ca management ms 2006

8/10/2019 CA Management Ms 2006

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Overview of ACLS

May 2006


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900,000 people in the U.S. experience anMI annually

~225,000 die

~125,000 die in the field

Most deaths are arrhythmic in etiology

Acute Myocardial Infarction

Data from: Ryan TJ et al. J Am Coll Cardiol . 1996;28:1333.


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Mechanisms of CA

80-90% of non-traumatic cardiac arrests inadults are due to VF or PVTThe key action is early defibrillationMost arrests in children are respiratoryThe key action is ventilation


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Success of Defibrillation is

Time-Dependent

0

1020

30

40

50

60

70

80

90

1 2 3 4 5 6 7 8 9

SUCCESS

Minutes to

Defibrillation

Success is reduced 7-10% per minute


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AED

The AED assesses therhythm and advisesshocks for VT/VF

After shocks resumeCPR and reassessrhythm after 5 cycles(two) minutesIf pulse returns, assessand assist breathing


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Pulseless VT/VFWitnessed: Consider precordial thump(optional, may be harmful)Unwitnessed: CPR for 2 minutes prior toshockShock 1 time. Level of energy withmonophasic shock: 360 J. Biphasic:

120-200J.Resume CPR immediately after shock.Check rhythm after 2 minutes


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Pulseless VT/VF Persists

After Shock Start DrugsThe key drug in CA mgmt is epinephrineFor every type of CA, epinephrine is

given every 3-5 minutes until a pulse isrestoredVasopressin ( 40 u) may be giveninstead of the first or second dose ofepinephrineSimultaneously, intubate, oxygenateventilate


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CPR Pointers

The compresssion rate is 100 per minute.Be sure compressions are full (1 - 2) andfast , but be sure that chest recoil iscomplete between compressions.Hand position is mid-sternal at nipple line


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CPR Pointers

Minimize all CPR interruptionsOnce the patient is intubated do notinterrupt chest compressions forventilationFollowing intubation: Ventilation rate is 8-10 per minute. Do not hyperventilate


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Pulseless VT/VF

Proceed with a drug/shock sequence. Do

CPR for 5 cycles (2 minutes) after a drug isadministered, then shockStill in VF: amiodirone 300 mg IV. May givean additional 150 mg if VF persistsMinimize interruptions in CPR for pulsechecks


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Anti-Arrhythmics for PVT/VF After amiodirone: Lidocaine 1-1.5 mg/kg IV, may repeat in 3-5min (max 3 mg/kg)

Magnesium sulfate : 1-2 gm IV for suspectedhypomagnesemia or torsades

Procaineamide: 30 mg/min or 100 mg q5min (max 17mg/kg)Consider bicarbonate: 1mg/kg for pre-existingacidosis, drug OD, prolonged code


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Endotracheal Drug Adm

VALEN: Vasopressin, atropine, lidocaine,epinephrine, naloxone

IV administration is preferable: indicatedonly when iv access cannot be obtainedDose is 2-5X the iv dose. Dilute in sterilewater


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Central vs Peripheral Line

Peripheral iv is preferred because of lessinterruption of CPR

Peripherally administered drugs should befollowed by fluid bolus and arm elevationto facilitate delivery to central circulation


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80 yo comes into ER with weakness.On exam he is pale and diaphoretic, butalert and oriented and complaining ofweakness. PMH: CABG, diabetesInitial EKG:


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Acute anterior MIInitial evaluation


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Evaluate ABCIf adequate start O2, monitor (EKG andpulse ox), IV (OMI)iv site-antecubital

Asa, heparin, pain control cardiologyconsult


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His rhythm changes


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What do you want to know?


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Stable or unstable-presence of serioussigns and symptoms?

In this case starts out with BP114/70, iestable


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Treat with amiodarone 150mg iv over 10minutes and then infusion of 1mg/min

Patient remains in VT-develops MSchanges and pulse weakensStable or unstable?Treatment


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VT with pulse, unstable-cardiovertThis means a synchronized shock-youpress the synch button on the defibConsider sedationStart with 100jPatient changes as machine is charging-now pulseless and apneic


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Shock 360j (or 200 biphasic) if the syncbutton is still pressed it wont work -turn off

Do CPR for 2 minutes before checkingrhythmVentilate with BVM and 100% O2, intubateStart iv, give epi or vasopressin


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Intubation

Secures the airway Allows administration of 100% oxygen and

correction of respiratory acidosis Allows administration of some medications(VALEN-3X iv dose)

What if you cant intubate??


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Laryngeal Mask Airway


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LMA

The LMA is insertedby slipping the mask

along the palate intothe hypopharynx withsubsequent inflationof the mask rim


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Epi-1 mg q3-5 min or vasopressin 40 unitsShock-still VF

Amiodarone 300mg-shock, then 150 mgthen infusion (max 2.2 grams per 24hours)Lidocaine 1-1.5 mg/kg. Repeat x1 max3mg/kg.


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How do you check that the ETT is properlyplaced?

How do you know CPR is adequate


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ETT placement

Listen over both lateral lung fields and thestomach

Use end tidal CO2 (but no CO2 if CPR isnot adequate)


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Adequate CPR

Palpable carotid or femoral pulsePulse oximeter or A-lineCO2 production


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Vasopressin in CA

Half life is 10-20 minutes, so considerwaiting at least 10 minutes to give

epinephrineComparing survival in out of hospitalarrest, no advantage of vasopressin over

epinephrine (in one study, it looked betterfor asystole)


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What if they come back with a pulse butinadequate BP?


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Low BP

Fluid bolusDopamine-5 micrograms/kg/min titrate (put200 mcg in 250cc and start at 30drops/min)


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When to Stop ?

CV unresponsivenessYou get more info about situation andcode status


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Asystole/PEA

Confirm asystole in more than one lead (uselead select to move between limb leads)

Transcutaneous pacing is ineffective for asystoleand is no longer recommendedEpinephrine: 1mg IV q3-5 min (or vasopressin*)

Atropine: 1mg IV q 3-5 min (up to 3 doses)


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Consider Causes: 6Hs

HypovolemiaHypoxiaHyper, hypokalemiaHydrogen ions (acidosis)HypothermiaHypoglycemia


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5Ts

ToxinsTamponade, cardiacTension pneumothoraxThrombosis (pulmonary, coronary)Trauma


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PEA

Thinking of and correcting one of thereversible causes of PEA early (eg chest

tube placement for pneumothorax) can belifesaving


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Improving Survival After Cardiac

Arrest After restoration of spontaneouscirculation, poor neurologic outcome is

one of major causes of death2 studies have now demonstratedimproved neurologic outcome post arrest

with the use of mild hypothermia


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Mild Hypothermia after VF

Arrest136 patients comatose after VF arrest (thearrest was witnessed) were randomized to

mild hypothermia, target 32-34 Cmeasured with a bladder probe. Patientswere sedated with fentanyl and midazolam

and paralyzed with pancuronium andtemperature was maintained for 32 hours


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SURVIVAL AFTER CA


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ACLS: Managementof Tachycardias andBradycardias


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Bradycardia and Tachycardia

AlgorithmsThe main important point is the distinction betweenstable vs unstable with serious signs and sxincluding:

HypotensionShockPulmonary edema

Loss of consciousness, confusion agitationMI , angina


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Tachycardia with a Pulse

Main distinction is wide vs narrow complextachycardia. Also consider LV function.

Assume wide complex tachycardia is VTand treat with amiodarone, lidocaine orprocaineamide if stable or synchronized

cardioversion if unstableSynchronized cardioversion: sedate first,start with 100j


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Wide Complex Tachycardia

Always assume it is VTThe drugs of choice for stable VT or widecomplex tachycardia of unknown origin areamiodarone and procaineamide

Adenosine and verapamil are

contraindicated for the treatment of widecomplex tachycardia


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Narrow Complex TachycardiaIdentify the rhythm (carotid massage,adenosine), consider cause, duration,LV function

Tachycardia may be secondary to fever,dehydration, hypoxemia-treat theunderlying cause rather than the rhythm

No cardioversion for: sinus tachycardia,MAT, junctional tachycardia Avoid using > one drug


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Atrial Flutter-Fibrillation >48h

Agents that control rate rather thanconvert the rhythm are preferred, unless

the patient is adequately anticoagulatedNormal LV function: diltiazem or betablockers (I)

Abnormal LV function(EF


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Atrial Fibrillation


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Avoid Panic on the First Day of

InternshipLearn the basics of ACLS including drugdoses

ca management ms 2006

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