Cardiovascular System Flashcards
(101 cards)
1
Q
Complete Darcy’s Law.
Flow =
A
Difference in Pressure ÷ Resistance
2
Q
Blood Pressure =
A
CO X TPR
3
Q
SAN Pacemaker Potentials. Outline
Stage 4
Stage 0
Stage 3
A
4 - If Na+ channel activated by hyperpolarisation
0 - VGCa2+C open, rapid depolarisaton
3 - VGK+C cause K+ efflux and repolarisation
4
Q
Atrioventricular APs. Outine Stage 4 Stage 0 Stage 1 Stage 2 Stage 3
A
4 - RMP maintained by Na/K pump
0 - VGNa+ open, Na influx, VGCaC start to open
1 - peak of AP, VGNa+ close
2 - VGCaC still open, VGK+C open - plateau phase
3 - VGCaC close, K+ effluxing so rapid repolarisation
5
Q
P wave of an ECG shows?
A
Atrial Depolarisaton
6
Q
T wave of an ECG?
A
Ventricular Repolarisation
7
Q
Stroke Volume =
A
EDV-ESV
about 120-40 = 80ml
8
Q
Ejection Fraction =
A
SV ÷ EDV
9
Q
A wave of jugular venous pressure is due to
A
Atrial Contraction
10
Q
X descent and Y descent can be seen as pulsatile collapse in the neck veins. What do these correspond to?
A
X descent - ventricular contraction
Y descent - atria contraction when tricuspid valve opens
11
Q
S1 lub is due to which valves closing?
A
Tricuspid/Mitral
12
Q
Why do you get greater energy of contraction with greater muscle fibre stretch at rest?
A
Starlings Law
- less overlapping of myosin/actin
- less mechanical interference
- increased Ca2+ sensitivity and more cross bridge formation potential
13
Q
Laplaces Law is determined by wall stress (S).
S =
A
P X ( r ÷ 2w )
Afterload = Pressure X ( radius ÷ 2xwall thickness)
14
Q
Laplaces law means that a small ventricle, will have greater wall curvature, so more wall stress is directed towards….
and ejection is….
A
the centre so there is less afterload
and ejection is better
15
Q
In a healthy heart Laplaces law facilitates ejection as during ventricular contraction, chamber radius decreases, reducing afterload and aiding ejection.
What happens in a failing heart?
Compensation
Effect on CO
What happens to S
A
- chambers are dilated so radius is higher, S increases.
- to compensate w is increased by hypertrophy
- this increases CO
- S is the same but is spread over a larger area
16
Q
How does NA increase ionotropy?
A
- acts on B1 receptors
- GaS pathway, increases PKA
- phosphorylates VGCC and RyR
- increased Ca and CICR so increased force of contraction
17
Q
Name 3 Negative Ionotropic Agents
A
- Hyperkalemia
- high H+/acidity as H+ competes for TnC sites
- hypoxia as leads to local acidosis ^
18
Q
Arrythmias result from
-Abnormal impulse generation or
-Abnormal conduction
Give 2 examples of each
A
Impulse: -automatic rhythms/increased SAN activity
-Triggered rhythms: EAD, DAD
Conduction: -heart block
-re-entry electrical circuits
19
Q
Two things anti-arrythmic drugs can target:
A
- reducing conduction velocity
- reducing automaticity
20
Q
Anti-Arrhythmic Drug Classes act at: I II II IV
Do they act nodally, non-nondally or both at the node and non-nodally?
A
I - Na+ channel blockers (non nodal)
II - B blockers (both)
III - K+ channel blockers (non nodal)
IV - CCB (both)
21
Q
How do Class III anti-arrhythmic drugs such as Amiodarone act?
A
Block K+ channels to maintain depolarisation.
Na+ channels are inactivated so the refractory period increases during which more APs cant fire
22
Q
4 passive transport processes
A
- diffusion
- osmosis
- convection (Pressure)
- Electrochemical flux
23
Q
What 4 things control the rate of solute transport?
A
- Passive diffusion properties (T = x2 / 2D)
- Properties of solvents and membranes
- Properties of capillaries
- Permeability
24
Q
What are the three types of capillaries?
A
- continous (e.g. BBB)
- fenestrated (e..g. kidneys)
- discontinous
25
What is the glycocalyx?
A negatively charged material covering the endothelium which blocks solute permeation
26
What controls diffusion rate? 3 things
- blood flow (less time for equilibration of grad)
- decreased interstitial concentration (bigger difference)
- recruitment of capillaries (increases SA and shorter distance)
27
Starling's principle of fluid exchange that balance between hydraulic and oncotic pressure regulates exchange, was revised to include the....
As...
Glycocalyx
As...plasma proteins move from the lumen to interstital space via a vesicle system not via intracellular spaces as the glycocalyx acts a barrier
28
Oedema results from promoted...
| e.g. due to
Filtration
| ..increased Pc/ increased Lp (how leaky endothelium is) / increased πg / decreased πp
29
Give 2 examples of conditions where filtration is promoted due to decreased πp.
- Nephrotic Syndrome - urinary protein loss
| - Liver disease - not enough albumin produced
30
Complete the equation for Bernoulli's Law of blood flow
| FLOW =
PRESSURE + KINETIC + POTENTIAL
| pv + pv2/2 + pgh
31
Name 3 Types of Blood Flow
- Laminar (normal)
- Turbulent (not linear flow due to velocity changes)
- Bolus (in capilaries, single file, low R)
32
Reynolds Number:
Re = pVD/u
describes what?
Re = p-density Velocity Diametre / Viscosity
Describes change from laminar to turbulent flow
if Re > 2000 turbulent e.g. bruits, ejection murmur
33
Give 3 parametres that affect BP
- CO
- Properties of arteries
- TPR (arterioles)
- viscosity (Ht)
34
Pulse Pressure =
Systolic BP - Diastolic BP
about 120-80=40mmHg
or SV / Compliance
35
Compliance =
Change in Volume / Change in Pressure
36
Poiseulle's Law
| Conduction =
πr4 / 8nL
| π radius4 / 8 viscosity length
37
Give 3 factors that control TPR
- radius^4, and length
- myogenic response
- blood viscosity
- pressure difference
38
Contrast bolus flow and flow in arterioles.
- bolus flow has low viscosity, and low resistance
| - arterioles are arranged in series so total resistance is greater
39
Outline the Bayliss Myogenic Response
increase in distention of a vessel causes constriction
increased constriction in a vessels causes dilation
-maintains local flow during changes in BP
40
What three factors determine viscosity (n)?
- blood velocity
- vessel diameter
- haematocrit (usually 45%)
41
How is viscosity affected in polycynthemia? (increased TPR & BP, slower blood flow)
Viscosity is higher
42
How is viscosity affected in anaemia? (decreased TPR & BP, HR increased)
Viscosity is lower
43
Name 3 ways blood returns from systemic circulation to the heart.
- Down Pressure grad. (flow = change in p / R)
- thoracic pump (inhalation increases BF by raising abdo pressure and forcing blood up
- Skeletal muscle pump
44
According to Bernouilli's law, how does blood return to the heart?
Also according to Bernouilli's law, change in pressure and pgh gradients cancel out but kinetic energy of blood allows it to return to heart.
45
According to Bernouilli's law, how does ejected blood overcome the pressure to reach the feet?
- ejected blood has a greater KE than at the feet
| - has higher potential energy at the heart
46
Arterial thrombosis tend to be coloured....due to being
Arterial = white due to being platelet rich
47
Venous thrombosis tend to be coloured....due to being
Venous = red due to being platelet poor
48
Virchow's Triad of Thrombosis:
- stasis
- vessel wall injury (smoking, HT, trauma)
- hypercoaguability (hereditary/aquired)
49
Outline 1ry and 2ndry haemostasis
1ry - platelet adhesion, aggregation and stabilisation of plug with fibrin
2ndry - blood coagulation, dissolution of clot, vessel repair and fibrinolysis
50
Warfarin and heparin do what
are anti-coagulants
51
Plasminogen activators, steptokinase do what?
"clot busters" break down clots
52
Go through what happens in the stages of Atheroma:
- initial lesion
- fatty streak
- ATHEROMA
- FIBROATHEROMA
- COMPLICATED LESION
- initial lesion-mo infiltration, isolated foam cell
- fatty streak-intracellular lipid accumulation
- ATHEROMA-"" + core of extracelluar lipid
- FIBROATHEROMA- ""lipid cores. Fibrotic/calcific layers
- COMP. LESION-surface defect, haematoma, thrombosis
53
Give 5 risk factors of developing atherosclerosis:
- age
- male (+post-menapause)
- smoking
- hyperlipidemia
- HT, diabetes...
& systemic inflammation
54
What is involved in the initiation of Atheroscleosis?
- inflammatory mediators activated eg. oxidised LDL
- increased expression of adhesion molecules
- hyper-reactive endothelial layer attracting circulating monocytes
55
What is involved in plaque formation of Atheroscleosis?
- mo takes up LDL and becomes a foam cell
- releases cytokines activating VSMC
- VSMCs migrate and proliferate in the intima
56
What is involved in plaque maturation of Atheroscleosis?
- some VSMC that take up LDL and become foam cells undergo apoptosis
- the lipids accumulate into a necrotic core
57
What is involved in calcification/instability stage of atheroscleosis?
- calcium deposits (from apoptotic foam cells) builds up
| - plaque starts to occlude the vessel/break into lumen
58
What is thrombosis?
- When a plaque ruptures and the lipid/necrotic core is released into the vessel, where it occludes flow
- endothelium disruption exposed TF initiating thrombin formation
59
Give 3 consequences of Atheroma
- occlusive thrombosis
- thromoembolism
- aneurysm
- peripheral vascular disease
60
Whats the difference between stable and unstable angina?
Stable-due to permanent flow limitation
| Unstable-due to transient thrombosis
61
Where are baroreceptors found?
| How do they sense BP?
Walls of carotid artery and aorta
| Sense BP by detecting arterial wall stress
62
What is the central sympathetic pathway starting from chemoreceptors in response to a low BP?
(Pressor response)
- chemoreceptors excite NTS
- NTS inhibits the CVLM (this is the inhibitory centre)
- CVLM disinhibits the RVLM
- RVLM -> spinal cord, increases sympathetic outflow to heart and blood vessels to increase BP
63
Why is HR faster on inhalation?
Inhalation switches off parasympathetic vagal nerves
64
Upon orthostasis, BP drops due but quickly recovers due to...the integration of which 3 changes?
- HR X3
- TPR X3
- Contractility X1.5
so massive increase in O2 uptake by increased pulmonary circulaton
65
What is postural hypotension?
Upon orthostasis, venous pooling in legs, fall in CVP, decreased SV and CO.
Decreased BP so poorer perfusion to brain
66
Orthostasis reflex response:
Decreased: baroreceptor stimulation
Switch off inhibitory fibres in the CVLM
RVLM increases symp drive to SAN increases HR
Increased contractility and TPR so BP increases
67
What 3 things make postural hypotension worse?
- a-adrenergic blockage/drugs that decrease vascular tone
- varicose veins
- reduced circulating blood volume
- increased core temperature-peripheral v.dilation
68
How does CVS respond to excercise?
-increase symp NS, decreased vagal
-HR x3
-SV x1.5
-(A-V)02 x3
so o2 uptake from the lungs is increased with the greater flow and conc grad. Despite normal BP.
69
What vessels vasodilate in moderate excercise?
-arterioles in active myocardium and skin
70
What are mechanoreceptors in skeletal muscles sensitive to?
-K+, H+ and lactate (these increase during excercise)
71
Name three vasoconstrictors?
Adrenaline
Angiotensin II
ADH
72
Name a vasodilator?
ANP
73
How do high levels of K+, adenosine, histamine...cause vasodilation?
They act on the pre-synaptic terminal
| And reduce release of NA hence vasodilation as vascular tone is reduced
74
Where does Adrenaline preferentially act?
| At high concentrations where else...
B2 receptors
| high concs also a1 receptors
75
Endothelin 1/ET1 released from endothelium and TXA2 released from aggregating platelets act where to cause what?
Act on VSMC
| To cause vasoconstriction
76
What 3 things stimulate RAAS system?
- low renal blood flow
- sympathetic nerve at B1 receptors
- low plasma NaCl
77
By which mechanism do a1, AT1, V1, ETA and TXA2 receptors cause vasoconstriction?
via Gaq: PIP2 via PLC --> IL3 and DAG
-increases membrane excitability by increased Na+ and VGCa2+ channels
-increased release of Ca2+ from SR
More calcium leads to more contraction
78
What causes ANP release?
| Where is it released from?
Stretch receptors in the atria detected excess vasoconstriction
Release from atrial specialised myocytes
79
Give 2 ways ANP acts to reduce BP?
- dilates renal afferent arterioles so more filtration and excretion to decrease blood volume
- at NP receptors on VSMCs it increases the c.GMP pathway causing vasodilation
- decreases RAAS system
80
How do the parasympathetic nerves e.g. ACh, VIP cause vasodilation?
- they act on endothelium
| - cause release of NO
81
Give 2 situation in which sudomotor fibres may release ACh/VIP (causing vasodilation)
- sympathetic mediated sweating, increased BF makes more sweat to cool down
- blushing
82
Where can SubP/CGRP released from C fibres act?
| What is the purpose of the vasodilation caused?
-on mast cells causing histamine release
-on endothelium and VSM
Both cause skin "flare" increasing WBC for repair
83
What are the 3 parts of the Lewis Triple Response?
- flare
- local redness
- wheal
84
How does NO cause vasodilation?
- via eNOS, NO is produced
- NO stimulates GC (guanylate cyclase)
- GMP-->c.GMP--> PKG causing vasodilation
85
PGI2 is released via COX action, how do they act?
| And why is this important in the kidney?
- via prostanoid receptor
- GaS pathway increasing PKA --> vasodilation
- in kidney this maintains BF in arterioles to maintain GFR
86
3 ways PKG/PKA cause vasodilation in VSMC.
- inhibits MLCK
- Increases SERCA activity
- increases K+ activity--> hyperpolarisation
87
How does local increases in K+ ions cause VSMC vasodilaton?
- switches on K+ channels
- increases Na/K+ ATPase so more Na+ extruded
- VSMC hyperpolarisation
88
Why do you get more vasodilation at the heart and skeletal muscle upon sympathetic activity but vasoconstriction at most other sites?
Coronary circulation and skeletal muscle have loads of B2 receptors - Adren acts here, PKA inhibits contraction of smooth muscle (VSMC)
Elsewhere have more a1 receptors leading to sympathetic mediated v.constriction
89
List 4 compensatory mechanisms in HF
- ventricular dilation
- increased myocardial contractility
- myocardial hypertrophy
- sympathetic stimulation
- RAAS
90
Explain each of the following disadv.s of prolonged compensatory mechanisms in HF:
- continous symp activation
- increased HR
- increased preload
- increased TPR
- continous symp activation - B-adrenergic downregulation/desensitisation
- increased HR - higher metabolic demand
- increased preload - pressure transmitted to pulmonary vasculature --> pulmonary oedema
- increased TPR - increased afterload --> decreased CO
91
What is peripheral oedema and raised JVP a sign of?
-Right sided HF
92
What is pulmonary oedema a sign of?
-Left sided HF
93
Give 3 symptoms of pulmonary oedema (Left sided HF).
- dysponea
- orthopnea
- paroxysmal nocturnal dysponea
94
What biomarker is used in the clinical diagnosis of HF?
| If elevated what could be requested?
NTproBNP
| -request echo/ECG
95
What is paradoxical cold vasodilation in cutaneous circulation?
After cold induced vasoconstriction, you will eventually get osscilations between this and vasodilation to protect skin damage.
Occurs by paralysis of symp. transmission
96
What is special functionally about the pulmonary circulation?
- has low vascular resistancs (1/8th vs normal)
- less symp influence
- low pressure aids gas exchange
- HPV
97
What is HPV-hypoxic pulmonary vasoconstriction?
- prevents blood going to poorly ventilated regions of the lungs as hypoxia increases vasoconstriction on the VSMCs
- optimises V:Q ratio
98
Where is pulmonary pressure lowest, what does this cause?
Lowest p at the apex so poor perfusion here
| Vessels can collapse slightly impairing oxygenation
99
How does O2 extraction more than double in skeletal muscle during excercise?
(+1 disadv)
- increased flow (+more filtration/oedema)
- capillary recruitment so more SA for exchange and reduced distance for exchange
- steeper conc gradient
100
Partial occlusion of coronary arteries show what on an ECG?
- NSTEMI
| - small ischaemic area doesnt depolarise so ST segment is depressed
101
Explain how parasympathetic nerves affect HR.
- Ach at M2 receptors (Gai)
| - decrease HR
