3-cardio Flashcards by Angelica J

what are 4 causes of dysrhythmia

delayed after depolarization
abnormal pacemaker activity
heart block
circus movement/ re-entry

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what can cause delayed after depolarization

catecholamine action or digitalis toxicity (ca2+ overload)

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what can cause abnormal pacemaker activity

altered autonomic effects or long QT syndrome

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what is heart block/ what can cause it

conduction block of AV node

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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

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draw the circus movement pathway

yes

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what do you want to do to the refractory period to reduce circus movement

increase refractory period (so it cant double back)

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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

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what is use dependent block

so first impulse gets through but impulses generated rapidly after first impulse are blocked

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is it hard to reduce excitability and rhythmicity without reducing contractility

yes because they are intimately linked

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how do doctors choose which antidysrhythmics to give the patient

its empirical - based on experience not so much theory

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why can antidysrhythmics create more issues

because precise rates and routes of conduction determine cardiac function, any type of disturbance easily promotes arrhythmia

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how do you want to best treat supraventricular dysrhythmias +what drug is best

increase AV block

something like propranolol

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how do you want to best treat ventricular dysrhythmias

best to preserve AV conduction to increase chance of sinus rhythm taking over

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what is another name for cardioversion

defibrillation

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what is another name for defibrillation

cardioversion

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why can defibrillation be better than antidysrhythmics drugs

because all antidysrhythmics have effects on other tissue that produce undesirable side effects

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why can cardioversion be better than antidysrhythmics drugs

because all antidysrhythmics have effects on other tissue that produce undesirable side effects

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what is an example of an undesirable effect of antidysrhythmics

lidocaine is a CNS depressant

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what can general anesthetics do to dysrhythmia

sensitive the myocardium to catecholamines (like beta1 adrenergics), which could cause a dysrhythmia

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who classified the antidysrhythmic drugs

vaughan-williams

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how did vaughan-williams base his drug classes

in vitro electrophysiological effects (in glass/ test tube)

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what do class 1A drugs do GENERALLY

membrane stabilizers which prolong refractory period

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what drug is a class 1A

quinidine

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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

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

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

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

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

what class is verapamil

what class are cardiac glycosides

what class is adenosine

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