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Human Diseases > W3 12 Drugs And The CVS > Flashcards

W3 12 Drugs And The CVS Flashcards

1
Q

Formula for cardiac output

A

Heart pumps to generate a cardiac output
Cardiac output = heart rate X stroke volume

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2
Q

What conditions can limit cardiac output?

A

Arrhythmias - can affect heart rate
Heart failure - lowers stroke volume

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3
Q

What is the function of vasculature?

A

Delivers blood so controls flow, by changing vascular resistance

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4
Q

What is TPR?

A

Total peripheral resistance - vascular resistance in blood vessels

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5
Q

What can occur if TPR is altered?

A

If TPR is too high, causes hypertension
If flow in coronary blood vessels doesn’t match metabolic demand - causes angina

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6
Q

What is the formula for arterial blood pressure?

A

ABP = CO X TPR

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7
Q

How is blood altered by volume?

A

Volume over a long time period is controlled by renal function. Too high blood volume would be associated with high BP. Diuretics will be used to try and remove volume to lower BP.

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8
Q

How is blood altered by its constituents?

A

Might not have enough RBCs to carry oxygen = anaemia
Blood is how immune cells travel - might cause immune problems
Clotting ability and coagulation to prevent abhorrent bleeding

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9
Q

How does the cardiac cycle electrical signals move through the heart?

A

Origin at SAN
This will spread over atria causing them to contract
Atria contraction needs to go before ventricle contraction, so AV node will add a small delay in this to allow this
Signal will pass through AV node and spread through Bundle of His and the Purkinje fibre to the ventricle and cause contraction

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10
Q

How does the autonomic nervous system control cardiac function - parasympathic? (PG114)

A

Vagus nerve (parasympathetic innervation) acts on the SAN to slow it down, inducing a bradycardia. With a slower firing of the SA node, we want to change the delay and make it longer at the AV node, to allow atrial contraction always before ventricle contraction.

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11
Q

How does the autonomic nervous system control cardiac function - sympathetic? (PG114)

A

Sympathetic nerve drives the SAN to fire more quickly (to increase HR), so delay needs to be shorted at the AV node.
Sympathetic nerves also have action in the muscle and increase force of contraction, increasing contractility.

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12
Q

What is force of contraction dependent on?

A

Force of contraction is dependent on how full it gets and the venous return with the end diastolic volume. As we increase filling, we get an increased force of contraction, and increased stroke volume and sympathetic nerves will change contractility.

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13
Q

What pathology occurs when there is less contraction of ventricular muscle?

A

If we are not causing as big a contraction of that ventricular muscle as we expect, stroke volume will be less, which is seen in heart failure.

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14
Q

What is the pathology of incorrect heart rate?

A

SAN could be firing too fast or too slow, causing an incorrect heart rate
Unstable muscle cells in heart might depolarise on their own causing ectopic beats
Altered conduction - re-entrants

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15
Q

How does an SAN action potential work?

A

Unstable prepotential = depolarises on its own until it reaches threshold, then fires an action potential

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16
Q

If the SAN is firing incorrectly I.e. altered pacemaker activity, how is it fixed pharmacologically - if we have to meet threshold and want it to go faster, what happens? PG115 IMG

A

Want to lower threshold to make it more negative to reach it earlier
Can start from a higher starting point, reaching threshold will be quicker
Slope of prepotential being more steep means we will reach threshold quicker
(all these things mean threshold is reached, so more frequent action potentials, so heart rate will increase)

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17
Q

If the SAN is firing incorrectly I.e. altered pacemaker activity, how is it fixed pharmacologically - if we want it to go slower, what happens? PG115 IMG

A

Parasympathetic vagus can slow everything down causing a:
Higher threshold
Lower starting point
Less of a slope

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18
Q

What is the more common arrhythmia and how do we fix it pharmacologically?

A

Heart going too fast and SAN a firing too quickly
Response to block the sympathetic response using beta blockers eg propanolol, atenolol = class II antiarrhythmics.

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19
Q

What drugs are used if SAN is going too slow?

A

Not very common. But want to block cholinergic receptors - atropine is given

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20
Q

Compare the action potential of a cardiac myocyte with a muscle twitch (PG 116 IMG)

A

Cardiac myocyte: action potential stable, followed by depolarisation. Calcium influx and plateau followed by repolarisation.
Muscle twitch: contraction peaks during refractory period so cannot stimulate another contraction on top of it.

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21
Q

If we extend the refractory period and make it longer, it will be longer before we can get another contraction. How do we increase the refractory period?

A

Slow down the rapid depolarisation and lessen the slope to extend refractory period
Extend (slow down) the repolarisation period

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22
Q

How do we slow down the rapid depolarisation to extend the refractory period?

A

Need to affect fast sodium ion channels. Blocking these/stabilising the membrane further will increase the refractory period. Use Class I antiarrhythmics - eg lidocaine or quinidine.

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23
Q

How do we extend the repolarisation period to increase refractory period?

A

Potassium efflux causes the repolarisation, so blocking potassium channels will cause an increased refractory period. Using Class III antiarrhythmics

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24
Q

Apart from increasing refractory period, how else can we alter myocyte action potential?

A

Slow down the conduction through the AV node, taking more time between ventricular contractions.

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25
Q

Which channels are affected when slowing down conduction in the AV node?

A

L-type calcium channels affected, to slow depolarisation in AVN and hence slow conduction

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26
Q

Which drugs have their affects on the L-type calcium channels to slow conduction in the AVN?

A

Nifedipine, verapamil - Class IV antiarrhythmics (blockers of L-type calcium channels)

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27
Q

If trying to block the AVN, why is it not useful if the origin of the arrhythmia is in the ventricle?

A

Because L-type calcium channels are also responsible for calcium influx in cardiac myocytes which causes muscle contraction, so reducing influx and having a reduced plateau, there would also be a negative ionotropic effect, so muscle would not contract as much.

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28
Q

Which drugs will inhibit the sodium potassium ATPase?

A

Cardiac glycosides

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29
Q

What is the action of cardiac glycosides?

A

Inhibiting the sodium potassium ATPase will cause a depolarisation. The vagus parasympathetic nerves that go to the SAN are sensitive to this. As it is inhibited, the vagus is depolarised, causing a transmitter release (ACh), which will slow the heart

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30
Q

Given an example of a cardiac glycoside

A

Digoxin

31
Q

Describe the Starling curve

A

As we increase venous return and filling of the heart causing increased end diastolic volume, the increased filling will cause cardiac muscle to contract more forcefully, leading to an increase in stroke volume.

32
Q

What happens to the Starling curve in heart failure?

A

There is a reduction in the curve. Any EDV will cause a reduced stroke volume.

33
Q

Describe physiologically how sympathetic nerves cause contraction of ventricles?

A

Sympathetic nerves go to cardiac muscle. When stimulated will act on b-receptors, which will increase calcium influx, allowing a stronger contraction. Ventricle contracts and has to eject blood into the vascular system, against peripheral resistance and blood pressure.

34
Q

What are the 2 strategies for heart failure?

A
  1. Positive ionotropic effect - using natural sympathetic nerves (increasing contractility)
  2. Can reduce cardiac workload
35
Q

What drugs can be used to have a positive ionotropic effect to bring the curve up a bit (in HF)?

A

Cardiac glycosides
Sympathomimetics

36
Q

What drugs can be used to reduce cardiac workload (in HF)?

A

ACE inhibitors - reduce blood pressure
b-blockers (chronic) - act on SAN to reduce HR, hence CO, and thus workload on heart
Diuretics - for hypertension treatment, reducing blood volume and thus pressure in vascular system
Vasodilators - reduce TPR and thus blood pressure

37
Q

Describe the ion movement that occurs when an action potential comes along in a cardiac myocyte

A

As the action potential comes, sodium channels open and get a sodium influx, depolarisation and causing voltage gated calcium channels to open, and calcium to influx into the cell.
Calcium then acts on the sarcoplasmic reticulum, with calcium stores. Calcium is released via calcium induced calcium release.
This calcium acts on the actin and myosin filaments to cause contraction.

38
Q

What happens to the calcium from cardiac myocytes after contraction?

A

It can be sequestration back into the SR ready for the following contraction
Or it can be pumped out of the cell via the sodium calcium exchange (3Na+ IN for Ca2+ OUT). This reduces intracellular calcium levels. Sodium is then pumped out via sodium potassium pump with K+ coming in (since don’t want sodium buildup).

39
Q

Cardiac glycosides inhibit the sodium potassium pump. What affect does this have on cardiac glycosides?

A

Less sodium would be pumped out, so less gradient for sodium to influx into the cell, so calcium would not be pumped out as fast. If levels of sodium get too high inside, the calcium sodium exchange can flip with sodium going out of the cell and calcium coming in. Both of these would result in higher intracellular calcium levels, increasing force of contraction and having a positive ionotropic effect.
BASICALLY INCREASES INTRACELLULAR CALCIUM SO INCREASES FORCE OF COTNRACTION!

40
Q

How can we control hypertension?

A

Inhibit vasoconstriction to reduce TPR

41
Q

What causes resistance in the vascular system?

A

Resistance vessels are arterioles. Resistance causes a fall in blood pressure after, so capillary pressure is lower than upstream pressure. Vasoconstriction causes a bigger drop in pressure, meaning upstream there is higher pressure from more resistance,

42
Q

What are the strategies for hypertension?

A

Vasodilate to reduce upstream pressure
Reduce cardiac output (since ABP = CO X TPR)

43
Q

What classes of drugs can be used to treat hypertension?

A

Beta blockers
Targeting the RAAS system - ACE inhibitors and Ang II antagonists
Ca2+ antagonists
a1 antagonists
Diuretics

44
Q

How do beta blockers affect hypertension?

A

Cardiac effects - reduce rate via SAN, negative ionotropic effect on cardiac myocytes, reducing stroke volume and thus CO
Renal effects - b-receptors stimulate renin release, so beta blockers decrease renin release

45
Q

What is the role of angiotensin in the RAAS system?

A

Angiotensin is a vasoconstrictor.

46
Q

What is the role of aldosterone in the RAAS system?

A

Aldosterone is linked with our sodium reabsorption in the kidney, leading to more fluid water coming back, increasing volume.

47
Q

What effects do ACE inhibitors have on hypertension?

A

They reduce the formation of angiotensin, so has vasodilatation effects

48
Q

Give examples of ACE inhibitors

A

Captopril, enalapril

49
Q

What effects do angiotensin antagonists have?

A

Block the receptors that the angiotensin are acting on, having effects on vasodilatation

50
Q

Give an example of an angiotensin antagonist

A

Losartan

51
Q

How do Ca2+ antagonists treat hypertension?

A

Can act in the heart because of calcium needed for muscle contraction, giving a negative ionotropic effect. Act directly on the vascular smooth muscle and have the same effect, reducing constriction in these blood vessels and have a dilation effect.

52
Q

How to a1 antagonists treat hypertension?

A

Blood vessels are under tone - they have vascular tone. A lot of this is mediated by sympathetic nerves acting via a1 receptors. So antagonists will block vasoconstrictor tone, causing a vasodilatation.

53
Q

Give some examples of diuretics

A

Thiazides, furosemide

54
Q

What effects do diuretics have on hypertension?

A

Lower the blood volume so lower pressure in the system. Thiazides will act on the DCT, furosemide will act on the Loop of Henle.

55
Q

What is a severe side effect of diuretics?

A

Hypokalaemia

56
Q

What is angina and what is the goal to treat it?

A

Angina is an imbalance between oxygen demand and supply to cardiac myocytes. Treatment is to get a better match - might be by reducing cardiac work to reduce metabolic demand, or increasing oxygen delivery to meet demand. Most drugs will reduce cardiac work TO REDUCE VO2 (consumption!)

57
Q

What are the drug types that can be used to treat angina?

A

Nitrates (eg GTN)
beta blockers
Ca2+ antagonists (L type)
Anticoagulants eg aspirin
Ranolazine
Trimetazidine

58
Q

What action do nitrates (eg GTN) have?

A

Vasodilatation on coronary blood vessels, increases blood flow

59
Q

What action do beta blockers have on angina?

A

Bradycardia increases diastole (coronary blood flow occurs during diastole, so increasing diastole increases blood flow)
Reduced contractility
(Both reduce work of the heart)

60
Q

What actions do Ca2+ antagonists have on angina?

A

Reduced contractility
Vasodilatation (or coronary blood vessels)

61
Q

What action do anticoagulants have on angina?

A

Inhibit platelet aggregation and clotting (reduces physical blocking of coronary blood vessels)

62
Q

What action does ranolazine have on angina?

A

Decreased Na+ current, reduces Ca2+ influx, so reduced workload

63
Q

What are some drug complications of ACE inhibitors?

A

Inhibit bradykinin metabolism - dry persistent cough.
Hyperkalaemia

64
Q

What are some drug complications of class IV antiarrhythmics (Ca2+ antagonists)?

A

Hypotension - dizziness - as can act as vasodilators and affect cerebral blood flow if too low
Oedema - flushing - dilating cutaneous blood vessels in the skin can lead to this

65
Q

What are some drug complications of diuretics?

A

Hypokalaemia - proarrythmogenic

66
Q

What are some drug complications of class V antiarrhythmics (glycosides)?

A

Increased efficacy in hypokalaemia
Proarrythmogenic
(don’t mix glycosides and diuretics!)

67
Q

What are some drug complications of class II antiarrhythmics (beta blockers)?

A

Asthma - might have a b2 agonist in their inhaler, so beta blockers might block the bronchodilator effect, inducing asthma attack
Arrhythmia - conductance block - beta blockers extend AVN delay, if too potent might block AVN
HF - oedema

68
Q

What dental patient considerations need to be made with drugs and the cardiac system?

A

Orthostatic hypotension
Ageing
Altering/defence response (anxiety)
Chair position - venous return

69
Q

What consideration has to be made with orthostatic hypotension?

A

Might have increased venous pooling if sat in chair for a while
Older patients have reduce baroreflex, so might get hypotension when standing
Gradual upright portion needed

70
Q

How should you consider age in dental practice?

A

Older people have a slow baroreflex
Older people have a lower PO2, need to be considered in GA which lowers PO2 more

71
Q

How does the alerting response need to be considered in dentistry?

A

Hypertension - response could exacerbate even further in patients with hypertension, increasing risks of stroke
Angina - response will increase HR and CO, maybe exacerbating an angina attack. Increases oxygen demand.

72
Q

How does chair position affect normal people.

A

As people are upright, will reduce venous return and EDV, and have effect on SV. As you lie them down, removes the effect of gravity on venous return and increases EDV.

73
Q

How does chair position affect patients with heart failure?

A

In HR, lying down can increase congestion in ventricles by filling them more, feeding back into promoting oedema. Eg in left ventricle failure, increased congestion will increase the pulmonary oedema, and patient will have dyspnoea, and find it more difficult to breathe. So more comfortable upright.

Human Diseases (75 decks)

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