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Pharmacology > Drugs and the heart > Flashcards

Drugs and the heart Flashcards

1
Q

Why is the action potential generation in the heart different to normal cells?

A

Depolarisation is mainly calcium dominated instead of sodium

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2
Q

What are the three ions with voltage gated channels that are important in the nodes?

A
  • If (hyperpolarisation activated cyclic nucleotide gated channel aka funny channels - sodium)
  • T type calcium channel/long lasting calcium channel (two different ones)
  • Ik (potassium channel)
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3
Q

Describe what happens during AP generation in the node

A
  • At around -60mV, you get spontaneous activation so the heart continues to always beat
  • At -60mV, the If channel opens -> Na enters the cell -> depolarisation
  • This is then propagated by calcium channels (T type first)
  • The major arm (upstroke) of the AP is driven by the long lasting (L type) calcium channels
  • Once the AP reaches above 0, the potassium channels open -> repolarisation
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4
Q

Which ion channels does the sympathetic nervous system affect and what does this do?

A
  • Increase cAMP -> increased If and ICa

- Promotes depolarisation

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5
Q

Which ion channels does the parasympathetic nervous system affect and what does this do?

A
  • Decrease cAMP -> increased Ik

- Prolongs repolarisation

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6
Q

Describe the sequence of membrane depolarisation involving calcium

A
  • AP causes calcium channels to open
  • Influx causes calcium induced calcium release via ryanodine receptor stimulation
  • Calcium binds to troponin
  • Allows actin-myosin cross bridging
  • Returned to SR and pumped out by NaCa exchanger
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7
Q

How is contractility of the heart maintained?

A

B1 stimulation -> increased cAMP -> increased PKA
PKA leads to:
- Phosphorylation of proteins in myofibril
- Induces CICR in the SR by stimulating calcium into SR

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8
Q

What is the main determinant of myocardial oxygen demands?

A

How much the heart is contracting

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9
Q

What would a high HR, high afterload and preload do to the force of contraction?

A

Increase - preload only causes a small increase

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10
Q

What do beta blockers, calcium antagonists and ivabradine affect (channels and the effect of that)?

A

B-blockers
- Decrease If and ICa

Calcium antagonist

  • Decrease ICa
  • Reduces depolarisation

Ivabradine

  • Decrease If
  • Decreases their opening so increases distance between APs

THEY REDUCE HEART RATE

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11
Q

What drugs affect heart rate and contractility?

A

calcium antagonists and beta blockers

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12
Q

What do beta blockers and calcium antagonists do to contractility and how?

A

B-blockers – decrease contractility
Reduces phosphorylation and cross-bridge formation

Calcium antagonists –decrease ICa
Stops further entry of calcium into myofibrils

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13
Q

What are the two classes of calcium antagonists?

A

Rate-slowing – cardiac + VSM

  • Phenylalkylamines (Verapamil)
  • Benzothiazepines (Diltiazem)

Non-rate slowing – VSM, more potent
- Dihydropyridines (Amlodipine)

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14
Q

How can the non rate slowing calcium antagonists affect heart rate?

A

The large amount of vasodilation can lead to reflex tachycardia

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15
Q

What are some drugs affecting myocardial oxygen supply/demand and how?

A
  • organic nitrates: they increase the amount of NO available -> increase cGMP -> smooth muscle relaxation -> dilation and better blood flow (may act as K channel opener so hyperpolarisation)
  • potassium channel opener: opens channel -> efflux -> prolonged hyperpolarisation

IMPROVE CORONARY BLOOD FLOW

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16
Q

What do organic nitrates and potassium channel openers do to afterload and preload?

A

Vasodilation = decreased afterload (less TPR)

Venodilation = decreased preload

They increase supply (more blood flow) and reduce the demand (preload and afterload)

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17
Q

What causes angina and what is the treatment for it?

A
  • Angina is chest pain
  • Mismatch of myocardial supply and demand
  • It is usually driven by atherosclerosis (narrowing of coronary arteries)
  • We usually start with a beta-blocker or calcium antagonist as background
  • Ivabradine is new specific treatment
  • Nitrates for symptomatic treatment e.g. during exercise
  • Others e.g. potassium channel openers if intolerant to others
18
Q

What causes the unwanted side effects of beta blockers?

A

Due to actions on beta 1 (and sometimes beta 2 receptors due to only partial selectivity)

19
Q

What are the side effects of beta blockers?

A
  • Worsening of cardiac failure (C.O. reduction, B1)
  • Bradycardia (B1)
  • Bronchoconstriction (blockade of β2 in airways) – be very careful with asthmatic patients
  • Hypoglycaemia (in diabetics on insulin, B2) due to decreased glycogenolysis/gluconeogenesis
  • Cold extremities and worsening of peripheral arterial disease (β2 blockade in skeletal muscle vessels)
  • Fatigue
  • Impotence (sexual dysfunction)
  • Depression
  • CNS effects e.g. nightmare
20
Q

What are the side effects of rate limiting calcium blockers and what causes them?

A

Bradycardia & AV-block –heart Ca2+channels blocked

Constipation – gut Ca2+channels blocked

21
Q

What are the side effects of non rate limiting calcium blockers and what causes them?

A

Ankle oedema –vasodilation means more capillary pressure in extremities

Headache/flushing –vasodilation

Palpitations – reflex SNS adrenergic activation due to vasodilation

22
Q

What are the side effects of potassium channel openers and nitrates and what causes them?

A

Ankle oedema –vasodilation means more capillary pressure in extremities

Headache/flushing –vasodilation

23
Q

What are the different types of arrhythmias?

A
  • supraventricular
  • ventricular
  • complex (supra and ventricular)
24
Q

What is the Vaughan Williams classification?

A 
Classes of anti-arrhythmic drugs
Class 1 – Na+-channel blockade
Class 2  - B-blockers
Class 3  –K+-channel blockade –prolong repolarisation
Class 4 –Ca2+-channel blockade

Limited significance as there are cross-overs between rhythm disturbances

25
Q

What is the aim of angina treatment?

A

reduce sudden death, alleviate symptoms, prevent stroke

26
Q

What is the use of adenosine in arrythmias?

A

Adenosine is used intravenously to terminate supraventricular tachyarrhythmias (SVT). Its actions are short-lived (20-30s hence safer as fewer long term SE

27
Q

How does adenosine work?

A

Activates A1 receptors in the SA and AV nodes -> Gi protein activation to reduce conversion of ATP to cAMP -> decreased cAMP -> decreased ionotropic and chronotropic effect

28
Q

Where are adenosine receptors found?

A

A2 on smooth muscle

A1 on nodal tissue

29
Q

What is the use of verapamil?

A

reduces ventricular responsiveness to atrial arrhythmias

30
Q

How does verapamil work?

A

blocks VGCC and thus depresses SA firing and subsequent AV node conduction

31
Q

What is the use of amiodarone?

A

In SVT and VT (often due to reentry)

32
Q

How does amiodarone work?

A
  • affects potassium and calcium channels
  • complex action by working on many ion channels
  • major effect due to potassium channel blockade
33
Q

What are the adverse effects of amiodarone?

A
  • Accumulation in body so side effects due to long half life
  • Skin rashes (photosensitive)
  • Hypo-or hyper-thyroidism
  • Pulmonary fibrosis
34
Q

What are re-entry arrhythmias?

A

In normal, healthy tissue, the AP would pass down on either side of the purkinje fibres, and if they crossed paths, they would meet and cancel eachother out. This ensures that the AP proceeds in one direction. You can get tissue block, leading to re-entry rhythm. As long as the tissue has undergone its repolarisation phase, APs can reactivate the tissue -> tachyarrhythmia

  • In re-entry rhythms, you see constant depolarisation
  • Instead of a nice repolarisation, there is consistent depolarisation and relaxation/contraction is not effective
35
Q

How can re-entry rhythm be overcome?

A
  • Prolong repolarisation
    When the re-entry AP comes into the tissue and reaches the AP point, the tissue hasn’t repolarised yet. Therefore the AP just dies – it cannot be propagated
  • This is done with a potassium channel blocker like AMIODARONE
36
Q

What is digoxin used for?

What is the drug class?

A
  • To treat arrhythmias commonly AF and flutter

- cardiac glycoside

37
Q

How does digoxin work?

A

Inhibition of Na-K-ATPase (Na/K pump). This results in increased intracellular Ca2+ via effects on Na+/Ca2+ exchange → positive inotropic effect

Central vagal stimulation by digoxin causes increased refractory period and reduced rate of conduction through the AV node (parasympathetic NS slows the heart)

38
Q

What does digoxin do?

A
  • slows down heart rate

- improves ventricular contraction

39
Q

Why does digoxin improve contraction?

A

Digoxin competes with potassium. Potassium and sodium exchange is therefore interfered with, because digoxin binds to the potassium-binding site. Less sodium is being exchanged (less is leaving the cell). There is a build up of sodium inside the cell, with digoxin.

You also have the sodium-calcium exchange protein in cardiac muscle. If you get a build up of sodium inside the cell, there is more sodium-calcium exchange. Therefore, more calcium comes into the cell. As a result, there is a powerful positive inotropic effect in the ventricles.

40
Q

What are some adverse effects of digoxin?

A

Dysrhythmias (e.g. AV conduction block, ectopic pacemaker activity)

If you have too much vagal stimulation, it can lead to conduction block

41
Q

Why is digoxin a problem in hypokalaemic patients?

A

Diuretics promote hypokalaemia (promote potassium loss). Digoxin competes with potassium, so if you have little potassium in your blood, then digoxin over-inhibits, its too powerful then. This is why hypokalaemia is dangerous with digoxin.

Pharmacology (26 decks)

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