CVS 9 Drugs and the CVS Flashcards Preview

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Flashcards in CVS 9 Drugs and the CVS Deck (43):

What are cardiovascular drugs used to treat?

Heart failure
Risk of thrombus formation


What can drugs alter in the CVS?

Rate and rhythm of heart
Force of myocardial contraction
Peripheral Resistance and blood flow
Blood volume


What are some abnormalities of heart rate or rhythm?

atrial flutter
atrial fibrillation
tachycardia (ventricular and supraventricular)
ventricular fibrillation


What can cause arrhythmia?

damaged area of myocardium depolarises and becomes spontaneously active
latent pacemaker region activated due to ischaemia dominating SAN
AFTERDEPOLARISATIONS-abnormal depolarisations following AP (triggered activity)
RE-ENTRY LOOP conduction delay
accessory pathway


What are the two types of afterdepolarisations?

Early after-depolarisations
Delayed after-depolarisations


When do delayed after-depolarisations occur?

After the action potential
More likely if intracellular Ca2+ high


When do early after-depolarisations occur?

At point where repolarisation would normally occur
Can lead to oscillations
More likely if AP prolonged
Longer AP - longer QT


What is the re-entrant mechanism for generating arrythmias?

Normally at points where impulses move against each other they cancel.
If there is a unidirectional block, conduction cannot occur down a pathway but can go round and move back up the pathway the wrong way and create more excitation in the other direction (as myocardium wont be in refractory period by this time)


Where are re-entry loops often found?

Several small entry loops in atria which lead to atrial fibrillation


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

I. Drugs blocking v-gated sodium channels
II. Antagonists of beta-andrenoceptors
III. Drugs blocking potassium channels
IV. Drugs blocking calcium channels


Give an example of a Sodium blocking drug

Blocks Na+ channels in open or inactive state then dissociates in time for next AP
This stops AP from firing too soon


When is lidocaine used?

Following MI if patient has ventricular tachycardia where damaged areas of myocardium may depolarise and fire automatically.
Not used prophylactically(to prevent) following MI


What do beta-blockers(beta-adrenoceptor antagonists) do?

Block sympathetic action by acting on beta-1 adrenoceptors in heart to decrease slope of pacemaker potential in SA node


Give some examples of beta blockers

propranolol, atenolol


When are beta blockers used?

Used following MI (as MI causes increased sympathetic activity), to prevent ventricular arrhythmias (may be partly due to inc sympathetic activity)
Used to reduce O2 demand to reduce myocardial ischaemia (beneficial following MI)
Slow conduction in AV node to prevent supraventricular tachycardia


How do drugs that block K+ channels work?

Prolong action potential to lengthen the absolute refractory period
In theory prevents another AP from firing to soon but in reality can be proarrythmic so not generally used


What are drugs blocking K+ channels used for?

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


What drug in class III (K+ blockers) is an exception to the fact that they are pro-arrhythmic?

Amiodarone as it has other actions too including being a beta antagonist and blocking Na+ channels


Give an example of a drug that blocks Ca2+ channels (IV)



How do Ca2+ channel blockers work?

Decrease slope of pacemaker action potential at SA node to decrease AV nodal conduction and reduce force of contraction (-ve inotropy)
Also causes some coronary and peripheral vasodilation


What are dihydropyridine Ca2+ channels used to do?

Not used in preventing arrythmias but do act on vascular smooth muscle


What does adenosine do and whats it used for?

Produced endogenously and can be administered pharmacologically
Acts on alpha1 receptors at AV node to:
enhance K+ conductance
decrease cAMP levels
It is a very short acting anti-arrhythmic administered intravenously


What is heart failure?

Chronic failure of the heart to provide sufficient output to meet the body's requirements


What are features of heart failure?

Reduced force of contraction
Reduced cardiac output
Reduced tissue perfusion


What drugs are used to treat heart failure?

Positive inotropes (inc CO) e.g cardiac glycosides and B-adrenergic agonists e.g dobutamine
Drugs reducing workload of heart by reducing preload and afterload


Name a cardiac glycoside, what do they do?

Digoxin, blocks Na+/K+ATPase (which decreases Ca2+ efflux as increases [Na+] so lower grad for Na+/Ca2+ exchanger)to increase inotropy
Improves symptoms but not long term outcome
Also increase vagal activity to slow AV conduction and heart rate


What do B-adrenoceptor agonists do and what are they used for?

Increase myocardial contractility by acting on b1 receptors e.g dobutamine
Used in cardiogenic shock and acute but reversible heart failure (e.g following heart failure)


How do ACE-inhibitors work?

Inhibit angiotensin converting enzyme preventing conversion of angiotensin I to angiotensin II
Angiotensin II acts on kidneys to inc Na+ and water reabsorption and is a vasoconstrictor
So ACE inhibitors decrease blood pressure and blood volume


What do ACE-inhibitors do?

Decrease vasomotor tone and so decreases blood pressure
Decreases fluid retention and so blood volume
Reduces preload of heart to reduce work load of heart


What types of drugs reduce work load of heart?

B-adrenoceptor antagonists
ACE inhibitors


What is angina?

Ischaemia of heart tissue giving chest pain
Usually pain with exertion
Due to narrowing of coronary arteries die to atheroma


How is angina treated?

Drugs that reduce workload of heart:
Beta blockers, Ca2+ channel antagonists, organic nitrates
Drugs improving blood supply to heart:
organic nitrates, Ca2+ channel antagonists


How do organic nitrates work?

React with thiols (SH groups) in vascular smooth muscle causes NO2- to be released which is reduced to NO which is a powerful dilator


How does NO cause vascular dilation?

NO activates guanylate cyclase
This increases cGMP
Lowers intracellular {Ca2+} relaxing vascular smooth muscle


How does dilation alleviate angina symptoms?

PRIMARY ACTION-Venodilation lowers preload
reduces workload of heart (reduces venous pressure and return)
heart fills less therefore lower force of contraction (starling's law) lowering O2 demand
SECONDARY ACTION- vasodilation of collateral coronary arteries improves O2 delivery to ischaemic myocardium


How does NO dilating collateral arteries and not arterioles increase blood flow to ischaemic myocardium?

Arterioles already fully dilated in ischaemic areas.
Dilation of collateral arteries allows more blood to bypass stenosed regions which previously limited flow


What heart conditions carry an increased risk of thrombus formation?

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves


What are some common anticoagulants, when are they used and how do they work?

Heparin (given intravenously and as subcutaneous injection)
-inhibits thrombin, used acutely for short term action
Warfarin (given orally) antagonises action of Vit K used long term


What drug is antiplatelet and when is it given?

following acute MI or when high risk of MI


What causes hypertension?

Increases blood volume (inc water and Na+ retention by kidneys)
Increase in TPR
pressure=flow x resistance


What three factors can we target to stop hypertension?

Lower blood volume (which also lowers CO by Starling's)
Lower CO directly
Lower peripheral resistance


What drugs are used to treat hypertension?

Diuretics- decrease blood vol by reduced Na+ and water retention
ACE inhibitors- decrease Na+ and water retention in kidney, decrease TPR via vasodilation
B blockers- decrease CO
Ca2+ blockers selective for VSM (dilation)-dihydropyridine
a1-adrenoceptor antagonist- vasodilation


How is blood pressure calculated?