Brainscape's Knowledge GenomeTM

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


See full index

Heart > 9 Drugs and the CVS > Flashcards

9 Drugs and the CVS Flashcards

1
Q

What are the action of drugs on the CVS? (what can the drugs alter?)

A
  1. rate and rhythm of heart
  2. force of myocardial contraction
  3. peripheral resistance and blood flow (changing PR affects BF)
  4. blood volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

do drugs only act at 1 site?

A

no

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

What are arrhythmias?

A

disturbance of cardiac rhythm

abnormality of HR or rhythm

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

What are the different types of arrhythmias?

A
  1. bradycardia - slow HR
  2. atrial flutter
  3. atrial fibrillation
  4. Tachycardia (ventricular + supraventricular)
  5. ventricular fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is atrial fibrillation? How does it arise?

A

damage to the atria causing multiple re-entry loops to generate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is supraventricular tachycardia?

A

tachycardia in the atria / AVN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is ventricular tachycardia?

A

tachycardia in the bundle of His / Purkinje fibres / ventricles

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

Explain how arrhythmias can arise

A
  1. ectopic pacemaker activity
  2. afterdepolarisations
  3. Re-entry loop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does ectopic pacemaker activity cause arrhythmia?

A
  1. damaged area of myocardium becomes DEPOLARISED and spontaneously active
  2. latent (hidden) pacemaker region activated due to ischaemia

(the damaged area of myocardium undergoes ischaemia, so latent pacemaker regions activated for pacemaker function - spontaneously active and depolarise, this latent pacemaker dominates over SAN)

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

How does afterdepolarisations cause arrhythmia?

A

abnormal depolarisations FOLLOWING the AP (triggered activity)
more likely to occur if intracellular Ca2+ high
if reaches a threshold, can trigger another AP causing arrhythmia

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

How does re-entry loop cause arrhythmia?

A
  1. through conduction delay (slow down conduction) and accessory (other) pathway
  2. incomplete conduction damage (unidirectional block) - excitation can take a long route to spread the wrong way through the damaged area, setting up a circus of excitation
    (block allows depolarisation to travel in 1 direction, NOT both, causing a loop of excitation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens in early after-depolarisations (triggered activity)? What can it lead to? When is it more likely to occur?

A

can lead to depolarisations (membrane hasn’t had a chance to fully repolarise)
can lead to oscillations (more likely to happen if AP prolonged)
longer AP = longer QT interval on ECG (because the depolarisation has been ‘extended’)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does multiple re-entry loops occur and what does it lead to?

A

e.g. several small re-entry loops in the atria (multiple foci) usually atrium damaged (e.g. from stretch - from volume overload)
leads to atrial fibrillation

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

Describe the classes of anti-arrhythmia drugs

A
  1. drugs that block voltage-sensitive Na+ channels
  2. antagonists of ß-adrenoreceptors (normally stimulatory of adenylyl cyclase)
  3. drugs that block K+ channels
  4. drugs that block Ca2+ channels
    all these drugs have ability to cause arrhythmia themselves because they mess with ion channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the principles of the therapeutic use of drugs which block voltage-dependent Na+ channels (class I)

A 
typical example: local anaesthetic 'lidocaine' class 1b
only blocks voltage-gated Na+ channels in open / inactive state (use-dependent block)
dissociates rapidly in time for next AP (little effect in normal cardiac tissue - only those constantly depolarised from ischaemic damage)

-block doesn’t occur at initiation of AP, but ONCE AP has taken place and is in the inactive state-

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

When is lidocaine used? why?

A

class I anti-arrhythmia, blocks Na+ channels

  1. used following MI, if pt shows signs of ventricular tachycardia (fast), given intravenously
  2. damaged areas of myocardium may be depolarised and fire automatically
  3. more Na+ channels are opened in depolarised tissue: lidocaine blocks these Na+ channels (use-dependent), preventing automatic firing of depolarised ventricular tissue

-NOT used prophylactically (as a prevention drug)-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the principle of the therapeutic use of ß-adrenoreceptor antagonist (class II)? and examples?

A

e.g. propranolol, atenolol (ß-blockers)
block sympathetic action: act at ß1-adrenoreceptors in the heart (reduce rate and force of contraction through reducing Ca2+ release / entering from L-type Ca2+ channels)
they decrease the slope of pacemaker potential in SAN (slow depolarisation) - takes longer for AP to be initiated (less Ca2+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When are ß-blockers used? Why?

A

used following MI, because of increased sympathetic activity (rapid HR)
ß-blockers prevent ventricular arrhythmias (block sympathetic?)
arrhythmias may be partly due to increased sympathetic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where does ß-blocker slow down conduction? why?

what else do ß-blockers do?

A
  1. slow down conduction in AVN: prevent supraventricular tachycardias (above ventricles), slows ventricular rate in patients in AF
    (so slows down SAN and AVN, slows down rate of pacemaker and rate of ventricles receiving that signal and transmitting it to the ventricles)
  2. reduce O2 demand: reduces myocardial ischaemia (less demand for O2, then less likely tissue will die), beneficial following MI (lack of O2 to myocardium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the principle of the therapeutic use of drugs that block K+ channels (class III anti-arrhythmics)?

A

prolong the AP: mainly blocking K+ channels: lengthens ARP

should prevent another AP occuring too soon, but in reality pro-arrhythmic (can block Na+ as well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which drug is used to treat Wolff-Parkinson-White syndrome? Which class of drug is it and what are it’s functions?

A

amiodarone
a type III anti-arrhythmic, but has other actions as well as blocking K+
used to treat tachycardia associated with W-P-W

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

briefly explain what Woldd-Parkinson-White syndrome is?

A

re-entry loop due to an extra conduction pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the principle of the therapeutic use of drugs that block Ca2+ channels? an example?

A

e.g. verapamil
decreases slope of AP at SAN (less influx of Ca2+)
decreases AVN conduction (less AP to travel to AVN from SAN)
decreases force of contraction (neg inotropy - due to lack of Ca2+)
some coronary + peipheral vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the function of Dihydropyridine Ca2+ channel blockers?

A

not effective in preventing arrhythmias, but DO act on vascular smooth muscle
e.g. amlopidine, felopidine, nicardipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is heart failure?

A

chronic failure of the heart to provide sufficient output to meet the body’s requirements

26
Q

What are the features of heart failure?

A
  1. reduced force of contraction

2. reduced cardiac output –> 3. reduced tissue perfusion –> 4. oedema

27
Q

How does reduced tissue perfusion from reduced cardiac output lead to oedema?

A

if right side of the heart has failure, then venous return will not be adequate, then congesting the venous system, increasing hydrostatic pressure, causing oedema peripherally

28
Q

What are the drugs used in the treatment of heart failure?

A
  1. positive inotropes increase cardiac output e.g. cardiac glycosides, ß-adrenergic agonists (dobutamine)
  2. drugs which reduce work load of the heart: reduce afterload and preload
29
Q

Describe the therapeuti use of ß-adrenoceptor antagonists

A
  1. ß-adrenoceptor antagonists can be used to reduce the force of contraction by preventing the action of sympathetically released NA: prevent the heart’s workload following an MI
  2. ß-adrenoceptors also reduce the HR following an MI, preventing any arrhythmias following an MI
  3. can also be used to treat angina
30
Q

Define the term ‘inotropic drug

A

drugs that affect the force of contraction

31
Q

What are the circumstances where inotropic drugs can be used?

A
  1. to increase cardiac output in heart failure e.g. cardiac glycosides
  2. cardiac glycosides inhibit: Na+-K+-ATPase: leading to increased [Na+] inside cell, so NCX can pump Ca2+ out of cell, so more intracellular store of Ca2+ for contraction, increasing the force of contraction
32
Q

What are examples of selective ß1-agonist that has inotropic effects? How do they work?

A

adrenaline + dopamine

INCREASE force of contraction + HR by activating ß1-adrenoreceptors

33
Q

explain the mechanisms by which organic nitrates elevate angina

A
  1. organic nitrates release nitric oxide (NO)
  2. NO is a powerful vasodilator: produced naturally by endothelial cells lining the blood vessels
  3. organic nitrates dilate the VEINS (venodilation), reducing central venous pressure (preload) - reducing workload of the heart
  4. organic nitrates do NOT alleviate angina by dilating arterioles
34
Q

What is a secondary effect of organic nitrates?

A

dilation of collateral coronary arteries, improving blood supply to the heart
all helping to alleviate angina

35
Q

What are drugs which increase myocardial contractility?

A

cardiac glycosides e.g. digoxin
improve symptoms but NOT long term
digoxin blocks Na+/K+ ATPase

36
Q

Describe the action of cardiac glycosides

A
  1. block Na+/K+ ATPase
  2. increase in Na+ concentration inside the cells, leading to an inhibition of NCX (due to decrease in conc. gradient)
  3. increase in [Ca2+] inside cardiac myocytes:
    positive inotropic effect - increasing force of contraction
    (more Ca2+ available for each contraction, AP shoots up higher)
37
Q

What is the action of cardiac glycosides on HR?

A

cause increased vagal activity:

  1. action via CNS to increase vagal activity
  2. slows AV conduction (via AVN?)
  3. slows HR
38
Q

What are drugs which increase myocardial contractility?

A

ß-adrenoreceptor agonists (ß-adrenoreceptors normally increase contractility by increasing adenylyl cyclase e.g. NA)
e.g. dobutamine, acts on ß1-receptor
used in: cardiogenic shock (used in inadequate cardiac output to perfuse tissues), acute but reversible heart failure (e.g. following cardiac surgery)

39
Q

What’s the best way to treat heart failure?

A

reduce workload of the heart

40
Q

What are examples of drugs which reduce the workload of the heart?

A

ACE-inhibitors
drugs which inhibit the formation of angiotensin converting enzyme (ACE)
prevent conversion of angiotensin I to angiotensin II
angiotensin II acts on kidneys: increase Na+ and water reabsorption (Increase in blood volume - heart works harder)
angiotensin II is a vasoconstrictor (constrict peripheral vessels to increase peripheral resistance: (increase?) afterload)

41
Q

How do ACE-inhibitors work in terms of heart load?

A
  1. reduce preload: decrease fluid retension from angiotensin II (Na+ & water reabsorption), decreasing blood volume
  2. Reduce afterload: decrease vasomotor tone (decrease BP - decrease peripheral resistance)

both reduce workload of the heart

42
Q

What are drugs which reduce the work load of the heart?

A
  1. ß-adrenoceptor antagonists (ß-blockers) - decrease contractility (less adenylyl cyclase)
  2. diuretics: reduce blood volume (less to pump out)
43
Q

When does angina occur?

A

when O2 supply to the heart doesn’t meet its need

limited to duration and doesn’t result in death of myocytes

44
Q

What happens in angina?

A

ischaemia of heart tissue (myocardial ischaemia) - leading to chest pain usually on exertion
due to narrowing of the coronary arteries (atheromatous disease)

45
Q

How do you treat angina?

A
  1. reduce work load of the heart:
    ß-adrenoreceptor blockers (ß-adrenoreceptors stimulate Heart)
    Ca2+ channel antagonists (reduce amount of Ca2+ entering heart via L-type Ca2+ channel, reducing CICR, reducing force of contraction)
    Organic nitrates (venodilator, reduce central venous pressure)
  2. improve blood supply to heart: organic nitrates, Ca2+ channel antagonists (reduce vascular SM contraction e.g. organs, vessels- reduce demand)
46
Q

How do organic nitrates become nitric oxide?

A

reaction of organic nitrates with thiols (-SH groups) in vascular smooth muscle causes NO2- to be released (endothelial cells)
NO2- is reduced to NO (nitric oxide)

47
Q

What are examples of organic nitrates?

A

glyceryl trinitrate
isosorbide dinitrate

powerful vasodilator

48
Q

Describe the types of drugs used to treat patients with common cardiovascular problems and their mechanisms of action

A
  1. anti-arrhythmia: treat atrial fibrillation, supraventricular tachycardia / ventricular tachycardia, by affecting Na+, K+, Ca2+ channels, ß-adrenoreceptor blockers
  2. inotropic drugs: treat force of contraction e.g. increase cardiac output in heart failure
  3. ACE-inhibitors treat chronic heart failure: promote vasodilation, reducing preload + afterload of heart
49
Q

How does nitric oxide cause vasodilation?

A

NO activates guanylate cyclase
increase cGMP –> PKG
lowers intracellular [Ca2+] - (phosphorylating L-type Ca2+ channels to shut them)
causes relaxation of vascular smooth muscle

50
Q

How does NO help to alleviate symptoms? (primary action)

A

acts on venous system venodilation to lower preload
more blood stored in veins, less in circulation, reducing pre-load heart fills less, doesn’t contract as hard (Starling’s Law), reducing the O2 demand when not contracting as hard

51
Q

How does NO help to alleviate symptoms? (secondary action)

A

act on coronary arteries: improve O2 delivery to ischaemic myocardium
acts on collateral arteries (joining arterioles) rather than arterioles

52
Q

Describe how organic nitrates work on dilating arterioles?

A

only helps in a minor contribution

as there aren’t that many collateral arteries, so increase in blood flow to ischaemic area is little

53
Q

What is the main action of organic nitrates?

A
  1. venodilation
    reducing venous pressure + preload (return to heart)
    reducing work of heart (less in , pump less) - Starling’s Law of the heart
54
Q

When are antithrombotic drugs used?

A

certain heart conditions carry an increased risk of thrombus formation

  1. atrial fibrillation (can move into LV –> systemic circulation, if carotid artery –> brain –> stroke)
  2. acute myocardial infarction
  3. mechanical prosthetic heart valves
55
Q

What are examples of antithrombotic drugs? action?

A

Anticoagulants:
1. heparin (intravenously): inhibits thrombin (acutely short term)
2. Warfarin (orally): antagonises vit K, can be long term
3. fractionated heparin (subcutaneous injection)
Antiplatelet drugs:
1. aspirin: following acute MI / high risk of MI (prevent thrombus which is platelet rich)

56
Q

What are risks of hypertension?

A
  1. associated with increases in blood volume: Na+ & water retention by kidneys
  2. increase in total peripheral resistance (TPR) - increasing BP
57
Q

How do you work out pressure?

A

pressure = flow x resistance

58
Q

how do you work out BP?

A

BP = cardiac output x total peripheral resistance

59
Q

How do you work out cardiac output?

A

stroke volume x HR

60
Q

What are possible targets for hypertension?

A
  1. lower blood volume: lowers cardiac output via Starling’s law (less in, contracts not as hard)
  2. lower cardiac output directly: reduce contractility / TPR
  3. lower peripheral resistance (pumping against less resistance, less force required)
61
Q

What are the different types of drugs that can be used to treat hypertension?

A
  1. Diuretics: decrease Na+ & water retention by kidney, decrease blood volume (decrease CO & TPR)
  2. ACE-inhibitors: decrease Na+ & water retention by kidney, decrease TPR (vasodilation)
  3. ß-blockers: decrease cardiac output (aren’t used to treat)
  4. Ca2+ blockers selective for vascular SM, vasodilation, reduce VSM contraction, reduce cardiac output through reducing peripheral resistance
  5. a1-adrenoceptor antagonist: vasodilation (decrease BP & TRP)
62
Q

Which common cardiovascular problems does cardiovascular drugs treat?

A
  1. arrhythmias - irregular rhythm
  2. heart failure
  3. angina - lack of oxygen to the myocardium –> chest pain upon exertion
  4. hypertension
  5. Risk of thrombus formation

Heart (18 decks)

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