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Flashcards in deck_652996 Deck (47):

What do drugs for the CVS have an effect on?

-- rate and rhythm of heart-- force on contraction-- peripheral resistance and blood flow-- blood volume


Define arrhythmia

an abnormality of heart rate or rhythm


Give 5 types of arrythmia

1. Bradycardia2. Atrial flutter3. Atrial fibrillation 4. Tachycardia (ventricular and supraventricular)5. Ventricular fibrillation -- no coordinated electrical activity so no coordinated contraction


What are the 3 causes of arrhythmias?

1. Ectopic pacemaker activity -- pacemaker activity not where it is meant to be 2. Afterdepolarizations3. Re-entry loop -- problem with conduction4. Sarah's Doctor Who Uno


Define afterdepolarisations

-- anything that prolongs the duration of the AP-- can trigger a premature action potential -- longer AP so longer QT interval -- could be due to increased intracellular calcium


GIve an example of re-entry loop and describe it

problem with conduction e.g. conduction delay There is a block of a branch of purkinje fibreIncomplete conduction damage -- unidirectional block-- excitation takes the long route to spread the wrong way setting up a circus of excitation-- can get several small re-entry loops in the atria which can cause atrial fibrilation


Describe ectopic pacemaker activity

Damaged area of myocardium because depolarised and spontaneously active. Latent pacemaker region activated due to ischaemiaDominate over SA node


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

1. Drugs that block voltage gated Na+ channels2. Antagonists of β-adrenoceptors3. Drugs that block K+ channels4. Drugs that block Ca2+channels


Give an example of a drug that blocks voltage-gated Na channels and what they do

lidocaineThey block channels in open or inactive state -- are able to dissociate rapidly before the next AP-- Prevents firing of AP too close to each other


When are class I drugs used and why?

After MI w/ ventricular tachycardia -- prevents the automatic firing of the depolarised, damaged area of the myocardium


Give an example if antagonists of B-adrenoceptors and what they do

Propranolol, atenolol -- block sympathetic action (B-1 adrenoceptors in heart) and decrease slope of pacemaker potential in the SA


When are class II drugs used?

Used after MI --> decreased sympathetic activity which prevent ventricular arrhythmias. -- reduces O2 demand to reduce the risk of myocardial ischaemia-- slows AV node conduction (prevents supraventricular tachycardias)


What do drugs that block K+ channels do?

-- prolong the AP to lengthen the absolute refractory period-- should prevent and AP from occurring too soon, but can be proarrhythmicAre not generally used


What class III drug is used regularly?

Amiodarone-- used to treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop due to extra conduction pathway)


GIve an example of a drug which blocks calcium channels and what they do

Verapamil-- Decreases the slope of pacemaker action potential at SA node and decreases AV node conduction. -- This causes a decrease in the force of contraction (negative ionotropy)-- Can cause coronary and peripheral vasodilation


What is adenosine?

Acts on A2 receptors at AV node to enhance K+ conductance (prevents conduction through the AV node) -- inhibits adenylyl cyclaseDoes not fit into the classes-- short half life of ~ 10 seconds -- Allows heart to get back to a synchronous rhythm h


What are the features of heart failure that have to be combatted?

– Reduced force of contraction – Reduced cardiac output– Reduced tissue perfusion– Oedema


What are positive ionotropes used for?Give an example of a positive ionotrope

Increase the cardiac outputCardiac glycosides


What are the general actions of cardiac glycosides?

Improve the symptoms of heart failureAre not good in the long term


What is the molecular action of cardiac glycosides?

--> blocks Na+/K+ ATPase so increases intracellular Na conc as well as intracellular Ca as the Na/Ca exchanger is inhibited--> increase vagal activity via CNS (slows AV conduction and heart rate


Give an example if antagonists of B-adrenoceptors and what they do

Propranolol, atenolol -- block sympathetic action (B-1 adrenoceptors in heart) and decrease slope of pacemaker potential in the SA


What is the effect of cardiac glycosides?

--> blocks Na+/K+ ATPase --> Na/Ca exchanger still works so [Na] increases--> increased [Na] causes Na/Ca to exchange less, so [Ca] increases--> increase [Ca] increases the force on contraction (positive ionotropic effect)INCREASE CARDIAC OUTPUTAlso cause increase vagal activity(slows AV conduction and HR)


What class of drugs increase myocardial activity and give an example

Beta-adrenoceptor agonistDobutamine


When are drugs which increase myocardial activity used?

1. Cardiogenic shock2. Acute but reversible heart failure, for example after heart surgery


What are ACE-inhibitors?

drugs which inhibit the action of angiotensin converting enzyme


What do ACE-inhibitors do?

They prevent the conversion of angiotensin I to angiotensin II-- angiotensin II acts on the kidneys to increase Na+ and H20 reabsorption. It is also a vasoconstrictor. – decrease Na+ and water retention by kidney (decrease blood volume)– decrease total peripheral resistance due to vasodilation- decrease blood pressure by decreasing vasomotor tone, reducing afterload


What does angiotensin II stimulate the release of?

Aldosterone from the adrenal cortex


Define angina

Occurs when O2 supply to the heart does not meet its needCauses Ischaemia of heart tissue Usually causes chest pain upon exertion which is due to narrowing of the coronary arteries


What are the general ways of treating angina

Reduce the work load of the heart andImprove the blood supply to the heart


What drugs reduce the work load of the heart?

– β-adrenoreceptor blockers– Ca2+ channel antagonists– organic nitrates


What drugs improve the blood supply of the heart?

– organic nitrates– Ca2+ channel antagonists


What is the general action of organic nitrates?

Reduce venous pressure due to venodilation and dilate the coronary arteries


Describe the molecular action of organic nitrates

The react with -SH groups in vascular smooth muscle causing the release of NO (powerful vasodilator)NO activates guanylate cyclase. This converts GTP to cGMP to lower [Ca]. Lower [Ca] relaxes the vascular smooth muscle --> venodilation


What is the primary action of organic nitrates?

Cause venodilation which lowers preload-- reduces work load, lowers force on contraction and lowers O2 demand


What is the secondary action of organic nitrates?

Acts to dilate the coronary arteries so improves O2 supply to ischaemic myocardium-- usually collateral arteries rather than arterioles to bypass atheromatous plaque


Which conditions carry an increased risk of a thrombus forming?

– Atrial fibrillation– Acute myocardial infarction– Mechanical prosthetic heart valves


What are the two classes of drugs that are antithrombitic drugs?

Anticoagulants and anti-platelet drugs


Give three anticoagulants and what they do

1. Heparin (given intravenously)-- inhibits thrombin and is used acutely (short term action)2. Fractionated heparin (subcutaneous injection)3. Warfarin (given orally)-- antagonises action of vitamin K so can be used long term


Give an antiplatelet drug

Aspirin-- taken following an acute MI of if someone has a high risk of an MI


What are possible treatments for hypertension?

– diuretics– ACE-inhibitors– β-blockers– Ca2+ channel blockers which act at vascular smooth muscle– α1-adrenoceptor antagonists


What characteristics are associated with hypertension?

Increased blood volumeIncreased TPR


What do diuretics do?

decrease Na+ and water retention by kidney therefore decrease blood volume


What do beta-blockers do?

Decrease the cardiac output


What do drugs that are Ca2+ channel blockers selective for vascular smooth muscle do?

Cause vasodilatation


What do alpha-one adrenoceptor antagonists do?

Cause vasodilation


What is the equation the links BP, TPR and CO?



What do organic nitrates not dilate?