ACLS Algorithms Slide

8/10/2019 ACLS Algorithms Slide

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Assess responsiveness (speak loudly, gentlyshake patient if no trauma - "Annie, Annie,

are you OK?"). Call for help/crash cart if unresponsive. ABCDs

irway Open airway, look, listen, and feel for

breathing. reathing If not breathing, slowly give 2 rescue

breaths.C irculation

Check pulse. If pulseless, begin chest compressions at100/min, 15:2 ratio. Consider no defibrillator nearby

Defibrillation Attach monitor, determine rhythm. If VF or pulseless

VT: shock up to 3 times. If not, basic CPR.

Then, move quickly to Secondary Survey.
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After initial (primary) assessment done Another set of ABCDs

irway Establish and secure an airway device (ETT, LMA,

COPA, Combitube, etc.).

reathing Ventilate with 100% O2. Confirm airway placement

(exam, ETCO2, and SpO2). Remember, nometabolism/circulation = no blue blood to lungs = noETCO2.

C

irculation Evaluate rhythm, pulse. If pulseless continue CPR,

obtain IV access, give rhythm-appropriate medications

D ifferential Diagnosis Identify and treat reversible causes.


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Treatment Consider bicarb, pacing early

icarb (NaHCO3)

Epinephrine 1 mg IV q3-5 min

tropine 1 mg IV q3-5 min. Max 0.04 mg/kg

Consider possible causesHypoxia, Hyperkalemia, Hypothermia, Drug

overdose (e.g., tricyclics), Myocardial Infarction

Consider termination. If patient had >10minwith adequate resucitative effort and notreatable causes present

Always Primary Survey- Secondary Survey: Confirmrhythm (check monitor, power, different lead)
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Primary Survey

Secondary Survey assess need for airway, oxygen, IV, monitor, fluids,

vitals, pulse ox

12-lead ECG, Consider Dx

If AV block:

2nd degree (type 2) or 3rd degree: standby TCP, prepare fortransvenous pacing.

If serious signs or symptoms, tropine

0.5-1.0 mg IV push q 3-5 min. max 0.04 mg/kg

Pacing

Use transcutaneous pacing (TCP) immediately if sx severe

Dopamine 5-20 g/kg/min

Epinephrine 2-10 g/min
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Primary Survey, Secondary Survey: Is patient

stable or unstable? stable: determine rhythm, treat accordingly unstable

=chest pain, dyspnea, decreased level of

conciousness, low BP, CHF, AMI If HR is cause of symptom (almost always HR>150):

cardiovert

Specific Rhythms Atrial fib/flutter

Narrow-Complex (Supraventricular) Tachycardia Wide-Complex Tachycardia, Unknown Type Stable Ventricular Tachycardia
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Generally not needed for HR150, prepare for immediate cardioversion.May give brief drug trial.

Steps: Prepare emergency equipment

Medicate if possible Cardioversion

monomorphic VT with pulse, PSVT, A fib, A flutter:

100-200-300-360 J* (Synchronized)

may try 50J first for PSVT or A flutter

may use equivalent biphasic (biphasic 70, 120, 150, and 170J)

if machine unable to synchronize and patient critical,defibrillate

polymorphic VT: use VT/VF algorithm


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Management:Control rate, consider rhythm

cardioversion, and anticoagulateas shown below,according to Category: 1, 2 or 3

Category 1. Normal EF

Rate control: Ca-blocker or beta-blocker.

Cardiovert: If onset < 48 hours, consider DC cardioversionOR with

one of the following agents: amiodarone, ibutilide,procainamide, (flecainide, propafenone), sotalol.

If onset > 48 hours: avoid drugs that may cardiovert(e.g. amiodarone). Either: Delayed Cardioversion: anticoagulate adequately x 3 weeks,

then cardioversion, then anticoagulate x 4 weeks

Early Cardioversion: iv heparin, then TEE, then cardioversionwithin 24 hours, then anticoagulate x 4 weeks

Transesofageal ekokardiogram
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Category 2. EF< 40% or CHF

Rate control: digoxin, diltizaem, amiodarone

avoid verapamil, beta-blockers, ibutilide,procainamide (and propafenone/flecainide)


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Category 3. WPW A fib

Suggested by: delta wave on resting EKG, very

young patient, HR>300 Avoid adenosine, beta-blocker, Ca-blocker, or

Digoxin

If < 48 hour:

If EF normal: one of the following for both rate controland cardioversion: amiodarone, procainamide,propafenone, sotalol, flecainide

If EF abnormal or CHF: amiodarone or cardioversion

If > 48 hour

Medication listed above may be associated with risk ofemboli Anticoagulate and DC cardioversionas in Category 1.

Sindrom Wolff Parkinson White


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If unstable, cardiovert No cardioversion for stable SVT with low EF.

Management 12-lead ECG, clinical exam

Vagal stimulation, adenosine. Consider esophageallead

Treat according to specific rhythm:

PSVT

MAT

Junctional
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EF normal Refleks Vagal

Ca-blocker> beta-blocker> digoxin> DCCardioversion.

Consider procainamide, sotalol, amiodarone.

If unstable proceed to cardioversion

EF < 40%, CHF No Cardioversion. Digoxin or amiodarone or

diltiazem.

If unstable proceed to cardioversion


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EF normal: amiodarone, beta-blocker, Ca-blocker

EF < 40%, CHF: amiodarone Notes

rare, most commonly misdiagnosed PSVT.

likely digoxin or theophylline OD, catecholamine

state no cardioversion


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If unstable, cardiovert Attempt to establish specific diagnosis

12 leads, esophageal lead, Clinical info

Note: the use of adenosine to differentiate SVT vs

VT is now de-emphasized.

If unable to make Dx, treat according to EF: EF normal: DC cardioversionor procainamide or

amiodarone

EF < 40%, CHF: DC cardioversionor amiodarone Note: no lidocaine and bretylium in protocol


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May proceed directly to cardioversion If not, treat according to morphology:

Monomorphic VT

EF normal: one of the following:

procainamide (2a), sotalol (2a) OR amiodarone (2b), lidocaine (2b)

EF poor

amiodarone 150 mg iv over 10 min OR lidocaine 0.5-0.75mg/kg iv push

Synchromized cardioversion


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Polymorphic VT

Baseline QT Normal

Possible ischemia (treat) or electrolyte (esp. low K, Mg)abnormality (correct)

EF normal: betablocker, amiodarone, procainamide, orsotalol

EF poor

amiodarone 150 mg iv over 10 min synchromized cardioversion

Prolonged QT baseline (torsade)

Correct electrolyte abnormalities.

Treatment options: magnesium, overdrivepacing, isoproterenol
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Primary Survey, then Secondary Survey: rule

out pseudo-PEA (handheld doppler: look forcardiac mechanical activities. If present treatagressively).

Problem

Search for the probable cause... Wide QRS: suggests massive myocardial injury,

hyperkalemia, hypoxia, hypothermia

Wide QRS+Slow: consider drug OD (tricyclics, beta-blockers, Ca-blockers, digoxin)

Narrow complex: suggests intact heart; considerhypovolemia, infection, PE, tamponade

... and treat as needed
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Consider fluid challenge empirically Consider bicarbonate

hyperkalemia K (Class 1)

bicarbonate responsive acidosis, tricyclic OD, to alkinalizeurine for aspirin OD (Class2a)

prolonged arrest (Class 2b)

not for hypercarbic acidosis

Epinephrine: 1 mg IV q3-5 min

tropine If bradycardia, 1 mg IV q3-5 min

max 0.04 mg/kg


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If you prefer a mechanistic approach (and areused to thinking about MAP, CO, SVR, etc.)think of things that affect forward flow... Decreased Preload: Hypovolemia, Tamponade,

Tension Pneumothorax Increased Afterload: Pulmonary Embolus

Decreased Contractility: Hypoxia, Hypothermia,Acidosis, Myocardial Ischemia

Altered Rate/Rhythm: Hyperkalemia, Drug Overdose


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Hypovolemia Assess: Collapsed vasculature Tx: Fluids

Hypoxia Assess: Airway, cyanosis, ABGs Tx: Oxygen, ventilation

Hydrogen ion (acidosis) Assess: Diabetic patient, ABGs

Tx: Bicarb 1 mEq/kg, hyperventilationHyperkalemia (preexisting)

Assess: Renal patient, EKG, serum K level Tx: Bicarb, CaCl, albuterol neb, insulin/glucose, dialysis,

diuresis, kayexalate

Hypothermia Assess: Core temperature Tx: Hypothermia Algorithm


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Tablets/toxins overdose Assess: Hx of medications, drug use Tx: Treat accordingly

Tamponade, cardiac Assess: No pulse w/ CPR, JVD, narrow pulse pressure

prior to arrest Tx: Pericardiocentesis

Tension pneumothorax

Assess: No pulse w/ CPR, JVD, tracheal deviation Tx: Needle thoracostomy

Thrombosis, coronary Assess: History, EKG Tx: Acute Coronary Syndrome algorithm

Thrombosis, pulmonary embolism Assess: No pulse w/ CPR, JVD

Tx: Thrombolytics, surgery


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Remember: initial stacked shocks are part of theprimary survey Implement the secondary surveyafter your stacked

shocks. Meds: Shock-drug-shock-drug-shock pattern.

Continue CPR while giving meds, and shock (360J or150J if biphasic) within 30-60 seconds. Evaluaterhythm and check for pulse immediately aftershocking.

Epi or vasopressin big drugs (may give either one asfirst choice). If VF/PVT persists, may move on to antiarrhythmics and

sodium bicarb max out one antiarrhythmic before proceeding to the next

in order to limit pro-arrhythmic drug-drug interactions.
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Shock 200J* If VF or VT is shown on monitor: shock immediately. Do not lift paddles from chest after shocking -

simultaneously charge at next energy level and evaluate

rhythm.Shock 200-300J*

If VF or VT persists on monitor, shock immediately. Do not check pulse, do not continue CPR, do not lift

paddles from chest. After shocking, simultaneously charge at next energy

level and evaluate rhythm.Shock 360J*

If VF or VT persists, shock immediately.

Epinephrine 1 mg IV q3-5 min. High dose epinephrine is no longer recommended

Vasopressin 40 U IV one time dose (wait 5-10 minutes before starting epi). Preferred first drug?
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Shock 360J*

miodarone (Class 2b) 300mg IV push.

May repeat once at 150mg in 3-5 min max cumulative dose = 2.2g IV/24hrs

Shock 360J*

Magnesium Sulfate (Class 2b) 1-2 g IV (over 2 min) for suspected

hypomagnesemia or torsades de pointes(polymorphic VT)


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Shock 360J*

icarbonate

1 mEq/kg IV for reasons below: Class 1: hyperkalemia

Class 2a: bicarbonate-responsive acidosis, tricyclicOD, to alkinalize urine for aspirin OD

Class 2b: prolonged arrest

Not for hypercarbia-related acidosis, nor for routineuse in cardiac arrest


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