CVS Session 9 Flashcards
What main methods of action can CVS drugs use?
Alter HR Alter heart rhythm Alter force of myocardial contraction Act on arterioles to alter TPR and blood flow Alter blood volume
What are CVS drugs used to treat?
Arrhythmias Heart failure Angina Hypertension High risk of thrombus formation
Can CVS drugs act at more than one site?
Yep
What is bradycardia?
Slow HR
What is atrial flutter?
Rapid depolarisation rate of atria
What is atrial fibrillation?
Unidentifiable depolarisation of atria on ECG
How does atrial fibrillation appear on an ECG?
Oscillating baseline
What is tachycardia?
Fast HR coupled with low BP as there is not enough time for filling of ventricles
What two types of tachycardia can occur?
Ventricular
Supraventricular
What causes supraventricular tachycardia?
Something in the atria causing rapid ventricular contraction e.g. Extra conduction loop, fast atrial contraction
What does ventricular fibrillation cause?
A severely reduced cardiac output which is incompatible w/life
What are the three causes of arrhythmias?
Actio is pacemaker activity due to damage
Afterdepolarisations (triggered activity)
Re-entry loop
How do damaged myocytes cause ectopic pacemaker activity?
They depolarise and become spontaneously active
How can an MI lead to tachycardia?
If area of ischaemia around infarct depolarises and becomes spontaneously active at a rate faster than the SAN
What is triggered activity?
Abnormal depolarisations after a normal AP
In what conditions are afterdepolarisations more likely?
If intracellular calcium is high
What can cause the firing of an early AP?
NCX or calcium-activated chloride conductance
When is an early after-depolarisation more likely?
In a long AP
What does a long QT make a cardiac myocyte more susceptible to?
Sodium channels recovered from inactivation
V-G calcium channels triggered
What causes oscillatory activity in early after-depolarisation?
Recovery of sodium channels and triggering of V-G calcium channels
What is a re-entry loop?
Accessory pathway - 2 paths b/w atria and ventricles or damaged area which causes condition delay
How does incomplete conduction damage cause a re-entry loop to form?
Unidirectional block formed which forces excitation to take long route to spread wrong way through damaged area
What circumstances must be present in order for a re-entry loop to exist normally in a person?
No delay in conduction and circuit set up
What can multiple re-entry loops around the pulmonary vein spread to give?
Atrial fibrillation
What method of action do Class I anti-arrhythmics use?
Block V-G sodium channels
What mechanism of action do Class II anti-arrythmics use?
Beta-adrenoreceptor antagonists
What method of action do Class III anti-arrhythmics use?
Block potassium channels
What method of action do Class IV anti-arrythmics use?
Block calcium channels
Give an example of a Class I anti-arrhythmic.
Lidocaine
Why is lidocaine described as ‘use-dependent’?
Can only block sodium channels when they are open/inactive
Do Class b V-G sodium channel blockers affect normal AP firing?
No, they do not affect the upstroke
Do Class b V-G sodium channel blockers dissociate rapidly or slowly?
Rapidly
Why are V-G sodium channel blockers given IV in ventricular tachycardia following MI?
Sodium channels are open in the damaged tissue so can be blocked to prevent automatic firing and therefore prevent ventricular fibrillation
Is lidocaine still used prophylactically after MI?
Nope
What other name are beta-adrenoreceptor antagonists known by?
Beta blockers
Give two named examples of beta-adrenoreceptor antagonists.
Propranolol
Atenolol
How do beta-blockers reduce heart rate?
Alter cAMP levels –> decrease funny current –> decrease slope of pacemaker potential –> slow SAN firing
Slow conduction at AVN