Session 7.2. Flashcards
(24 cards)
What are the causes of tachycardia?
- ectopic pacemaker activity by damaged areas of myocardium
- afterdeoplarisations which follow the AP
- atrial flutter/fibrilation
- re entry loop: conduction delay/ accessory pathway
What causes bradycardia?
- sinus bradycardia
- conduction block
How do delayed after depolarisations differ from early after depolarisations?
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.
What is the re entrant mechanism for generating arrhythmias?
- 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
What does lidocaine do?
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
What do B blockers do?
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.
What do drugs that block k+ channels do?
- prolong the action potential = longer absolute refractory period
- prevents another AP occuring to soon
E.g amiodarone - effective against ventricular arrhythmia’s
What do drugs that block ca2+ channels do?
- Decrease slope of AP at SA node
- Decrease AV nodal conduction
- Negative intropy
- help against ventricular arrhythmia
What does adenosine do?
Acts on A1 receptors at AV node
Enhances K+ conductance
Anti- arrhythmic
Why are ace inhibitors bad to give to asthmatics?
Can cause a dry cough as you have express bradykinin
Why are ace inhibitors valuable in the treatment of heart failure?
- decrease vasomotor tone = decrease blood pressure
- reduced afterload of heart
- decreased fluid retention = decreased blood volume
- reduced preload
= decreased overall work load of heart
Why would angiotensin II receptor blockers Be used?
In patients that cant tolerate ace inhibitors
Treat heart failure and hypertension
What are the role of diuretics?
Treat heart failure and hypertension
- e.g furosemide reduced pulmonary and peripheral oedema (heart failure causes oedema)
What do Ca2+ channel blockers do?
- 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
What do positive inotropes do?
Increase contractility and thus cardiac output
E.g glycosides and B adrenergic agonists
What’s the role of cardiac glycosides?
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.
What do b adrenoreceptors agonist Do??
Stimulate B1 receptors on SA and AV node and ventricular myocytes
Uses cardiogenic shock
What would you use to treat heart failure?
ACE inhibitors or ARBs
Diuretics
Beta blockers
All help reduce workload
Why are nitrates used to treat angina (myocardial ischaemia)?
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
How does NO cause vasodilation?
NO activates guanylate cyclase
Increases cGMP
Lowers intracellular Ca
Causes relaxation of vascular smooth muscle
How does vasodilation help alleviate symptoms of angina?
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)
So how would you treat angina?
Reduce workload of heart
- organic nitrates
- B blockers
- Ca channel antagonist
Improve blood supply
- Ca channel antagonist
- minor effect of organic nitrates
Name 3 conditions hat carry an increased risk of thrombus formation.
Atrial fibrillation
Acute myocardial infarction
Mechanical prosthetic valves
What’s the role of antithrombotic drugs?
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)
