30 - arrhythmic drugs Flashcards
movement or procedure with uniform or patterned
recurrence of a beat, accent, or the like
rhythm
Heartbeat is irregular, too fast, or too slow
cardiac arrhythmia
in atrial fibrillation, the tracing shows tiny, irregular “fibrillation” waves btw heart beats
the rhythm is irregular and erratic
Contraction of _
ventricle sends O2
depleted (and CO2
rich) blood to the lungs.
Contraction of the _
ventricle sends O2
rich blood to the other tissues.
Electrical signals
coordinate cardiac
muscle contraction
right ventricle - O2 depleted and CO2 rich
left ventricle - O2 rich to other tissues
the sum total of action potentials traveling
through the heart creates the _
EKG
Diagnostic components of the EKG
_ reflects
depolarization of SA
node
P wave
Diagnostic components of the EKG
_describes the time it takes for the
impulse to travel from sinus node through AV node
PR interval
Diagnostic components of the EKG
_ reflects depolarization of right and left ventricles (lots of muscle mass, big signal).
QRS complex
Diagnostic components of the EKG
_ segment Ventricles depolarized
ST segment.
J point - ventricles depolarized - J point is important because it is the start of the ST segment. The J point must be assessed for:
absolute position: it can be elevated or depressed
shape: it can be notched or slurred
Diagnostic components of the EKG
Repolarization
of ventricles
T wave.
Diagnostic components of the EKG
repolarization of
interventricular
septum.
U wave
Four main types of arrhythmias Extra beats Supraventricular tachycardias Ventricular arrhythmias bradyarrhythmias
extra beats - Premature atrial contractions, Premature ventricular contractions
supraventricular tachycardas - Atrial fibrillation
Atrial flutter
Paroxysmal supraventricular tachycardia
ventricular - Ventricular fibrillation
Ventricular tachycardia
bradyarrhythmias - less than 60bpm
Classification of arrhythmias by _ Atrial Junctional Ventricular AV Heart blocks (atrioventricular node)
site of origin
_ arrhythmia
Conduction between the atria and ventricles is blocked or slowed
PR interval lengthened beyond 0.2 seconds
primary AV block
200msec or longer
_ arrhythmia
Conduction between the atria and ventricles is blocked or slowed
Disturbance, Delay, Interruption of atrial
impulse conduction through the AV node to the ventricles
PR interval - 0.12-0.2sec
secondary AV block
2,3,or 4 P wave before each QRS
PR interval - 0.12-0.2sec - little delay
QRS <0.12s
_ arrhythmia
Conduction between the atria and ventricles is blocked or slowed
aka complete heart block. Impulse generated
in SA node does not propagate to the ventricles.
tertiary AV block
none of the pwaves conduct to ventricles (P-P and QRS-QRS are independent)
cardiac arrhythmias result from disorders of impulse _ or impulse_ or both
disorders of impulse formation or
impulse conduction or both
causes of arrhythmias ~cardiac ischemia ~excessive discharger or sensitivity to autonomic transmitters ~exposure to toxic substances ~unknown ?
_ puts little delay on the wave on Ap’s thru heart
AV node
atrial first then ventricles
sum total of AP’s traveling thru heart - but at different times
ECG/EKG
if patient has an arrhythmia
Can always be a secondary problem of _ - when blood isn’t moving smoothly thru system
clotting
4 classes of drugs for arrhythmic drugs
Class 1 - block Na channels
Class 2 - beta anatagonists
Class 3 - prolong AP and refractory period
Class 4 - Ca channal antagonist
which phase of heart
1 - phase 0, depolarization Na coming in
2 - phase 4 - resting potential K+
3 - between phase 1 and 3 - working on K channels
4 - phase 2 - blocking Ca
phases of cardiac AP
0-4
0- Na coming in steep rise 1 - K+ and Cl- out 2 - Ca++ in K+ out 3 - K out 4- resting potential
Class 1 antiarrhythmic drugs block _
block Na channel
Drugs with intermediate lengths bind to Na channels - not shutting down but tweaking enough to cause little change
When injecting Lidocaine - we block entire Na channel and prevent AP all
We are tweaking the depolarization (Na channel) and changing AP stop
Class 1 Na channel blockers
Lengthen duration of action potential.
Bind more selectively to the open state of the channel.
Dissociate from channel with intermediate kinetics.
class 1 A
increase QRS and QT
Class 1 Na channel blockers
Shorten duration of action potential.
Bind primarily to inactivated state of
the channel.
Dissociate from the channel with rapid kinetics.
class I B
decrease QT
Class 1 Na channel blockers
Minimal effect on duration of action potential.
Bind more selectively to the
open state of the channel.
Dissociate from channel with slow kinetics.
class 1 C
increase QRS duration most
which ABC of class 1 antiarrhythmic drugs
Procainamide. Effective against atrial and ventricular arrhythmias.
Frequent dosing (t1/2 = 3 hrs) limits its utility. Can produce lupus like
symptoms.
class 1 A
Lengthen duration of action potential.
Bind more selectively to the open state of the channel.
Dissociate from channel with intermediate kinetics
which ABC of class 1 antiarrhythmic drugs
Lidocaine. One of the less toxic antiarrhythmic drugs. Used in
conjunction with arrhythmias associated with myocardial
infarctions. Very short t1/2. Administered by infusion
class 1 B
Shorten duration of action potential.
Bind primarily to inactivated state of
the channel.
Dissociate from the channel with rapid kinetics
which ABC of class 1 antiarrhythmic drugs
Flecainide and Propafenone. Used to treat supraventricular arrhythmias
class I C
Minimal effect on duration of action potential. Bind more selectively to the
open state of the channel. Dissociate from channel with slow kinetics.
class _(1-4) of antiarrhythmic drugs diminish phase 4 depolarization, thus depressing automaticity, prolonging AV conduction and decreasing HR and contractility
class 2
beta-adrenergic antagonists
beta 2 atagonist if heart is beating too fast
how do class 2 betablockers work
they can diminish both _ and _ currents
diminsh both Na and Ca
phase 4 of the cardiac AP
which receptor
- increase force of heart contraction, increase rate of contraction, excessive stimulation leads to arrhythmias
beta 1
what kind of beta adrenergic drug do we use if that patients heart is beating too fast
beta 2 antagonist
class _ antiarrhythmic drugs
block potassium K+ channels and thus prolonging AP
delayed repolarization
class 3 K+ channel blockers
in contrast to the sodium-channel blockers, _ and _ drugs are increasing in use
class 2 - Beta blockers and class 3 K channel blockers
Class _ antiarrhythmic drugs
block Ca++ channels
decrease inward Ca current, decreasing rate of phase 4 spontaneou depolarization
slow conduction in tissues dependent on Ca current (AVnode)
MAJOR EFFECTS ON VASCULAR SM AND HEART THOUGH
class IV blocking Ca channels
major systemic effects though
slow conductiong and increase refractory period
verapamil
