L16: Cardiovascular Pharmacology - Coronary Heart Disease (Angina) Flashcards

1
Q

How can coronary artery disease be treated by treating the symptoms (angina)?

A
  • organic nitrates
  • beta blockers
  • K+ channel activators
  • Ca2+ channels blockers
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2
Q

What is Angina Pectoris?

A

Intermittent chest pain caused by miscmatch between demand of oxygen by the heart and supply of oxygen to the heart.
O2 supply decreased by: coronary artery disease (also anaemia)
O2 demand increased by: exercise, tachycardia (high HR), hypertension

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3
Q

What can help reduce O2 demand during acute Angina?

A

During the attack:
- rest
- organic nitrates: act on guanylate cyclase, which converts GTP to cGMP. It inhibits calcium ions intake and causes relaxation

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4
Q

Where can nitrates act in?

A
  • venous circulation: decrease venous return and preload
  • coronary arteries: improves supply if coronary spasm, can dilate collaterals and redistribute blood
  • arterioles

Acute only, chronic use leads to tolerance

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5
Q

What can help reduce O2 demand during chronic Angina?

A

To prevent the atack:
- beta-adrenoreceptor antagonists
- calcium channel blockers
- potassium channel activators

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6
Q

How do beta-adrenoreceptor antagonists act during angina?

A
  • reduce heart rate and O2 demand
  • decrease preload (blood volume) and O2 demand
  • increase duration of diastole (greatest coronary blood flow) and increase O2 supply
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7
Q

How do calcium channel blockers act during angina?

A
  • block entry of calcium ions into cells via L-type calcium channels
  • cardioselective phenylethylalkamine
  • reduce force of contraction in cardiomyocytes and therefore O2 demand
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8
Q

How do potassium channel openers act during angina?

A

Opens K(ATP) channel in smooth muscle to cause relaxation and vasodilation (by closing voltage sensitive calcium channels). Side effects: can cause headache, flushing and diziness, therefore only used short term while awaiting angioplasty

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9
Q

What is cardiac arrythmia caused by?

A
  • genetics
  • lifestyle (caffeine, smoking)
  • disease: hyperthyroid (increased rate), hypertension (fibrosis), coronary heart disease (ischaemia, MI), ageing, medication
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10
Q

What does cardiac arrythmia result in?

A
  • dizziness and fainting
  • cardiac arrest and death (ventricular fibrillation following myocardial infarction)
  • stroke (secondary to clots forming in pooling atrial blood, atrial fibrillation)
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11
Q

What are the changes in cardiac arrythmias? What happens during CA?

A

In cardiac arrythmias ionic balances become fluctuating. Disturbances in the rhythm of the heart due to abnormal pulse generation or abnormal impulse conduction

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12
Q

How are cardiac arrythmias usually classified?

A

according to:
- site of origin of abnormality e.g. atrial, junctional or ventricular
- whether the rate is increased (tachycardia) or decreased (bradycardia) or disorganised (fibrillation)

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13
Q

What are the possible sites of origin of abnormality for cardiac arrythmias?

A

Atrial, junctional, ventricular

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14
Q

What is tachycardia?

A

Type of cardiac arrythmia, when the rate is increased

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15
Q

What is bradycardia?

A

Type of cardiac arrythmia, when the rate is decreased

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16
Q

What is fibrillation?

A

Type of cardiac arrythmia, when the rate is disorganised

17
Q

What are the types of cardiac arrythmias?

A
  • Re-entry arrythmia: cardiac impulse fails to stop i.e. reexcites the myocardium after refractory period (no repolarization period) MAIN TYPE
  • Delayed after depolarisation (DAD). Additional depolarisation of non-excitable cells before previous repolarisation is complete (depolarisation prolonged)
18
Q

What is the treatment of cardiac arrythmias?

A
  • cardioversion: electrical resynchronisation to sinus rhythm if serious ventricular arrythmia
  • surgery: tissue ablation or placement of an artificial pacemaker
  • drug intervention: anti-arrythmic drugs
19
Q

What are the four classes of drugs used for treatment of cardiac arrythmias?

A
  • class I: block voltage sensitive sodium channels and therefore reduce the maximum rate of depolarisation during phase O of cardiac potential. Organized into classes based on their interaction with Na channels (depending on where on the channel they act) e.g. flecainide
  • class II: beta-blockers - beta adrenoreceptor antagonists block effects of the sympathetic nervous system and therefore slow the heart, by actions on pacemaker potential (phase 4) e.g. propanolol
  • class III: prolong the action potential by blocking K+ channels and inhibiting repolarisation, increasing the refractory period and making re-entry more difficult. e.g. amiodarone, sotalol
  • class IV : ‘Calcium-antagonists’. Decrease Ca2+, slow conduction in SA and AV nodes, suppress extra beats and re-entry. e.g. verapamil
20
Q

What is the action of class I anti-arrythmic drugs? What is their example?

A

class I: block voltage sensitive sodium channels and therefore reduce the maximum rate of depolarisation during phase O of cardiac potential. Organized into classes based on their interaction with Na channels (depending on where on the channel they act) e.g. flecainide

21
Q

What is the action of class II anti-arrythmic drugs? What is their example?

A

class II: beta-blockers - beta adrenoreceptor antagonists block effects of the sympathetic nervous system and therefore slow the heart, by actions on pacemaker potential (phase 4) e.g. propanolol

22
Q

What is the action of class III anti-arrythmic drugs? What is their example?

A

class III: prolong the action potential by blocking K+ channels and inhibiting repolarisation, increasing the refractory period and making re-entry more difficult. e.g. amiodarone, sotalol

23
Q

What is the action of class IV anti-arrythmic drugs? What is their example?

A

class IV : ‘Calcium-antagonists’. Decrease Ca2+, slow conduction in SA and AV nodes, suppress extra beats and re-entry. e.g. verapamil

24
Q

What are the class I of drugs used for treatment of cardiac arrythmias?

A

sodium channel blockers

25
Q

What are the class II of drugs used for treatment of cardiac arrythmias?

A

beta-blockers

26
Q

What are the class III of drugs used for treatment of cardiac arrythmias?

A

drugs that prolong repolarisation

27
Q

What are the class IV of drugs used for treatment of cardiac arrythmias?

A

calcium channel-blocking drugs

28
Q

What’s the damage of myocardial infarction to the heart?

A
  • remaining ventricle
  • remodels to maintain cardiac output (reduces damage, but no repair, not sufficient)
  • initially compensates, but eventually heart fails
  • damaged tissue is replaced by non-contractile collagen scar