CVS L01-L14 Flashcards
1
Q
What is the value for normal pulse pressure? L02
A
40mmHg
2
Q
Define cardiac output L02
A
Volume of blood pumped per min
3
Q
What happens if Right CO > Left CO? L02
A
Pulmonary oedema
4
Q
Define stroke volume L02
A
Volume ejected per contraction
5
Q
What happens if Left CO > Right CO? L02
A
Peripheral oedema
6
Q
What arrangement are vascular beds in? L02
A
Parallel
7
Q
What arrangement are the right and left sides of the heart? L02
A
In series with each other
8
Q
Define systole L02
A
Phase of ventricular contraction and ejection
9
Q
What is the equation for cardiac output? L02
A
CO = SV x HR
10
Q
Define diastole L02
A
Phase of ventricular relaxation and filling
11
Q
What do you feel when you take someone’s pulse? L02
A
Pulse pressure
12
Q
What determines blood pressure? L02
A
- Resistance to blood flow
2. Blood volume
13
Q
What are the three different cardiac action potentials? L04
A
Sino-atrial node, atrio-ventricular node, and non-nodal potentials
14
Q
What is the primary pacemaker of the heart? L04
A
The sino-atrial node
15
Q
What is the resting membrane potential of SAN cells? L04
A
They do not have a true resting membrane potential
16
Q
Why do SAN cells not have a true resting membrane potential? L04
A
So they can generate regular, spontaneous action potentials
17
Q
Do SAN cells contains fast Na+ channels? L04
A
No, there are no fast Na+ channels in either the SAN or AVN
18
Q
What 3 things happen in phase 4 of an SAN cell action potential? (the pacemaker potential) L04
A
- Na+ influx through slow Na+ channels causing depolarisation
- Then Ca2+ influx by T-type calcium channels at around -50mv
- Then Ca2+ influx by L-type calcium channels at around -40mV
19
Q
What is the rough value of the membrane potential of SAN cells? L04
A
-60mV
20
Q
What type of calcium channels predominate depolarisation in phase 0 of an SAN cell action potential? L04
A
L-type; they increase Ca2+ conductance causing further depolarisation. The rate of depolarisation is slower than phase 4 because the number of open T-type calcium channels close.
21
Q
What channels open in phase 3 (repolarisation) of an SAN cell action potential? L04
A
K+ channels
22
Q
What happens to the L-type calcium channels in phase 3 of an SAN cell action potential? L04
A
They become inactivated and close, decreasing gCa2+
23
Q
How are SAN cell action potentials similar to AVN action potentials? L04
A
Neither use fast sodium channels
Both are determined by slow Ca2+ influx and K+ efflux
24
Q
What is the intrinsic firing rate for the SA node? L04
A
100 bpm
25
What predominates in determining HR? L04
Vagal tone
26
What receptor do the catecholamines act upon in heart muscle? L04
Beta1 receptors
27
What neurotransmitter and its receptor does the parasympathetic nervous system stimulate in heart muscle? L04
Acetylcholine (Ach) on M2 receptors
28
What effect does sympathetic stimulation have on the heart rate? L04
Positive chronotropic effect (increases HR). It does this by increasing the slope of the pacemaker potential.
29
What effect does parasympathetic stimulation have on the heart rate? L04
Negative chronotropic effect (decreases HR). It does this by hyperpolarisation (opens K+ channels) thus decreasing the slope of the pacemaker potential.
30
What junctions are present in the heart for conducting action potentials between myocytes and what is the name of this mechanism? L04
Gap junctions; Excitation-Contraction Coupling (ECC)
31
What is the speed for SA node action potential conduction? L04
0.5m/sec
32
What is the speed for AV node action potential conduction? L04
0.05m/sec
33
Why is the AVN conduction rate slower than the SAN conduction rate? L04
AV delay; to ensure complete atrial depolarisation and contraction (systole)
34
What is the speed for the Bundles of His action potential conduction? L04
2m/sec
35
What is the speed for Purkinje fibre action potential conduction and what is the reason for this? L04
4m/sec; for rapid ventricular depolarisation
36
Which interval will decrease on an ECG if you increase AVN contraction due to sympathetic stimulation? L04
The P-R interval
37
What is the resting membrane potential of non-nodal cells in the heart? L04
-90mV
38
Why is the resting membrane potential of non-nodal cells very stable and negative? L04
So you do not have spontaneous contraction; you do not want it contracting until necessary so it is therefore far away from threshold level
39
What is the absolute refractory period for a non-nodal cell action potential? L04
200ms
40
What is the relative refractory period for a non-nodal cell action potential? L04
50ms
41
Why is there long refractory periods in cardiac muscle compared to skeletal muscle? L04
As you do not want temporal summation in cardiac muscle
42
Atrial and ventricular myocytes and Purkinje fibres conduct what type of action potential? L04
Non-pacemaker action potentials; they are fast response with a true resting membrane potential
43
What is happening in phase 4 of a non-pacemaker action potential? L04
K+ channels are open meaning a negative membrane potential
| Both Na+ and L-type calcium channels are closed
44
What causes the initial depolarisation in phase 0 of a non-pacemaker action potential? L04
Na+ channels open causing Na+ influx and K+ channels close
45
What causes the initial repolarisation in phase 1 of a non-pacemaker action potential? L04
Transient K+ channel opening causing K+ efflux
46
Why is there a plateau in phase 2 of a non-pacemaker action potential? L04
Large increase in slow Ca2+ influx through L-type Ca2+ channels means repolarisation is delayed
47
What happens in phase 3 of a non-pacemaker action potential? L04
Inactivation of Ca2+ channels
48
What are 5 things that can change the rate of SAN firing? L04
1. Changes in autonomic activity
2. Circulating hormones
3. Serum ion concentrations e.g. hyperkalaemia causes bradycardia
4. Cellular hypoxia
5. Drugs e.g. CCBs cause bradycardia by inhibiting slow Ca2+ channels
49
When does systole begin and end? L06
Begins with contraction of the ventricles and ends when ejection ceases
50
When does diastole begin? L06
Begins when ejection ceases, filling starts after sufficient relaxation
51
If the pressure in the atrium is less than in the ventricle is the AV valve open or closed? L06
Closed
52
If the pressure in the aorta is more than in the left ventricle is the aortic valve open or closed? L06
Closed
53
Which valves are open in atrial systole? L06
AV valves only
54
What does the P wave on an ECG represent? L05/6
Atrial depolarisation
55
Why does blood not flow back into the vena cava? L06
Inertial effects of venous return
56
When does EDV occur? L06
At the end of atrial systole
57
What is the typical left ventricular EDV? L06
120ml; represents ventricular pre-load
58
What does the QRS complex on an ECG represent? L05/6
Ventricular depolarisation
59
What causes the first heart sound (S1)? L05/6
Closure of the atrio-ventricular valves when ventricular P > atrial P
60
Which valves are open during rapid ejection of the ventricles? L06
Semilunar valves only
61
What does the T-wave represent? L05/6
Ventricular repolarisation
62
Why does outward flow of blood still occur when atrial pressure exceeds ventricular pressure at the end of systole? L06
Kinetic/inertial energy of the blood; blood continues to eject due to momentum
63
What causes the second heart sound (S2)? L05/6
The semilunar valves closing
64
What is the typical left ventricular ESV? L06
50ml
65
What is the equation for stroke volume? L06
SV = EDV - ESV
66
What is a typical value for normal stroke volume? L06
120ml - 50ml = 70ml
67
What is the equation for ejection fraction and what percentage should it be above for healthy heart function? L06
Ejection fraction = stroke volume/EDV
| It should be above 55%
68
Why is the right side of the heart less muscular? L06
It only has to overcome the pressure of the pulmonary arteries, which is a low resistance pressure system
69
Why do the ventricles never fully empty? L06
The blood is pushing against TPR, and it allows the SV to increase or decrease
70
What happens to EDV in an
a) increase in pre-load
b) increase in after-load
c) increase in contractility? L07
a) Increases
b) No change
c) No change
71
What happens to ESV in an
a) increase in pre-load
b) increase in after-load
c) increase in contractility? L07
a) No change
b) Increases
c) Decreases
72
What happens to SV in an
a) increase in pre-load
b) increase in after-load
c) increase in contractility? L07
a) Increases
b) Decreases
c) Increases
73
The intrinsic regulation of the energy of cardiac contraction is due to the effects of what, and what is the name of this law? L08
Stretch; Starling's law
74
What are the two factors affecting the muscle-length tension relationship? L08
Number of crossbridges formed and sarcomere length
75
When does peak tension of cardiac muscle occur? L08
At optimum sarcomere length there is maximum overlap leading to maximum number of cross bridges; so there is peak tension
76
What is pre-load? L08
Initial stretching of the cardiac myocytes prior to contraction
77
If you increase pre-load, what effect does this have on SV? L08
Increases SV
78
Name some factors that will increase pre-load. L08
Increase in CVP
decrease in venous compliance
increase in thoracic blood volume
Decrease in HR
Increase in atrial contractility (from symp. or filling)
Increase in ventricular compliance
Increase in aortic pressure
79
Name some factors that will increase CVP. L08
```
Moving from standing to lying down (decreased pooling)
Increase in skeletal muscle pump
Increase in venous constriction
Increase in respiratory muscle pump
Increased total circulating volume
```
80
What is the main function of Starling's law? L08
To balance the SV for the two ventricles
81
How does a high HR affect EDV? L08
Decreases EDV because passive filling time is reduced (P-P interval shortens)
82
What is the Frank-Sterling mechanism? L08
The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
83
What is contractility/inotropy? L08
Change in force of contraction at any given EDV; due to altering intracellular Ca2+ level (NOT due to stretch)
84
What determines the level of intracellular Ca2+? L08
Sympathetic nerves and circulating agents
85
What effect does increasing levels of intracellular Ca2+ have on contractility? L08
Increases it/ Positive inotropic effect
86
What is negative inotropy? L08
A decrease in cardiac contractility
87
What can decrease contractility? L08
Hypoxia, ischaemia, heart failure
88
How do you increase SV by Starling's law? L08
Increase pre-load
89
How do you increase SV by inotropy? L08
Increase intracellular Ca2+ levels
90
If there is an increase in force due to increased filling pressure- is this Starling's law or increased contractility? L08
Starling's law
91
Why does high afterload cause hypertrophy? L08
A larger ventricle is needed to overcome the higher afterload; needed with high ABP
92
What do class I anti-arrhythmics do and what effect do they have? L09
V-gated Na+ channel blockers
| They slow depolarisation
93
What is an example of a class I anti-arrhythmic? L09
Lidocaine
94
What do class II anti-arrhythmics do and what effect do they have? L09
Beta-blockers
| Takes longer time to reach threshold
95
What is an example of a class II anti-arrhythmic? L09
Propanolol
96
What do class III anti-arrhythmics do and what effect do they have? L09
K+ channel blockers
| They prolong repolarisation
97
What is an example of a class III anti-arrhythmic? L09
Amiodarone
98
What do class IV anti-arrhythmics do and what effect do they have? L09
Slow Ca2+ channel blockers
| Slow action potential
99
What is an example of a class IV anti-arrhythmic? L09
Verapamil
100
What class of drug is Digoxin and what is its mechanism? L09
Cardiac glycoside
| Partial inhibition of Na+/K+ ATPase means slow Na+ accumulation and less Ca2+ efflux
101
What is the mechanism for Adenosine? L09
Opens K+ channels and causes hyperpolarisation
102
What is an example of a Phosphodiesterase inhibitor (PDE)? L09
Milirinone, Enoximone
103
How do PDEs work? L09
Increased cAMP leads to increased Ca2+ entry so an increase in contractility
104
What happens in the aorta during systole? L10
It distends to accomodate SV and energy is stored
105
What happens in the aorta during diastole? L10
The aortic walls recoil to propel blood forward
106
What are the features of laminar flow? L10
Normal pattern, highly efficient, follows Poiseuille's law, cannot hear
107
What are the features of turbulent flow? L10
Where flow velocity is high, inefficient, not Poiseuille's law, can hear (murmurs and Korotkoff sounds)
108
What determines systolic pressure? L10
Stroke volume
109
What factors will increase systolic pressure? L10
Increased preload, increased afterload, and increased contractility
110
What determines diastolic pressure? L10
Arteriolar resistance and HR
111
What factors will increase diastolic pressure? L10
Increased vasoconstriction, atherosclerosis and very high HR
112
What happens to pulse pressure with age? L10
It increases as arterial compliance decreases
113
How do endothelial factors affect vasoconstriction/dilation of blood vessels? L10
Nitric oxide, EDHF, and prostacyclin cause vasodilation
| ET-1 causes vasoconstriction
114
How do local factors affect vasoconstriction/dilation of blood vessels? L10
Metabolic: Increased metabolism due to active/functional hyperaemia increases blood flow from dilation
Myogenic: Reflex vasoconstriction in response to higher intravascular pressure e.g. in kidney
115
What is the cerebral autoregulatory range? L10
Mean arterial pressure between 60-170mmHg
116
How do central neural mechanisms affect vasoconstriction/dilation of blood vessels? L10
SNS activity:
Norad on alpha-1 receptors on blood vessels causes vasoconstriction
Norad on beta-2 receptors on skeletal muscle causes vasodilation (fight/flight)
117
How do hormonal mechanisms affect vasoconstriction/dilation of blood vessels? L10
Adren on alpha-1 receptors causes vasoconstriction
Adren on beta-2 receptors causes vasodilation
ADH and AGII cause vasoconstriction
118
What is the thickness of a capillary wall? L11
Single endothelial cell; 0.5µm
119
What is the velocity in a capillary? L11
1mm/sec
120
What are the three exchange mechanisms in a capillary? L11
Diffusion, vesicular transport and bulk flow
121
What is diffusion in a capillary used for? L11
Lipid-soluble substances
122
What is the equation for Fick's Law? L11
Rate of diffusion = Permeability coefficient x conc. grad. x area
123
What is vesicular transport in a capillary used for? L11
Lipid-insoluble substances e.g. proteins, antibodies
| Use other methods e.g. pinocytosis
124
What is bulk flow in a capillary used for? L11
Water, electrolytes, small molecules
125
What are the size of the fenestrations in fenestrated capillaries? L11
60nm
126
What are the forces that counteract filtration in a capillary? L11
Starling forces
127
At what hydrostatic pressure (Pc) does blood enter the arteriolar end of a capillary? L11
35mmHg
128
What is capillary osmotic pressure (πc)? L11
25mmHg
129
At what hydrostatic pressure (Pc) does blood leave the venous end of a capillary? L11
15mmHg
130
If Pc > πc in a capillary, what happens? L11
Filtration out the capillary
131
If Pc < πc in a capillary, what happens? L11
Reabsorption into the capillary
132
What percentage of blood does the venous system hold? L11
60-80%
133
What is the equation for compliance? L11
change in volume/ change in pressure
134
What effect does a fall in venous capacitance have on venous return? L11
Increased venous return
135
Which receptors are responsible for vasoconstriction on blood vessels? L12
Alpha-1 and alpha-2 adrenoceptors
136
Which receptors are responsible for renin release? L12
Beta-1 adrenoceptors
137
Antagonist for alpha receptors? L12
Phentolamine
| Doxazosin
138
What effects on the heart will beta-receptor activation have? L12
Positive chronotropic effect (increased HR)
Positive inotropic effect (increased contractility rate)
Increased automaticity
139
How does a beta-agonist e.g. adrenaline affect the heart? L12
Increased Ca2+ channel opening
| Increased K+ conductance for faster repolarisation
140
What is adrenaline used to treat? L12
Asystole
Ventricular fibrillation
Anaphylaxis
141
What is dobutamine (beta-1 agonist) used to treat? L12
Cardiogenic shock
142
What is phenylephrine (alpha-1 agonist) used to treat? L12
Nasal congestion
143
What is doxazosin (alpha-1 antagonist) used to treat? L12
Hypertension
| Raynaud's syndrome
144
What are beta-blockers used for? L12
Angina
Heart failure
Arrhythmias
Hypertension
145
How do beta-blockers lower blood pressure? L12
Decrease CO
Block renin release (beta-1 receptors in kidney)
Inhibit catecholamine effects
146
What is the effect on the cardiovascular system of parasympathetic stimulation? L12
Negative chronotropic effect on SAN
Slow AVN conduction
(Limited vasodilation due to limited innervation)
147
Which receptors does atropine block? L12
Cardiac M2 receptors
148
Blood flow to coronary muscle is _____ L13
Intermittent
149
When is 85% of the blood flow to the left side of heart? L13
During diastole
150
What happens during systole in the left side of the heart's coronary vessels? L13
They are compressed by the high pressure in the ventricle = extra vascular compression
151
What determines the left side coronary flow during diastole? L13
Aortic pressure
152
When is right side coronary flow highest? L13
During systole
153
Name some examples of local factors that increase blood flow. L13
Adenosine
Prostaglandins
Nitric Oxide
Potassium
154
Name the dense capillary network of the brain. L13
Circle of Willis
155
Functional adaptations of cerebral flow? L13
High basal flow (15% of CO)
Peripheral vasoconstriction to protect cerebral circulation
Autoregulation between 60-170mmHg
Very responsive to CO2 levels
Neuronal activity-evoked functional hyperaemia e.g. local factors to increase blood flow
156
What is CPP? L13
Cerebral Perfusion Pressure
157
What exists in cutaneous circulation to allow blood to go quickly through ateriolar network? L13
AV anastomoses
158
What is bradykinin? L13
Local vasodilator
159
Describe Raynaud's syndrome. L13
"Overreactive" skin vessels
Cold or emotional stimuli causes extreme vasoconstriction
Numbness, pain and burning sensation in hands and feet
160
What do indirect vasodilators do? L14
Block vasoconstriction
161
What do direct vasodilators do? L14
Affect calcium channels
162
Drugs used in angina pectoris? L14
```
Beta-blockers
Ivabradine
GTN
Isosorbide mononitrate
Ca2+ channel blockers e.g. verapamil
```
163
How does GTN work? L14
Increased cGMP levels to cause relaxtion in systemic vessles
164
Side effects of GTN? L14
Hypotension; syncope, headaches
165
5 uses of vasodilators? L14
```
Hypertension
Angina pectoris
Peripheral vascular disease e.g. Raynaud's
Impotence
Hair loss
```
