ACLS

Special ResuscitationsDr. Michelle Welsford

Introduction

Hypothermia Traumatic Cardiac Arrest Electrical Shock and Lightning Cardiac Arrest associated with Pregnancy Toxicologic Cardiac Emergencies

Hypothermia

Severe hypothermia: T < 30C Often unresponsive to defibrillation and

pacemaker CBF and O2 requirement, Cardiac

Output, arterial pressure may appear clinically dead because CNS

depression and CVS depression

Hypothermia Continued

Peripheral pulses and respiration may be difficult to detect

Take 30-45 seconds to confirm pulselessness or profound bradycardia

Bradycardia is usually physiologic and pacing not indicated until warmed

V fibrillation – Try 3 shocks but may be unsuccessful until rewarmed– Can repeat defib when temperature rises > 32 C

Hypothermia Continued

Handle gently to avoid precipitating v. fib Intubate gently; Avoid NG, pacer, etc Warming

– “warm and dead” – try to rewarm to 34 C but use judgment

– if dead – wont’ be able to warm completely – External warming – Internal warming

Hypothermia Continued

Metabolism of medications is slowed– < 30 C - only one round of medications– > 30 C usual meds but at greater intervals – Bretylium – ? DOC in hypothermic V fib

because raises fibrillation threshold

Traumatic Cardiac Arrest

Don’t need to begin resuscitation if: – Hemicorporectomy– Decapitation– Total body burns– Obvious severe blunt trauma without vital signs– Deep penetrating cranial injuries– Penetrating injuries, asystole and transfer time > 15

minutes to trauma centre

Blunt Trauma Cardiac Arrest

Exsanguinations often difficult to treat Survival nearly nil except:

– Ventilate high spinal cord injury– Clear Airway obstruction– Relief of Tension pneumo– Fluid/Blood resuscitation of single organ injury– Defibrillation of VF that may have caused trauma

Penetrating Trauma Arrest

Directly to trauma centre if < 15 minutes from arrest

Intubation IV en-route In general, don’t worry about meds/defib Rapid fluid resuscitation after control of

hemorrhage surgically

Electrical Shock & Lightning

Alternating current:– Ventricular fibrillation common

Direct current:– Asystole common

Electrical Shock & Lightning Continued

Respiratory arrest may be prolonged long after cardiac rhythm restored

Respiratory arrest secondary to:– Inhibition of central medullary respiratory centre– Tetanic contraction of the diaphragm and chest wall

musculature during current exposure– Prolonged paralysis of respiratory muscles

With electic/lightning injuries - use reverse triage and treat nonbreathing, pulseless patients first

Electrical Shock & Lightning Continued

Management:– Ensure safety– CPR –young, healthy people may have good survival

even after as long as 1 hour of CPR– Ventilation– Treat burns:

• Lightning: rarely have cutaneous/muscle injury• Electric: often have cutaneous burns, muscle, etc

– Myoglobinuria will require fluid resuscitation +/- bicarbonate

Cardiac Arrest in Pregnancy

Physiologic changes in pregnancy Maternal CO by up to 50% HR, minute ventilation, O2 consumption Pulmonary functional residual capacity, systemic

and pulmonary vascular resistance– less tolerant to respiratory and cardiovascular insults– when supine, gravid uterus may compress inferior

vena cava and abdominal aorta resulting in hypotension and in CO (by 25%)

Cardiac Arrest in Pregnancy Continued

Precipitants of cardiac arrest:– pulmonary embolus– amniotic fluid embolus– trauma– peripartum hemorrhage– congenital and acquired cardiac disease– complications of tocolytic therapy including

arrhythmia, CHF, AMI

Cardiac Arrest in Pregnancy Continued

Management:– standard resuscitation followed– if VF then defibrillation– CPR as usual, Meds as usual– Wedge under Right hip to displace uterus to

left

Cardiac Arrest in Pregnancy Continued

Potential fetal viability up to 20 minutes, best if < 5 minutes

If no maternal response within 4 minutes, then should consider perimortem C-section (if in neonatal center)

Delivery within 4-5 minutes of arrest May result in viable fetus/infant; best survival for

mother

Toxicologic Cardiac Emergencies – Cocaine

Physiology:– Stimulates release and blocks reuptake of NE, E,

dopamine and serotonin BP, HR, euphoria, CNS stimulation, myocardial

contractility, coronary artery spasm, seizures, death coronary artery flow due to spasm and O2

consumption leading to cardiac ischemiaHTN and SVT

Cocaine Continued

Management: – HTN

• O2 and diazepam, nitro/nitroprusside, Labetalol; not B-blockers!

– PSVT, A fib, A flutter • O2 (don’t usually require treatment because short-

lived)• if persistent, often responds to benzos eg:

Diazepam: blunts hypersympathetic state centrally

Cocaine Continued

ventricular irritability –runs of VT, PVCs– O2, benzos, lidocaine, B-blocker– often transient but may require benzos if

continue eg: VT– standard ACLS with LIDO but may increase

risk of seizures

– selective B1-blockers may be better (esmolol)

Cocaine Continued

Ventricular fibrillation– Standard ACLS except increase interval

between epi and avoid high dose epi– Lidocaine 1 dose only– If non-responsive try selective B-blocker– Magnesium

Cocaine Continued

AMI– Treat with benzodiazepines and nitroglycerin– B-blockade causes unopposed alpha

stimulation so avoid– Ischemia/infarction may be due to spasm,

therefore angioplasty may be better than thrombolysis

Toxicologic Cardiac Emergencies – TCAs

One of the most cardiotoxic medications Sinus tach, prolonged QT widened QRS,

hypotension, ventricular arrhythmias, VT, torsades, seizures

Management:– Alkalinization:Ph 7.45-7.55 with bolus NaHCO3– Decrease free unbound form and overrides the Na-

channel blockade of phase I action potential– Avoid procainamide; may use lidocaine if necessary

(true VT)

Summary

ACLS guidelines for majority of arrhythmias and resuscitations

Some special resuscitations require deviation from guidelines

Questions ?