3-cardio Flashcards
what are 4 causes of dysrhythmia
delayed after depolarization
abnormal pacemaker activity
heart block
circus movement/ re-entry
what can cause delayed after depolarization
catecholamine action or digitalis toxicity (ca2+ overload)
what can cause abnormal pacemaker activity
altered autonomic effects or long QT syndrome
what is heart block/ what can cause it
conduction block of AV node
what are 3 pathological requirements for circus movement
circular conducting pathway
branch of circuit with UNIDIRECTIONAL conduction block
refractory period of re-entry region < propogation time around pathway
draw the circus movement pathway
yes
what do you want to do to the refractory period to reduce circus movement
increase refractory period (so it cant double back)
what are 5 desirable features of antidysrhythmic drugs
1-convert 1 way block to 2 way block 2-increase refractory period 3-block effects of catecholamines 4-reduce excitability and rhythmicity (without reducing contractility) 5-produce "use-dependent" block
what is use dependent block
so first impulse gets through but impulses generated rapidly after first impulse are blocked
is it hard to reduce excitability and rhythmicity without reducing contractility
yes because they are intimately linked
how do doctors choose which antidysrhythmics to give the patient
its empirical - based on experience not so much theory
why can antidysrhythmics create more issues
because precise rates and routes of conduction determine cardiac function, any type of disturbance easily promotes arrhythmia
how do you want to best treat supraventricular dysrhythmias +what drug is best
increase AV block
something like propranolol
how do you want to best treat ventricular dysrhythmias
best to preserve AV conduction to increase chance of sinus rhythm taking over
what is another name for cardioversion
defibrillation
what is another name for defibrillation
cardioversion
why can defibrillation be better than antidysrhythmics drugs
because all antidysrhythmics have effects on other tissue that produce undesirable side effects
why can cardioversion be better than antidysrhythmics drugs
because all antidysrhythmics have effects on other tissue that produce undesirable side effects
what is an example of an undesirable effect of antidysrhythmics
lidocaine is a CNS depressant
what can general anesthetics do to dysrhythmia
sensitive the myocardium to catecholamines (like beta1 adrenergics), which could cause a dysrhythmia
who classified the antidysrhythmic drugs
vaughan-williams
how did vaughan-williams base his drug classes
in vitro electrophysiological effects (in glass/ test tube)
what do class 1A drugs do GENERALLY
membrane stabilizers which prolong refractory period
what drug is a class 1A
quinidine
what is quinidine
class 1A
how do patients typically use quinidine
prophylactically for atrial and ventricular dysrhythmia
what do class 1A do to refractory period
increase
how does quinidine work
blocks na+ and k+ channels
what does quinidine do to threshold
increases
how does quinidine slow rate of rise of Na+ dependent phase 0
use dependent effect
how does quinidine effect phase 4
decreases slope (Na/K dependent)
what are some off target effects in all class 1A agents
anticholinergic (like atropine)
-independent of antidysrhythmic action
which drugs have anticholinergic effects that are independent of antidysrhythmic action
class 1A agents
what does quinidine do to conduction velocity
decrease
what does quinidine do to automaticity
decrease
what does quinidine do to action potential duration
increase
what does quinidine do to QT interval
increase
what does quinidine do to refractory period
increase
what does quinidine do to one-way conversion blocks
abolished re-entry - turns it into a two way block
what does quinidine do to contractility and HOW
decrease via negative ionotropic effect
what is the negative inotropic effect
SA node slows sinus rate, GIRK channels hyperpolarized Sa node, decrease slope in phase 4
what happens with block by quinidine with more activity
increases the degree of block
what do class 1B drugs do GENERALLY
membrane stabilizers which shorten refractory period
what is an example of 1B drug
lidocaine
what class is lidocaine
1B
when is lidocaine used
emergency treatment of ventricular dysrhythmias
how does lidocaine work
blocks Na channels
what does lidocaine do to threshold
increase
what does lidocaine do to phase 4
decreases rate of rise of NaK dependent phase 4 pacemaker
what does lidocaine do to phase 3
shorten
what does lidocaine do to phase 0
slows rate of rise ONLY IN DAMAGED TISSUE
how does lidocaine affect phase 0
use dependent effect - inactivated state blocker
what does lidocaine do to ECG in healthy people
little effect
what does lidocaine do to automaticity and where
decreases automaticity and especially in purkinje fibres
what does lidocaine do to automaticity
decreases automaticity and especially in purkinje fibres
does lidocaine have the same effects on healthy and ischemic tissues
no
what does lidocaine do to one way block and where
converts it into a two way block in ischemic tissue
what does lidocaine do to one way block
converts it into a two way block in ischemic tissue
what does lidocaine do to ADP
decrease
what does lidocaine do to ERP
decrease
why do you use lidocaine if it decreases ADP and ERP
because its still a really good antidysrhythmic
what do class 1C drugs do GENERALLY
membrane stabilizers which do not affect refractory period
what is an example of a 1C drug
flecanide
what is flecanide
1C
when do you use flecanide
prophylaxis of atrial dysrhythimas
what does flecanide do to phase 0
slows rate of rise
what does flecanide do to APD
nothing
what does flecanide do to ERP
nothing
what does flecanide do to ventricular dysrhythmias
worsen
what are class 2 drugs GENERALLY
anti adrenergics and membrane stabilizers
what are 2 examples of class 2 drugs
propranolol and acebutolol
what is acebutolol
b1 blocker, class 2
how are class 2 drugs used
in adjunct to other therapies
what 4 catecholamine effects to anti-adrenergics antagonize
1-delayed afterdepolarizations
2-purkinje fibre automaticity
3-increased AV conduction
4-shortened ventricular AP
what do class 2 do to delayed afterdepolarizations
stops them
what do class 2 do to purkinje fibre automaticity
reduce
what do class 2 do to AV conduction
decrease
what do class 2 do to ventricular AP
increase
what 3 situations are B blockers contraindicated
severe heart failure
asthma
dysrhythmias with AV block
why dont you use B blockers in dysrhythmias with AV block
because beta blockers already decrease AV
which class of drugs is beta blockers
2
what do class 3 drugs do GENERALLY
prolong ADP and ERP, no effect on rise time
what is amiodarone (class)
class 3
what is sotalol
b blocker AND class 3
what are examples of class 3 drugs
amiodarone and sotalol
how does amiodarone work
thyroxine antagonist which prolongs refractory period
what is the duration of action for amiodarone
long, more than 30 days
what does sotalol do to heart AP
prolongs the ERP and APD
what kind of beta blocker is sotalol
non selective
why would amiodarone be a thyroxine antagonist/ what is this good for
thyroxine usually juices things up, so its an antagonist so it will downregulate the sympathetic effects
what are class 4 drugs GENERALLY
slow channel blockers
what are 2 class 4 drugs
verapamil and diltiazem
what kind of dysrhythmia are class 4 drugs good for
supraventricular dysrhythmias (not ventricular)
are class 4 drugs good for ventricular dysrhythmias
noooo
how do class 4 drugs work
cardioselected L-type calcium channel blocker to block AV conduction
what are the 2 main types of class 5 drugs
cardiac glycosides and adenosine
what is an example of cardiac glycosides
digoxin
what is another name for the cardiac glycosides
digitalis glycosides
what is the therapeutic action of cardiac glycosides
decrease conduction through the AV node
what class is diltiazem
4
what class is verapamil
4
what class are cardiac glycosides
5
what class is adenosine
5
where does adenosine occur naturally
in blood
what does adenosine do to the heart
decrease sinus rate and decrease AV conduction
what are the electrophysiological effects of adenosine similar to
ACh
what do class 6 drugs do
enhance vagal activity
what are “channelopathies”
individuals with genetic disorders with mutations in cardiac potassium channels
what are 3 types of people with long Q-T syndrome
people with “channelopathies”, some diabetics and people with cardiovasc disorders
what does long Q-T mean/entail
prolonged ventricular action potentials
what can long Q-T syndrome cause
fatal dysrhythmias
can people with long Q-T take sotalol and why
no becaus it increases refractory period
why do people with long Q-T have to be careful with lots of drugs
because lots of eve non-cardiovasc drugs can precipitate long Q-T in susceptible individuals
how can fibres with long Q-T cause dysrhythmias
if they are adjacent to fibres with normal refractory period, they can be re-excited by the fibre with a long refractory period
