Ischaemic Heart Disease Flashcards

1
Q

What is a heart attack?

A

Blockage of blood vessels
= heart starved of oxygen

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2
Q

What dos increased myocardium demand increase?

A

Coronary artery blood flow

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3
Q

What is the equation for oxygen demand?

A

Blood flow X arteriovenous O conc difference

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4
Q

Why does O act as a vasoconstrictor?

A

O deficiency dilates coronary arteries

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5
Q

Decsribe what happens during hypoxia

A

AMP cannot be regenerated to ATP =
Adenosine rises in myocardium
Adenosine acts as direct vasodilator
Accumulation of lactate H+ ions + prostacyclin = vasodilation

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6
Q

When does myocardia ischaemia occur?

A

Myocardial oxygen demand exceeds myocardial oxygen supply

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7
Q

What is myocardial oxygen supply affected by?

A

Diastolic perfusion pressure
Coronary vascular resistance
O-carrying capacity

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8
Q

What is myocardial oxygen demand affected by?

A

Wall tension
HR
Contractility

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9
Q

What are the causes of ischaemic heart disease?

A

Atherosclerosis
Arteritis
Embolism + endocarditis
Coronary artery wall thickening
Coronary spasm
Congenital arterial disease

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10
Q

Describe what stenosis does

A

Increases resistance to floe
O supply may not be able to meet demand
Diminished coronary reserve
Raised resistance

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11
Q

What happens when the coronary arteries are narrowed?

A

Blood flow to heart slows or stops
= myocardial ischaemia + hypoxia pain

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12
Q

What is a result from ischaemic heart disease?

A

Chest pain
SOB
Myocardial infarction

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13
Q

What are the modifiable risk factors?

A

Hypertension
Hypercholesterolaemia
Smoking
Diabetes
Sedentary lifestyle
Obesity

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14
Q

What are non-modifiable factors?

A

Age
Male gender
Family history

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15
Q

What is the primary symptom associated with ischaemic heart disease?

A

Chest pain

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16
Q

Why is pain caused?

A

Pain from myocardium after switching to anaerobic metabolism (low O supply)

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17
Q

What is stable angina?

A

Experienced on exertion or emotional stress
Relieved by rest

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18
Q

What is unstable angina?

A

Incomplete occlusion-angina on minor exertion
Blockage = angina at rest

19
Q

What is variant angina?

A

Diffuse coronary vasospasm

20
Q

Describe what happens as a consequence of ischaemia
ATP deficiency

A

ATP produced non-aerobically
= lactic acid produced
Dissociates into H+ + lactate
Low ATP + high H+ = abnormal ventricular contraction

21
Q

What can happen as a consequence of persistent ischaemia?

A

Infarction

22
Q

What are the consequences of myocardial ATP deficiency?

A

Impairment of ventricular systolic pumping action
Decreased compliance of myocardium during diastole
Pulmonary congestion + dyspnea

23
Q

What does extended myocardial ischaemia lead to?

A

Myocardial necrosis (infarction)

24
Q

What is the development of myocardial infarction promoted by?

A

Turbulence + rupture of atheroma
Thrombocyte activation
Abnormal function of endothelium
Sympathetic nervous stimulation increases cardiac work

25
Q

How can you identify myocardial infarction?

A

Enzyme markers

26
Q

What are the main enzyme markers?

A

Troponin
= signify rupture of cardiomyocyte

27
Q

What are the therapy principles?

A

Reduce O demand
OR
Increase O supply

28
Q

Describe smooth muscle relaxation
Nitric oxygen

A

ACh binding to G protein receptors = IP3 production
IP3 releases Ca2+
Ca2+ + calmodulin form complex which stimulate NO synthase to produce NO
NO diffuses from cell to muscle cells
NO activates guanylyl cyclase kinase to make cGMP
cGMP activates protein kinase G
Activates myosin light chai phosphatase
Dephosphorylates myosin light chains = smooth muscle relaxation

29
Q

What are examples of nitrates?

A

Glyceryl Trinitrate (GTN)
Isosorbide nitrate

30
Q

What are nitrates indication?

A

Stable angina
Variant angina
Acute coronary syndrome

31
Q

What are the side effects of nitrates?

A

Tachycardia
Headache
Postural hypotension

32
Q

Describe the mechanism of action for nitrates

A

Acts directly on smooth muscle through cGMP mechanism
Coronary microvessels contain enzyme to convert NO

33
Q

What is the dose of nitrates dependent on?

A

Dilation of coronary vessels

34
Q

What is the 1st part of Nicorandil mechanism?
Dual mechanism

A

Relaxation of venous vasculature
Systemic + epicardial arteries
Coronary blood flow maximised, pre-load + afterload reduced

35
Q

What is the 2nd part of Nicorandil mechanism?
Dual mechanism

A

Opens ATP-dependent K+ channels
Hyperpolarisation = arterial dilation
Cardiac repolarisation = reduced cardiac work

36
Q

What are examples of beta-blockers in angina treatment?

A

Atenolol
Carvedilol
Propranolol

37
Q

What is the indication of beta-blockers?

A

Stable angina
Variant angina

38
Q

What is the mechanism of action of beta-blockers?

A

Block beta-1 adrenoreceptor
+ reduced generation of intracellular cAMP
= decreased HR
= reduce force of contraction
= reduce O demand

39
Q

What are the side effects of beta-blockers?

A

Bronchospasm
Hypoglycaemia
Interact with CCB

40
Q

What are examples of CCB?

A

Verapamil
Nifedipine
Diltiazem

41
Q

What is the indication of CCB?

A

Stable angina
Variant angina

42
Q

What is the mechanism of action of CCB?

A

Peripheral vasodilation
Reduced cardiac work

43
Q

What are the side effects of CCB?

A

AV blockage
Oedema
Hypotension