Session 7.2.

Question 1

What are the causes of tachycardia?

Answer 1

• ectopic pacemaker activity by damaged areas of myocardium
• afterdeoplarisations which follow the AP
• atrial flutter/fibrilation
• re entry loop: conduction delay/ accessory pathway

Question 2

What causes bradycardia?

Answer 2

• sinus bradycardia

- conduction block

Question 3

How do delayed after depolarisations differ from early after depolarisations?

Answer 3

Delayed

• more likely to happen if intracellular Ca2+ high, especially in stores
• small bump after depolarisation

Early
- can lead to oscillations, more likely to happen if AP prolonged = longer QT interval.

Question 4

What is the re entrant mechanism for generating arrhythmias?

Answer 4

• block of conduction through damaged area
• excitation takes a longer route to spread the wrong way through the damaged area, setting up a circus of excitation

Several loops = atrial fibrillation

Question 5

What does lidocaine do?

Answer 5

Blocks voltage dependant Na+ channels
Preferentially blocks damaged depolarised tissue = damaged areas of myocardium. More Na channels are open in depolarised myocardium = prevents automatic firing.
Given after MI if there’s ventricular tachycardia

Question 6

What do B blockers do?

Answer 6

Block B1 adrenoreceptors and slow AV node conduction

• prevent superventricular tachycardia
• slows ventricular rate in patients with AF
• MI = increased sympathetic activity, combats this.
• reduced o2 demand = reduced myocardial ischaemia, beneficial following MI.

Question 7

What do drugs that block k+ channels do?

Answer 7

• prolong the action potential = longer absolute refractory period
• prevents another AP occuring to soon

E.g amiodarone - effective against ventricular arrhythmia’s

Question 8

What do drugs that block ca2+ channels do?

Answer 8

• Decrease slope of AP at SA node
• Decrease AV nodal conduction
• Negative intropy
• help against ventricular arrhythmia

Question 9

What does adenosine do?

Answer 9

Acts on A1 receptors at AV node
Enhances K+ conductance
Anti- arrhythmic

Question 10

Why are ace inhibitors bad to give to asthmatics?

Answer 10

Can cause a dry cough as you have express bradykinin

Question 11

Why are ace inhibitors valuable in the treatment of heart failure?

Answer 11

• decrease vasomotor tone = decrease blood pressure
• reduced afterload of heart
• decreased fluid retention = decreased blood volume
• reduced preload

= decreased overall work load of heart

Question 12

Why would angiotensin II receptor blockers Be used?

Answer 12

In patients that cant tolerate ace inhibitors

Treat heart failure and hypertension

Question 13

What are the role of diuretics?

Answer 13

Treat heart failure and hypertension

- e.g furosemide reduced pulmonary and peripheral oedema (heart failure causes oedema)

Question 14

What do Ca2+ channel blockers do?

Answer 14

• decrease peripheral resistance
• decrease arterial BP
• reduce workload of heart by reducing afterload
• can also act to for a negative inotropy
• useful to treat hypertension, angina, coronary artery spasms and SVTs

Question 15

What do positive inotropes do?

Answer 15

Increase contractility and thus cardiac output

E.g glycosides and B adrenergic agonists

Question 16

What’s the role of cardiac glycosides?

Answer 16

Block Na/K ATPase
Leads to a rise in intracellular Na
This causes decreased activity of Na/Ca exchanger which brings Na in
Causes increase in intracellular Ca
Therefore get increased force of contraction

Also increase Vegal activity via CNS, slowing AV conduction and thus heart rate.

Question 17

What do b adrenoreceptors agonist Do??

Answer 17

Stimulate B1 receptors on SA and AV node and ventricular myocytes
Uses cardiogenic shock

Question 18

What would you use to treat heart failure?

Answer 18

ACE inhibitors or ARBs
Diuretics
Beta blockers

All help reduce workload

Question 19

Why are nitrates used to treat angina (myocardial ischaemia)?

Answer 19

Reaction of organic nitrates with thiols on vascular smooth muscle causes NO2- to be released
This is reduced to NO which is a powerful vasodilator, particularly on veins

E.g GTN spray

Question 20

How does NO cause vasodilation?

Answer 20

NO activates guanylate cyclase
Increases cGMP
Lowers intracellular Ca
Causes relaxation of vascular smooth muscle

Question 21

How does vasodilation help alleviate symptoms of angina?

Answer 21

Primary action

• lowers preload = lower workload of heart
• less filling of heart = force of contraction reduced
• lowers o2 demand

Secondary
- action on coronary collateral arteries (but not arterioles) improves o2 delivery to the ischaemic myocardium (only by a little)

Question 22

So how would you treat angina?

Answer 22

Reduce workload of heart

• organic nitrates
• B blockers
• Ca channel antagonist

Improve blood supply

• Ca channel antagonist
• minor effect of organic nitrates

Question 23

Name 3 conditions hat carry an increased risk of thrombus formation.

Answer 23

Atrial fibrillation
Acute myocardial infarction
Mechanical prosthetic valves

Question 24

What’s the role of antithrombotic drugs?

Answer 24

Anticoagulants
Prevent venous thromboembolism

Heparin

• intravenous
• inhibits thrombin short term

Warfarin

• oral
• antagonises actions of vitamin k

Antiplatelet drugs

• aspirin
• clopidogrel (following acute/high risk MI)