Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular System > Angina treatment > Flashcards

Angina treatment Flashcards

1
Q

Characteristic distribution of angina pain

A

chest, arm, jaw
brought on by exertion, cold or excitement
chemical factors that cause pain in skeletal muscle may be responsible (K, H, adenosine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Two types of treatment for angina (general)

A

reduce chest pain symptoms

prolong survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the coronary window?

A

during diastole, where the coronary arteries are filing.

The aortic pressure > ventricular pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 things that shrink the coronary window

A
  1. shortening diastole (increased HR)
  2. increased ventricular end diastolic pressure (eg. progressive decline in ventricular emptying, aortic stenosis)
    If cannot eject properly, will have residual blood in ventricles: higher blue line.
  3. reduced diastolic arterial pressure (eg. mitral or aortic valve incompentence, heart failure) ie. if backflow of blood into ventricles due to valve rather than into resistant small artery system.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do we match tissue demand (exercise) to blood flow

A

by altering flow at arteriolar level
This is achieved by metabolic control: muscle cell produces byproducts (eg. adenosine) which triggers relaxation of vascular smooth muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • Neural vasoconstrictors
  • Hormonal vasoconstrictors (3)
  • Local vasoconstrictors
A
  • sympathetic nerves
  • adrenaline, angiotensin 2, vasopressin
  • myogenic response, endothelin 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • 2 hormonal vasodilators

- Local vasodilators

A
  • acetylcholine, atrial-natriuretic peptide (ANP)

- K, CO2, H+, decreased O2, adenosine, NO, bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Coronary ischaemia is usually the result of which process?

A

atherosclerosis (which then causes angina)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sudden ischaemia is usually caused by which process?

A

Thrombosis (which then may result in cardiac infarction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aside from coronary ischaemia, what can also cause angina?

What is this called?

A

coronary spasms

variant angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Following ischaemia, what happens in terms of calcium levels?

A

get cellular calcium overload.

may cause cell death and dysrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 Classes of angina

A
  1. Variant Angina (vasospasm - is a supply ischaemia)
  2. Chronic stable angina (fixed stenosis - is a demand ischaemia)
  3. Unstable angina (thrombus - is a supply ischaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do antianginal drugs work?

2 broad types

A

to decrease the metabolic demand of the heart

Organic nitrates, nicorandil and Ca antagonists are vasodilators (decrease preload or afterload)

Beta-blockers and ivabradine slow down the heart (decrease metabolic demand of muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Preload determined by

A

the venous pressure

venous return to the heart (end-diastolic pressure/volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Afterload determined by

A

aortic or pulmonary artery pressures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Action of beta-blockers

2 examples

A
  • decrease cardiac oxygen consumption by SLOWING THE HEART
    [They are blocking ability of sympathetic NS via B1 adrenogenergic recetors to modulate activity of F-type Na channels]
  • also have antidysrhythmic action

Eg. bisoprolol, atenolol

17
Q

Action of calcium antagonists

A
  1. prevent opening of voltage-gated L-type calcium channel
    - therefore block Ca entry
    - (inhibits Ca entry upon muscle cell depolarisation)
  2. vasodilator effect mainly on resistance vessels (reduces afterload)
18
Q

2 Types of calcium antagonists

A
  1. Dihydropyridine derivatives eg. amplodipine and lercanidipine
  2. Rate-limiting eg. verapamil, diltiazem.
    These allow less Ca to come in each time a muscle contracts, reducing workload.
19
Q

Why are calcium antagonists important in treatment of variant angina?

A

as they dilate the coronary vessels

20
Q

Which calcium antagonists can reduce and impair AV conduction and myocardial contractility

A

rate-limiting: verapamil/diltiazem

21
Q

Main drivers at different stages of myocardial depolarisation

A

(pi like)
upshoot driven by Na
plateau phase driven by calcium
repolarisation driven by K

22
Q

Describe SA node depolarisation (neuronal).

A

Phase 1: gradual drift increase in RMP due to increase Na as funny-type Na channels open (and decrease in K as K channels slowly close). This oscillating flux of Na into cell provides pacemaker potential.
Transient Ca channels help with the final push

Phase 2: moderately rapid depolarisation due to Ca entry via slow L channels

Phase 3: rapid repolarisation as elevated internal Ca stimulates opening of K channels, and get increase in K

23
Q

What keeps the SA node rate down?

A

parasympathetic NS

through AV node

24
Q

What calcium antagonist would you use in a patient with heart failure?

A

Dihydropyridine derivatives eg. amplodipine and lercanidipine

25
Q

If using a beta-blocker, which calcium antagonist type would you avoid using?

A

Rate-limiting: diltiazem or verapamil

also contraindicated in HF, bradycardia, AV block

26
Q

Side effects of calcium antagonists

A

headache, constipation, ankle oedema

27
Q

Antidysrhythmic using calcium antagonist

A

Verapamil

  • slows ventricular rate in rapid AF
  • prevents recurrence of supraventricular tachycardia
  • no effect on ventricular arrhythmias
28
Q

How does GTN spray work?

A

Glyceryl trinitrate is a vasodilator.
IS metabolised to NO and relaxes smooth muscle

  • Acts on veins to decrease preload
  • In higher concentrations, can affect arteries and decrease afterload
  • dilates collateral coronary vessels decreasing cardiac workload. This is particularly useful in variant angina
29
Q

Organic nitrate not GTN

A

Isosorbide mononitrate

30
Q

How do endothelial cells regulate vascular tone?

A

if shearing stress to endothelial cell - causes NO production, which acts on soluble gyanylate cyclase enzyme in smooth muscle, which acts to convert GTP -> GMP to cause relaxation

31
Q

K Channel Activator

A

Nicorandil

  • combines activation of KATP channels with nitrovasodilator actions
  • arterial and venous dilator
32
Q

Give 4 conditions where you might use organic nitrates

A
  1. stable angina (prevention with GTN, or isosorbide mononitrate long before exercise)
  2. unstable angina (IV GTN)
  3. acute heart failure (IV GTN)
  4. chronic heart failure (isosorbide mononitrate with HYDRALAZINE in patients of African American origin)
33
Q

Action of Ivabradine

A

inhibits f-type channels in the heart

reduces cardiac pacemaker activity (inhibits heart rate)

34
Q

Action of Ranolazine

A

unique anti-anginal used as last resort

Cardiovascular System (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions