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ESA 2: Cardiovascular > Cardiovascular: Session 10 > Flashcards

Cardiovascular: Session 10 Flashcards

1
Q

What are cardiavascular drugs used to treat?

A
  • Arrhythmias
  • Heart Failure
  • Angina
  • Hypertension
  • Risk of thrombus formation
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2
Q

What can cardiovascular drugs alter?

A
  • The rate and rhythm of the heart
  • The force of myocardial contraction
  • Peripheral resistance and blood flow
  • Blood volume

Some drugs can act at more than one site

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3
Q

What can cause disturbances of cardiac rhythm?

A

Abnormality of heart rate or rhythm

  • Bradycardia
  • Atrial flutter
  • Atrial fibrillation
  • Tachycardia (ventricular tachycardia, supraventricular tachycardias)
  • Ventricular fibrillation
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4
Q

How is tachycardia caused? (arrhythmia)

A

Due to ectopic pacemaker activity

  • Damaged area of myocardium becomes depolarised and spontaneously active.
  • This Latent pacemaker region activated due to ischaemia dominates over the SA node
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5
Q

What causes arrhythmia?

A
  • Ectopic pacemaker activity
  • After depolarisation
  • Atrial flutter/atrial fibrillation
  • Re-entry loop
  • Sinus Brady cardia
  • Conduction block
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6
Q

What is the mechanism of action of an ectopic pacemaker activity in the causation of an arrhythmia?

A
  • Damaged area of myocardium becomes depolarised and spontaneously active
  • Latent pacemaker region activated due to ischaemia and dominates over SA node
  • This causes tachycardia and can lead to an arrhythmia
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7
Q

When are delayed after-deplarisation more likely to happen?

A

High intracellular Calcium

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8
Q

When are early after depolarisation more likely to happen?

A

When the action potential is prolonged. Can lead in oscillations

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9
Q

How does a longer action potential present on an ECG?

A

Long Q-T interval

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10
Q

What is the normal spread of excitation?

A
  • Splits at the branch point in two different directions

- Cancels out in the midline due to refractory period of tissue as it has already depolarised

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11
Q

What is the re-entrant mechanism for generating arrhythmia?

A
  • Incomplete conduction damage

- Excitation can take a long route to spread the wrong way through the damaged area setting up a circus of excitation

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12
Q

What can lead to atrial fibrillation?

A

Several re-entrant loops in the atria leading to atrial fibrillation.

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13
Q

What can cause AV nodal re-entry?

A

Fast and slow pathways in the AV node create a re-entry loop.

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14
Q

What can cause ventricular Pre-excitation?

A

An accessory pathway between atria and ventricles creates a re-entry loop such as in owl-parkinson-white syndrome

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15
Q

What are the basic classes of anti-arrhythmic drugs?

A
  • Drugs that block voltage sensitive sodium channels
  • Antagonists of beta adreno-receptors
  • Drugs that block potassium channels
  • Drugs that block calcium channels
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16
Q

What is the mechanism of action for a voltage dependant Na+ channels?

A
  • Use dependant block. Blocks voltage gated Na+ channels in open or inactive state - therefore blocks damaged depolarised tissue.
  • Has a little effect on normal cardiac tissue as it dissociates rapidly.
  • Blocks during depolarisation but dissociates in time for the next action potential
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17
Q

How is lidocaine used in the clinical setting?

A
  • Sometimes given intravenously following Myocardial infarction if the patient shows signs of ventricular tachycardia
  • Damaged areas of the heart may be depolarised and fire automatically
  • More Na+ channels are open in depolarised tissue. Lidocaine blocks these Na+ channels and prevents automatic firing of depolarised ventricular tissue
  • Not used prophylactically following MI even in patients showing ventricular tachycardia. Tend to use other drugs
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18
Q

What is the mechanism of action of beta-adrenorecptor antagonists?

A
  • Block sympathetic action by acting at beta 1 adrenoreceptors in the heart
  • Decreases slope of pacemaker potential in SA and slows conduction at AV node. Can prevent supra ventricular tachycardias and slows ventricular rate in patients with atrial fibrillation
  • Used following myocardial infarction. Myocardial infarction causes increased sympathetic activity. They prevent ventricular arrhythmias and arrhythmia may be partly due to increased sympathetic activity
  • Also reduced oxygen demand so reduced myocardial ischaemia which is beneficial following myocardial infarction
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19
Q

What is the mechanism of action of drugs that block K+ channels?

A
  • They prolong action potential

- Lethens the absolute refractory period. in theory this prevents another Action potential occurring too soon

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20
Q

Why aren’tdrugs that block K+ channels generally used?

A

Can be also pro-arhythmic due to the prolonged action potential

21
Q

What is the exception K+ blocking drugs?

A

Amiodarone

22
Q

What is the action of amiodarone?

A
  • It is a type 3 anti-arrhythmic but has other actions in addition to blocking K+ channels
  • Beta blocker, Calcium Channel blocker
  • Used to treat tachycardia associated Wolff-parkinon-White syndrome
  • Effective for suppressing ventricular arrhythmias post myocardial infarction
23
Q

What is mechanism of action of drugs the block Ca2+ channels?

A
  • Decreases slope of action potential at SA node
  • Decreases AV nodal conduction
  • Decreases force of contraction
  • Also some coronary and peripheral vasodilation

-Dihydropyridine Ca2+ channel blockers are not defective in preventing arrhythmias but do act on vascular smooth muscle (less effect on the heart compared to verapamil)

24
Q

How does adenosine work?

A
  • Produced endogenously but can also be administered intravenously
  • Acts on alpha 1 receptors at AV node but has a very short half-life
  • Enhances K+ conductance . Hyperpolarises cells of conducting tissue
  • Anti-arrhythmic. Useful for terminating re-entrant supra ventricular tachycardia
25
What is heart failure?
Chronic failure of the heart to produce sufficiency output to meet the body's requirements
26
What are the features of heart failure?
- Reduced force of contraction or reduced filling - Reduced cardiac output - Reduced tissue perfusion - Oedema
27
What are the type s of drugs used in the treatment of heart failure?
Positive inotropes to increase cardiac output - Cardiac glycosides - Beta adrenergic agonist Drugs that reduce workload of the heart - reduce after load and preload
28
What is the action of cardiac glycosides (Digoxin)?
- Physiologically Ca2+ extruded via Na+/Ca2+ which is driven by Na+ moving down contraction gradient - Cardiac glycoside block Na+/K+ ATPase which leads to rise in intracellular Na+. - This leads to decrease in a activity of Na+/Ca2+ exchanger - Cause increase in Ca2+ intracellular so more Ca2+ stored in SR - Increased force of contraction - Cardiac glycoside also cause increase in vagal activity. - Action via central nervous system to increase vagal activity - Slows AV conduction - Slows heart rate
29
When are cardiac glycosides used?
May be used in heart failure when there is an arrhythmia such as atrial fibrillation
30
What is the action of beta adrenergic agonists?
- Acts on beta 1 receptors | - Used in cardiogenic shock and acute but reversible heart failure
31
Why can't cardiac glycoside and beta adrenergic agonist be used long term?
- Making the heart work harder is not good in the long run. | - Better to reduce workload
32
Why can't cardiac glycoside and beta adrenergic agonist be used long term?
- Making the heart work harder is not good in the long run. | - Better to reduce workload
33
Which Drugs reduce workload of the heart?
- ACE-inhibitors - Diuretics - Beta adrenoreceptor antagonists
34
What is the action of the ACE inhibitors?
- Inhibit the action of angiotensin converting enzyme which is important in the treatment of heart failure - Prevent the conversion of angiotensin 1 to angiostensin 2 - Decrease in vasomotor tone (decrease in blood pressure) - Reduce afterload of the heart - Reduce preload of the heart - Reduce work load of the heart - Decrease fluid retention (decrease in blood volume)
35
How do diuretics reduce workload of the heart?
-Reduce blood volume
36
What causes angina?
- Occurs when O2 supply to the heart does not meet its need - Ischaemia of heart tissue so pain - Usually pain is on exertion - Due to narrowing of the coronary arteries due to atheromatous plaque formation
37
How do you treat angina?
-Reduce workload of the heart (beta-adrenoreceptor blockers, Ca2+ channel antagonists, organic nitrates) -Improve the blood supply to the heart (organic nitrates, Ca2+ channel antagonists)
38
What is the action of organic nitrates?
- Reaction of organic nitrates with thiols in vascular smooth muscle causes (NO2)- to be released - (NO2)- is rescued to NO - NO is a powerful vasodilator
39
How does nitric oxide cause vasodilation?
- NO activates granulate cyclase - Increase cGMP - Lowers intracellular [Ca2+] - Causes relaxation of vascular smooth muscle
40
How does NO alleviate symptoms of angina?
Primary - Action on the venous system. Venodilation reduces the venous pressure so lowers preload - Reduced workload of the heart - Heart fills less therefore force of contraction reduced - This lower O2 demand - The heart works less Secondary Action - Action on coronary collateral arteries improves O2 delivery to ischaemic myocardium - Acts on collateral arteries not arterioles
41
Why do organic nitrites preferentially act on veins?
- Probably because there is less endogenous nitric oxide in veins - Most effective on veins>arteries - Little effect on arterioles
42
Which heart conditions carry an increased risk of thrombus formation?
- Atrial fibrillation - Acute myocardial infarction - Mechanical prosthetic heart valves
43
What are the antithrombotic drugs?
- Anticoagulants | - Antiplatelet drugs
44
What is the mechanism of action of anticoagulants?
- Heparin given intravenously which inhibits thrombin. It is used acutely for short term action - Fractionated heparin - Warfarin is given orally. It antagonises the action vitamin - Direct acting oral thrombin inhibitors such as digabatran
45
What is the mechanism of action for antiplatelet drugs?
-Aspirin following acute MI or high risk of MI
46
What is hypertension associated with?
- Increases in blood volume (Na+ and water retention in kidneys) - An increase in total peripheral resistance
47
What are the possible targets for treatment of hypertension?
- Lowers blood volume (lower cardiac output via Starling's laws) - Lower cardiac output directly - Lower peripheral resistance
48
What are the type of drugs for Hypertension?
- ACE inhibitors - Decrease Na+ and water retention by kidney and decreases total peripheral resistance (vasodilation) - Ca2+ channel blockers slevetive for vascular smooth muscle - vasodilation - Diuretics - decrease Na+ and water retention by kidney so decrease in blood volume Not routinely used - Beta blockers - decreases cardiac output - Alpha 1 adrenoreceptor antagonist - vasodilation

ESA 2: Cardiovascular (11 decks)

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