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s2 - Embryo, Cardio, Endo, GI, Neuro, Pharm > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

Complete Darcy’s Law.

Flow =

A

Difference in Pressure ÷ Resistance

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2
Q

Blood Pressure =

A

CO X TPR

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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

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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

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5
Q

P wave of an ECG shows?

A

Atrial Depolarisaton

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6
Q

T wave of an ECG?

A

Ventricular Repolarisation

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7
Q

Stroke Volume =

A

EDV-ESV

about 120-40 = 80ml

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8
Q

Ejection Fraction =

A

SV ÷ EDV

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9
Q

A wave of jugular venous pressure is due to

A

Atrial Contraction

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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

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11
Q

S1 lub is due to which valves closing?

A

Tricuspid/Mitral

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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
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13
Q

Laplaces Law is determined by wall stress (S).

S =

A

P X ( r ÷ 2w )

Afterload = Pressure X ( radius ÷ 2xwall thickness)

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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

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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
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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
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17
Q

Name 3 Negative Ionotropic Agents

A
  • Hyperkalemia
  • high H+/acidity as H+ competes for TnC sites
  • hypoxia as leads to local acidosis ^
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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

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19
Q

Two things anti-arrythmic drugs can target:

A
  • reducing conduction velocity

- reducing automaticity

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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)

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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

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22
Q

4 passive transport processes

A
  • diffusion
  • osmosis
  • convection (Pressure)
  • Electrochemical flux
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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
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24
Q

What are the three types of capillaries?

A
  • continous (e.g. BBB)
  • fenestrated (e..g. kidneys)
  • discontinous
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25
Q

What is the glycocalyx?

A

A negatively charged material covering the endothelium which blocks solute permeation

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26
Q

What controls diffusion rate? 3 things

A
  • blood flow (less time for equilibration of grad)
  • decreased interstitial concentration (bigger difference)
  • recruitment of capillaries (increases SA and shorter distance)
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27
Q

Starling’s principle of fluid exchange that balance between hydraulic and oncotic pressure regulates exchange, was revised to include the….
As…

A

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

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28
Q

Oedema results from promoted…

e.g. due to

A

Filtration

..increased Pc/ increased Lp (how leaky endothelium is) / increased πg / decreased πp

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29
Q

Give 2 examples of conditions where filtration is promoted due to decreased πp.

A
  • Nephrotic Syndrome - urinary protein loss

- Liver disease - not enough albumin produced

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30
Q

Complete the equation for Bernoulli’s Law of blood flow

FLOW =

A

PRESSURE + KINETIC + POTENTIAL

pv + pv2/2 + pgh

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31
Q

Name 3 Types of Blood Flow

A
  • Laminar (normal)
  • Turbulent (not linear flow due to velocity changes)
  • Bolus (in capilaries, single file, low R)
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32
Q

Reynolds Number:
Re = pVD/u
describes what?

A

Re = p-density Velocity Diametre / Viscosity
Describes change from laminar to turbulent flow
if Re > 2000 turbulent e.g. bruits, ejection murmur

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33
Q

Give 3 parametres that affect BP

A
  • CO
  • Properties of arteries
  • TPR (arterioles)
  • viscosity (Ht)
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34
Q

Pulse Pressure =

A

Systolic BP - Diastolic BP
about 120-80=40mmHg

or SV / Compliance

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35
Q

Compliance =

A

Change in Volume / Change in Pressure

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36
Q

Poiseulle’s Law

Conduction =

A

πr4 / 8nL

π radius4 / 8 viscosity length

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37
Q

Give 3 factors that control TPR

A
  • radius^4, and length
  • myogenic response
  • blood viscosity
  • pressure difference
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38
Q

Contrast bolus flow and flow in arterioles.

A
  • bolus flow has low viscosity, and low resistance

- arterioles are arranged in series so total resistance is greater

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39
Q

Outline the Bayliss Myogenic Response

A

increase in distention of a vessel causes constriction
increased constriction in a vessels causes dilation
-maintains local flow during changes in BP

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40
Q

What three factors determine viscosity (n)?

A
  • blood velocity
  • vessel diameter
  • haematocrit (usually 45%)
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41
Q

How is viscosity affected in polycynthemia? (increased TPR & BP, slower blood flow)

A

Viscosity is higher

42
Q

How is viscosity affected in anaemia? (decreased TPR & BP, HR increased)

A

Viscosity is lower

43
Q

Name 3 ways blood returns from systemic circulation to the heart.

A
  • 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
Q

According to Bernouilli’s law, how does blood return to the heart?

A

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
Q

According to Bernouilli’s law, how does ejected blood overcome the pressure to reach the feet?

A
  • ejected blood has a greater KE than at the feet

- has higher potential energy at the heart

46
Q

Arterial thrombosis tend to be coloured….due to being

A

Arterial = white due to being platelet rich

47
Q

Venous thrombosis tend to be coloured….due to being

A

Venous = red due to being platelet poor

48
Q

Virchow’s Triad of Thrombosis:

A
  • stasis
  • vessel wall injury (smoking, HT, trauma)
  • hypercoaguability (hereditary/aquired)
49
Q

Outline 1ry and 2ndry haemostasis

A

1ry - platelet adhesion, aggregation and stabilisation of plug with fibrin

2ndry - blood coagulation, dissolution of clot, vessel repair and fibrinolysis

50
Q

Warfarin and heparin do what

A

are anti-coagulants

51
Q

Plasminogen activators, steptokinase do what?

A

“clot busters” break down clots

52
Q

Go through what happens in the stages of Atheroma:

  • initial lesion
  • fatty streak
  • ATHEROMA
  • FIBROATHEROMA
  • COMPLICATED LESION
A
  • 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
Q

Give 5 risk factors of developing atherosclerosis:

A
  • age
  • male (+post-menapause)
  • smoking
  • hyperlipidemia
  • HT, diabetes…

& systemic inflammation

54
Q

What is involved in the initiation of Atheroscleosis?

A
  • inflammatory mediators activated eg. oxidised LDL
  • increased expression of adhesion molecules
  • hyper-reactive endothelial layer attracting circulating monocytes
55
Q

What is involved in plaque formation of Atheroscleosis?

A
  • mo takes up LDL and becomes a foam cell
  • releases cytokines activating VSMC
  • VSMCs migrate and proliferate in the intima
56
Q

What is involved in plaque maturation of Atheroscleosis?

A
  • some VSMC that take up LDL and become foam cells undergo apoptosis
  • the lipids accumulate into a necrotic core
57
Q

What is involved in calcification/instability stage of atheroscleosis?

A
  • calcium deposits (from apoptotic foam cells) builds up

- plaque starts to occlude the vessel/break into lumen

58
Q

What is thrombosis?

A
  • 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
Q

Give 3 consequences of Atheroma

A
  • occlusive thrombosis
  • thromoembolism
  • aneurysm
  • peripheral vascular disease
60
Q

Whats the difference between stable and unstable angina?

A

Stable-due to permanent flow limitation

Unstable-due to transient thrombosis

61
Q

Where are baroreceptors found?

How do they sense BP?

A

Walls of carotid artery and aorta

Sense BP by detecting arterial wall stress

62
Q

What is the central sympathetic pathway starting from chemoreceptors in response to a low BP?
(Pressor response)

A
  • 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
Q

Why is HR faster on inhalation?

A

Inhalation switches off parasympathetic vagal nerves

64
Q

Upon orthostasis, BP drops due but quickly recovers due to…the integration of which 3 changes?

A
  • HR X3
  • TPR X3
  • Contractility X1.5

so massive increase in O2 uptake by increased pulmonary circulaton

65
Q

What is postural hypotension?

A

Upon orthostasis, venous pooling in legs, fall in CVP, decreased SV and CO.
Decreased BP so poorer perfusion to brain

66
Q

Orthostasis reflex response:

A

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
Q

What 3 things make postural hypotension worse?

A
  • a-adrenergic blockage/drugs that decrease vascular tone
  • varicose veins
  • reduced circulating blood volume
  • increased core temperature-peripheral v.dilation
68
Q

How does CVS respond to excercise?

A

-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
Q

What vessels vasodilate in moderate excercise?

A

-arterioles in active myocardium and skin

70
Q

What are mechanoreceptors in skeletal muscles sensitive to?

A

-K+, H+ and lactate (these increase during excercise)

71
Q

Name three vasoconstrictors?

A

Adrenaline
Angiotensin II
ADH

72
Q

Name a vasodilator?

A

ANP

73
Q

How do high levels of K+, adenosine, histamine…cause vasodilation?

A

They act on the pre-synaptic terminal

And reduce release of NA hence vasodilation as vascular tone is reduced

74
Q

Where does Adrenaline preferentially act?

At high concentrations where else…

A

B2 receptors

high concs also a1 receptors

75
Q

Endothelin 1/ET1 released from endothelium and TXA2 released from aggregating platelets act where to cause what?

A

Act on VSMC

To cause vasoconstriction

76
Q

What 3 things stimulate RAAS system?

A
  • low renal blood flow
  • sympathetic nerve at B1 receptors
  • low plasma NaCl
77
Q

By which mechanism do a1, AT1, V1, ETA and TXA2 receptors cause vasoconstriction?

A

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
Q

What causes ANP release?

Where is it released from?

A

Stretch receptors in the atria detected excess vasoconstriction
Release from atrial specialised myocytes

79
Q

Give 2 ways ANP acts to reduce BP?

A
  • 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
Q

How do the parasympathetic nerves e.g. ACh, VIP cause vasodilation?

A
  • they act on endothelium

- cause release of NO

81
Q

Give 2 situation in which sudomotor fibres may release ACh/VIP (causing vasodilation)

A
  • sympathetic mediated sweating, increased BF makes more sweat to cool down
  • blushing
82
Q

Where can SubP/CGRP released from C fibres act?

What is the purpose of the vasodilation caused?

A

-on mast cells causing histamine release
-on endothelium and VSM
Both cause skin “flare” increasing WBC for repair

83
Q

What are the 3 parts of the Lewis Triple Response?

A
  • flare
  • local redness
  • wheal
84
Q

How does NO cause vasodilation?

A
  • via eNOS, NO is produced
  • NO stimulates GC (guanylate cyclase)
  • GMP–>c.GMP–> PKG causing vasodilation
85
Q

PGI2 is released via COX action, how do they act?

And why is this important in the kidney?

A
  • via prostanoid receptor
  • GaS pathway increasing PKA –> vasodilation
  • in kidney this maintains BF in arterioles to maintain GFR
86
Q

3 ways PKG/PKA cause vasodilation in VSMC.

A
  • inhibits MLCK
  • Increases SERCA activity
  • increases K+ activity–> hyperpolarisation
87
Q

How does local increases in K+ ions cause VSMC vasodilaton?

A
  • switches on K+ channels
  • increases Na/K+ ATPase so more Na+ extruded
  • VSMC hyperpolarisation
88
Q

Why do you get more vasodilation at the heart and skeletal muscle upon sympathetic activity but vasoconstriction at most other sites?

A

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
Q

List 4 compensatory mechanisms in HF

A
  • ventricular dilation
  • increased myocardial contractility
  • myocardial hypertrophy
  • sympathetic stimulation
  • RAAS
90
Q

Explain each of the following disadv.s of prolonged compensatory mechanisms in HF:

  • continous symp activation
  • increased HR
  • increased preload
  • increased TPR
A
  • 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
Q

What is peripheral oedema and raised JVP a sign of?

A

-Right sided HF

92
Q

What is pulmonary oedema a sign of?

A

-Left sided HF

93
Q

Give 3 symptoms of pulmonary oedema (Left sided HF).

A
  • dysponea
  • orthopnea
  • paroxysmal nocturnal dysponea
94
Q

What biomarker is used in the clinical diagnosis of HF?

If elevated what could be requested?

A

NTproBNP

-request echo/ECG

95
Q

What is paradoxical cold vasodilation in cutaneous circulation?

A

After cold induced vasoconstriction, you will eventually get osscilations between this and vasodilation to protect skin damage.
Occurs by paralysis of symp. transmission

96
Q

What is special functionally about the pulmonary circulation?

A
  • has low vascular resistancs (1/8th vs normal)
  • less symp influence
  • low pressure aids gas exchange
  • HPV
97
Q

What is HPV-hypoxic pulmonary vasoconstriction?

A
  • prevents blood going to poorly ventilated regions of the lungs as hypoxia increases vasoconstriction on the VSMCs
  • optimises V:Q ratio
98
Q

Where is pulmonary pressure lowest, what does this cause?

A

Lowest p at the apex so poor perfusion here

Vessels can collapse slightly impairing oxygenation

99
Q

How does O2 extraction more than double in skeletal muscle during excercise?
(+1 disadv)

A
  • increased flow (+more filtration/oedema)
  • capillary recruitment so more SA for exchange and reduced distance for exchange
  • steeper conc gradient
100
Q

Partial occlusion of coronary arteries show what on an ECG?

A
  • NSTEMI

- small ischaemic area doesnt depolarise so ST segment is depressed

101
Q

Explain how parasympathetic nerves affect HR.

A
  • Ach at M2 receptors (Gai)

- decrease HR

s2 - Embryo, Cardio, Endo, GI, Neuro, Pharm (6 decks)

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