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CVS > CVS 6 Arrthymias And CVS Drugs > Flashcards

CVS 6 Arrthymias And CVS Drugs Flashcards

1
Q

What is the primary mechanism by which GTN spray alleviates myocardial ischaemia in a patient with stable angina?

A

Dilation of systemic veins

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2
Q

Causes of tachycardia

A
  • ectopic pacemaker activity - damaged area of myocardium takes over from SAN
  • afterdepolarisations - abnormal depolarisations following the AP
  • atrial flutter/atrial fibrillation
  • re-entry loop - conduction delay
    - accessory pathway
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3
Q

Causes of bradycardia

A
  • sinus bradycardia - SAN does depolarise quick enough - Sick sinus syndrome
  • Drugs e.g. B blockers, Ca2+ channel blockers
  • conduction block - issue at AVN or bundle of His
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4
Q

Types of tachycardias

A

Ventricular
Supraventricular - above ventricles

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5
Q

Does hypokalaemia or hyperkalaemia cause early after depolarisations?

A

Hypokalaemia - delays repolarisation&raquo_space; can cause early after depolarisations

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6
Q

When are early after depolarisations more likely to occur?

A

When AP is prolonged
(Longer QT interval)

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7
Q

When are delayed after depolarisations more likely to occur?

A

If intracellular Ca2+ conc is high

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8
Q

What happens in incomplete conduction damage?

A

Excitation can take longer route to spread the wrong way through damaged area
This sets up a circus of excitation

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9
Q

What happens in AV nodal re-entry?

A

Fast and slow pathways in the AVN create a re-entry loop
Ventricles stimulated too soon

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10
Q

What happens in ventriuclar pre-excitation?
Example of where this is seen

A

An accessory pathway between atria and ventricles
creates a re-entry loop
e.g. Wolff-Parkinson-White syndrome

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11
Q

What causes atrial fibrillation?

A

Multiple small re-entry loops in the atria

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12
Q

What are the 4 classes of anti-arrhythmic drugs?

A
  • drugs that block voltage gated Na+ channel
  • antagonists of B-adrenoreceptors (B blockers)
  • drugs that block K+ channels
  • drugs that block Ca2+ channels
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13
Q

Mechanism of lidocaine

A
  • Blocks voltage gated Na+ channel when open or inactive state
  • Blocks VGNC in damaged myocardium spontaneously depolarising after AP&raquo_space; prevents initiation of another AP
  • dissociates quickly
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14
Q

What can lidocaine be used for?

A

Ventricular tachycardia

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15
Q

Example of drugs which blocks voltage gated Na+ channels

A

lidocaine

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16
Q

Suffix of Beta blockers

A

-olol

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17
Q

How do beta blockers work?
Effect on SAN + AVN

A
  • Block sympathetic action - B1 adrenoreceptors in heart
  • which decreases heart rate due to:
  • Decreases slope of pacemaker potential in SAN
  • Slows Conduction at AVN by reducing voltage gated Ca2+ channel activity in upstroke of AP
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18
Q

When can B blockers be used?

A

Prevent supraventriclar tachycardia
Atrial fibrillation
Following myocardial infarction
To reduce O2 demand - reduces myocardial ischamia
Heart failure

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19
Q

How are beta blockers useful after a myocardial infarction?

A
  • MI often increases sympathetic activity - B blockers block sympathetic activity
  • increased sympathetic activity can cause arrhythmias
  • prevent ventricular arrhythmias
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20
Q

How fast does lidocaine dissociate and what is the importance of this?

A

<0.5ms
- Bound long enough to prevent inappropriate depolarisations + dissociates in time for next AP
- This means myocardium can depolarise normally + heart beats efficiently

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21
Q

Mechanism of drugs that block K+ channels

A
  • prolong AP
  • this lengthens the absolute refractory period
  • in theory would prevent another AP occurring too soon but can be pro-arrhythmic - prolonged QT interval
22
Q

Why are drugs that block K+ channels not generally used?

A

Can be pro-arrhythmic

23
Q

Mechanism of amiodarone

A

Blocks K+ channels
Has other actions so can cause side effects

24
Q

Examples of drugs that block Ca2+ channels

A

Verapamil
Diltiazem

25
Q

Mechanism of drugs that block Ca2+ channels

A

On myocardium:
- Decreases slope of AP at SAN
- Decreases AVN conduction
- Decreases force of contraction

On smooth muscle:
- dilation of blood vessels&raquo_space; reduces TPR

26
Q

3 groups of Ca2+ channel blockers and what they act on

A
  • benzothiazapines - act on heart to give negative inotropic + chronotropic effects
  • phenylalkamines - act on heart to give negative inotropic + chronotropic effects + dilate vessels to reduce TPR
  • dihydropyridine - mainly act on vasculature to reduce TPR
27
Q

What type of drug are dihydropyridines and why aren’t they use to treat arrhythmias?

A

Ca2+ channel blockers
Act mainly on peripheral vasculature not the heart

28
Q

Mechanism of adenosine

A

Act on a1 receptors at AVN
Enhances K+ conduction - hyperpolarises cells&raquo_space; ‘resets the SAN’

29
Q

Uses of adeonsine

A

Terminating re-entrant supra-ventricular tachycardia

30
Q

What do patients need to be warned of when given adeonsine?

A

It will feel like their heart has stopped

31
Q

Suffix of ACE inhibitors

A

-pril

32
Q

Mechanism of ACE inhibitors

A
  • Inhibitors action of angiotensin converting enzyme
  • prevents conversion of AngI > AngII - reduces effect of RAAS system
  • vasodilation > reduces afterload
  • reduced ADH and aldosterone release > reduces preload
33
Q

Side effect of ACE inhibitors
Explain why

A

Dry cough
- inhibits ACE
- prevents breakdown of bradykinin&raquo_space; build up causes a dry cough

34
Q

Suffix of angiotensin II receptor blockers

A

-sartan

35
Q

Mechanism of angiotensin II receptor blockers

A
  • Blocks Ang receptor 1 which prevents AngII from binding
  • reduces effect of RAAS system:
  • vasodilation - reduces afterload
  • reduces ADH + aldosterone release - reduces preload
36
Q

Similarity+ difference between ACE inhibitors and angiotensin II receptor blockers

A

Have the same effect - both reduce effect of RAAS system

Ang II receptors don’t prevent bradykinin breakdown - only ACEi have dry cough, not ARBs

37
Q

How are ACE inhibitors and ARBs useful in heart failure?

A
  • decreased BP&raquo_space; reduces afterload
  • decreases fluid retention (blood volume)&raquo_space; reduces preload

Both of these decrease the work load on the heart

38
Q

What diuretic is used to treat congestive heart failure? Example
What does it do?

A

Loop diuretic e.g. furosemide
Reduces pulmonary and peripheral oedema

39
Q

What types of Ca2+ channel blockers are better at treating arrhythmias?

A

Benzothiazapines e.g. diltiazem
Phenylalkamines e.g. verapamil

40
Q

Examples of dihydropyridine Ca2+ channel blockers

A

amlopidine
nicardipine

41
Q

Uses of Ca2+ channel blockers

A

Hypertension
Angina
Coronary artery spasm
Supraventricular tachycardia

42
Q

What do positive inotropes do?

A

Increase contractility - heart beats harder&raquo_space; increases CO

43
Q

Primary mode of action of cardiac glycosides

A

Block Na+/K+ ATPase&raquo_space; rise in intracellular [Na+]
This causes an increases in intracellular [Ca2+]&raquo_space; increases force of contraction (positive inotropic)

44
Q

Difference in use of propanolol and bisoprolol

A

propanolol - non selective B1/B2 antagonist
- B1 - slow HR + reduces force of contraction
- B2 - bronchoconstriction

bisprolol - selective B1 antagonist
- less risk of bronchoconstriction

45
Q

What drugs are used to treat angina?

A

Nitrates&raquo_space; NO
- glyceryl trinitrate spray - sprayed under tongue

46
Q

What does NO do?

A

Vasodilator - particularly effective on veins

47
Q

Mechanism of nitric oxide

A
  • NO activates guanylate cyclase
  • Increases cGMP
  • Lowers intracellular [Ca2+]
  • Relaxation of vascular SM
48
Q

How does nitric oxide help alleviate symptoms of angina?

A
  • venodilation - lowers preload > reduces work load + contraction > lowers O2 demand
  • action on coronary arteries improves O2 delivery to ischaemic myocardium
49
Q

What heart conditions have an increased risk of thrombus formation?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

50
Q

Examples of anticoagulants

A

IV heparin - inhibits thrombin
Oral warafin - antagonises action of vit K
Oral dabigatran - thrombin inhibitor

51
Q

Examples of anti platelet drugs

A

aspirin
clopidogrel

52
Q

Selectivity of beta blockers

A

A-N: cardio-selective B1 blocker
O-Z: non-selective B1+B2 blocker

If suffix is close to olol but not exact: beta + alpha blocker

CVS (17 decks)

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