker potential
- Effect on Heart Rate
Sympathetic nervous system
- Sympathetic nerves release noradrenaline
- Plus circulating adrenaline from adrenal medulla
- Both act on β1 receptors on sinoatrial node
- Increases slope of the pacemaker potential
- Increases heart rate = tachycardia
49
How does the parasympathetic nervous system regulate HR:
- What hormones are released?
- What receptors do they act on?
- Effect on pacemaker potential
- Effect on Heart Rate
Parasympathetic nervous system
- Vagus nerve releases acetylcholine
- Acts on muscarinic receptors on sinoatrial node
- Hyper-polarises cells and decreases slope of pacemaker potential
- Decreases heart rate = bradycardia
50
What does Starling’s Law state?
Starling’s Law states - The energy of contraction is proportional to the initial length of the cardiac muscle fibre
51
In vivo, what is preload of the heart affected by?
In vivo, preload is affected by the end diastolic volume.
52
Effect of increased venous return on stroke volume
Effect of decreased venous return on stroke volume
What does this help to ensure?
Increased venous return = Increased EDV = Increased SV
Decreased venous return = Decreased EDV = Decreased SV
This ensures self regulation - matches SV of left & right ventricles.
53
What is the after load of the heart?
After load is the load against which the muscle tries to contract. This can be seen in NOTION 3.7.
54
What is the effect of an increase in Total Peripheral Resistance (TPR)?
If TPR increases = Aortic Pressure will increase = Ventricle will have to work harder to push open the aortic valve = Less energy left to do the useful bit of ejecting blood ie. SV will decreases.
55
How does the sympathetic nervous system regulate SV:
- What hormones are released?
- What receptors do they act on?
- What is the effect on contractility?
- What is the effect on contraction?
Sympathetic nervous system
- Sympathetic nerves releasing noradrenaline
- Plus circulating adrenaline from adrenal medulla
- Both act on β1 receptors on the myocytes
- Increases contractility (an inotropic effect)
- Gives stronger, but shorter contraction
56
Effect of the parasympathetic nervous system on Stroke Volume
Parasympathetic nervous system
- Little effect
- Probably because the vagus nerve does not innervate the ventricular muscle
57
What are the 3 factors which impact/ regulate Stroke Volume?
3 main factors:
- Preload
- Contractility
- Afterload
NOTION 3.8
58
Equation for Cardiac Output
Cardiac Output = Heart Rate x Stroke Volume
Increasing heart rate (e.g. with electronic pacemaker) causes a small increase in cardiac output but stroke volume starts decreasing.
59
Why does stroke volume decrease with an increase in HR?
- The shortened cardiac interval cuts into the rapid filling phase
- The reduced end diastolic volume reduces preload
- So according to Starling’s law, stroke volume is reduced
60
Summary of Control of Cardiac Output
HR increases:
- Via decreased vagal tone
- Increased sympathetic tone
Contractility increases:
- Via increased sympathetic tone
- Alters Ionotropic state & shortens systole
Venous return increases:
- Via venoconstriction and skeletal skeletal/ respiratory pumps
- Maintains preload
Total peripheral resistance falls:
- Due to arteriolar dilation in muscle, skin & heart
- Reduces afterload
61
How can you measure arterial pressure?
What are the advantages and disadvantages of this method?
Auscultation of Korotkoff sounds using a sphygmomanometer and stethoscope.
Disadvantages = Discontinuous, accuracy, needs care/skill
Advantages = Non invasive, cheap
NOTION 4.1
62
What would you hear through a stethoscope when measuring the arterial pressure?
NOTION 4.2
63
What is another method by which arterial pressure can be recorded?
What are some advantages/ disadvantages of this method?
Using an oscillatory blood pressure measurement:
- Turbulent blood flow sets up vibrations (oscillations) in the blood vessel wall
- Transducer monitors those vibrations
- Maximum vibrations occur at the mean arterial pressure
- Algorithm estimates diastolic and systolic pressures
Disadvantages = discontinuous, accuracy, needs care
Advantages = non-invasive, cheap
NOTION 4.3
64
What do elastic arteries act as?
They act as a pressure reservoir (Damps down pressure variations).
65
What is the pressure wave affected by?
Pressure wave is affected by:
- Stroke volume
- Velocity of ejection
- Elasticity of arteries
- Total peripheral resistance
66
Graph of pressure in elastic arteries vs time
NOTION 4.4
67
What is the effect of age on arterial pressure?
Graph displaying this.
Arterial pressure (especially pulse pressure) increases with age.
A graph displaying this, can be found on NOTION 4.5
68
Graph displaying Pressure and flow from arteries to veins
NOTION 4.6
69
1. By how much does pressure decrease through the arteries?
2. What about through the arterioles?
3. And finally, through the veins?
1. Small drop through arteries (from 95 to 90 mmHg)
- Low Resistance conduit
2. Large drop through arterioles (from ~90 to 40 mmHg)
- Resistance vessels
3. Leaves a small pressure difference pushing blood back through the veins (from ~20 to 5 mmHg)
- The systemic filling pressure
70
Pulmonary circulation pressure vs systemic
Pulmonary circulation pressure ~ 1/5th of systemic
71
What is velocity related to, and what does this then mean?
Velocity is related to total cross-sectional area (Fastest in aorta and vena cava, slowest in capillaries).
72
Graph displaying velocity (of blood flow) and cross sectional area of the different vessels
NOTION 4.7
73
Why do external influences affect flow in the veins?
Is pressure high or low in the veins?
Veins are distensible and collapsible (Therefore external influences affect flow).
Pressure is low in the veins (Therefore ΔP driving blood back to the heart is low).
74
Effect of gravity on driving pressure from arteries to veins
Gravity does not affect driving pressure from arteries to veins
75
Gravity causes venous distension in legs. What is the effect of this?
Gravity causes venous distension in legs:
-↓ EDV, ↓ preload, ↓ SV, ↓ CO, ↓ MAP
76
Image displaying effects of standing up, on blood pressure throughout the body
NOTION 4.8
77
When some people stand up, their blood pressure drops by a significant degree. What is this known as?
Orthostatic (Postural) Hypotension
78
What is the effect of the skeletal muscle pump?
Skeletal muscle pump
- Rhythmic contraction increases venous return and EDV
- Significance:
- Rhythmic vs. static exercise
- Deep vein thrombosis
79
What is the effect of the respiratory pump?
Respiratory pump
- Increased respiratory rate and depth increase venous return and EDV
80
What is the effect of venomotor tone?
Venomotor tone:
- Is the state of contraction of the smooth muscle surrounding the venules and veins
- Mobilises capacitance and increases EDV
81
What is the effect of the systemic filling pressure?
Systemic filling pressure:
- Pressure created by ventricles and transmitted through vascular trees to the veins
82
So therefore, overall, what are the 5 main factors which impact on venous pressure?
- Gravity
- Skeletal muscle pump
- Respiratory pump
- Venomotor tone
- Systemic filling pressure
83
Equation for MAP
Effect of Low MAP
Effect of High MAP
MAP = CO x TPR
Too low = fainting
Too high = Hypertension
84
Where are the 2 main baroreceptors?
- Carotid sinus baroreceptors
- Aortic arch baroreceptors
85
What is the effect of increased/ decreased arterial pressure on the firing rate of the main baroreceptors?
NOTION 5.1
86
What nerve transmits information from the aortic arch baroreceptors to the medullary cardiovascular centres?
Vagus nerve
87
What nerve transmits information from the carotid sinus baroreceptors to the medullary cardiovascular centres?
Glossopharyngeal nerve
88
Where is the parasympathetic outflow from the medullary cardiovascular centre?
What is the effect of this?
It travels via the Parasympathetic nerve (Vagus).
Activation of this nerve leads to a decrease in HR.
89
Where is the sympathetic outflow from the medullary cardiovascular centre?
What is the effect of this?
It travels via the sympathetic nerve.
And results in an increase in HR & Contractility.
It also travels to the adrenal medulla (releasing adrenaline & noradrenaline).
And overall results in venoconstriction & arteriolar constriction.
90
What are 5 other inputs to the medullary cardiovascular centres?
1. Cardiopulmonary baroreceptors (Sensing central blood volume)
2. Central chemoreceptors (Sensing arterial pCO2 & pO2)
3. Chemoreceptors in muscle (Sensing metabolite concentrations)
4. Joint receptors (Sensing joint movement)
5. Higher centres (Hypothalamus & cerebral cortex)
91
Overall what helps provide short term control of arterial blood pressure?
The arterial baroreflex is responsible for the short term control of arterial blood pressure.
92
What is the Valsalva manoeuvre?
The Valsalva manoeuvre = forced expiration against a closed glottis
93
What is the effect of the Valsalva manoeuvre?
Stage I: Increased thoracic pressure is transmitted through to aorta -hence the immediate jump
Stage II: Increased thoracic pressure reduces the filling pressure from the veins, which therefore decreases VR, decreases EDV, decreases SV, decreases CO, decreases MAP
Late Stage II: The reduced MAP is detected by baroreceptors which initiate a reflex increase in CO & TPR
Stage III: At the end of the manoeuvre, the decrease in thoracic pressure is transmitted through to the aorta, hence the drop
Stage IV: VR is restored so SV increases, but reflex effects have not worn off
NOTION 5.2
94
What is the clinical significance of the Valsalva manoeuvre?
This can be used as a test of autonomic function.
The response to Valsalva manoeuvre may be reduced in:
- Older people
- Autonomic neuropathy
The manoeuvre can also help control supra-ventricular tachycardia.
It can, however, increase the risk of myocardial infarction.
95
What are capillaries?
What is their abundance within the human body?
What is the structure of a capillary?
- They are specialised for exchange
- There are lots of them
- Every tissue within ~100 µm of one
- They are thin-walled
-Presents a small diffusion barrier
- They have a small diameter
- Big surface area:volume ratio
96
What are the gap junctions like in the capillaries?
What does transcytosis involve?
Continuous vs fenestrated capillaries
NOTION 6.1
97
Where are continuous capillaries found, and what is their structure?
Where are fenestrated capillaries found, and what is their structure?
Where are discontinuous capillaries found, and what is their structure?
Continuous
- No clefts or pores e.g. brain (hence the blood-brain barrier)
- Clefts only e.g. muscle, and most other capillaries
Fenestrated
- Clefts and pores e.g. intestine and kidney, specialised for fluid exchange
Discontinuous
- Clefts and massive pores e.g. liver
98
How does most exchange in capillaries take place via?
What is another, less common, mechanism?
What is bulk flow determined by?
Most exchange is via diffusion:
- Self regulating
- Non - saturable
- Non-polar susbtances across the phospholipid membrane
- Polar susbtances through clefts/ pores
Carrier mediated transport:
- E.g glucose transporter in the brain
Bulk flow:
- Determined by Starling’s Forces
99
Starling’s forces in the capillaries
How much litres are lost from the capillaries each day?
And how many litres are regained?
What happens to the remaining litres?
Bulk flow is determined by Starling’s Forces:
- Capillary Hydrostatic pressure vs ISF hydrostatic pressure
- Plasma osmotic pressure vs ISF osmotic pressure
- Net filtration pressure =
(Hc - Hif) - (pi_c - pi_if)
This varies between capillary beds!
Overall 20 litres is lost and 17 litres are regained each day.
The remaining 3 litres travel into the lymphatic system.
100
What is oedema?
What can oedema be due to?
Oedema = accumulation of excess fluid
This could be due to:
- Raised CVP
- e.g due to ventricular failure
- Lymphatic obstruction
- e.g due to filariasis, surgery
- Hypoproteinaemia
- e.g due to nephrotic syndrome, liver failure, malnutrition
- Increased capillary permeability
- Inflammation e.g rheumatism
101
What are 2 laws related to the control of peripheral blood flow?
1. Darcy’s Law
2. Poiseuille’s Law
NOTION 6.2
102
How can an equation for MAP be obtained from Darcy’s Law?
/\ Pressure = Flow x Resistance
MAP - CVP = CO x TPR
MAP = CO x TPR (Since CVP is very small!)
103
Visual diagram displaying Darcy’s Law
NOTION 6.3
104
What is a major factor important for regulating peripheral blood flow?
Controlling the radius (and therefore the resistance) of arterioles is doubly important.
Arteriolar radius affects flow through individual vascular beds, and it affects mean arterial pressure.
105
What are the 2 main levels of control over smooth muscle surrounding arterioles?
This is achieved by two levels of control over the smooth muscle surrounding arterioles:
- Local (intrinsic) mechanisms - concerned with meeting the selfish needs of each individual tissue
- Central (extrinsic) mechanisms – concerned with ensuring that the total peripheral resistance (and therefore MAP) of the whole body stays in the right ball park
106
What are the 4 main intrinsic controls of arteriolar smooth muscle?
1. Active (metabolic) hyperaemia
2. Pressure (flow) autoregulation
3. Reactive hyperaemia
4. The injury response
107
Active (metabolic) hyperaemia & local control of arteriolar smooth muscle
Trigger is an increase local metabolism:
• ↑ metabolic activity causes ↑ concentration of metabolites
• Triggers release of paracrine signal (e.g. EDRF/NO)
• Causes arteriolar dilation
• ↑ flow to wash out metabolites
• An adaptation to match blood supply to the metabolic needs of that tissue
108
Pressure autoregulation & local control of arteriolar smooth muscle
Trigger is a decrease in perfusion pressure:
• ↓ MAP causes ↓ flow
• Metabolites accumulate
• Triggers release of paracrine signal (e.g. EDRF/NO)
• Arterioles dilate and flow is restored to normal
• An adaptation to ensure that a tissue maintains its blood supply despite changes in MAP
109
Reactive hyperaemia & control of arteriolar smooth muscle
Trigger is occlusion of blood supply:
• This causes a subsequent increase in blood flow
• An extreme version of pressure autoregulation
110
Injury Response & control of arteriolar smooth muscle
NOTION 6.4
111
What hormones are released by Sympathetic nerves?
What receptor do they bind to?
What is the effect on arteriolar diameter?
And, therefore, what happens to the flow through the tissue?
Sympathetic nerves
• Release noradrenaline
• Binds to α1receptors
• Causes arteriolar constriction
• Therefore ↓ flow through that tissue and tends to ↑ TPR and ↑ MAP
112
What is the effect of parasympathetic nerves on arteriolar diameter?
What is an exception?
Parasympathetic nerves
• Usually no effect
• Genitalia and salivary glands are the exception (↑ flow)
113
What are some exceptions to the receptors expressed on arteriolar smooth muscle?
What is the effect of this?
In some tissues, e.g. skeletal and cardiac muscle also activates β2 receptors
• Causes arteriolar dilation
• Therefore ↑ flow through that tissue and tends to ↓ TPR
• Significant during exercise
114
What is the blood supply in the coronary circulation interrupted by?
How does it cope with increased demand during exercise?
What type of receptor is expressed in arteriolar smooth muscle of the heart?
Coronary circulation
• Blood supply is interrupted by systole
• But still has to cope with increased demand during exercise
• Shows excellent active hyperaemia
• Expresses many β2 receptors
• These swamp any sympathetic arteriolar constriction
115
What is special about the cerebral circulation?
Cerebral circulation
• Needs to be kept stable, whatever
• Shows excellent pressure autoregulation
116
Effect of low oxygen levels on the diameter of arterioles in the lungs. What does this ensure?
Pulmonary circulation
• ↓ O2 causes arteriolar constriction
• i.e. the opposite response to most tissues
• Ensures that blood is directed to the best ventilated parts of the lung
117
What is special about renal circulation?
Renal circulation
• Main job is filtration
• Filtration rate kept relatively constant during normal fluctuations in MAP
• Due to excellent pressure autoregulation
