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PHA222 > Angina > Flashcards

Angina Flashcards

1
Q

What is Angina?

A

Acute/chronic ischaemic heart disease characterised by transient chest pain due to decreased blood flow to the heart as a result of an imbalance of myocardial supply and demand

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2
Q

What is the underlying pathology of SCAD?

A

Reversible mismatch between myocardial supply and demand leading to reduced blood flow to the heart.

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3
Q

What are the two clinical subtypes?

A
  1. Angina with obstructive CAD
  2. Angina without obstructive CAD
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4
Q

Describe Angina with obstructive CAD.

A
  • Partial obstruction of coronary artery by atherosclerotic plaque
  • Chest pain on exertion
  • ST-segment depression
    E.g. Classic/Stable Angina
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5
Q

Describe Angina without obstructive CAD.

A
  • At rest/at night and during exercise
  • Focal or diffuse spontaneous coronary artery spasm.
  • ST-segment elevation
    E.g. Variant/ microvascular
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6
Q

Describe the CCS classification of Angina.

A

Class I - doesn’t cause angina
Class II - slight limitation
Class III - marked limitation
Class IV - unable to carry out physical activities and angina present at rest

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7
Q

Describe subendocardial ischemia.

A
  • Only penetrates through 1st layer to the heart muscle
  • Causes ST segment depression.
  • The natural flow of current is to flow towards the septum, in this case the current is going opposite direction - causing an ST segment depression.
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8
Q

Describe Transmural ischemia.

A
  • Penetrates completely through the heart muscle
  • Causes ST segment elevation due to the fact that the current is moving towards the septum.
  • The normal flow of the current is to flow towards the septum, in transmural ischemia this current is added on.
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9
Q

What are the symptoms of Angina?

A

Breathlessness, dizziness, chest pain that eases at rest, clammy/cold, nausea/vomiting, radiation to neck ,upper arms/ lower jaw

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10
Q

List and describe the pathology of the clinical features on SCAD.

A

Breathlessness and dizziness due to ischaemia induced LV dysfunction

Metabolic lactate production due to anaerobic metabolism

ECG - ST-segment depression or elevation

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11
Q

What is Classic angina?

A
  • Partial obstruction of coronary artery by atherosclerotic plaque
  • Increase myocardial demand
  • Cheat pain on execration
  • segment depression
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12
Q

What is Variant angina?

A
  • Spontaneous, transient coronary artery spasm due to increase vasoconstriction
  • Decreased myocardial supply
  • Chest pain during sleep and rest
  • ST-segment elevation
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13
Q

What is microvascular angina (unstable)?

A
  • Primary structural/functional dysfunction to small coronary blood vessels.
  • Decreased myocardial supply
  • Chest pain at at rest and during exercise
  • ST-segment depression
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14
Q

What are the triggers of angina?

A
  • exercise/stress
  • heavy meals
  • exposure to cold
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15
Q

If a patient has angina what are some lifestyle changes would you recommend?

A
  • Increase physical activity min 30mins a day
  • Lose weight if needed
  • Smoking cessation
  • Alcohol moderation
  • Healthy diet - low salts and fats
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16
Q

The revascularisation to restore blood flow in the coronary artery by increasing myocardial supply can be achieved by..

A
  • Percutaneous coronary intervention (PCI) - balloon angioplasty, coronary stenting
  • Coronary artery bypass grafting (CABG)
17
Q

Describe the NICE pathway of treating angina.

A
  • Treat acute episodes with GTN spray
  • 1st line - BB or CCB e.g. atenolol or Verapamil
  • Add dihydropyridine CCB e.g. amlodipine
  • Switch to long acting nitrate e.g. ISDN OR miscellaneous agent such ivabradine, ranolazine, nicorandil
18
Q

Describe the mechanism of action of 1st line treatment of angina

A

BBs
- Atenolol antagonises the effects of adrenaline and noradrenaline at B-adrenoceptors
- Decreasing HF, BP and contractility which decreases myocardial demand
- Increased diastolic filling time increases myocardial perfusion
- Anti-arrhythmic activity increases electrical stability

19
Q

What are the side effects of BBs?

A

Fatigue
Headaches
sleep disturbnaces
cold hands and feet
bronchoconstriction
sexual dysfunction in males

20
Q

Describe the mechanism of action of anti anginal drug Dihydropyridine CCBs

A
  • Inhibit Ca+ influx into voltage gated channels into arterioles which leads to arteriole dilation and vasodilation decreasing SVR
  • Coronary dilation increases blood flow to heart preventing/reversing spasm and decrease HR, BP and contractility which decrease myocardial demand
21
Q

What are the side effects of dihydropyridine CCBs?

A
  • swollen ankles
  • flushing
  • headaches
  • dizziness
22
Q

Describe the vascular effects of CCBs

A

Block of Ca influx into arterioles leading to arteriolar dilation
- Peripheral vasodilation resulting in decreased SVR leading to decreased arterial BP.
- Coronary dilation which leads to increased coronary blood flow reversal/prevention of spasm

23
Q

Describe the Cardiac effects of the CCBs phenylalkyamines (verapamil) and Benzothiazepines (diltaizem)

A
  • Block of Ca influx into cardiac muscle cells leading to decreases cardiac contractility.
  • Block of Ca influx into nodal and conducting cells leading to decreased HR.
24
Q

Describe the mechanism of action of anti anginal drug - Long acting nitrate

A
  • ISDN/ISMN directly acts on blood vessels causing vasorelaxation and vasodilation to decrease SVR and increase blood flow
  • venodilation decreases preload and myocardial demand
  • arterial dilation decrease preload and myocardial oxygen demand
  • coronary vasodilation increases blood flow and prevents/reverse spasm
25
Q

What are the side effects of long acting nitrate?

A

flushing
throbbing headaches
postural hypotension
reflex tachycardia

26
Q

Describe the mechanism of action of anti anginal drug - miscellaneous

A

Nicorandil - venodilation and arterial dilation decreases preload and after load which decreases myocardial demand

Ivabradine - inhibits If which decreases HR and myocardial demand

Ranolazine - inhibits INa having anti-ischaemic effects

27
Q

Define modified release drug therapy.

A

delivery of drug to a target with delayed effect after administration

28
Q

Why should we avoid MR formulations in nitrate therapy? Describe how tolerance can be overcome.

A

Avoid SR formulations as it exposes the body to nitrates for longer, speeding up depletion of thiol (-SH) groups. This leads to nitrate tolerance.

29
Q

How would you counsel a patient taking nitrates?

A

begin with small dose then establish dose threshold. Have nitrate free interval by splitting dose e.g. 8am and 2pm

PHA222 (13 decks)

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