Cardiovascular Drugs & Dentistry Flashcards

1
Q

What does ‘acutely’ mean?

A

Progresses rapidly

Lasts for a short period

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2
Q

What is acute myocardial infarction caused by?

A

Thrombosis

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3
Q

What can acute myocardial infarction lead to?

A

Heart failure

Arrhythmias

Sudden cardiac death

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4
Q

What affects the heart’s energy status and viability?

A

Coronary artery blood flow

Sympathetic stimulation

Peripheral arterioles/TPR

Central venous pressure sets inotropic state/resting ventricular pressure

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5
Q

How does sympathetic stimulation affect cardiac output?

A

b1-adrenoceptors activated

Increased rate and force of pumping

Increased cardiac output

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6
Q

What factors improve the energy status of the ventricles?

A

Increased energy supply

Reduced energy demand

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7
Q

What can increase the energy supply of the heart?

A

Increased coronary artery supply

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8
Q

What can decrease the energy demand of the heart?

A

Reduced afterload/TPR

Reduced preload/CVP

Negative inotropy

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9
Q

What is the aetiology of IHD?

A

Coronary atherosclerosis

Thrombosis

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10
Q

What is coronary atherosclerosis?

A

Lesion in coronary arteries and laying down of lipid leading to a fat lump

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11
Q

What is acute thrombosis?

A

Platelets suddenly start clumping on a fissure of an atherosclerotic plaque causing obstruction of vessel

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12
Q

What can provoke angina pectoris?

A

Increased sympathetic stimulation (eg. exercise)

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13
Q

What are the causes of death in IHD?

A

Ventricular fibrillation

Heart failure

Stroke

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14
Q

What may be the cause of angina pectoris?

A

Adenosine (local mediator, ATP metabolism)

Accumulates due to lack of washout

Stimulates nerves = pain

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15
Q

What are the three types of angina pectoris?

A

Stable angina

Unstable angina

Inappropriate coronary vasospasm (Prinzmetal’s variant)

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16
Q

What is stable angina?

A

Fixed partial blockage (atheroma)

Exercise or stress causes pain; alleviated by rest

17
Q

What is unstable angina?

A

Atheroma fissures and thrombus forms causing full blockage of artery

18
Q

How do you treat acute angina attacks?

A

Sublingual GTN/nitroglycerin

19
Q

Why is GTN not given orally?

A

Liver metabolises GTN too quickly

20
Q

What is the mechanism of GTN?

A

Venodilatation (in capacitance veins)

Reduces central venous pressure/preload

Decreases inotropic state

Decreased energy/oxygen demand

21
Q

Why does exercise/stress trigger stable angina?

A

At rest, coronary supply meets demand

Exercise/stress = increased sympathetic stimulation and heart works harder

Vasodilatation

Atheroma cannot dilate so limits maximum flow

Coronary supply cannot meet demand

22
Q

How do the pharmacokinetics of GTN allow it to work?

A

Denitrated in bloodstream

NO produced

NO diffuses into smooth muscle and initiates cascade involving cGMP => smooth muscle relaxation

23
Q

What is a heart attack?

A

Sudden, symptomatic episode of acute myocardial ischaemia (loss of coronary blood flow) in patients with IHD

24
Q

What is morphine used for?

A

Acute myocardial infarction

Reduces stress-related catecholamine drive

25
How is morphine administered?
Intravenously
26
What is the major side effect of morphine?
Nausea
27
What is a ventricular premature beat?
Mild ventricular arrhythmia Next normal beat is very powerful due to prolonged diastolic interval
28
What is the most severe type of arrhythmia?
Ventricular fibrillation
29
Why does ventricular fibrillation cause death?
Disturbed electrical physiology due to a region of ischaemia Electrical waves fragmented = vibration instead of contraction No cardiac output so no blood to brain
30
What should you do when ventricular fibrillation occurs in a patient?
Mechanical defibrillation CPR Intravenous lignocaine Dial 999
31
What do a1-adrenoceptor antagonists do?
Block sympathetic reflex to constrict arteries/arterioles
32
Why might someone be taking a1-adrenoceptor antagonists?
For hypertension
33
What is an example of an a1-adrenoceptor antagonist?
Prazosin
34
What can a1-adrenoceptors cause?
Orthostatic/postural hypotension