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CVS * > S7 Understanding Arrhythmias and the Action of Drugs on CVS > Flashcards

S7 Understanding Arrhythmias and the Action of Drugs on CVS Flashcards

1
Q

What can cause tachycardia?

A
  • ectopic pacemaker activity
  • after depolarisations
  • atrial flutter
  • re-entry loops
  • sinus tachycardia
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2
Q

What can cause bradycardia?

A
  • sinus bradycardia

* conduction block

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3
Q

What are the abnormalities in heart rate/rhythm (arrhythmias)?

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

What are cardiovascular drugs used to treat?

A
  • arrhythmias
  • heart failure
  • angina
  • hypertension
  • risk of thrombus formation
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5
Q

When are delayed after-depolarisations more likely to happen?

A

More likely to happen if intracellular Ca2+ is high

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6
Q

What are delayed after-depolarisations depolarisations?

A

Abnormal depolarisations that occur before the next depolarisation should occur (if they reach threshold, it triggers an earlier action potential) causes ventricular tachycardia

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7
Q

What are early after-depolarisations? What can it lead to?

A

Abnormal depolarisation leads to production of an action potential before repolarisation is complete

Can lead to oscillations

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8
Q

When are early after-depolarisations likely to happen? When does someone have this?

A

More likely to happen is the action potential is prolonged

If they have a longer QT interval

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9
Q

What is re-entry?

A

When a propagating impulse fails to die out after normal activation of the heart so it persists to re-excite the heart after the refractory period has needed - leads to arrhythmias

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10
Q

What normally happens to the impulses in the spread of excitation?

A

Reach a point where they cancel out

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11
Q

What happens if there is incomplete conduction damage?

A

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

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12
Q

What does a re-entrant mechanism arise from in the AV node?

A

The slow and fast pathways in the AV node

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13
Q

How can re-entrant circuits lead to atrial fibrillation?

A

You can get multiple small re-entry loops in the atria

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14
Q

How does ventricular pre-excitation occur? What is this syndrome called?

A

An accessory pathway between the atria and ventricles creates a re-entry loop

Wolff-Parkinson-White syndrome

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15
Q

What are the 4 classes of anti-arrhythmic drugs?

A
  1. Drugs that block voltage-sensitive sodium channels
  2. Antagonists of beta-adrenoreceptors
  3. Drugs that block potassium channels
  4. Drugs that block calcium channels
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16
Q

What is an example of a drug that blocks voltage-dependent Na+ channels (class I)? How does it work?

A

Lidocaine (anaesthetic)

Blocks voltage-gates Na+ channels in the open/inactivated states so blocks damaged depolarised tissue and has little effect in normal cardiac tissue due to it’s quick dissociation (in time for next AP in normal tissue)

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17
Q

When is lidocaine used following a MI? How is it given?

A

If the patient has ventricular tachycardia

Intravenously

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18
Q

What does lidocaine prevent?

A

Prevents automatic firing of depolarised ventricular tissue (damaged) by blocking Na+ channels

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19
Q

What are some examples of beta-adrenoreceptor antagonists (class II)?

A

Propranolol
Atenolol

(Both are beta blockers)

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20
Q

What do beta-adrenoreceptors do?

A

Blocks sympathetic action by acting on beta-1 adrenoreceptors and decreases the slope of the pacemaker potential in the SA node and slows conduction at the AV node

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21
Q

What can beta-blockers be used for?

A
  • prevents supraventricular tachycardia by slowing conduction in the AV node so slows the ventricular rate of patients with atrial fibrillation
  • used after myocardial infarction
  • reduces the oxygen demand
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22
Q

What do drugs that block K+ channels (class III) do?

A

They prolong the action potential by blocking K+ channels and hence lengthen the absolute refractory period to prevent another AP from occurring too soon

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23
Q

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

A

They produce a prolonged QT interval which is pro-arrhythmic rather than anti-arrhythmic

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24
Q

What is the K+ channel blocker drug that is used? What is is usually used to treat?

A

Amiodarone (has other actions as well as blocking K+ channels)

Treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry lop due to extra conduction pathway) and effective for suppressing ventricular arrhythmias post MI

25
Q

What are some drugs that can block Ca2+ channels in the heart?

A

Non-dihydropyridine types: verapamil and dilitiazem

26
Q

What do non-dihydropyridine type Ca2+ channel blockers do?

A
  • decrease the slope of the AP at the SA node
  • decrease AV nodal conduction
  • decrease force of contraction (negative inotropy)
27
Q

Where do dihydropyridine Ca2+ channel blockers act?

A

Act on vascular smooth muscle

28
Q

How is adenosine produced usually?

A

Produced endogenously at physiological levels but can be administered intravenously

29
Q

What does adenosine act on?

A

Alpha-1 receptors at the AV node (but have a short half life)

30
Q

What does adenosine do?

A
  • enhances K+ conductance (hyperpolarises cells of conducting tissue)
  • anti-arrhythmic - terminates re-entrant supraventricular tachycardias
31
Q

What do ACE inhibitors do?

A
  • inhibit action of angiotensin converting enzyme
  • prevents conversion of angiotension I into angiotensin II
  • involved in treatment of hypertension and heart failure
32
Q

What is a disadvantage of ACEi?

A

Can cause a dry cough due to excess bradykinin (ACE breaks down bradykinin)

33
Q

What is the advantage of inhibitor production of angiotensin II?

A

Angiotensin II increases reabsorption of Na+ and water in kidneys meaning an increase in blood volume and lead to vasoconstriction.

So inhibiting this means less reabsorption so decreased blood volume and increased vasodilation.

34
Q

What is the benefit on the heart of decreasing blood pressure (deceasing vasomotor tone) and blood volume (decreasing fluid retention)?

A
  • blood pressure - reduces afterload of the heart
  • blood volume - reduces preload of the heart

Both of these reduce the work load of the heart

35
Q

What type of drug has similar affects of ACEi? When are these used?

A

Angiotensin II receptor blockers (ARBs) e.g. losartan

Used if a patient can’t tolerate ACEi due too the dry cough

36
Q

What heart issues are diuretics used to treat?

A

Treat heart failure and hypertension

Loop diuretics are useful in congestive heart failure (fluid building up around the heart) - increase loss of Na+ and water from the kidneys

37
Q

What is the advantage of vascular smooth muscle Ca2+ channel blockers in heart problems?

A
  • decrease peripheral resistance
  • decrease arterial blood pressure

So reduce workload of heart by reducing afterload

38
Q

What do positive inotropes do?

A

Increased contractility and cardiac output

39
Q

What are the two types of positive inotropes?

A
  • cardiac glycosides

* beta-adrenergic agonists

40
Q

What is a type of cardiac glycoside?

A

Digoxin

41
Q

What do cardiac glycosides block?

A

Na+/K+ ATPase

42
Q

How do cardiac glycosides work to increase contractility?

A
  1. Na+/K+ ATPase is blocked by cardiac glycosides
  2. Leads to a rise in intracellular Na+ conc.
  3. This rise leads to decreased activity of the Na+-Ca2+ exchanger
  4. So increase in intracellular Ca2+ conc. (more Ca2+ is stored in SR)
  5. This leads to an increased force of contraction
43
Q

What is the action of cardiac glycosides on heart rate? When can they be used in heart failure?

A
  1. Increases vagal activity (via CNS)
  2. This slows the AV conduction
  3. Which slows heart rate

If there is an arrhythmia like atrial fibrillation

44
Q

What is an example of a beta-adrenoceptor agonist? What does it stimulate?

A

Dobutamine (a selective beta-1 adrenoceptor agonist)

Stimulates beta-1 receptors at the SA node, AV node and ventricular myocytes

45
Q

When are beta-adrenoceptors used?

A
  • cardiogenic shock

* acute but reversible heart failure e.g. after cardiac surgery

46
Q

Why would you not use cardiac glycosides as a long term treatment for heart failure?

A

It makes the heart conduct faster, but this isn’t good in the long run

47
Q

When does angina occur?

A

When oxygen supply to the heart doesn’t meet it’s need - results in pain with exertion and ischaemia of heart tissue (chest pain)

48
Q

How can you treat angina?

A

With organic nitrates

49
Q

What is the effect of NO on veins? Why do they act preferentially on veins?

A

Vasodilation of veins (venodilation)

Because there is less endogenous nitric oxide in veins?

50
Q

How does NO cause vasodilation of veins?

A
  1. NO activates guanylate cyclase
  2. This leads to an increase in cGMP
  3. This lowers the intracellular Ca2+ conc
  4. And so causes relaxation of vascular smooth muscle
51
Q

How does dilation of smooth muscle vasculature help alleviate angina symptoms?

A
  • venodilation lowers preload so workload of heart is decreased so heart fills less so reduced force of contraction (Starling’s Law) and so oxygen demand of heart is lowered
  • action of coronary collateral arteries improves oxygen delivery to ischaemic myocardium
52
Q

Why don’t organic nitrates work by dilating arterioles?

A

Because in the ischaemic region, the arterioles are already fully dilated and if you increase the dilation of the normal arterioles will have a negative impact

53
Q

What types of drugs do you use to treat angina by reducing the workload of the heart?

A
  • organic nitrates (venodilation)
  • beta-adrenoreceptor blockers
  • Ca2+ channel antagonists
54
Q

What types of drugs do you use to treat angina by improving the blood supply to the heart?

A
  • Ca2+ crabbed antagonists

* minor effect of organic nitrates

55
Q

Which heart conditions carry an increased risk of thrombus formation?

A
  • atrial fibrillation
  • acute myocardial infarction
  • mechanical prosthetic heart valves
56
Q

What are the two types of antithrombotic drugs?

A
  • anticoagulants

* antiplatelet drugs

57
Q

What is a type of antiplatelet drug?

A

Aspirin

58
Q

What anticoagulants prevent venous thromboembolism?

A
  • heparin (via IV)
  • fractionated heparin (subcutaneous injection)
  • warfarin (orally)

CVS * (17 decks)

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