9/29 Narrow complex Tach- treatment

what mechanism is responsible for the following rhythms

PSVT (PAT, PJT)

Non-p tachycardias

A flutter

A fib

sinus tach

PSVT (PAT, PJT)- Av nodaln reenty

Non-p tachycardias- enhanched automaticity/ttiggered activity

A flutter- atrial reentry at one site

A fib- atrial reentry at many sites

sinus tach- compensatory

4 components of perfusion that should be evaluated first with any patient with signs of poor perfusion

rate problem

pump problem

volume problem

PVR problem

when is it NOT a rate problem (at least on paper)

heart rates less than 150 or greater than 50. If symptoms exist, it is likely a compensation for something else.

PSVT vs sinus tach

PSVT

150 or greater

absent or abnormal p waves

rate does not vary

abrupt onset

ST

less than 150

p waves normal

rate varies

gradual onset

S/S of unstable

Acute changes in mental status

SBP <90mmHg

s/s shock

acute pulmonary edema

ischemic chest pain

how does the vagal mauever actually work

increases inta-amdominal pressure which increases aortic pressures which are sensed by baroreceptors. Parasympathetic tone is increased which slows HR and conduction through AV node

Methods for doing vagal maneuver vs modified vagal

cough, bear down, blow through straw/syringe, push hand off abdomen, ice to brow or bridge of nose

for 15 seconds

Modified vagal- same as above steps with inclusion of lowering patientto supine and raising their legs immediately

what are the interventions we can use for SVT

VOMIT

VADMV

Vagal

Adenosine

dilltiazem

motoprolol

Verapamil

cardiovert if unstable

• If they have chest pain w/o hypotension, you MAY consider a drug first.

how do the following help with narrow complex tachy

cardioversion

valsalva

adenosine

metoprolol/deltiazem/verapamil

cardioversion- short acting termination of reentry anywhere in the heart

valsalva- short acting termination of reentry through the AV node

adenosine-short acting termination of reentry through the AV node

metoprolol/deltiazem/verapamil - long acting termination of reentry in atria and AV node. Rate control by decreasing AV node conduction thus decreasing impulses conducted from atria to ventricles, thus decreasing hr.

a fib/flutter treatment if longer than 48 hours and explain why

stable- monitor them

unstable- cardiovert

we only shock if unstable because clots may form in the atria. termination could cause emboli to circulate. Anticoagulation therapy should ne completed first. However, if they are unstable, the benefits outweigh the risks.

synchronized cardioversion steps for zoll and lifepack

hit “sync” (must do this each time)

zoll 100-120-150-200

lifepack 100-200-300-360

stay at level that was effective if it reoccurs

what level do we start at for a fib to cardiovert? Why

120 joules because there are lots of pacemakers

STABLE scenarios format

V- stable

O- maintain

M- interpret (SVT)

I- Establish Iv access, NS TKO

T- 12 lead- Now

vagal maneuvers

adeonsine 6mg IVFP, repeat x2@ 12 mg q 1-2 mins

diltiazem- 0.25mg/kg IV over 2 mins., rpt. x1 @ 0.35mg/kg q 15

Metoprolol- 5mg IV over 1-2 mins., q 5 , 15 mg max

verapamil- 2.5-5 mg IV over 2 min., rpt @ 5-10 mg q 15-30 min.

Unstable scenarios format

V- Unstable

O- depends on scenario

M- interpret rhythm

I- Establish IV access, NS TKO

T- later

consider sedation

cardiovert 100-360J (120-360 if irregular)

what should be included in the drugs section on scenarios

dose, route, rate, repeat

WPW syndrome

LGL syndrome

there is an accessory pathway called the bundle of kent in the left ventricle that signals can pass through. Bc part of the LV starts depolarizing early (before AV node finishes the delay), their is a ramped appearence- the delta wave. We dont wanna give certain meds like diltiazem to them in tachydysrhythmias bc it completely shuts off the AV node and then all the signals go to the accessory pathway. This could put the heart into vtach or v fib

LGL is similar but the accessory pathway is closer to normal pathway so no ramp, just a shortened PRI.