Cardiovascular Pharmacology Flashcards
(55 cards)
Do do positive and negative inotropes do, what are positive inotroped used to treat?
Positive inotropes- increase contractility
Used for dilated cardiomyopathy
Negative inotropes- decrease contractility
What do lusiotropes, positive and negative chronotropes do and what are they used to treat?
Lusiotropes- relax ventricles- used for hypertrophic and restrictive cardiomyopathy
Positive chronotropes increase HR- used for AV block
Negative chronotropes decrease HR- used for atrial fibrillation
What is heart rate determined and altered by?
CV centre in medulla oblongata
Autonomic nervous system
What is the conduction of the action potential of the heart dependent on?
Normal activity of Na, K, Ca2+ channels
Normal intracellular and extracellular concs of ions
Correct function off intercalated disks
Why can control of HR go wrong?
Ectopic pacemakers
Damage to conducting tissue
Depression of CV centre
Why are tachycardias a problem?
Reduced diastolic filling time
Lower end diastolic ventricular volume
Lower stroke volume= lower cardiac output
Increased cardiac work= hypertrophy
What is the name of the classes of antidysrhythmics and what are the different classes?
Vaughan-Williams classification
Classes- I, II, III, IV, mis (V)
What does each class (I ,II, III, IV) do?
I- sodium channel blockers
II- Beta blockers
III- Drugs which prolong AP by blocking some K channels
IV- calcium channel blockers
What do class I drugs bind to and what do they cause?
Bind to and block fast sodium channels- use dependent Na channel blockade (open over resting)
Cause reduced heart rate in tacyarrhythmias while not significantly affecting normal heart rates
What does the efficacy of class I sodium channel blockers depend on?
Normal concentration of extracellular K
Hypokalaemia reduces their function
Hyperkalaemia increases their function
What are the three sub-classes of Class I sodium channel blockers and how do their actions differ?
Ia- old, intermediate rate of dissociation
Ib- bind during phase 0, begin to dissociate for the next AP, prevents premature beats
Ic- bind and dissociate slowly, reach steady state and reduce His-purkinje system
Name an example of each sub-class of sodium channel blockers?
Ia- quinidine- increase effective refractory period
Ib- lidocaine - decrease effective refractory period
Ic- flecainide- doesn’t affect effective refractory period
How is quinidine (class Ia) administered and what are its adverse effects?
Oral or parenteral- not IV
Adverse- Various rhythm disturbances as blockage persists, negative inotropy and vasidilation, GI signs, nervousness, depression
How is lidocaine administered and what are its adverse effects:
Parenteral (slow IV) as almost complete first pass hepatic metabolism
Adverse- CNS- excitation, disorientation, seizures, nausea
What is the effect of class II antidyshrthmics?
B2 blockade- some vasoconstriction
Slow pacemaker potential by slowing calcium influx
Slow conduction through AV bundle- increase refractory period
Negative isotropy and reduced myocardial relaxation
What are class II antidysrythmics used for?
Supraventricular or ventricular tachycardias
Hypertension
What is an example of class II and what are its adverse effects?
Atenolol- beta 1 selective
Adverse effects limited to CNS
What are the 2 modes of actions of class III?
Prolong cardiac AP
Block K+ channels- slows repolarisation, increases refractor period
Name an example of class III antidysrhythmics and what is it made up of and what are its adverse effects?
Sotalol Racemic mixture of isomers I and D I- non-selective beta blocker D- inhibits K channels Adverse- hypotension, bradycardia, GI signs
What is the mode of action of class IV and therefore their effect?
Block ca channels of cardiomyocytes, nodal tissue, vascular and smooth muscle
Effect- shorten plateau phase, slow conduction in SAN and AVN
Negative inotropes and positive lusiotropes
Name an example of class IV, how is it administered?
Diltiazem
Oral and parenteral administration
Toxicity- myocardial depression, hypotension, AV block
Name an example of Class ‘V’, what is its mode of action, how is it administered, what are its adverse effects?
Digoxin
MOA- chronotropic effects without negative inotropy
Oral admin
Adverse- myocardial toxicity, GI toxicity
How are bradyarrythmias treated?
Most require pacemaker if causing clinical signs Sympathomimetics Anticholinergics Methylxanthines PDE III inhibitors
What are examples of categories of sympathomimetics and anticholinergics and what do they do?
Beta 1 agonists- dobutamine- inotropic
Beta 2 agonists- terbutaline- +ve chronotropy
Muscarinic antagonists- atropine- +ve chronotropy
