DPT II Exam 6

ion movement produced currents that form

action potential

what do voltage gated/ion gated channels prevent

free diffusion

phase 4 SA Node

the cell undergoes spontaneous depolarization (pacemaker potential) which triggers an action potential once the membrane reaches between -40 and -30mV

hypocalcemia

prolongs the QT interval

hypercalcemia

shortens the QT interval

channelopathies

inherited arrythmogenic disease, autoimmune or inflammatory K channelopathies or long QT syndrome or short QT syndrome

catecholaminergic polymorphic ventricular tachycardia

involve multiple genes and ion channels

disturbance in impulse formation

increases automaticity and causes afterdeoplarizations

disturbance in impulse conduction

blocks in conduction, unilateral blocks

a phase of myocytes action potential characterized by slow inward calcium current

phase 2

abnormal impulse conduction tachyarrhytmia

reentrant

torsades de pointes is an example of

afterdepolarizations

abnormal impulses generation tacchyarthmias

automatic

an ECG wave that represents signal travels through venticrles

QRS

activates acetylcholine-sensitive potassium current in atrium

adenosine

phase of SA node action potential characterized by potassium moving out of the cells

repolarization.

block the repolarizing K current and prolong AP duration

dofetilide

an ECG wave that represents ventricle contraction

RST

a phase of myocytes action potential characterized by slow Na influx and slowing of K outflow

phase 4

phase 0 SA node

this is depolarization phase where action potential is initiated

phase 3 SA node

cell repolarizes and once it reaches around -60mV, the cycle starts again

t type

pacemaker ca channel (in SA node)

Phase 0 (myocytes)

rapid depolarization (inflow of Na)

phase 1 (myocytes)

partial (early) repolarization. (inward Na current deactivated, outflow of K)

phase 2 (myocytes)

plateau (slow inward calcium current) triggers contraction

phase 3 (myocytes)

repolarization (ca current inactivates, k outflow)

phase 4 (myocytes)

resting membrane potential

L type

non pacemaker ca channel in myocytes

ECC

process where an action potential triggers a myocyte to contract followed by a subsequent relaxation

p wave

atrial depolarization

PR interval

wave and segment, current moves from SA node to AV node (atrial contract)

QRS complex

signal travels through ventricles ventricular muscle depolarization

RST interval

ventricles contract

t wave

repolarization of ventricles

QT interval

reflects the duration of the ventricular action potential

what is flecanide C/E in

MI

what drugs do we use for class IV HF rhythm maintenance

amiodoorone or dofenilide

what do we do as a first line therapy in acute SVT

adenosine or vagal maneuvers

if the adenosine is unresponsive, what do we give next in SVT

diltiazem, verapamil, BB

catheter ablation is used in

rhythm control (afib) / recurrent fib

how do we tx sustained VT with pulse

amiodorne, procanimde, lidocaine

how do we tx non sustained VT with symptoms

BB

how do we tx symptomatic PVC

B blockers and reduce catecholamines

how to tx 2nd and 3rd degree AV block

atropine, dobutamine, dopamine, pacemaker

mobitz 1

PR gets increasingly longer until depolarization

mobitz 2

consistent PR with occasional non conducted depolarization

sinus bradycardia tx

atropine, pacemaker, B agonist

effect of quinidine that has tinnitus, blurred vision, flushed skin

cinchonism

which classes are used for ease control of supra ventricular arrhythmia

class II and IV

which class of antiarrythmics has the greatest effect on QTc interval

class III

most efficacious atiarrythmic

amiodorne

atropine MOA

antimuscaranic, comp antagonist of acetylcholine, direct vagolysis (decreases PR)

ivabradine MOA

sinus node inhibitor, blocks HCN channel responsible for the if current

adenosine moa

binds puringeric G protein receptors (flat line tx)

digoxin MOA

vagal stimulation, blockade of Na/K ATPase pump, increases PR

dofretilide drug interactions

HPCVTMKZ

HCTZ

Prochloprerazine

cimetidine

verapamil

TMP

Megestrol

ketoconazole

zoprasidone

rate controlling drugs

control the ventricular rate in pts with supraventricular tachyarrythmias

rhythm controlling drugs

to convert or maintain normal sinus rhythm

if you decrease PR

you increase HR

EAD

phase 3 (Na opens)

DAD

phase 4 (ca release= digoxin tox)

class Ia act on

supra ventricular and ventricular

class Ib acts on

only ventricular

class Ic acts on

supra ventricular and ventricular

class II

supraventicular

Class IV

supraventricular