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CVS > CVS 6 Arrthymias And CVS Drugs > Flashcards

CVS 6 Arrthymias And CVS Drugs Flashcards

(52 cards)

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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

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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?

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A

Can be pro-arrhythmic

23
Q

Mechanism of amiodarone

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A

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

24
Q

Examples of drugs that block Ca2+ channels

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A

Verapamil
Diltiazem

25
Mechanism of drugs that block Ca2+ channels
**On myocardium**: - Decreases slope of AP at SAN - Decreases AVN conduction - Decreases force of contraction **On smooth muscle**: - dilation of blood vessels >> reduces TPR
26
3 groups of Ca2+ channel blockers and what they act on
- **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
What type of drug are dihydropyridines and why aren’t they use to treat arrhythmias?
Ca2+ channel blockers Act mainly on peripheral vasculature not the heart
28
Mechanism of *adenosine*
Act on a1 receptors at AVN Enhances K+ conduction - hyperpolarises cells >> ‘resets the SAN’
29
Uses of *adeonsine*
Terminating re-entrant supra-ventricular tachycardia
30
What do patients need to be warned of when given *adeonsine*?
It will feel like their heart has stopped
31
Suffix of ACE inhibitors
-pril
32
Mechanism of ACE inhibitors
- 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
Side effect of ACE inhibitors Explain why
**Dry cough** - inhibits ACE - prevents breakdown of bradykinin >> build up causes a dry cough
34
Suffix of angiotensin II receptor blockers
-sartan
35
Mechanism of angiotensin II receptor blockers
- Blocks Ang receptor 1 which prevents AngII from binding - reduces effect of RAAS system: - vasodilation - **reduces afterload** - reduces ADH + aldosterone release - **reduces preload**
36
Similarity+ difference between ACE inhibitors and angiotensin II receptor blockers
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
How are ACE inhibitors and ARBs useful in heart failure?
- decreased BP >> reduces afterload - decreases fluid retention (blood volume) >> reduces preload Both of these decrease the work load on the heart
38
What diuretic is used to treat congestive heart failure? Example What does it do?
Loop diuretic *e.g. furosemide* Reduces pulmonary and peripheral oedema
39
What types of Ca2+ channel blockers are better at treating arrhythmias?
**Benzothiazapines** *e.g. diltiazem* **Phenylalkamines** *e.g. verapamil*
40
Examples of dihydropyridine Ca2+ channel blockers
*amlopidine* *nicardipine*
41
Uses of Ca2+ channel blockers
Hypertension Angina Coronary artery spasm Supraventricular tachycardia
42
What do positive inotropes do?
Increase contractility - heart beats harder >> increases CO
43
Primary mode of action of cardiac glycosides
Block Na+/K+ ATPase >> rise in intracellular [Na+] This causes an increases in intracellular [Ca2+] >> increases force of contraction (positive inotropic)
44
Difference in use of *propanolol* and *bisoprolol*
*propanolol* - non selective B1/B2 antagonist - B1 - slow HR + reduces force of contraction - B2 - bronchoconstriction *bisprolol* - selective B1 antagonist - less risk of bronchoconstriction
45
What drugs are used to treat angina?
Nitrates >> NO - *glyceryl trinitrate spray* - sprayed under tongue
46
What does NO do?
Vasodilator - particularly effective on **veins**
47
Mechanism of nitric oxide
- NO activates guanylate cyclase - Increases cGMP - Lowers intracellular [Ca2+] - Relaxation of vascular SM
48
How does nitric oxide help alleviate symptoms of angina?
- venodilation - lowers preload > reduces work load + contraction > lowers O2 demand - action on coronary arteries improves O2 delivery to ischaemic myocardium
49
What heart conditions have an increased risk of thrombus formation?
Atrial fibrillation Acute MI Mechanical prosthetic heart valves
50
Examples of anticoagulants
IV *heparin* - inhibits thrombin Oral *warafin* - antagonises action of vit K Oral *dabigatran* - thrombin inhibitor
51
Examples of anti platelet drugs
*aspirin* *clopidogrel*
52
Selectivity of beta blockers
**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

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