EMRESIDENT

Lessons in Emergency Medicine

[emresident]

Transvenous Pacing, other tips and tricks

Which site? Right IJ or Left subclavian. Prefer Right IJ so that the Left subclavian can later be used for a permanent pacemaker. 

Pacer generator setup: the pacer has 2 sterile wires (the generator has 1 nonsterile wire). The proximal (shorter) wire inserts into the positive port (Proximal = Positive). The longer wire (distal) inserts into the negative port  

set to demand

turn rate to 30 bpm greater than intrinsic rate - often ~ 80

Sensitivity = 0 

set initial current high: 20-25 mA

Insert the Cordis

Insert the pacer wire: Put the swan sheath (the plastic sterile thing) on first. 

insert wire to 20cm

inflate balloon with 1.5cc of air 

advance (with the balloon up) observing ECG for changes in ECG morphology and capture of pacing rate (direct wire to RV apex)

approximate depth 35-40cm

once pacing captured deflate balloon

then decrease mA to find threshold - then double (usually this is ~ 5mA)

secure. Extend swan sheath (plastic sterile thing) and lock onto cordis hub

[emresident]

transvenous pacemaker, video 2

[emresident]

Technique for inserting transvenous pacemaker. 

[emresident]

Very basic transcutaneous pacing video (with lifepack) 

[emresident]

Transcutaneous Pacing

Indications: symptomatic bradycardia (3rd degree, sinus, mobitz 2 + unstable), overdrive pacing.

How to:

-place pads (anterior and posterior)

-set to demand (if the following steps fail to capture/pace, then try “fixed” mode)

-choose rate ~20-30 above intrinsic, often start at 80

-Increase mA as needed to achieve capture.

     -if arrest situation, set mA at max setting and then decrease

     -otherwise, set at 70, increase until capture is achieved

-when is capture achieved?

     -spike then wide QRS

     -increased pulse rate, improvement in clinical status

-once capture achieved, increase mA by 5-10.

[emresident]

[emresident]

PTX on CXR

TIPS TO LOOK for

-thin white line (visceral pleural line)

-then no lung markings (looks black) distally or peripherally (air in pleural cavity)

-deep sulcus sign 

-may see more clearly in expiratory film (normal lung gets smaller, ptx lung does not)

tension pneumothorax

tracheal deviation

heart/mediastinal shift 

diaphragm (on side of ptx) is depressed

[emresident]

Reflexes

General principles:

How a refex works

strike tendon --> stretch fibers --> sensory nerves --> spinal cord --> lower motor neuron --> muscle 

Grading of reflexes

0 - no movement

1 - decreased but present (hyporeflexic)

2 - normal

3 - increased (hypereflexic)

4 - clonus: 1 stimulation, repetitive shortening of muscle

reflexes - to cover this week

achilles

patellar

biceps

brachoradialis

triceps

babinski / Hoffman

[emresident]

Bundles, LAFB, and LPFB

[emresident]

LAFB, LPFB

LAFB

What is happening?

left bundle branch composed of  left anterior fascicle and left posterior fascicle

LAFB - anterior fascicle blocked

initial impulse downward and rightward, then upward/leftward

EKG:

-left axis deviation (+I, -avF, -II)

-look at II, III, avF: rS (small r, deep S)

-look at I, avL: small q waves, tall R waves

-avL: prolonged R wave to peak time

-increased QRS voltage in limb leads

-slight QRS widening (80-110)

LPFB

What is happening?

-initial vector upward and leftward, then vector downward and rightward

-less common than LAFB (many bundles of fibers, more resistant)

EKG

Right axis deviation (-I, +avF)

no RVH, no other cause for Right axis deviation

look at I, avL: rS (small r, deep S)

llook at II, III, avF: small Q, tall R. Also prolonged R wave to peak time  in avF

QRS normal or slightly prolonged (80-110)

increased QRS voltage in limb leads

Bifascicular block

Technically LBBB = bifascicular block as both fascicles are blocked

RBBB + LAFB (RBBB + LAD)

OR RBBB + LPFB (RBBB + RAD)

significance - conduction to ventricles from 1 remaining fascicle

[emresident]

EKG - low voltage

definition = QRS <5mm in all limb leads OR QRS <10mm in all precordial leads

Ddx

pericardial effusion

pleural effusion

obesity

infiltrative cardiac disease

myxedema

obesity

severe COPD

previous massive MI

severe cardiomyopathy

[emresident]

Ddx Hypotension

-cardiac (tachycardia, bradycardia, arrhythmia, decreased contractility, ischemia, valvulopathy)

-hypovolemia (dehydration [vomiting, diarrhea, poor po intake, diuresis, hyperglycemia, hyperthermia, pancreatitis, burn], hemorrhage [chest, abdomen, retroperitoneum, GI]

-obstruction (tension ptx, cardiac tamponade, pe, lung hyperinflation)

-decreased arterial tone (sepsis, anaphyalxis, neurogenic shock)

-metabolic etiology (adrenal insufficiency, hypo/hyperthyroid, hypoCa)

-toxicologic (CCB/BB, opiates/sedatives, TCA)

[emresident]

CORONARY ARTERY ANATOMY

from Smith, The EKG in Acute MI: An Evidence Based Manual of Reperfusion Therapy.

[emresident]

Wellens Syndrome

Definition: deeply inverted or biphasic T waves V2-V3, specific for LAD stenosis

Nuances

See characteristic T waves in V2-V3 but may extend V1-V6

ST segment normal

normal R wave progression V1-V6 / no precordial Q waves

often patient’s have history of chest pain/angina, but you see these EKG findings when they are pain-free

(be wary of Wellen’s mimic in young men - see high voltage EKG, “fish hook” then concave ST with sudden drop to T)

Pathophysiology

sudden occlusion of LAD - chest pain! anterior STEMI (but often don’t capture on EKG)

reperfusion of LAD, chest pain resolves, ST elevation improves, T waves become biphasic/inverted

however if reperfusion unstable, LAD may reocclude (T waves pseudonormalize, go from biphasic/inverted to upright) and if LAD remains occluded, will develop anterior STEMI

2 types

type A/type II Wellens: biphasic

type B/type I Wellens: inverted 

Treatment

cath lab (don’t do exercise stress)

[emresident]

[emresident]

SVT

Tachycardia + narrow complex + regular

DDX = sinus tachycardia, SVT, Atrial Flutter 2:1 

sinus tachycardia - P waves (upright in I, II, III, avF, downward in avR)

maximum sinus rate 220-age

SVT - no P or inverted. VERY regular.

may see ST depression in inferior/lateral leads that will resolve when rate controlled 

A flutter 2:1 - think when HR ~ 150

TYPES of SVT 

orthodromic 

down AV node and up accessory pathway

narrow complex 

rx: procainamide (decreases conduction through accessory pathway), amiodarone, cardioversion 

antidromic 

down accessory pathway, up AV node

wide complex 

WHAT ABOUT WPW

classic EKG findings = short PR***, wide QRS, delta wave

some electricity through AV pathway, some through accessory pathway (no pause through accessory pathway - therefore delta wave) 

TREATMENT

vagal maneuvers

infant - ice on the face 

toddler - 

adult - valsalva 

adenosine 

transient AV nodal block (A1R receptor, decrease cAMP)

6 mg then 12 mg

go up on the dose of patient has NO response to 6mg

if adenosine terminates tachycardia then tachycardia restarts, then it doesn’t make sense to go up on the dose, can give another 6mg dose, but you also need to think about doing something else. 

0.1 mg/kg as initial dose in peds

consider 3mg if given via central line, or transplanted heart

consider starting with 12mg if patient on a lot of caffeine 

CCB

diltiazem, verapamil

verapamil second line (if age OK) - AV nodal blocking but less abruptly (give 5 minutes), will last a little longer (1 hour), consider if patient has brief response to adenosine. 

dose = adults, 2.5mg, 5mg, 10mg

peds (>2 -5 years old) = 0.1mg/kg for first dose 

diltiazem 0.25 mg/kg for first dose 

be careful in PEDS 

don’t use < 2 years old (some people recommend not using if <5 years old!)

infants have limited ability to store Ca in sarcoplasmic reticulum, so CCB may cause CV collapse 

Beta Blocker 

don’t use if have already given CCB

cardioversion - 

if unstable

start with 50J in adults 

1J/kg in peds up to 2J/kg 

type IA antiarrhythmics 

procainamide 

ADULT: 20-50 mg/min until 17mg/kg given, maintenance 1-4 mg/min 

PEDS: 15 mg/kg load over 30-60 minutes 

amiodarone 

ADULTS: 150 mg first dose, then 1mg/min for first 6 hours 

PEDS: 5 mg/kg load over 30-60 minutes 

                (don’t give procainamide and amiodarone together)

[emresident]

traumatic cardiac arrest

Evidence of chest/epigastrium trauma - open the chest right away 

Is there a medical component (MI leading to car accident)? - consider ACLS (If no medical cause- no compressions ! ) 

circulation - 

            control hemorrhage (external, pelvic, long bone) + give blood

            tamponade? (Thoracotomy, not needle aspiration), 

tension pneumothorax, needles, chest tubes 

oxygenation (airway)