S10) Arrythmias & CVS Drugs Flashcards Preview

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Flashcards in S10) Arrythmias & CVS Drugs Deck (45):

Outline, briefly, the possible action of drugs on the cardiovascular system

CVS drugs can alter:

- The rate and rhythm of the heart

- The force of myocardial contraction

- Peripheral resistance and blood flow

- Blood volume 


What are arrhythmias/dysrhythmias?

Arrythmias are abnormalities of heart rate or rhythm


Provide 5 examples of arrythmias

- Bradycardia

- Tachycardia (ventricular/supraventricular)

- Atrial flutter

- Atrial fibrillation

- Ventricular fibrillation 


Describe four causes of arrhythmia which manifest as tachycardia

- Ectopic pacemaker activity – latent pacemaker region activated due to ischaemia and dominates over SAN

- After depolarisations – abnormal depolarisations following the action potential

- Atrial flutter / atrial fibrillation

- Re-entry loop – conduction delay due to accessory pathway 


Describe two causes of arrhythmia which manifest as bradycardia

- Sinus bradycardia

I. Intrinsic SAN dysfunction

II. Extrinsic factors e.g. drugs (beta blockers, CCBs)

- Conduction block

I. Problems at AVN / bundle of His

II. Slow conduction at AVN due to extrinsic factors e.g. drugs


When are delayed after-depolarisations likely to happen?

Delayed after-polarisations are more likely to happen if intracellular Ca2+ high 

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When are early after-depolarisations likely to happen?

- Early after-polarisations are more likely to happen if AP prolonged

- Longer AP = longer QT 

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Describe the re-entrant mechanism for generating arrhythmias

- Incomplete conduction damage (unidirectional block)

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

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How does atrial fibrillation occur?

Atrial fibrillation arises due to several small re-entry loops in the atria

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Briefly, explain how AV nodal re-entry occurs

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

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Briefly, explain how ventricular pre-excitation occurs

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

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There are 4 basic classes of anti-arrhythmic drugs affecting the rate and rhythm of the heart. 

What are they? 



- Drugs that block voltage-sensitive Na+ channels

- β-adrenoreceptors antagonists

- Drugs that block K+ channels

- Drugs that block Ca2+ channels


Describe the action of drugs which block voltage-dependant Na+ channels (Class I) 

- Only blocks voltage-gated Na+ channels in open/inactive state, thus preferentially blocks damaged depolarised tissue

- Blocks during depolarisation but dissociates in time for next action potential

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In four steps, describe the action of β-adrenoreceptor antagonists (class II) 

⇒ Act at β1-adrenoreceptors in the heart

⇒ Block sympathetic action

⇒ Decrease slope of pacemaker potential in SAN

⇒ Slows conduction at AVN 

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Describe the effects of beta blockers

Beta blockers slow conduction in AV node:

- Prevent supraventricular tachycardias (decrease in SNS activity)

- Slows ventricular rate in patients with AF


Explain why beta blockers are beneficial following myocardial infarction

- MI causes increased sympathetic activity

- β-blockers reduce O2 demand, hence reducing myocardial ischaemia


Describe the action of drugs that block K+ channels (class III)

- Block K+ channels

- Prolong the action potential 

- Lengthens the absolute refractory period

- Preventing another action potential occurring too soon (can be pro-arrhythmic)

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Describe the actions of drugs that block Ca2+ channels (class IV)

- Decreases slope of action potential at SAN

- Decreases AV nodal conduction

- Decreases force of contraction (negative inotropy)

- Some coronary and peripheral vasodilation


What is heart failure?

Heart failure is the chronic failure of the heart to provide sufficient output to meet the body’s requirements 


Identify 4 features of heart failure

- Reduced force of contraction or reduced filling

- Reduced cardiac output

- Reduced tissue perfusion

- Oedema 


Which types of drugs are used in the treatment of heart failure? 

- Positive inotropes to increase cardiac output (not routinely used)

- Drugs which reduce work load of the heart (afterload and preload)


Which drugs increase myocardial contractility in the treatment of heart failure?

- Cardiac glycosides

- β adrenoreceptor agonists 


In 5 steps, explain how cardiac glycosides increase myocardial contractility

⇒ Ca2+ is extruded via the Na+-Ca2+ exchanger 

⇒ Cardiac glycosides block Na+/K+ ATPase 

⇒ Rise in [Na+]i decreases activity of Na+-Ca2+ exchanger

⇒ Causes increase in [Ca2+]i 

⇒ Increased force of contraction 

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Cardiac glycosides may be used in heart failure when there are arrythmias.

Describe the action of cardiac glycosides on heart rate

- Action via CNS to increase vagal activity

- Slows AV conduction

- Slows the heart rate


Describe two uses of β – adrenoreceptor agonists

- Cardiogenic shock

- Acute but reversible heart failure e.g. following cardiac surgery


Which drugs reduce the work load of the heart?

- ACE inhibitors

- Diuretics

- β – adrenoreceptor antagonists


Describe the action of ACE-inhibitors

Prevent the conversion of angiotensin I to angiotensin II:

- Reduce Na+ and H2O reabsorption

- Vasodilation of systemic vasculature


Explain why ACE inhibitors are so useful in the treatment of hypertension

- Decrease vasomotor tone (blood pressure)

- Reduce afterload of the heart

- Decrease fluid retention (blood volume)

- Reduce preload of the heart


What is angina?

Angina is a condition arising due to insufficient O2 supply to the heart for a limited duration caused by artheromatous plaque formation in the coronary arteries

- It results in heart tissue Ischaemia which presents as chest pain 


How does one treat angina?

Reduce the work load of the heart:

I. β blockers


III. Organic nitrates

- Improve the blood supply to the heart:

I. Organic nitrates



Describe the action of organic nitrates

Reaction of organic nitrates with thiols in vascular smooth muscle causes NO2- to be released

- NO2- is reduced to nitrous oxide

- NO is a powerful vasodilator


How does nitrous oxide cause vasodilation?

⇒ NO activates guanylate cyclase

⇒ Increases cGMP

⇒ Lowers [Ca2+]i

⇒ Causes relaxation of vascular smooth muscle 

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In four steps, describe the primary action of nitrous oxide

Acts on venous system (venodilation):

⇒ Reduced venous pressure

⇒ Reduced filling → reduced contractility (Starling’s Law)

⇒ Lowers O2 demand 

⇒ Reduces work load of the heart 


What is the secondary action of nitrous oxide?

Acts on coronary collateral arteries to improve O2 delivery to the ischaemic myocardium


Why do organic nitrates preferentially act on veins?

Less endogenous nitric oxide in veins:

- Most effective on veins > arteries

- Little effect on arterioles 


Illustrate how venodilation by organic nitrates is a major contribution to their overall action

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Illustrate how the dilation of collateral coronary arteries by organic nitrates is only a minor contribution to their overall action

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Provide an example of an organic nitrate

Glyceryl trinitrate (GTN spray – sublingual)


Why do we need antithrombotic drugs?

To treat certain heart conditions which carry an increased risk of thrombus formation e.g. atrial fibrillation, AMI, mechanical prosthetic heart valves 


What are the two types of antithrombotic drugs?

- Anticoagulants 

- Antiplatelet drugs


Identify some anticoagulants and describe their actions

- IV Heparin – inhibits thrombin (short term)

- Oral Warfarin – antagonises action of vitamin K (long term)

- Other: fractionated subcutaneous heparin, oral thrombin inhibitors


What is the most common antiplatelet drug and when is it given?

Aspirin – following AMI / in high risk of MI 


What is hypertension?

Hypertension is the persistent elevation of blood pressure


What are the possible targets of hypertensive drugs?

- Lower blood volume

- Lower cardiac output directly

- Lower peripheral resistance 


Identify 5 hypertensive drugs and describe their respective actions

- ACE-inhibitors – decrease Na+ and H2O retention and TPR

- CCBs – vasodilation in vascular smooth muscle

- Diuretics – decrease Na+ and H2O retention

- β-blockers – decrease cardiac output (not routinely used)

- α1 adrenoceptor antagonist – vasodilation (not routinely used)