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CVS > 14. Drugs On CVS > Flashcards

14. Drugs On CVS Flashcards

1
Q

What can cause tachycardia?

A

Ectopic pacemaker activity
Afterdepolarisations
Atrial flutter/atrial fibrillation
Re-entry loop

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2
Q

What can cause bradycardia?

A 
Sinus bradycardia (sick sinus syndrome or drugs)
Conduction block (problems at AV node or bundle of His, slow conduction at AV node due to extrinsic factors)
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3
Q

What are delayed afterdepolarisations?

A

Can trigger action potentials which if repeated can lead to tachycardia
More likely to happen if intracellular Ca2+ high

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4
Q

What are early afterdepolarisations?

A

Can lead to oscillations
More likely to happen if AP prolonged
Longer AP - longer QT so more prone to arrhythmias

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5
Q

What is the re-entrant mechanism for generating arrhythmias?

A

Incomplete conduction damage (unidirectional block)

Excitation can take a long out to spread the wrong way through the damaged area, setting up a circus of excitation

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6
Q

Describe the AV nodal re-entry

A

Fast and slow pathways in AV node create a re-entry loop

Sets up tachycardia

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7
Q

Describe ventricular pre-excitation

A

An accessory pathway between atria and ventricles creates a re-entry loop such as in Wolff-Parkinson-White syndrome

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8
Q

What are the 4 basic classes of anti-arrhythmic drugs?

A

Drugs that block voltage-sensitive sodium channels
Antagonists of beta-adrenoceptors
Drugs that block potassium channels
Drugs that block calcium channels

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9
Q

How do drugs which block voltage-dependent Na+ channels work?

A

Use-dependent block, only blocks voltage gated Na+ channels in open or inactive state, therefore preferentially blocks damaged depolarised tissue
Little effect in normal cardiac tissue because it dissociates rapidly
Blocks during depolarisation but dissociates in time for next AP
E.g. lidocaine

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10
Q

When is lidocaine used?

A

Sometimes used following MI if patient shows signs of ventricular tachycardia but generally use other drugs

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11
Q

How does lidocaine work?

A

Damaged areas of myocardium may be depolarised and fire automatically
More Na+ channels are open in depolarised tissue, lidocaine blocks these and prevents automatic firing of depolarised ventricular tissue

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12
Q

Describe beta-adrenoceptor antagonists

A

Block sympathetic action, act at beta 1-adrenoceptors in heart
Decrease slope of pacemaker potential in SA and slows conduction at AVN
E.g. propranolol, atenolol

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13
Q

What are beta-blockers?

A

Can prevent supraventricular tachycardia by slowing conduction in AVN and ventricular rate in patients with AF
Reduces O2 demand to reduce myocardial ischaemia which is beneficial following MI

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14
Q

When are beta-blockers used?

A

Following MI
MI ofte causes increased sympathetic activity, arrhythmias may be partly due to increased sympathetic activity
Beta blockers prevent ventricular arrhythmias

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15
Q

Describe drugs that block K+ channels

A

Class 3 anti-arrhythmics
Prolong action potential by blocking K+ channels
Lengthens absolute refractor period
In theory would prevent anotherAP occurring too soon but in reality can be pro-arrhythmic and prolong QT interval
Can cause EAD
Only amiodarone used, used to treat tachycardia associated with Wolff-Parkinson-White syndrome

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16
Q

Describe drugs that block Ca2+ channels

A

Decreases slope of action potential at SAN
Decreases AV nodal conduction
Decreased force of contraction
Dihydropyridine Ca2+ channel blockersnot effective in preventing arrhythmias but do act on vascular smooth muscle (e.g. amlodipine)
Non-dihydropyridine types - verapamil, diltiazem

17
Q

Describe adenosine

A

Produced endogenously at physiological levels bu can be administered IV
Act of A1 receptor at AVN but as short half life
Enhances K+ conductance - hyperpolarises cells of conduction tissue
Anti-arrhythmic

18
Q

Describe ACE-inhibitors

A

Inhibits action of angiotensin converting enzyme
Important in treatment of hypertension and heart failure
Prevents conversion of angiotensin 1 to angiotensin 2
Can cause a dry cough due to excess bradykinin
Reduces after load and preload and decreases fluid retention
Both effects reduce work load on heart
E.g. perindopril

19
Q

What is the role of angiotensin 2?

A

Acts on kidneys to increase Na+ and water reabsorption

Also a vasoconstrictor

20
Q

Describe angiotensin 2 receptor blockers

A

In patients who cant tolerate ACEi can use AT1 receptor blocker
Used in treatment of heart failure and hypertension
E.g. losartan

21
Q

What are diuretics?

A

Used in treatment of heart failure and hypertension
Loop diuretics useful in congestive heart failure
E.g. furosemide
Reduces pulmonary and peripheral oedema

22
Q

Describe Ca2+ channel blockers

A

Dihydropyridine Ca2+ channel blockers not effective in preventing arrhythmias, but ac on vascular smooth muscle
E.g. amlodipine, nicardipine - decrease peripheral resistance, decrease arterial BP and reduce workload of heart by reducing afterload
Verapamil and diltiazem act on heart by reducing force of contraction
Useful in hypertension, angina, coronary artery spams, SVTs

23
Q

What are positive inotropes?

A

Increase contractility and thus cardiac output
Cardiac glycosides e.g. digoxin
Beta-adrenergic agonists e.g. dobutamine

24
Q

Describe cardiac glycosides

A

Used to treat heart failure and improves symptoms but not long term outcome
Digoxin is prototype
Primary mode of action is to block Na+/K+ ATPase

25
Q

Describe the action of cardiac glycosides

A

Ca2+ is extruded vis Na+-Ca2+ exchanger, driven by Na+ moving down concentration gradient
Cardiac glycosides lock Na+/K+ ATPase
Leads to rise in [Na+]in
Rise in intracellular Na+ leads to decrease in activity of Na+-Ca2+ exchanger
Causes increase in [Ca2+]in
Increased force of contraction

26
Q

What is the effect of cardiac glycosides on heart rate?

A

Cause increased vagal activity
Slow AV conduction
Slows heart rate
May be used in heart failure when there is an arrhythmia

27
Q

What are beta-adrenoceptor agonists?

A

Dobutamine
Selective beta 1-adrenoceptor agonist - stimulates beta 1 receptors present in SA node, AV node and on ventricular myocytes
Uses: cardiogenic shock, acute but reversible heart failure

28
Q

What are the best drugs for heart failure?

A

ACEi or ARBs and diuretics

Beta blockers can also reduce workload of heart

29
Q

What is angina?

A

Occurs when O2 supply to heart does not meet its need
Ischeamia of heart tissue
Usually pain with exertion
Does not result in death of myocytes

30
Q

How do you treat angina?

A

Reduce work load of heart using organic nitrates, beta-adrenoceptor blockers, Ca2+ channel antagonists
Improve blood supply to heart using Ca2+ channel antagonists, minor effect of organic nitrates

31
Q

What are organic nitrates?

A

Reaction of organic nitrates with thiols in vascular smooth muscle causes NO2- to be released
NO2- is reduced to NO (nitric oxide)
Nitric oxide is released endogenously from endothelial cells
NO is powerful vasodilator particularly effective on veins

32
Q

Why do organic nitrates preferentially act on veins?

A

Less endogenous nitric oxide in veins
At normal therapeutic doses it is most effective on veins - less of an effect on arteries
Very little effect on arterioles

33
Q

How does nitric oxide cause vasodilation?

A

NO activates granulate cyclase in vascular smooth muscle cell
Increases cGMP
Lowers intracellular [Ca2+]
Causes relaxation of vascular smooth muscle

34
Q

How does vasodilation due to nitric oxide help alleviate symptoms?

A

Venodilation lowers preload - reduced work load of heart, heart fills less therefore force of contraction reduced, lowers O2 demand
Action on coronary collateral arteries improves O2 delivery to ischaemic myocardium

35
Q

Which heart conditions carry an increased risk of thrombus formation?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

36
Q

What are the antithrombotic drugs?

A

Anticoagulants
Prevention of venous thromboembolism - heparin, fractionated heparin, warfarin, direct acting oral thrombin inhibitors such as dabigatran
Antiplatelet drugs - aspirin, clopidogrel

CVS (21 decks)

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