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Medicine > CVS > Flashcards

CVS Flashcards

1
Q

What is the main function of the CVS?

A

Transport

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2
Q

What are the transport functions the CVS carries out?

A

1) External to internal environment- oxygen from the respiratory system and nutrients and water from the GIT.
2) Cell to cell- waste products are taken to the liver, immune cells and antibodies are taken to other cells in need of them, hormones are taken to their target cells.
3) Materials leaving the body- metabolic waste to the kidneys, heat and thermoregulation done by circulation to the skin, CO2 is got rid of by perfusion of the lungs.

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3
Q

What is the arrangement of the CVS?

A

Left heart, arterial system, systemic circulation, venous system, right heart.

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4
Q

What is the relationship between the right and left sides of the heart?

A

They are in series with eachother. Output of RV into pulmonary circulation = output of LV into systemic circulation.

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5
Q

What is the relationship between the vascular beds?

A

They are in parallel. All beds get blood with the same level of oxygenation, prevents changes in blood flow in in one organ affecting flow in other organs.

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6
Q

What is systole?

A

Phase of ventricular contraction and ejection

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7
Q

What is diastole?

A

Phase of ventricular relaxation and filling

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8
Q

What is the formula for CO?

A

SV x HR

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9
Q

What is cardiac output and what is a typical value?

A

Volume of blood pumped per minute. 5Lmin-1

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10
Q

What is CO determined by and what are the typical values for these

A

Heart rate- 70bpm and stroke volume- 70ml

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11
Q

True or False, left CO = right CO

A

True

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12
Q

What is the formula for pulse pressure?

A

SP-DP

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13
Q

What does a strong pulse indicate?

A

A high pulse pressure

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14
Q

What percentage of the cardiac cycle is diastole?

A

60%

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15
Q

What is the formula for mean ABP?

A

Mean ABP= (SP-DP)/3 + DP

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16
Q

What happens to pressure through the system?

A

Pressure drops because there is resistance to flow

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17
Q

What determines pressure in the arterial system?

A

1) Resistance to blood flow
2) Blood volume in the arterial system
ABP= CO x TPR

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18
Q

How do arterioles control blood flow to organs?

A

Vasoconstriction or vasodilation changes resistance and controls flow. Vasodilation increases flow and vasoconstriction decreases it.

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19
Q

What are the functions of veins and how are these achieved?

A 
Carry blood at v low pressure
Thin walls
Muscle control by ANS
Wide lumen to accommodate large volumes
Reservoirs used to adjust ventricular filling
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20
Q

What are the functions of arteries and how are these achieved?

A 
Carry blood at high pressure
Thick muscular walls
Elastic layers
Narrow lumen
High pressure conduits
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21
Q

What are the functions of arterioles and how are these achieved?

A

Carry blood at modest pressure
Thick, muscular walls
Muscle under influence of local factors and ANS
Function to control flow to tissues

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22
Q

What are the functions of capillaries and how are these achieved?

A

Carry blood at low pressure
Single endothelial cell wall
Maximise exchange between blood and tissue

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23
Q

What are the functions of venules and how are these achieved?

A

Low pressure
Resemble capillaries
Low pressure conduits

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24
Q

How is ABP maintained?

A

Negative feedback control. ABP= CO x TPR
= (SV x HR) x TPR
ANS causes cardiac stimulation, vascular constriction (if ABP decreases) Kidneys change blood volume.

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25
Q

What is important about cardiac muscle cells?

A

They have myogenic or auto rhythmicity. Conductoin then occurs in a highly coordinated way.

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26
Q

What are the 3 types of cardiac action potentials?

A

SA and AV nodes
Atrial muscle
Purkinje fibres and ventricular muscle

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27
Q

What is the pacemaker rate?

A

100 AP/min

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28
Q

Where is the SAN?

A

Wall of the R atrium near the entrance on the vena cava, a group of excitable cells.

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29
Q

Why is there no ‘resting’ membrane potential?

A

The cells constantly cause APs, there is a pacemaker potential.

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30
Q

How are cardiac cells depolarised?

A

Opening of T type calcium channels
Closure of K+ channels
Opening of slow Na+ channels
Opening of fast Na+ channels

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31
Q

Which ions are responsible for the PACEMAKER POTENTIAL in the SA node?

A

Inward movement of Na+ (not fast v-g current)
Inward movement of Ca2+
Decreased conductance of K+ by closure of K+ channels
These changes slowly work towards threshold and cause an AP
If the cell uses v-g fast channels then it depolarises v quickly, not for cardiac cells. This is calcium mediated depolarisation. T (transient) channels in the pacemaker. Further decrease in K+ conductance, mostly Ca entering the cell.

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32
Q

Which ions are responsible for the ACTION POTENTIAL in the SA node?

A

Long action potential, calcium mediated.
Inward movement of Ca2+ (through different channels to those involved in the pacemaker potential
Further decrease in K+ conductance
Outward movement of K+

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33
Q

What is the autonomic control like in the SAN?

A

Antagonistic
Intrinsic rate is 100 AP/min, but HR= 60-70bpm. This is because vagal outflow reduces resting heart rate. Vagus- heart- short postganglionic neuron. Sparse innervation to the ventricles. Vagal tone predominates.

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34
Q

How does autonomic control of heart rate occur?

A

By altering the pacemaker potential
Increased parasympathetic activity decreases heart rate. ACh at M2 receptors. 1) Hyperpolarises the cell (opens K+ channels) 2) Reduces the slope of the pacemaker potential
Negative chronotropic effect.
Increased sympathetic activity increases HR. Gets closer to threshold a lot quicker, AP- slow depolarisation changed to much quicker. Increased slope of pacemaker potential increases Na and Ca conductance.

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35
Q

How do APs spread through atrial muscle?

A

Current flows to adjoining cells through gap junctions to depolarise adjacent cells. Current spreads so quickly that it contracts as one. From SA to atrium.

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36
Q

What is the speed of conduction through atria?

A

0.5m/s

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37
Q

What happened in atrial depolarisation?

A

Activity spreads through atrial muscle, complete within 0.09s of SAN firing. As activity spreads it generates APs myocytes contract.

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38
Q

What is the pathway of conduction from the SAN to the ventricle?

A

SAN-atria-AVN. The fastest pacemaker at any point drives HR. AVN ensures conduction is in the correct order.

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39
Q

What is AV delay?

A

AVN is a different tissue and has poorer conduction, the delay ensures the ventricles have the chance to fill.

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40
Q

What is the order of depolarisations?

A

Depolarise atria, depolarise bundle of His, depolarise bundle branches, depolarise purkinje fibres and ventricular muscle, depolarise ventricles from endocardium to epicardium.

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41
Q

What are the phases of ventricular myocyte AP?

A

Rapid depolarisation- Inward movement of Na+ through fast V-G channels
Partial repolarisation- Inactivation of Na+ channels
Plateau- Inward Ca2+ movement AND outward K+ movement
Repolarisation- Outward movement of K+

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42
Q

What are the refractory periods like for the ventricles?

A

Absolute- long time, 200ms
Relative- 50ms
Important to have a long refractory period because if there wasn’t one, there would be tetanic contraction of the muscle as it is stimulated, it wouldn’t relax fully.

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43
Q

What are the ECG leads?

A

6 limb leads and 6 precordial chest leads, both together would make up a 12 lead egg

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44
Q

Where should the electrodes be placed?

A

On the fleshy parts of the limbs, not over bones or joints

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45
Q

What are the leads on a limb ecg?

A

RA (R) Right wrist, red
LA (L) Left wrist, yellow
RL (N) Right leg, black, neutral, wire filters other electrical activity
LL (F) Left leg, green

3 standard (bipolar) limb leads and 3 augmented (unipolar) limb leads.

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46
Q

What are the points of Einthoven’s triangle for recording standard bipolar limb leads?

A

Electric flows along sides of a triangle. Right arm, left arm and pubic symphysis.

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47
Q

How is a dipole generated?

A

A dipole is charge separation. The body is a good conductor of electricity. The heart contracts due to APs, a wavefront of electrical activity moves across the heart and results in a - to + dipole, this creates an electrical field that can be recorded by electrodes on the skin.

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48
Q

What do the ECG waves represent?

A 
P- atrial depolarisation
Q- down bundle of His
R- mass of ventricle spreads
S- up side of ventricles, away from the leg
T- repolarisation
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49
Q

What does QRS wave show?

A

Ventricular depolarisation

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50
Q

What does PR interval show?

A

AVN delay

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51
Q

Outline the cardiac cycle physiological principles

A

1) Pressure will increase in a chamber when muscle around it contracts
2) Valves will open when there is a P gradient across them, Patrial>Pventricular
3) Blood will flow down a pressure/ energy gradient
4) When valves are open, changes in P in neighbouring chambers change together
5) When valves are closed, pressures in neighbouring chambers can be different

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52
Q

What is ventricular diastole rapid filling?

A

Rapid filling
AV (mitral) valve opens Patrial>Pventricular
Aortic valve closed Pventricular Patrial> Pventricular

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53
Q

What part of ventricular diastole is it when atrial contraction increases Patrial and contributes ~5ml to ventricular filling?

A

Atrial systole and ventricular filling in ventricular diastole

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54
Q

What is ventricular systole?

A

Isovolumetric contraction

1) Ventricular contraction increases Pventricular, causes AV valve to close
2) AV valve closes Pvent> Patrial
3) Aortic valve closed, PventPaortic will cause the ejection of blood into the aorta
4) Aortic valve opens (Pvent>Paortic )
5) Ventricular ejection into the aorta

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55
Q

What happens after ventricular systole?

A

Ventricular Diastole, Isovolumetric relaxation
Ventricular relaxation causes Pvent to decrease. Momentum of blood slows, lose positive energy gradient and aortic valve closes. AV valve closed Pvent> Patrial

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56
Q

What are the phases of ventricular diastole?

A

Isovolumetric relaxation
Rapid filling- AV valve open
Atrial systole, ventricular filling- Atrial contraction
SYSTOLE

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57
Q

What are the phases of ventricular systole?

A

Isovolumetric contraction

Ejection

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58
Q

Important pressures of the L cardiac cycle:

a) Aortic Pressure
b) Ventricular Pressure
c) Atrial Pressure
d) ESV
e) EDV
f) SV

A

a) 80-120mmHg
b) 0-120mmHg
c) 0-10mmHg
d) ~50ml
e) ~120ml
f) EDV-ESV

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59
Q

What does the ESV do?

A

Gives a reserve of blood if SV needs increasing

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60
Q

Give 2 formulae for CO

A 
HR x SV
HR x (EDV - ESV)
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61
Q

How can you increase SV?

A

Increase EDV &/ decrease ESV

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62
Q

What is excitation contraction coupling?

A

Ca2+ regulates the number of actin-myosin cross bridges formed and therefore the force of contraction.
The force of contraction (number of cross bridges formed) can be increased by:
1) Increasing the Ca2+ sensitivity of the contractile apparatus (Starling’s law of the heart - EDV)
2) Increasing the concentration of Ca2+ in the cell (changing contractility/inotropy)

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63
Q

What is Starling’s law of the heart?

A

Increasing EDV stretches the heart and enables generation of a greater force of contraction.
It is an intrinsic property of cardiac muscle, in isolated muscle cells, stretching the sarcomere increases the force of contraction. This is a LENGTH DEPENDENT increase in Ca2+ sensitivity and results in a greater number of cross bridges.

‘Force of ventricular contraction is dependent on the length of ventricular muscle fibres in diastole.’

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64
Q

How does increased EDV lead to increased SV?

A

Increased sarcomere stretch leads to a greater EDV, length dependent Ca2+ sensitivity increase, stronger contraction due to more cross bridges. So greater SV.

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65
Q

How is EDV regulated?

A

Venous return and CVP

Increased VR and CVP increases cardiac filling of the R heart and so increases R SV and therefore L SV.

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66
Q

What pathology causes the following?

a) RSV>LSV
b) LSV>RSV

A

a) Congestion of pulmonary circulation

b) Congestion of systemic circulation

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67
Q

Which factors affect venous return to the right ventricle?

A

1) Blood volume
2) Skeletal muscle pump
3) Respiratory pump
4) Venous tone
5) Gravity

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68
Q

How does blood volume affect venous return?

A 
Increased BV (renal failure) leads to increased VR
Decreased BV (dehydration/ haemorrhage) leads to decreased VR
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69
Q

How does the skeletal muscle pump affect venous return?

A

Postural muscles encourage blood to move back towards the heart

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70
Q

How does the respiratory pump affect venous return?

A

Blood moves back to the heart because inspiration decreases thoracic pressure and increases abdominal pressure

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71
Q

How does venous tone affect venous return?

A

Increased simp activity causes venoconstriction, reduces volume of blood in veins at a given pressure.
Venoconstriction increases venous return.

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72
Q

How does gravity affect venous return?

A

Supine- uniform distribution of blood across the body, CVP and VR maintained
Standing- Redistribution of blood due to gravity, venous pooling in lower extremities, reduced thoracic volume, CVP and VR fall, EDV and SV fall.

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73
Q

What is preload?

A

Any factor influencing the stretch of cardiac muscle cells before contraction

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74
Q

What factors affect EDV (pre load)?

A

CVP, VR, atrial contraction, HR

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75
Q

How is ESV regulated?

A

Increased contractility/ inotropy
Increased sympathetic nerve activity and NA and A stimulate beta 1 receptors.
Increased Ca influx during AP and increased Ca induced Ca release.
Increased cross bridge formation and binding affinity for TN-C
Increased force of contraction and SV, decreased ESV

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76
Q

What is after load?

A

The load against which the heart must contract to eject the SV

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77
Q

What affects after load?

A

Aortic/ pulmonary pressure
High aortic/ pulmonary pressure makes it more difficult to eject the SV eg. in hypertension
Increased resistance in peripheral/ pulmonary circulation increases the P upstream and therefore increases after load

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78
Q

How to increase SV by Starlings law

A

Same Ca influx, length dependent increase in sensitivity of contractile apparatus to Ca2+, more cross bridges, greater for of contraction, increased SV.

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79
Q

How to increase SV by increasing contractility

A

Increases Ca influx from SR, length independent increase in sensitivity of contractile apparatus to Ca (more TN-C binding affinity), more cross bridges, greater for of contraction, increased SV.

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80
Q

CO = HR x ( EDV - ESV ) REGULATION

A

EDV- intrinsic, preload, VR, CVP. atrial contraction, HR > 180bpm
ESV- extrinsic, contractility

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81
Q

How can drugs affect the heart?

A

Directly- rate, rhythm, force of contraction

Indirectly- Vasculature, blood, volume, composition, renal

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82
Q

Why do we need drugs that affect rate/rhythm?

A

Abnormal generation or conduction in arrhythmias- disorders of rate or rhythm.

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83
Q

Types of arrhythmias?

A

Atrial, supraventricular, junctional, ventricular, tachycardia, bradycardia. Label relates to location then rate.

84
Q

How do class 1 anti arrhythmic drugs work?

A

eg. Lidocaine, flecainide
Local anaesthetic on V-G Na+ channels with anti arrhythmic effects. Affects depolarisation phase, looks at contractile cells. Causes less steep depolarisation. VG channel blocker. Affect big depolarisation spike.

85
Q

How do class 2 anti arrhythmic drugs work?

A

eg. Propanolol,

Beta blockers, decrease sympathetic affect

86
Q

How do class 3 anti arrhythmic drugs work?

A

eg. Amiodarone (contains iodine, can change thyroid function), sotalol
Prolongation of AP, ?K+ channel block, makes cells refractory for longer.

87
Q

How do class 4 anti arrhythmic drugs work?

A

eg. Verapamil
Ca2+ channel blockers
Depolarisation in nodal cells, particularly AVN are Ca dependent so they affect depolarisation. Relative cardioselectivity, cardiac myocytes for more effect on slope.

88
Q

How does adenosine act as an anti arrhythmic?

A

Non- classified drug
Receptors in SA and AV, binds to receptors, K+ channels open, hyperpolarisation, increased refractory period and nodal contraction slowed.

89
Q

How does digoxin act as an anti arrhythmic?

A

Cardiac glycoside
CNS, increases vagal activity, increases PSNS, decreased AV conduction rate, decreased ventricular rate, normalise rhythm as well.

90
Q

Adverse effects of anti arrhythmic drugs?

A

Can cause arryhthmias or make them worse, because arrhythmias are diverse with lots of channels.

91
Q

Why might we need drugs to affect the force of contraction?

A

Anaphylaxis- CV collapse, increase the force of contraction

Heart failure- CO insufficient for metabolic needs of the body, many therapeutic options.

92
Q

How can drugs increase contractility?

A

Inotropic drugs- increases intracellular Ca2+.
Sympathomimetics
Cardiac glycosides
Phosphodiesterase inhibitors

93
Q

How do cardiac glycosides increase contractility?

A

eg. Digoxin
Partial inhibition of Na+/K+ Atlases so slows it down. Reduction in Na/Ca protein activity so Ca remains in cells, an inotrope.
When depolarised, Na+ enters the cardiac myocytes so ATPase pumps Na+ out. If reduced function, slowly increases the intracellular Na+, decreases conc grad so less Ca can leave.

94
Q

What are the adverse effects of cardiac glycosides?

A

Ionic disturbance- increased excitability, cause arrhythmia, neurological disturbance, GIT smooth muscle affected.
Gynaecomastia- off target effect, not to do with the Na/K ATPase. Fools oestrogen receptors because of steroid part, so can have breast growth. Psych impact on males and can have low compliance.

95
Q

Clinical use for digoxin?

A

Subset of heart failure patients, dose tailoring, not universally used. Can be combined with diuretics which decrease K+, but may cause hypokalaemia although this does increase the effect of digoxin.

96
Q

Examples and mechanism of phosphodiesterase inhibitors?

A

eg. milrinone and enoximone

cAMP/cGMP breakdown, inhibit PDE, more signalling molecules. cAMP affects Ca channels so they’re open for longer.

97
Q

PDE type 3 -heart
Adverse effects?
When used?

A

Arrhythmias

Emergencies only clinically

98
Q

Why are diuretics, vasodilators and ACE inhibitors also used for HF?

A

Decrease BV, Increase systemic volume, decrease HR

99
Q

How is the driving pressure from the ventricles sustained during diastole?

A

Windkessel effect
Elastic wall of the aorta distends during systole and stores energy.
It then recoils during diastole to propel blood forward (energy released)
Driving pressure sustained during diastole, continuous blood flow.

100
Q

What are the 2 major functions of elastic arteries?

A

Dampen pulsatile pressure to ensure continuous flow into the circulation
Ensure blood pressure is maintained during diastole

101
Q

What are the effects of ageing on pulse pressure?

A

Ejection of the same or even reduced SV leads t increased SP, reduced elastic recoil leads to lower DP. So pulse pressure, SP - DP increases with age.

102
Q

What is the formula for flow?

A

Flow= (changeP x r^4)/n x L

103
Q

What is laminar flow?

A

In most vasculature the centre of the vessel is the fastest and the edges next to the walls are slowest due to the friction. Normal pattern of flow highly efficient, follows Poiseuille’s Law.

104
Q

What is resistance to blood flow determined by?

A

1) Vessel length
2) Blood viscosity
3) Radius

105
Q

What is turbulent flow?

A

Where flow velocity is high, inefficient, random and spiral pattern followed by RBC. Cannot apply Poiseuille’s law. eg. at large artery branches, pregnancy exercise. Vibrations heard as sounds- korotkoff or murmurs

106
Q

What is a common cause of turbulence?

A

Heart valves

107
Q

What determines SP?

A

1) SV
2) Aortic/ arterial distensibility
3) Ejection velocity
4) DP of previous beat
So increases in the following increase SP:
- EDV - Contractility - Decreased aortic compliance - Increased ejection velocity -

108
Q

What determines DP?

A

1) Arteriolar resistance
2) Heart rate
So increases in the following increase DP:
- Vasoconstriction - Arteriosclerosis - Atherosclerosis - Very high HR increases DP -

109
Q

How is driving force for flow determined?

A

Blood volume in the arterial system (CO)

Resistance to blood flow (TPR)

110
Q

How do vasoconstriction and vasodilation of arterioles occur?

A
  • endothelial factors
  • local mechanisms
  • central neural mechanisms
  • hormonal mechanisms
111
Q

What happens to the flow of blood to an organ when the arterioles to that organ constrict?

A

Decreased blood flow

112
Q

What happens to blood flow when there is constriction of arterioles to multiple organs?

A

Increase TPR and therefore ABP

113
Q

What local factors cause changes in blood flow?

A

Myogenic mechanisms- reflex vasoconstriction in response to increased intravascular pressure.
Autoregulation- metabolic and myogenic

114
Q

Which forms of endothelial control cause constriction?

A

Endothelins- due to Ang-II or trauma, thromboxane, PGF. Cause increased Ca2+ in the muscle.

115
Q

Which forms of endothelial control cause dilation?

A

NO- due to ACh, substance P, ATP, bradykinin, thrombin, bacterial endotoxins, shear/stress and prostaglandins, PGE, PGI2, EDHF, cause a decrease in Ca2+

116
Q

What are the central neural mechanisms of the vascular muscle?

A

Most has a tonic vasomotor tone due to symp nerve activity. Decreased SNA=vasodilation, increased SNA=vasoconstriction. All vessels start off slightly constricted so can change diameter in both directions.

117
Q

What local factors affect the metabolic mechanisms?

A

K+, adenosine, lactate, CO2, H+. Diffuse into the resistance vessel and cause vasodilation.

118
Q

Which are the receptors for NA in the blood vessels and what effect does it have on the smooth muscle activity?

A

alpha1 in all vessels (including skeletal muscle), increased sympathetic activity causes vasoconstriction. Beta2 in skeletal muscle binds weakly and causes vasodilation. In response to increased SNA the alpha1 effect predominates in skeletal muscle.

119
Q

Which are the receptors for adrenaline in the blood vessels and what effect does this have on smooth muscle activity?

A

alpha1 in all vessels binds weakly to cause vasoconstriction and beta2 in skeletal muscle to cause vasodilation. In response to circulating adrenaline, beta2 predominates in skeletal muscle.

120
Q

What effect does ADH have on the blood vessel diameter?

A

Vasoconstricts

121
Q

What effect does angiotensin II have on the blood vessel diameter?

A

Vasoconstricts

122
Q

What are the main types and roles of the blood vessels in the systemic circulation?

A

Arteries- Distribution/ resistance
Capillaries- Exchange
Veins- Capacitance

123
Q

What is a capillary’s structure and function?

A

Single endothelial wall, basal lamina, lumen diameter = RBC. No elastin, no smooth muscle, slow velocity

124
Q

What is Fick’s law of diffusion?

A

Rate = Permeability coefficient x concentration gradient x area

125
Q

Why must there be a low flow in the capillaries?

A

To increase the time for exchange. Thye have no innervation so cannot constrict or dilate, only 25% open at one time, increased VO2 opens more capillaries and flow is determined by the arterioles.

126
Q

What mechanisms of exchange are there in the capillaries?

A

Diffusion
Vesicular transport- large charged molecules-proteins and antibodies
Bulk flow- through fenestrations- water, electrolytes, small molecules

127
Q

In the capillaries there is filtration and reabsorption. What are these affected by?

A

1) Blood enters the capillary with a hydrostatic P of 35mmHg.
2) Hydrostatic P in the interstitium is very low- 0mmHg
3) Interstitial oncotic P is also very low
4) Capillary oncotic P of 25mmHg due to plasma proteins
5) Blood leaves with a hydrostatic pressure of 15mmHg
If at the arteriolar end of the capillary Pc>OncPc then fluid leaves
If at the venous end of the capillary Pc

128
Q

What happens to excess fluid?

A

It is removed by the lymphatic system

129
Q

What are capacitance vessels?

A

Where 60-80% of the blood volume is found, veins.

130
Q

What determines cardiac filling (CVP)

A

Venous return

131
Q

What determines venous return?

A

Venous compliance, dV/dP. Veins are very compliant and can act as a reservoir. A fall in capacitance increases venous return.

132
Q

What are the ganglionic and post ganglionic neurotransmitters for the PSNS and SNS respectively?

A

PSNS- ACh in both

SNS- ACh then NA

133
Q

Cardiovascular effects of sympthetic stimulation?

A

Increased HR and contractility (beta1)
Vasoconstriction (alpha 1 and 2)
Some vasodilation (beta2)
Regulation of renin for vol control (beta1)

134
Q

What are the agonists and antagonists for alpha receptors?

A

Agonists: NA>A>isoprenaline
Antagonists: Phentolamine

135
Q

What are the agonists and antagonists for beta receptors?

A

Agonists: NA<a></a>

136
Q

What are the selective agonists and antagonists for alpha and beta 1 and 2?

A

Agonist Antagonist
Alpha 1 Phenylephrine Doxasosin
Alpha 2 Clonidine -
Beta 1 Dobutamine Metoprolol
Beta 2 Salbutamol -

137
Q

What are the effects of the beta adrenoceptor on the heart?

A

Increased HR, positive chronotropic effect
Increased contractility rate, positive inotropic effect
Increased automaticity
Fast relaxation and recovery, lusitropic effect

138
Q

Mechanism of beta receptor activation

A

Increased Ica,L (calcium channel)for greater Ca2+ entry.
Increased Ik for faster depolarisation
Increased Na+/K+ ATPase
Increased funny current for positive chronotropy
Increased ER Ca2+ uptake
Increased Ca2+ sensitivity

139
Q

What are the clinical uses of agonists?

A

Adrenaline- beta and alpha
Treats asystole, VF and other severe arrhythmias
Anaphylaxis
Local injection causes vasoconstriction, for local anaesthetics
Dobutamine
beta1
Treats cardiogenic shock with inotropic support.

140
Q

Mechanism of alpha1 receptor activation

A

Classical- IP3- mediated Ca2+ release from SR

Alternative- Through PKC and Rho kinase

141
Q

Use for phenylephrine

A

alpha1 agonist
vasoconstriction
Sudafed
Nasal congestion

142
Q

Clinical uses of antagonists:

alpha1, beta1 and 2

A

Alpha 1: Doxasosin, vasodilation, treat hypertension, Raynaud’s
Beta1/2: Propanolol, beta1: atenolol, negative chronotropic actions, negative inotropic actionc, inhibots automaticity, decreases wd by heart, anti platelet aggregation, treats angina, HF, arrhythmias, hypertension

143
Q

What is carvedilol used for?

A

Mixed beta and alpha adrenoceptor antagonist, inhibits cardiac K+ channel, heart failure

144
Q

Why do beta blockers decrease BP?

A

Decrease CO, ma lead to resetting of baroreceptors. Beta 1 in the kidneys lead to renin release which leads to production of angiotensin, vasoconstriction and fluid retention. Inhibit the trophic effects of catecholamines in the heart and inhibit cardiac hypertrophy.

145
Q

What are the cardiovascular effects of PS stimulation?

A

Heart- negative chronotropic action at SAN
Slow AVN conduction
little effect on contractility

BVs- limited vasodilation

146
Q

What are the 2 muscarinic signalling pathways in the heart?

A

1) direct GPCR activation of KACh

2) Inhibition of adenylate cyclase opposing PKA-mediated actions on a range of channels.

147
Q

What are the cardiovascular uses of muscarinic antagionists?

A

Atropine- block cardiac M2 receptors, decreased secretions, bronchodilation, constipation, urinary retention, treat supra ventricular bradycardia

148
Q

What are the tasks of the coronary circulation?

A

1) Maintain secure oxygen supply to the coronary muscle (low capacity for anaerobic metabolism)
2) Alter local flow according to activity functional hyperaemia

Flow can increase 4-5x when CO increases, this is coronary reserve.

149
Q

Is blood flow to the heart muscle continuous?

A

No, it is intermittent because when ventricular P > aortic P, blood will not flow

150
Q

Describe the pressure changes in the left side of the heart.

A

During systole, vessels are compressed by high pressure in the ventricle (Pout). Most blood flows to the left myocardium during diastole. Aortic pressure (Pin) during diastole determines flow. It is max during early diastole and at a high HR, diastole is shortened and reduces time for perfusion.

151
Q

How is coronary flow controlled?

A

Coronary arterioles exhibit myogenic autoregulation in the pressure range 60-180mmHg. Some sympathetic control but overridden by local control. Metabolic hyperaemia is the dominant form of regulation. Adenosine is the most important, it diffuses back and dilates resistance arterioles along with prostaglandins and low O2 forming chemical signals. K+ and NO also affect blood flow.

152
Q

What are the tasks of the cerebral circulation?

A

1) Maintain totally secure O2 supply to the brain tissue (myogenic auto regulation)
2) To alter local flow according to activity functional hyperaemia (metabolic regulation)

153
Q

What are the structural adaptations of the cerebral circulation?

A

Short arterioles, dense capillary network, relatively high vascular resistance, cerebral perfusion maintained if the carotid artery is obstructed.
High capillary density aids gas exchange, similar density to the myocardium. Multiple transport pathways in systemic capillaries.

154
Q

What is the cellular basis of the BBB?

A

Tight junctions between endothelial cells makes it hard to get in and out of the brain.

155
Q

What is the BBB?

A

Blood brain barrier, protects the cerebral environment. Cerebral capillaries form tight junctions (no bulk flow) and no vesicular transport. This protects neurones and maintains the environment. This is responsible for the long lasting effects of heroin.

156
Q

What are the functional adaptations of cerebral circulation?

A

1) High basal flow- 15% of CO and high O2 extraction.
2) Regulation of other organs safeguards cerebral circulation- peripheral vasoconstriction except the heart can maintain arterial pressure.
3) Autoregulation - a change in BP is met by a change in resistance to maintain perfusion.
Autoregulatory range is 60-170mmHg
4) Cerebral vessels are very responsive to arterial CO2
Vasodilation with hypercapnia- 1mmHg increase in CO2 causes a 2-4% increase in flow. Vasodilation due to endothelial NO and a fall in myocyte pH- H+. Vasoconstriction of hypocapnia.
5) Cerebral vessels are less responsive to levels of arterial O2.
Moderate hypoxia evokes little change in blood flow and severe hypoxia leads to vasodilation.
6) Neuronal activity evoked functional hyperaemia- CO2, K+ increase due to increased permeability, adenosine, NO are important in coupling tissue metabolism to local flow.
7) Nervous control- sympathetic stimulation can increase resistance by 20-30%. Baroreceptors have little influence on cerebral flow and sympathetic stimulation shifts auto regulatory curve to the right.

157
Q

What are the problems related with cerebral vasculature?

A

Raised intracranial P (ICP)

  • increased by intracranial bleeding, cerebral oedema and a tumour
  • Increased ICP causes collapsed veins, decreases effective cerebral perfusion pressure (CPP = ABP - ICP) and reduces blood flow.

Postural syncope if baroreflex/ autonomic activity is impaired e.g. ageing.
Cerebral ischaemia- stroke
Vascular dilation- headaches, migraine due to vascular dilation

158
Q

What are the tasks of the cutaneous circulation?

A

1) Regulate body temperature as skin is the major thermoregulator
2) Respond to trauma

159
Q

What are the structural adaptations of cutaneous circulation?

A

Receives ~10% of CO and has moderately high resistance, has a unique microvascular network.
1) Arterioles of cutaneous circulation-
When warm, removal of alpha adrenoceptor mediated sympathetic tone leads to cutaneous vasodilation and heat loss.
2) AV anastamoses in the hands, feet and face- ears, nose and lips. 50um diameter with thick smooth muscle, shunt blood from arterioles - venules, alpha1 adrenoceptors. Warm, decreased alpha1 symp activity, dilated AV anastomoses, increased blood flow to venous plexus, heat loss.
3) Vasodilation by bradykinin leads to decreased systemic vascular resistance, leads to decreased ABP, increased HR and increased CO

160
Q

How does a drop in temperature cause heat gain?

A

Stimulation of alpha adrenergic receptors, vasoconstriction leading to heat gain.

161
Q

What is the effect of ambient temperature on skin blood flow?

A

Cold induced vasoconstriction when there is a decrease in temperature followed by a paradoxical cold vasodilation due to paralysis of neurogenergic transmission. Low temp increases Hb affinity for O2 making blood look oxygenated.

162
Q

What is countercurrent exchange?

A

Cold blood in veins returning from extremities can be cooler than trunk by 13deg.Radiation from warm arterial to cold venous blood flowing in the opposite direction. This ‘traps’ heat near the trunk.

163
Q

What is Raynaud’s disease?

A

Skin vessels are overactive to cold or stress when there is a sympathetic response. Cold or emotional stimuli lead to vasoconstriction (ischaemic attacks) white, blue (lack of O2) then red. Numbness, pain and a burning sensation.

164
Q

What is the triple response?

A

Pointed object drawn over the skin or a small burn

1) white reaction- blanching due to mechanical stimulation
2) red reaction- local vasodilation and histamine
3) flare- wider intense vasodilation
4) Wheals/local oedema

165
Q

What do vasodilator drugs do?

A

They have physiological control over vascular tone which is normally controlled by autonomic innervation, circulating hormones and local mediators acting on smooth muscle.

166
Q

What are indirect vasodilators?

A

Drugs which block vasoconstriction- ANS- sympathetic blockade (a1) = indirect vasodilation and RAAS- angiotensin II vasoconstrictor.

167
Q

What are direct vasodilators?

A

Intracellular Ca is necessary for contraction, enters through vg Ca channels and affects membrane potential. These affected by drugs and how easily they open.

168
Q

What are the clinical uses of vasodilators?

A

1) Hypertension
2) Angina pectoris
- Pain due to inadequate coronary blood flow
- Atheromatous obstruction
- Arterial spasm
Drugs increase coronary BF and decrease cardiac work
3) Peripheral vascular disease- Raynaud’s syndrome
4) Impotence via NO and cGMP so use of a phosphodiesterase inhibitor because PDE inhibits cGMP.
5) Hair loss
6) Improved cerebral function

169
Q

Which drugs are used in angina pectoris?

A
  • Beta blockers, ivabradine, decrease cardiac work
  • Organic nitrates, glyceryl trinitrate (GTN), NO on all systemic vessels, venous>arterial, decrease cardiac work and increase coronary flow. SE= excess dilation, hypotension, other smooth muscle affected. Sublingual admin but transdermal for prophylaxis.
  • Ca channel blockers e.g.. DHPs- dihydropyridines
170
Q

What is the action of organic nitrates?

A

NO dilates systemic vessels, venous> arterial, decreaes cardiac work and increases coronary flow. The nitrates spontaneously decompose to NO which interferes with cGMP which inhibits Ca channels so decreases Ca and inhibits actin-myosin interaction.

171
Q

What are the side effects of organic nitrates?

A

NO in excess
Excess vasodilation, hypotension- syncope, headache, reflex tachycardia and systemic vasodilation and also affects other smooth muscle in the bronchi and GIT

172
Q

How is glyceryl trinitrate administered?

A

Sublingual- Avoids first pass metabolism, fast but short duration
Transdermal for prophylaxis- avoids first pass metabolism, short acting
Can get physiological and pharmacological tolerance

173
Q

What are the non-reflex responses in the CVS which influence BP?

A

Heart- (HR, SV), intrinsic beating and Starling’s Law
Arterioles- (resistance), endothelial, myogenic, metabolic influences
Capillaries- diffusion and filtration
Veins- (capacity), gravity, respiratory pump, muscle pump
CNS may also modulate reflex responses
CNS may initiate cardiovascular and respiratory responses- emotion, previous experience, volition

174
Q

What are the roles of the forebrain, midbrain and hindbrain?

A

Forebrain- cortical influences, emotion and volition
Midbrain- Complex reflex patterns, exercise/ feeding/ satiety/ alert/defence/ thermoregulation/ reproduction
Hindbrain- Simple reflexes

175
Q

What are baroreceptors?

A

Stretch receptors. Found in the walls of the carotid sinus and aortic arch. They are tonically firing and firing rate changes with changes in blood pressure. Afferent activity is sent to the NTS.

176
Q

What is the threshold for baroreceptors?

A

60mmHg. Below this they cannot fire, they are sensitive to level and frequency

177
Q

What is the baroreceptor reflex to a fall in ABP?

A

Decreased ABP
Decreased baroreceptor activity
CNS NTS
Increased sympathetic outflow to the arterioles
Arteriolar constriction causing an increase in TPR and decreased capillary hydrostatic pressure.
Increased sympathetic outflow to the veins causing constriction.
This leads to greater cardiac filling and so increased EDV
Increased sympathetic outflow and decreased parasympathetic outflow to the SAN
This causes increased contractility
This leads to decreased ESV and so a greater SV
It also increases the HR and so these together increase the CO.
With an increased CO and TPR, ABP is increased because CO x TPR = ABP

178
Q

How do the nerves run in the baroreceptor reflex pathway?

A

The afferent nerves from the baroreceptors, the vagus and the glossopharyngeal signal to the NTS. If ABP is too high, increased firing causes outflow from the NTS to the supraoptic and paraventricular nuclei which fire an inhibitory response to the pituitary, decreasing ADH secretion. A nerve from the NTS synapses in the pre optic hypothalamus which then send inhibitory signals to the RVLM decreasing the sympathetic outflow from here to the pre ganglionic sympathetics which act on the BVs and heart.

179
Q

What are volume receptors?

A

Stretch receptors in the right atrium are affected by changes in CVP and distension of the veins.
Afferents via vagus to the NTS then PVN.
Affected by real changes in blood volume and distribution.

180
Q

What happens when there is an increased stretch of volume receptors?

A

Bainbridge reflex- increases simp activity to the heart and transiently increases the HR, protective mechanism to stop the heart overfilling.
There is decreased symp to the kidney, so renal perfusion is increased via vasodilation, decreased ADH release and increased urine production.

If there is a decreased stretch, the opposite occurs, apart from the Bainbridge reflex

181
Q

What are the respiratory influences on the heart?

A

Mechanical interaction- inspiration leads to increased venous return on the right side which increases R SV which then increases left EDV and SV
Neural interaction- inspirartion increases heart rate, sinus arrhythmia

182
Q

What are the 2 main mechanisms of near interaction with the heart?

A

1) Central nervous mechanisms. Central inspiratory neurones exert inhibitory influence on vagal activity to the heart and increase HR.
2) Reflex initiated by pulmonary stretch receptors in respiratory airways- vagal afferents. Pulm stretch receptors cause NTS to fire inhibitory signals to the NA which inhibits the vagus to the heart and increases HR.

183
Q

What is systemic hypoxia?

A

PaO2 decreases below 60mmHg (8.1kPa)

184
Q

What are the responses to systemic hypoxia?

A

Reflex- peripheral chemoreceptors sense the fall in PaO2
The reflexes are superimposed on local influences.
Peripheral chemoreceptors are stimulated by a decreased PaO2 and increase the afferent activity to the NTS. This causes a reflex depending on whether respiration can be increased.

185
Q

What is the reflex when respiration cannot be increased?

A

Primary cardiovascular reflex, HR is decreased and vessels are constricted apart from in the brain. Peripheral chemoreceptors fire through CN IX or X and promote signalling at the NTS. This sends a stimulatory signal to the central inspiratory neurones which stimulate the inspiratory motor neurones, but rest cannot increase further so the NTS stimulates nerves in the RVLM which increase the sympathetic stimulation to the vessels to cause constriction and no change to the sympathetic innervation to the heart, HR decreases to preserve O2.

186
Q

What is the reflex when respiration can be increased?

A

NTS sends inhibitory signals to the NA so the inhibition of the sympathetics to the heart is reversed. Central inspiratory neurones do the same. Inspiratory drive from the inspiratory motor neurones occurs as controlled by the central inspiratory neurones and an increase in aspiration increases the stretch in pulmonary stretch receptors which fire more and so stimulate the NTS.

187
Q

Give examples of systemic hypoxia when respiration cannot be increased

A

Under muscle relaxant, paralysed for an operation
High spinal transection
Long dive underwater
Foetus in utero
Severe respiratory disease (blue bloater)

188
Q

What happens in systemic hypoxia with no respiratory adjustments?

A

Chemoreceptors stimulated and afferent activity to the NTS increases, reflex HR decrease and constriction to preserve O2.
This is superimposed on depressed contractility, cerebral vasodilation, muscle vasodilation, pulmonary vasoconstriction which are local effects of hypoxia. O2 is directed to the brained pulmonary vasoconstriction may lead to pulmonary oedema and R ventricular failure. Patient remains hypoxic.

189
Q

What happens in systemic hypoxia with respiratory adjustments?

A

Reflex effects of peripheral chemoreceptor stimulation on the heart are overcome by effects of increased respiration on HR. Increased resp and HR and constriction restore PaO2. Tissues do not become hypoxic.

190
Q

Give examples of systemic hypoxia when respiration cannot be increased

A

Hypoxic atmosphere
High altitude
Less severe respiratory disease

191
Q

What happens when respiration decreases?

A

Decreased HR. Reflex evoked by trigeminal receptors, cold water on face/nose- doing reflex.
Stimulation of trigeminal afferents to NTS. Inhibit central insp neurones and cause expiratory apnoea. Decrease HR by increasing vagal activity + vasoconstriction

192
Q

What are the characteristics of response to mental stress?

A

Stimuli- emotion, visual, sound, pain, novel events, strong peripheral chemoreceptor stimulation.
Size of response- graded with stimulus strength
Increased respiration, decreased parasymp and increased symp activity to the heart, increased symp to cause vasoconstriction to the kidney, GIT and skin. Vasodilation of skeletal muscle due to decreased symp NA activity, increased A to muscle.
Increased ABP, HR with increase in blood flow to muscle.

193
Q

What are the characteristics of response to emotional or mental stress?

A

Can show habituation or sensitisation
Can be conditioned
During alerting or defence response the baroreceptor reflex is dampened so ABP can reach very high values.

194
Q

Describe the integrating areas for an alerting/defence response.

A 
Prefrontal cortex (modulation) 
Amygdala,ventral hypothalamus, midbrain periaqueductal grey, dorsal medulla have afferents feeding in and inhibit the baroreceptor reflex at the NTS.
Ventral medulla, RVLM, respiratory neurones, NA. Have efferent outflow symp, parasymp vagal to heart and respiratory.
195
Q

What is the clinical significance of an alerting/defence response?

A

Increased arousal and apprehension
Increased cardiac output redistributed to muscle
Split second advantage to fight or run
Increased ABP has acute risk for those with CHD- MI, aneurysm, fragile cerebral BVs.
Chronically repeated emotional stress may lead to essential hypertension if not habituated quickly.

196
Q

What is the mechanism for essential hypertension?

A

Increased ABP due to environmental steers via defence areas, genetic and environmental influences modulate it. This leads to hypertrophy of the vascular smooth muscle in arterioles which increases TPR and increases ABP in a cycle.

197
Q

What is vasovagal syncope?

A

Emotional fainting
Preceded by an alerting defence response or strenuous exercise or haemorrhage
Sudden increase in vagal activity to the heart and decrease in symp to BVs
Bradycardia and vasodilation
Fall in ABP

198
Q

What is the vasovagal reflex response?

A

Strong defence response leads to increased HR and ventricular contractility
Ventricles contract v strongly but low filling, decreased EDV especially if upright
Torsion or twisting of the ventricle stimulates mechanoreceptors with vagal afferents
Afferent via vagus to NTS and lat hypothal
Increased vagus to heart, decreases HR
Decreased symp to vessels leads to vasodilation
Decreased ABP, faints

199
Q

What is the significance of vasovagal syncope?

A

Emotional stress can cause it
May cause cardiac arrest and death in profound fear
may also occur in strenuous exercise and post sudden haemorrhage.

200
Q

What are the local effects in exercising muscle?

A

Exercise hyperaemia- local vasodilation
K+, Pi, adenosine, decreased TPR
Increased BF is rhythmic in dynamic exercise
Tends to decrease TPR
Muscle blood flow may not increase during static exercise
Hyperaemia occurs after contraction
TPR increases in static contraction

201
Q

What is the exercise reflex?

A

K+ and adenosine stimulate the metaboreceptors in exercising muscle and joint receptors are stimulated in dynamic exercise.
Afferent to CNS
Subthalamic locomotor region
Reflex- increased respiration
Increased HR and contractility
Increased CO
Sympathetic NA to GIT, kidney, skin and all skeletal muscle
increased TPR
Via connections with central respiratory neurones, cardiac vagal motor neurones, RVLM to sympathetic pre-ganglionic neurones
Central command- from cortex- to SLR reinforces reflex

202
Q

What are the CVS responses to acute exercise?

A

Increased CO and metabolic dilation of BVs by adenosine, K+, H+, ATP, Pi

203
Q

What are the CVS responses to chronic exercise?

A

Increased ability to meet energy demands, benefit to the CVS

204
Q

How is CVS performance determined?

A

Maximum rate of O2 transport from lungs to mitochondria

205
Q

What is VO2 max?

A

The rate of max O2 uptake from the air or the rate of max O2 use by mitochondria.

206
Q

What is VO2 max dependent on?

A

Max achievable CO, haematocrit, resting VO2.

207
Q

How is SV increased by exercise?

A

Eccentric hypertrophy- added sarcomeres in series with current sarcomeres. Stimulated by insulin like GF

Medicine (15 decks)

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