cardiac conduction basics, supravent tachy, etc-- V FIB

list conduction pathway

sa node— av node—bundle of his— bundle branches— perkinje

sa node rate

60-100 bpm

av node rate

40-60 bpm

purkinje system rate

30 -40 bpm

what is p wave represent

atrial depolarization

what does qrs wave represent

ventricule depol

what does T wave represent

vent repolar

what are the subjective measures of v fib

dyspnea, fatigue, dizzy, angina, chest pressur,e etc

what are some objective measures of v fib clinical history

tachypnea (fast breathing), tachycardia, labile BP, cardic death

what does vagus manuevers mean

carotid sinus can

–Valsalvais mean doht what does

reset vagus nerve

• act like going to poop

• flushed face

supposed to reset PNS/stimualte ACh

dose/admiinistration of adenosine

6 mg RAPID iv line via peripheral line

• followed by rapid saline flush

adenosine is half life short or long

short— like 3 seconds or smth

if giving adenosine in central line what is dose

3 mg

if adenosine doesnt work what is dose

12 mg

adverse effects of adenosine

chest pressure/discomfort— impending doom

prolonged systole (flatline for a smidge— if its over 6 seconds need to do CPR)

HA

flushing

what are signs of hemodynamic instability

• hypotension

• acute altered mental status

• signs of shock

• ishcmiec chest discomfort

• acute heart failure

so if vagal maneuvers don’t work and pt is hemodynamically unstable what give

direct current cardioversoin

if hemodynamics stable and QRS is narrow what give

• BB

• ndhp ccb

what is third line if adenosine, BB, and ndhp ccb don’t work for narrow QRS (NCT— narrow complex tachy)

• amiodarone

• digoxin

what are the two types of wide QRS complex

regular — needs adenosine or antiarrythmic

irregular— procainamide, amiodarone, sotatol

class for procainamid

class 1a antiarr

procainamide CI

• avoid in strucutral heart disease

• relies on kidneys AND liver for elimination

• can develop lupus like symptoms, blood dyscrasias, etc

procainamide MOA

Na channel blockers

• 1a is prolonged refractoriness

amiodarone moa

class 3 antiarry

• block K channels

• but has effects of like everything

how long give procainamide to

• arrhthmia stops

• hypotension cocurs

• QRS increase by more than 50%

• max dose of 17 mg/kg given

heart failure is basically a CI— no in structural heart disease

amiodarone can you use in heart failure

safe in HFrEF

DOC for v fib with heart failure

amiodarone

what is drawback to amiodarone

SO MUCH AD EFF

• gi

• hep tex

• blue skin

• optic tox

• thyroid destroyed

• myopathys

• cardiac tox

sotalol class

class 3 anti

• K channel blocker

• with some beta blocker effects

how is sotalol elminated

renal

which drug has hugeeee torsades (TdP) risk

sotalol

can you use sotalol in MI and HFrEF

nope

answer to slide 29

B— adenosine first line for ALL svt

answer to slide 30

b

what are the diseases associated with sa node dysfunction

• Sinus bradycardia, sinus pause, ectopic atrial bradycardia

• Tachycardia-bradycardia syndrome

• Chronotropic incompetence

av blocks associated with what diseases

• first degree

• second degree (type 1 and 2)

• third degree

conduction tissue disease is associated with

• bundle branch blocks

• either right or left side

• complete or incomplete

what can CAUSE bradycardia

• sa node disease

• increased PNS tone

• drugs

what drugs rly a probelm for causing av blocks

beta blockers

calcium channel blockers

how does av block present on EKG

prolonged PR interval

• rate varies, rhythm is normal

what is the first type of second degree AV block caused by and what called

mobitz type 1

• caused by PNS tone and drugs

• “wenkebach“

how does mobitz type 1 (wenkeback) present

pr interval gets progressively longer until you drop the beat

• longer longer longer DROP thats called a wenkebach

av block second degree is what mobitz type 2 look like

• pr can be normal or not

• caused by organic lesion in conduction pathway

av block third degree causes

extensive conduction system disease

third degree presentatoin

• qrs interval is wide

• pr can vary

• atrial and ventricular rates dissociated,

• vent rate is slow

how is av blocked treated

remove reversible causes

list some anti-HTN that cause av block

• bb

• clonidine

• ndhp cc

what are some antiarr that can cause av block

• adenosine

• amiodarone

• disopyramide

• dronedarone

• flecainde

• procainamide

• propafenone

• quinidine

• sotalol

what are some antidep that cause av block

• citalopram

• escitalopram

• fluoxetine

AChI that cause av block

• donepezil

• neostigmine

• physostigmine

• pyridostigmine

a

antiPlt that cause av block

• dipyridamole

• ticagrelor

anesthetic what can cause av blocks

bupivaciaine

propofol

first line for av block w/ symptoms

iv push atropine

second line after atropline for av block

cont infusion of epi or DA

what use for av block if on bb or ccb

glucagon

what is antidote for digoxin od that causes av block

digifab

atropine dose

1 mg IV push every 3-5 min

• max dose 3 mg

w

what is max dose atropine

3 mg

when atropine no work

• heart transplant

• second or third degree av block

MOA isoproterenol

beta-1 AND beta-2 ag

• iv infsion

• not a treatment of choice

glycopyrrolate MOA

reverse vagal reflexes taht can cause bradycardia by blocking acetylcholine

• antiAch effects

answer for slide 47

c, a

answer for slide 48

c

which temporary cardiac pacing often used after cabg

transvenous

Ventricular fibrillation (VF)

what is sudden cardiac arrest

sudden cessation of cardiac activity where pt unresponsive

• guppy breathing

what is sudden cardiac death

sudden unexpected death from heart stopping

what are the types of ventricular arrhythmias

• non sustained or sustained ven tachy

• torsades

  • v fib

risk factors for v arrs

• cad

• long qt’s

• hyperlipid

• HTN

• cardiomyopathy

• LV hypertrophy

• obesity t2dm

• genetic

• tobacco, ilicit drugs

where can palpitations be felt

chest throat or neck

• these pts stable

if unstable what are manifestations

• syncope

• v fib

• sca

• scd

treat like in cardiac arrest

how treat v fib when unstable

cpr if no pusle

defibriliation still otherwise

v fib tachy how present

wide qrs that all look same

• no p waves

polymorphic v tachy how present on ekg

many foci are depolarizing so the wide intervals are not uniform

what is torsades a subset of

polymorphic v tachy

risk factors for post-MI shock

• age > 70 ye4ars

• symptoms < 12 hours with stemi

• sbp < 120 mmHg

• HR >100 bpm

if have these cannot give BB for secondary prevent

proph for vent arrhythmias

• beta blockers have shown reduction in moratlity both primary and secondary

  • UNLESS have risk factor for post-mi shock

• optimzie GDMT for HF and CAD, ascvd

do you use iv lidocaine to PREVENT VT

no — but can be used for treatment

CAST Tiral provided which drugs showed should not be used to treat

encainide or flecainide

what williams-vaughn classes can we use for treating v tachy

• all of class 3

• amiodarone or sotatlol (class 2)

• classes 1 and 4 not recommended

answer to slide 21 on second deck

b (beta blockers)

HUGE ci to amiodarone

do. not. push. amiodarone in pts that have a pulse

what are class 1a agents used for

to get things under control— not long term effects

which class 1a has antiAch effects

disopyramidine

which class 1a does not have interchangable salt forms and can cause drug induced lupus

quinidine

which class 1a increases dig levels

quinidine

what kind of antibiotics can quinidine not be used with

quinolone antibiotics

procainamide what is its metaboilte and what is its probelm

NAPA; problemn in renal imparitment