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ESA 2 SK > CVS 9 Drugs and the CVS > Flashcards

CVS 9 Drugs and the CVS Flashcards

1
Q

What are cardiovascular drugs used to treat?

A 
Arrhythmias
Heart failure
Angina
Hypertension
Risk of thrombus formation
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2
Q

What can drugs alter in the CVS?

A

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

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3
Q

What are some abnormalities of heart rate or rhythm?

A 
bradycardia
atrial flutter
atrial fibrillation
tachycardia (ventricular and supraventricular)
ventricular fibrillation
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4
Q

What can cause arrhythmia?

A

ECTOPIC PACEMAKER ACTIVITY-
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

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5
Q

What are the two types of afterdepolarisations?

A

Early after-depolarisations

Delayed after-depolarisations

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6
Q

When do delayed after-depolarisations occur?

A

After the action potential

More likely if intracellular Ca2+ high

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7
Q

When do early after-depolarisations occur?

A

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

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8
Q

What is the re-entrant mechanism for generating arrythmias?

A

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)

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9
Q

Where are re-entry loops often found?

A

Several small entry loops in atria which lead to atrial fibrillation

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10
Q

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

A

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

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11
Q

Give an example of a Sodium blocking drug

A

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

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12
Q

When is lidocaine used?

A

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

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13
Q

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

A

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

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14
Q

Give some examples of beta blockers

A

propranolol, atenolol

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15
Q

When are beta blockers used?

A

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

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16
Q

How do drugs that block K+ channels work?

A

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

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17
Q

What are drugs blocking K+ channels used for?

A

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

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18
Q

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

A

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

19
Q

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

A

Verapamil

20
Q

How do Ca2+ channel blockers work?

A

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

21
Q

What are dihydropyridine Ca2+ channels used to do?

A

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

22
Q

What does adenosine do and whats it used for?

A

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

23
Q

What is heart failure?

A

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

24
Q

What are features of heart failure?

A

Reduced force of contraction
Reduced cardiac output
Reduced tissue perfusion
Oedema

25
Q

What drugs are used to treat heart failure?

A 
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
26
Q

Name a cardiac glycoside, what do they do?

A

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

27
Q

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

A

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)

28
Q

How do ACE-inhibitors work?

A

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

29
Q

What do ACE-inhibitors do?

A

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

30
Q

What types of drugs reduce work load of heart?

A

B-adrenoceptor antagonists
ACE inhibitors
Diuretics

31
Q

What is angina?

A

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

32
Q

How is angina treated?

A

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

33
Q

How do organic nitrates work?

A

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

34
Q

How does NO cause vascular dilation?

A

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

35
Q

How does dilation alleviate angina symptoms?

A

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

36
Q

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

A

Arterioles already fully dilated in ischaemic areas.

Dilation of collateral arteries allows more blood to bypass stenosed regions which previously limited flow

37
Q

What heart conditions carry an increased risk of thrombus formation?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

38
Q

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

A

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

39
Q

What drug is antiplatelet and when is it given?

A

Aspirin

following acute MI or when high risk of MI

40
Q

What causes hypertension?

A

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

41
Q

What three factors can we target to stop hypertension?

A

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

42
Q

What drugs are used to treat hypertension?

A

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

43
Q

How is blood pressure calculated?

A

BP=CO x TPR

ESA 2 SK (35 decks)

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