Drugs for IHD Flashcards

1
Q

What is O2 supply dependent on?

A
  • Whether coroanry blood flow is adequate
  • O2 carrying capacity of blood
  • Anatomy of coronary arteries (lumen size-affected by atherosclerosis)
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2
Q

What is O2 demand affected by?

A
  • Preload & afterload
  • Wall thickness
  • Contractility and heart rate
  • Left ventricular volume and diameter
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3
Q

What causes ischaemia?

A

Inadequate coronary blood flow

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4
Q

What are the IHD categories?

A
  • Chronic coronary artery disease (CAD)
    • Stable Angina
  • Acute coronary syndromes
    • Unstable angina
    • NSTEMI (Non-ST elevation MI; subendocardial)
    • STEMI (ST-elevation MI; transmural)
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5
Q

What is a myocardial infarction?

A

A damaged area of heart muscle resulting from a sustained block of coronary blood supply by a thrombus

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6
Q

Which serum proteins are used to indentify MI?

A
  • 1-2 hours post MI: Elevated myoglobin
  • 2-4 hours: elevated Troponins, CK-MB
  • 3-6 hours: CK-MB

CK-MB levels peak after 24 hours, whereas troponin keeps building up then decreases just before 48 hours post MI

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7
Q

How does a transmural MI cause sudden death?

A
  • Transmural MI results in patches of necrotic/ apoptotic tissue failing to conduct wave of depolarisation.
    • this produces Q wave (ST) changes
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8
Q

Whatare the symtpoms of MI?

A
  • Central chest pain radiating to neck and arms
    • not relieved by sublingual GTN
  • Shortness of breath, nausea
  • High pulse rate
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9
Q

What should you first aim to do after an MI like presentaion?

A
  1. Aim to re-establish O2 supply. We can do this by increase the duration of diastole (using a beta blocker), and by decreasing coronary resistance.
  2. And we need to decrease myocardial O2 demand (MVO2) to prevent more ischaemia and necrosis.
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10
Q

When we used drugs that wil reduce preload, what physiological effects does this have?

A

We reduce preload by Increasing peripheral venodilaton, decreasing venous return allowing a reduction in end diastolic volume and improved coronary perfusion.

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11
Q

When we use drugs to reduce afterload, what physiological effects does this have?

A

By reducing BP or decreasing peripheral arteriolar resistance

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12
Q

When treating acute coronary syndrome we do MONA what does this mean?

A

MONA

  • Morphine - reduce pain & anxiety
    • May need to give antiemetic (metoclopramide)
  • Oxygen - only use if O2 sats below 90
  • Nitroglycerin - S/L or spray, if pain unresolved use morphine to relieve pain if no asthma/COPD (can get respiratory depression)
  • Aspirin
    • high dose initially, then low dose daily
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13
Q

After how long does irreversible loss of myocardial tissue occur?

A

After 45 mins of ischaemia

Death common within first 2 hours following symptoms

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14
Q

What 3 classes of drugs should be give to improve symtpoms in MI patients quickly and to reduce their pain?

A
  • Morphine
  • Nitrates
  • Low dose aspirin
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15
Q

Why are nitrates (GTN) given for IHD?

A

Nitrates decrease myocardial demand

they release NO causing vasodilation and venodilation, which decreases preload and afterload. (It’s primarily venous dilation but also does arterial dilation).

  • The venodilation decreases venous return/preload (improves diastolic duration and subendocardial perfusion.
  • The vasodilation on the arterial system decreases afterload.
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16
Q

What are the anti-ischaemic effects of GTN?

A
  • Decreased preload, afterload and MVO2
  • Increased VF threshold
  • Decreased size, and extension of MI
  • Antiplatelet with valuable enhancement of thrombolytic
  • Dilation of stenotic coronary arteries

GTN may alter platelet function at clinically relevant doses.

17
Q

How can nitrates be given?

A

Oral, buccal, transdermal

Isosorbide mononitrate/dinitrate: oral

18
Q

What is the main benefit of aspirin for IHD patients who have had an MI?

And what should be taken with aspirin for the first 4 weeks

A

Prevents thrombus formation by decreasing platelets ability to adhere and aggregate at the site of injury.

use clopidogrel 75mg daily reccomended in combination with aspirin for 1st 4 weeks

19
Q

Summary of management of acute MI

A
20
Q

What is does tenecteplase do for patients with MI?

A

Its purpose is to acutely destroy (lyse) or prevent thrombus formation that occurs within the coronary artery at the time of myocardial infarction.

(Facilitates the coversion of plasminogen to plasmin)

Should be used acutely within 12 hours from onset of ischaemia if no prior contraindications

21
Q

What are the three main side effects of using thrombolytic agents to increase myocardial O2 supply

A
  • They aren’t tissue specific -> blood clotting ability in entire body is altered.
  • Cerebro-vascular incidents
  • GI bleeding
22
Q

If a patient can’t use tenecteplase what should be used?

A

LMWH enoxaparin

23
Q

When should B blockers not be used for patients with acute MI

A

We need to make sure they are haemodynamically stable because we decrease their CO.

We cannot use beta blockers if there is evidence of hypotension, bradycardia, heart block, cardiogenic shock or asthma.

Early aggressive use of beta blockers are no longer reccomended.

24
Q

What benefits do B blocks have on acute MI patients?

A
  • they are -ve chronotropes, therefore they prolong diastole and improve CF
  • They are also -ve inotropes, they decrease myocardial-wall stress
  • They decrease blood pressure at rest and during exercise
  • The end result is decreased MVO2. This limits infarct size
  • Also reduces chest pain - since it reduces O2 consumption
25
Q

Why do you need to be careful giving L-type CCBs?

A

Verapamil can cause excessie bradycardia, impaired electrical conduction (AV block) and depressed contractility

Dihydropyridines drop vascular pressure and may actually cause tachycardia and +ve inotropy

26
Q

What should an acute MI patient be sent home with post hospital

A

SAAB

  • Statin
  • ACE inhibitor
  • Low dose apspirin & clopidogrel
  • Beta blocker long term

And some nitrates for symtpom relief

27
Q

Effects of statins?

A
28
Q

What are the effects of ACE inhibitors?

A
29
Q

How is stable angina managed?

A
30
Q

Which drugs are used for the management of stable angina?

A
31
Q

What is the pharmacological management of untable angina and NSTEMI?

A
32
Q

Look at summary slides for pharmacolological management of STEMI

A