Circulation Flashcards
0
Q
What is recruitment?
A
More capillaries open
1
Q
What happens to pulmonary vascular resistance when pulmonary vascular pressure rises?
A
Resistance falls
2
Q
What is distension?
A
Capillaries widen
3
Q
How are capillaries used to control VQ mismatch?
A
Capillaries to underventilated alveoli can constrict, forcing the blood to flow elsewhere.
4
Q
What is a pulmonary embolus?
A
An obstruction to the pulmonary arterial system. Usually a thrombus.
5
Q
What is blood pressure?
A
Blood pressure = cardiac output x peripheral resistance
6
Q
What may cause pulmonary hypertension?
A
High cardiac output
High pulmonary vascular resistance
7
Q
What increases vascular resistance?
A
Vasoconstriction
Obstruction
Damaged vascular bed
8
Q
What does the p wave represent on an ECG?
A
Atrial systole
9
Q
What does the QRS complex show?
A
Ventricular systole
10
Q
What does the t wave represent?
A
Ventricular repolarisation
11
Q
What is an isovolumic contraction?
A
Ventricular pressure rises but the volume is constant.
12
Q
What is isovolumic relaxation?
A
The ventricular pressure decreases but the volume is constant.
13
Q
What is S1?
A
AV valves closing
14
Q
What is S2?
A
Semilunar valves closing
15
Q
What is S3?
A
Rapid ventricular filling
16
Q
What is S4?
A
Atrial systole
17
Q
Why are capillaries good for diffusion?
A
Large cross sectional area so they are low velocity.
Thin walls.
18
Q
What is Darcy’s law?
A
Blood flow = MABP/TPR
Same as saying that Arterial BP = CO x TPR
19
Q
What causes resistance to blood flow?
A
Vessel radius
Viscosity
20
Q
What determines viscosity?
A
Haematocrit - proportion of blood that is RBCs
Plasma protein concentration and type
21
Q
What is turbulence?
A
Stenotic vessels cause blood to flow in a disorganised way (not laminar flow)
22
Q
What determines vascular tone?
A
Intrinsic regulation (stretch and chemicals) Extrinsic regulation (hormones and nerves)
23
Q
How does NO cause vasodilation?
A
Ca2+ causes NO Synthase to produce NO which activates Guanylyl cyclase. GC causes GTP to be converted into cGMP which phosphorylates Myosin, causing the vascular muscle to relax.
24
What is the vascular response to an increase of metabolic rate in a tissue?
Increased metabolism leads to an increase of metabolites which causes a local vasodilation and increased blood flow to remove the excess metabolites.
25
Does sympathetic activity cause vasoconstriction or vasodilation?
Vasoconstriction
26
Does sympathetic activity increase or decrease peripheral resistance?
Increase
27
What is the effect of parasympathetic activity on vascular tone?
Causes vasodilation
28
What are baroreceptors?
Receptors which detect the blood pressure depending on the stretch of the vessel walls
29
Where are baroreceptors found?
Aortic arch and carotid sinuses
30
What is dynamic sensitivity?
Rate of pressure rise
31
What is static sensitivity?
Magnitude of pressure
32
What would be the autonomic result of an increase in BP?
Increase parasympathetic and decrease sympathetic.
This causes vasodilation and a decrease in HR and CO.
MABP falls
33
What determines the rate of diffusion?
Rate of diffusion = permeability x SA x concentration gradient
34
What is hydrostatic pressure?
Where fluid moves from an area of high pressure to an area of low pressure
35
What is colloid oncotic pressure? (Osmotic pressure)
Movement of fluid from an area of low [protein] to an area of high [protein]
36
When does oedema occur?
When the capillary filtration rate is faster than the lymphatic drainage
37
Describe Cardiac muscle.
Striated, multinucleate, branched, intercalated discs, Myogenic activity
38
Can recruitment alter strength of contraction in the heart?
No, all fibres in the heart contract together anyway.
39
Does the frequency of action potentials control heart rate?
Not really, the heart has an automatic rhythmic control system (SAN)
40
What ion increases the strength of a contraction in the heart?
Ca2+
41
What types of drugs increase the intracellular concentration of Calcium ions?
Positive Ionotropic drugs
42
List 3 ways of increasing intracellular calcium ion concentration.
1. Ca2+ enters from the outside of the cell
2. Intracellular stores allow 'quick release'
3. Calcium induced calcium release
43
How can you decrease intracellular calcium concentration?
1. Active Na+/Ca2+ exchange on cell membrane
| 2. Active uptake to Sarcoplasmic reticulum
44
How do calcium ions cause cardiac muscle contraction?
Ca2+ binds to Troponin-c which causes Tropomyosin to move out of the Myosin binding site. Actin-Myosin cross bridges form. Actin filament moves along Myosin and the Myosin head disengages, Repeat!
45
In a Cardiac Action potential, which ions are responsible for each stage?
Depolarisation - Na+ influx.Partial Repolarisation - K+ efflux
Plateau - Ca2+ influx
Repolarisation - K+ efflux
Pacemaker depolarisation - Na+ channels reactivation
46
What is the purpose of the plateau phase of the action potential?
Prevents tetanic contraction to maintain rhythmic contraction
47
How do beta agonists work as Positive Ionotropic drugs?
Speed up Ca2+ uptake to cellular stores, making it more availible
48
How do Glycosides work as Ionotropic drugs?
Inhibits Na+/K+ ATPase, increasing intracellular Na+, which causes a decrease in Na+/Ca2+ exchange. This allows the Ca2+ intracellular concentration to increase
49
Name 2 examples of Negative Ionotropic drugs.
Ca2+ channel blockers
| Beta blockers
50
What is Preload?
The stretching of cardiac myocytes prior to contraction (due to venous return)
51
What increases preload?
1. Gravity - inc. preload
2. Thoracic pump
3. Muscle pump
4. Co-localisation
5. Blood volume
6. Venomotor tone
52
How does the muscle pump increase preload?
Veins are compressed by surrounding muscles which increases venous return
53
What is Co-loacalisation?
Pulsating arteries massage veins, thus increasing venous return
54
What is the equation for Cardiac Output?
Cardiac output = Heart rate x Stroke Volume
55
What limits the cardiac output?
Venous return
56
How is Cardiac Output measured?
By looking at the volume of oxygen taken in, the O2 saturation of both arterial and venous blood and the Hb concentration. This calculates the lung blood flow which is equal to the cardiac output.
57
What is a possible impact of a fast heart rate on the coronary blood supply?
It may decrease as blood only flows in the coronary arteries during diastole. In severe cases, this may lead to ischaemia.
58
Is the SNS or the PNS mostly in charge of heart rate under normal conditions?
PNS
59
What is starlings law?
The stroke volume is dependent upon the stretch of the ventricular muscle fibres.
Stretching the fibres (from increased preload) increases the force with which the mucle contracts.
61
What is decompensation?
When the muscle is stretched too much, cross bridge formation is reduced and so the force of contraction decreases.
62
What is contractility?
The force of contraction caused by Calcium ions.
63
What is heart failure?
An inability to maintain a sufficient Cardiac output at a normal filling pressure (preload).
64
What is Dynamic/Isotonic exercise?
Rhythmic contraction of muscles (aerobic)
65
What does dynamic/Isotonic exercise do to the muscle length?
It shortens it.
66
What is static/Isometric exercise?
Continued muscle tension (e.g. weight lifting).
| No muscle shortening.
67
What muscle types are there?
Slow twitch and fast twitch
68
What are slow twitch muscle fibres?
Dependent upon Oxidative Phosphorylation.
Good blood supply
Lots of mitochondria
Mostly used for posture.
69
What are fast twitch muscle fibres?
Dependent upon Creatine Phosphate to regenerate ATP.
Lots of Glycolytic enzymes
Used in explosive exercise!
70
How do you measure the intensity of exercise?
By O2 uptake
71
What is oxygen debt?
The O2 which is used up readily before Cardiopulmonary adaptations start shortly after exercise begins.
72
How does Oxygen debt occur?
ATP and Creatine Phosphate are depleated and lactic acid builds up.
73
How is O2 debt repaid?
Fast - rephosphorylation of ADP and Creatine
Slow - lactate is converted back to Glucose/Glycogen
Very slow - Increased metabolic rate after exercise
74
What Cardiovascular changes occur during exercise?
Increased HR
Increased SV
Increased Arterial BP
Decreased Peripheral resistance
75
Why does peripheral resistance decrease during exercise?
Resistance is dependent upon vascular tone.
| Increased metabolism leads to increased vasodilation which decreases the resistance.
76
During exercise, where is more of the CO directed to?
Heart, muscle, skin (to a certain extent)
77
What happens to the proportion of the CO going to the brain during exercise?
It remains the same as before!
78
What respiratory changes are there during exercise?
Increased respiratory rate
| Increased tidal volume
79
Do ABGs change during exercise?
No
80
What triggers cardiopulmonary changes in exercise?
Central control of locomotor areas of the brain increase HR and Respiratory rate!
Barorecpetors detect 'stretch' to maintain a good BP.
81
What is the limiting factor of the pathway of O2 during exercise?
O2 delivery by cardiovascular system
82
What happens to muscles when they are trained?
Hypertrophy.
More myofibrils
More mitochondrial enzymes
More ATP, Phosphocreatine and Glycogen
83
What happens to the CVS as a result of training?
Bradycardia
Cardiac remodelling
Decreased blood pressure
Increased Myoglobin and BPG
84
What happens to the respiratory system as a result of training?
Decreased ventilation rate at the same level of exercise.
85
What is VO2max?
The functional capacity of the CVS and pulmonary system.
86
What does the Renin-Angiotensin system do?
Regulates blood pressure and blood volume.
87
What is Angiotensin 1 formed from?
Angiotensinogen
88
What enzyme helps convert Angiotensinogen into Angiotensin 1?
Renin
89
What is Angiotensinogen?
A physiologically inactive protein, produced and secreted continuously by the liver.
90
What enzyme helps convert Ang1 to Ang2?
Angiotensin converting Enzyme (ACE)
91
What product can be formed from Ang2?
Aldosterone
92
What does Ang2 do?
Vasoconstriction (short term control)
| Produces Aldosterone.
93
What does Aldosterone do?
Promotes salt and water retention. (Long term BP control)
94
Where is Renin secreted from?
The juxtoglomerulus apparatus in the kidney
95
How often is ACE secreted?
Continuously secreted in the same quantity.
96
Aside from converting Ang1 into Ang2, what does ACE do?
Breaks down Bradykinin.
97
What affect does Bradykinin have on vascular tone?
It causes vasodilation
98
Where is Aldosterone released from?
The adrenal cortex.
99
What is the regulatory control of the Renin-Angiotensin system?
Renin (under sympathetic control)
100
Where does Renin originate from?
The kidneys
101
When is Renin released?
Low BP (SNS via Baroreceptor reflex and via Intrarenal stretch receptors)
Low blood volume
Altered Na+ handling
102
What controls whether the Renin-Angiotensin system is on or off?
Renin
103
Where does Ang 2 mostly bind?
AT1 receptors
104
What happens when AT1 receptors are activated?
Vasoconstriction and inc BP
Promotes cell division and growth
Profibrotic
105
What happens when Ang 2 binds to AT2 receptors?
Vasodilation and decreased BP
| Anti-mitogenic
106
How does AT1 activation cause vasoconstriction?
Works directly on smooth muscle. Increases sympathetic activity by increasing NA release but blocking it's re-uptake back into the pre-synaptic knob.
107
When AT1 is activated, Aldosterone is released. What are the affects of Aldosterone?
Salt and water retention.
| Increased ADH secretion and thirst.
108
How does AT2 cause vasodilation?
NO release
| Increases Bradykinin levels
109
What equation represents MABP?
MABP = CO x TPR
110
Why would you want to block the Renin-Angiotensin system?
Reduce BP or Heart failure.
111
What drugs can be used to block RAS?
Beta blockers
Renin Inhibitors
ACE inhibitors
AT1 antagonists
112
How do beta blockers block RAS?
Reduces Sympathetic production of Renin.
