CVS - Arrrhythmia Drugs Flashcards Preview

CJ: UoL Medicine Semester Two (ESA2) > CVS - Arrrhythmia Drugs > Flashcards

Flashcards in CVS - Arrrhythmia Drugs Deck (28)
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What possible effects can drugs have on the CVS?

They can alter:
1) rate and rhythm of heart
2) force of myocardial contraction
3) peripheral resistance and blood flow
4) blood volume


Give some causes of tachycardia

- ectopic pacemaker activity
- afterdepolarisations
- atrial flutter/fibrillation
- re-entry loop


Give some causes of bradycardia

- sinus bradycardia (may be due to sick sinus syndrome or drugs)
- conduction block


What is delayed after-depolarisation?

Extra depolarisation which occurs after the main depolarisation. Usually due to high intracellular Ca2+


What are early after-depolarisations?

Extra depolarisations which occur at the end of the plateau phase of depolarisation. More likely to occur when action potential is prolonged, so there is a prolonged QT interval


How can a unidirectional block of conduction due to myocardial damage lead to an arrhythmia forming?

The impulse cannot travel down through the affected area, so the equivalent impulse from the other side of the heart (as there are two mirrored impulses) spreads upwards through the area, setting up a 'circus' of depolarisation


What can be caused by multiple re-entrant circuits in the atria?

Atrial fibrillation


How does lidocaine work?

It blocks voltage-dependent Na+ channels


Why does lidocaine have little effect on normal cardiac tissue?

It preferentially blocks open/inactive Na+ channels, which are most present in damaged depolarised tissue


Why would lidocaine be given (CVS causes)?

Sometimes used following MI if someone has ventricular tachycardia


How do beta blockers work?

They block sympathetic action at the B1 adrenoceptors in the heart, which slows conduction at the AV node and decreases the slope of the pacemaker potential


Why would beta blockers be used?

- prevent supraventricular tachycardias because they slow the conduction at AV node
- used after MI
- they reduce O2 demand, so they can be used to reduce myocardial ischaemia following MI


What is the effect of drugs that block K+ channels?

They lengthen the absolute refractory period, which can have pro-arrhythmic effects


Give an example of a drug which blocks K+ channels



What is the effect of drugs which block Ca2+ channels?

- decrease slope of action potential at SA node
- decrease AV node contraction
- decrease force of contraction


What is adenosine?

Substance which is produced endogenously, which acts on alpha-1 receptors at the AV node. It enhances K+ conductance and is an antiarrhythmic


How can drugs be used to treat heart failure?

Can give:
- positive inotropes to increase cardiac output (not routine)
- drugs which reduce afterload and preload


How do cardiac glycosides work?

- inhibit Na+Ka+ATPase, so [Na+] in the cell rises
- this means the Na+Ca2+ exchanger doesn't work as well, as it relies on the sodium gradient
- [Ca2+] rises and it is stored in the sarcoplasmic reticulum
- more Ca2+ available, so increased force of contraction

They also cause increased vagaries activity, slowing the heart rate


When would beta-adrenoceptor agonists be used?

They act on beta-1 receptors and are used in cardiogenic shock or acute but reversible heart failure


How do ACE-inhibitors work?

They reduce the workload of the heart by inhibiting the action of angiotensin converting enzyme. This reduces vasoconstriction and blood volume


Why are ACE inhibitors particularly useful in heart failure?

They decrease both afterload and preload of the heart


How do organic nitrates work?

NO2- is reduced to nitric oxide, which is a powerful vasodilator. They lower the intracellular [Ca2+], causing relaxation of vascular smooth muscle


How does nitric oxide help angina?

- causes VENOdilation which lowers preload and reduces work load of heart
- acts on coronary collateral arteries to improve O2 delivery to ischaemic myocardium


True or false - NO works on arterioles?

It doesn't!


Which heart conditions carry a higher risk of thrombus formation?

Atrial fibrillation, acute myocardial infarction, mechanical prosthetic heart valves


Give some examples of antithrombotic drugs

- anticoagulants (heparin, fractionated heparin, warfarin, oral thrombin inhibitors)
- antiplatelet drugs (aspirin)


How does warfarin work?

Antagonises the action of vitamin K


How does heparin work?

Inhibits thrombin

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