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Semester 3 > Drugs used in angina and MI > Flashcards

Drugs used in angina and MI Flashcards

1
Q

Define angina pectoris

A

Chest pain when blood supply to part of the myocardium is inadequate for its needs. Usually caused by atheroma

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2
Q

Causes of angina

A
  • Coronary atheroma
  • Aortic stenosis
  • Severe anaemia Infection (arteritis, syphillis)
  • Absent coronary circulation
  • Toxins
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3
Q

Strategies to prevent and treat angina

A

Reduce CV risk factors: BP, Cholesterol, smoking, LVH

Decrease metabolic demand of LV

Increase coronary blood flow

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4
Q

Major determinants of LV work

A

Heart rate

Arterial pressure

Ventricular size

Drugs relieve angina work by reducing the metabolic demands of the heart, which means reducing the work of the LV.

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5
Q

Drugs which reduce ventricular dimension

A

Nitrovasodilators e.g. glyceryl nitrate, isosorbide mononitrate, amyl nitrate.
These relax smooth muscle and preferentially affect veins. Leads to increase in venous capacitance with small falls in arteriolar resistance. This reduces the heart size

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6
Q

Mechanism of nitrovasodilators

A

Broken down or metabolised to nitric oxide in endothelial cells. This activates guanylate cyclase in vascular smooth muscle to cause an increase in cGMP, reducing [Ca}i and causing vascular relaxation.

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7
Q

Effect of organic nitrates on circulation

A

Increase in venous capacitance

Fall in CVP

Small decrease in arteriolar resistance

Reduction in cardiac size

Reduced CO

Fall in CO and TPR = Reduced LV work

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8
Q

Administration or nitrates in angia

A

GTN: given sublingually, when swallowed undergoes extensive first pass metabolism in the liver and is inactive. When sucked it is rapidly absorbed in the buccal mucosa into the systemic circulation. Action within 1-2mins that lasts for 15-20mins

Isosorbide mononitrate: sublingual or oral. Isosorbide DI-nitrate is converted to mononitrate in the liver by first pass metabolism. Long acting drugs that last for several hours.

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9
Q

Unwanted effects of nitrovasodilators

A

Vascular headaches as a result of dilation of the muscular intracranial arteries.

Prolonged exposure to nitrates results in tolerance. vsmc becomes resistant to dilator effects and following withdrawal may result in abnormal constriction.

Reflex tachycardia in response to vasodilation which offsets some of the benefit of the drugs.

Potential for dilating sites of atheroma leading to further reduction in coronary circulation

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10
Q

Drugs given to reduce heart rate

A

Beta blockers - slow the heart rate and attenuate increase in heart rate in respone to exercise and stress

Ivabradine - slows the heart by inhibiting If ion channels in the SA node but does not affect contractility of ventricles. Used in patients intolerant of beta blockers

Ca2+ channel blockers - slow the heart rate by reducing Ca2+ entry into pacemaker cells.

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11
Q

Efffects of beta blockers on the heart

A

Blocks b1 receptors of the sympathetic nervous system.

Reduces HR increases with exercise and other stress

Reduces contractility and arterial pressure

Reduces oxygen needs of the myocardium at a given level of exercise or stress

Reduces the metabolic needs of the heart.

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12
Q

Unwanted effects of beta blockers

A

Increase LV size which increases LV work, offsets benefits of the drugs.

Slows heart rate

Leads to cold peripheries (acts of b3Rs)

Contraindicated in asthmatics (causes bronchoconstriction)

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13
Q

Effects of Ca2+ channel blockers

A

Reduce calcium entry to cells through L-type VG-Ca2+ channels.

Reduced Ca2+ entry into pacemaker cells reduces the heart rate

Reduced Ca2+ entry into cardiac myocytes reduces the force of contraction

Reduce Ca2+ entry to vascular myocytes, resistance arteries relax, systemic vascular resistance decreases, bp falls.

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14
Q

Unwanted effects of Ca2+ channel blockers

A

Heart: Bradycardia, Heart failure, Oedema

Arterial pressure: Flushing, headaches, ankle swelling, reflec tachycardia (nifedipine only)

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15
Q

Drugs given to reduce arterial pressure

A

Ca2+ channel blockers: Nifedipine, Diltiazem, Verapamil

Work by reducing Ca2+ influx through VG-Ca2+ channels in peripheral vasculature. Leads to relaxation of resistance vessels and a fall in TPR.

Heart has to pump against a lower pressure so the work of the heart is reduced.

Ca2+ channel antagonists also prevent calcium entry in coronary vessels and may prevent vaso-spasm

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16
Q

Potassium channel openers

A

e.g. Nicorandil

Drugs that open K-ATP channels in vascular smooth muscle. This hyperpolarises the cell, closing Ca2+ channels. Low Ca2+ causes vessel relaxation.

More targeted towards arteries and arterioles which have a higher smooth musle tone.

May also cause headaches, flushing and dizziness. Used in conjuction with beta blockers to limit reflex tachycardia

17
Q

Ranolazine

A

Blocks late inward sodium currents in cardiomyocytes. In ischemic myocardium, late inward sodium currents contribute to an elevation in [Na]i which increases [Ca]i via the Na/Ca exchanger.

Ca2+ overload in ishemic cells leads to impaired relaxation and compresses microcirculation in the walls of the ventricle. Coronary blood flow is reduced and ischemia worsens.

Blocking late inward sodium currents reduces Ca levels, therefore stress on the heart and improves coronary flow.

Also inhibits fatty acid oxidation, promotes carbohydrate metabolism.

18
Q

Treatment for stable angina

A

First line: beta blocker or calcium channel blocker

If not tolerated: Long acting nitrate, ivabradine, nicorandil, ranolazine

19
Q

Treatment for unstable angina

A

Antiplatelt treatment asap. Aspirin (clopidogrel 2nd line)

Antithrombin treatment: Heparin or direct thrombin inhibitor

Nitrates

20
Q

Treatment immediately following MI

A

Rapid admission to coronary care unit

Early clot-busting treatment (PTCA, thrombolysis)

Aspirin (anti-platelet)

Beta blockers

Prevent thrombo-embolism

21
Q

Aims of treatment post-MI

A

Reduce morbidity:

  • Relieve pain
  • Minimise size of infarct
  • Prevent recurrence of heart attack
  • Treat heart failure
  • Anticipate and treat arrhythmias
  • Improve hyper-coagulable state

Reduce mortality:

  • arrhythmias
  • heart attack
  • embolism (venous or arterial)

Reduce complications

22
Q

Common abnormalities in ECG of patients with acute MI

A

LBBB

Anterior ST elevation

Posterior ST elevation

ST depression

Normal

23
Q

Treatment of a patient with acute MI but no ECG evidence

A

Pain relief: morphine, anti-emetic

Aspirin: to reduce risk of further clot formation

Rapid transfer to hospital

24
Q

Contraindications for clot-busting drugs

A

Previous harmorrhagic stroke

Recent major surgery

Peptic ulceration/internal bleeding

Oesophageal varices

Pregnancy

Any stroke within 6 months

25
Q

Drug interventions to prevent recurrent MI

A

Anti-platelet treatment - prevent clotting

Beta blockers - reduce heart rate, reduce blood pressure

ACE-inhibitors/ARBs - reduce fluid retention

Statins - reduce cholesterol

Lifestyle interventions: Diet, weight reduction, stop smoking

26
Q

Risks of using streptokinase

A

Re-perfusion arrhythmia

Development of neutralising antibodies (no re-use after 1 year of treatment)

Allergic reaction

Not to be used if patient has had recent streptococcal infection.

27
Q

Briefly describe the fibrinolytic pathway

A

Plasminogen is made in the liver and is incorporated into a fibrin clot as it forms. t-PA is released from the surrounding endothelium and cleaves plasminogen to plasmin. Plasmin cleaves the fibrin mesh into fragments which are cleared by proteases, kidney and the liver.

28
Q

Name 3 clot-busting drugs

A

Streptokinase

urokinase

tPA

reteplase

29
Q

Why are beta blockers given as an early treatment in acute MI?

A

Reduces SNS drive

Prevents cardiac rupture

Less risk of ventricular fibrillation

Infarct size decreased

30
Q

What is coronary steal?

A

Occurs as a complication of using vasodilator drugs.

Attempts may be made to dilate the narrowed artery to increased blood flow, however in atheroma there is a fixed narrowing which does not respond to drugs. The vasodilators may then dilate other more healthy vessels and decrease blood flow through the narrowed vessel making ischemia worse.

31
Q

What is a complication increasing coronary flow in atheromatous vessels and how can it be reduced?

A

Some atheromatous vessels may go into spasm when coronary flow is increased, reducing blood flow and precipitating an attack of angina.

Occurs when platelets and white cells adhere to the damaged vesel wall.

Anti-anginal drugs prevent vasospasm by causing vasodilation or preventing platelet activation

32
Q

Drug strategy for treating acute MI

A

Restore coronary blood flow:

  • Dilate coronary arteries
  • Inhibit vasospasm
  • Coronary thrombolysis
  • Inhibit clotting and platelet activation

Decrease myocardial oxygen consumption:
(decrease HR and contractility)

Pain management (analgesics)

Post MI:
Inhibit cardiac remodelling (inhibit sympathetic system and angiotensin)

33
Q

Two commonest types of tachyarrhythmia

A

Atrial fibrillation - heart beat is completely irregular

Supraventricular tachycardia - heart beat is rapid but regular.

Semester 3 (85 decks)

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