13 - Drugs on the CVS Flashcards

1
Q

What are some causes of arrhythmias?

A

Tachycardia: Ectopic pacemaker, afterdepolarisations, AF, re-entry loop

Bradycardia: sick sinus syndrome, drugs, AV block

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

What are the two different types of after depolarisations?

A

Delayed: if intracellular Ca high more likely to occur as reverses NCX and can lead to tachycardia

Early: depolarisation as recovery occuring, if AP prolonged (long QT)

EACH OF THESE CAN TRIGGER AN ACTION POTENTIAL

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

What is the rentrant mechanism of generating arrhythmias?

A

If you have multiple reentrant circuits you will get atrial fibrillation

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

What is AV nodal reentry?

A

Leads to tachycardia

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

What is ventricular pre-excitation?

A

Accessory pathway between atria and ventricles so impulse reaches ventricles earlier than it should so tachy

e.g Wolff-Parkinson-White syndrome

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

What are the four different classes of anti-arrhythmic drugs?

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

How do voltage-depend Na channel blockers prevent arrhythmia?

A

e. g Lidocaine
- They block depolarised tissue preventing automatic firing so A.P refractory period is longer, decreasing heart rate
- Damaged myocardium may be depolarised and fire automatically but these drugs stop this

- May give IV if patient has VT after MI to stop VF but not used prophylatically

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

How do B-adrenoreceptorr antagonists help treat arrhythmias and what are some examples?

A
  • Atenolol, Propranolol
  • Block sympathetic action. Decrease slope of pacemaker potential in SA and slow conduction at AV
  • Stops SVTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do K+ channel blockers prevent arrhythmias?

A
  • Prolong action potential, increasing absolute refractory period and heart rate but actually pro-arrythmic
  • NOT VERY GOOD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the absolute refractory period of the ventricles corresponding with on the ECG?

A
  • QT syndrome
  • Longer QT can lead to torsades (ventricular tachycardia) which can turn into VF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the only K+ channel blocker that is used?

A
  • Amiodarone as non selective to K+
  • Treats tachycardia associated with reentry loop syndrome called Wolff-Parkinson-White
  • Can supress ventricular arrhythmias post MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do Ca channel blockers prevent arrhythmias and what are some examples?

A
  • Verapamil, diltiazem (Non-hydropyridines)
  • Decrease slope of action potential at SAN, decrease AV nodal conduction and decreases force of contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do dihydropyridine Ca channel blockers differ to nondihydropyridines?

A

Dihydropyridines act on vascular smooth muscle, e.g nifedipine, to act as anti-hypertensive

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

How does adenosine act as an anti-arrhytmic drug?

A
  • Produced endogenously but can be given IV
  • Act on A1 receptors at AV node (short half life)
  • Enhances K+ conductance hyperpolarising cell
  • Terminates reentry SVT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the definition of heart failure?

A

Chronic failure of the heart to provide sufficient output to meet the body’s requirements - can lead to peripheral and pulmonary oedema

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

What is an example of an ACE inhibitor, what is it used to treat in the heart, and how does it do this?

A
  • Perindopril
  • Treat hypertension and heart failure by inhibiting ACE
  • Decreases vasomotor tone as angiotensin II is a vasoconstrictor
  • Reduces afterload of heart
  • Decrease fluid retention so decreased preload

REDUCING WORK LOAD OF THE HEART

17
Q

What can you give a patient who cannot tolerate ACE inhibitors, e.g because of a cough?

A
  • Losartan
  • Angiotensin II receptor blocker so can be used for heart failure and hypertension
18
Q

What can diuretics be used to treat?

A
  • Heart failure and hypertension
  • Mainly loop diuretics like furosemide in congestive heart failure to decrease blood volume and workload of heart
  • In mild congestive heart disease thiazide diuretics
19
Q

How can Ca channel blockers be used in the CVS apart from as an anti-arrhythmic?

A
  • Dihydropyridines like nicardipine, nifedipine, amlodipine
  • Decrease peripheral resistance, decrease arterial b.p, decreasing afterload and therefore workload

- Treat hypertension, angina, coronary artery spasm, SVTs

20
Q

What are examples of positive inotropes and what do they do to the heart?

A
  • They increase the contractility
  • B1 agonists
  • Cardiac glycosides
21
Q

How do cardiac glycosides work on the heart and when would they be used?

A
  • Improve symptoms of heart failure but not good in long run (horse anecdote)

- Positive inotrope and negative chronotrope

  • Digoxin precursor
  • Blocks Na/K ATPase so NCX reverses, increasing Ca in the cell, and therefore increasing force of contraction as more Ca stored in SER
  • Increase vagal activity slowing AV conduction and heart rate so can be used in heart failure when arrhythmia
22
Q

How do B agonists act as positive inotropes?

A
  • Dobutamine selective B1
  • Stimulates receptors at SA, AV and myocytes
  • Used in acute but reversible heart failure (e.g after surgery) or in cardiogenic shock
23
Q

What are the best and worst drugs to treat heart failure?

A

Worst: Cardiac glycosides and B agonists as they increase workload of heart whilst increasing cardiac output

Best: ACE inhibitors, ARBs, diuretics, beta blockers

24
Q

When does angina occur?

A

When the O2 supply to the heart does not meet the demand, usually due to ischemia with no death of myocytes

25
Q

What is the most common way to treat angina and how does it work?

A
  • Organic nitrates as they react with thiols in vascular smooth muscle to form NO for venodilation
  • ONLY ACTS ON VEINS NOT ARTERIOLES!!!!!!!
  • Lowers preload, lowers force of contraction of heart and lowers O2 demand
26
Q

What is the primary and secondary actions of organic nitrates in treating angina?

A

- Primary: VENODILATION, decreasing venous pressure and return of blood to heart so decreasing preload, decreasing force of contraction due to Starling and decrease O2 demand

- Secondary: Dilation of colateral arteries causing minor contribution

27
Q

What are the main ways to treat angina?

A

- Decrease workload of the heart: organic nitrates, beta blockers, ca channel antagonists

- Improve blood supply to heart: ca channel antagonists and organic nirates

28
Q

What are the main actions of beta-blockers?

A
29
Q

What heart conditions lead to an increased risk of thrombus formation?

A
  • Atrial fibrillation
  • Acute MI
  • Prosthetic heart valves
30
Q

What are some examples of antithrombotic drugs?

A

- Anticoagulants (VENOUS): heparin IV/subcutaneous, warfarin oral, dabigatran oral thrombin inhibitor

- Antiplatelet drugs (ARTERIAL): Aspirin, clopidogrel (after or high risk of MI)

31
Q

What is the difference between anti-platelet and anticooagulant drugs?

A

Anticoagulants slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing.

Antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing

32
Q

What are some examples of vasodilator drugs?

A
  • Nitric oxides
  • Ca channel blockers
  • ACE inhibitors
  • A1 antagonists
33
Q

How would a beta blocker help a tachycardia?

A
  • Slows conduction of SA node
  • Blocks Gas so less cyclic AMP, less HCN channels open so slower depolarisation
34
Q

How can mitral valve stenosis lead to AF?

A
  • Left atrium hypertrophy
  • Myocardium damaged so can spontaneously depolarise
35
Q

How does lidocaine help with VF and what drug is usually used instead of lidocaine now?

A

- Blocks Na channels, especially those in damaged tissues so they cannot spontaneously depolarise

- Amiodarone now used which blocks K+ channels to lengthen refractory period

36
Q

What is the action of digoxin and what patient setting is it used in?

A
  • Inhibits sodium pump so more calcium stored in ER due to NCX reversal
  • Patients with AF and heart failure as relieves symptoms but in long run not good as increases workload of heart
37
Q

Why are patients whose coronary blood flow is compromised treated with beta adrenoreceptor antagonists?

A
  • Negative inotropy
  • Decreased oxygen deman
  • Less blood flow needed from arteries
38
Q

Which parts of the myocardium will be affected if the following arteries are occluded:

  • Right coronary artery
  • Circumflex
  • Left coronary artery
  • LAD
  • Right marginal artery
A