ACLS

(Advance Cardiac Life Support)

Terminology
Cardiac arrest Loss of cardiac mechanical activity
Signs indication loss of circulation No pulse, unresponsiveness, apnea (early signs)
PEA Pulse electrical activity (absence of a pulse despite EKG)
Heart on the monitor has activity but not in the pt when you take the pulse manually (still some
electrical activity)
Non-shockable rhythm
Asystole Total lack of electrical activity in the heart (flat line on EKG)
Slow progressive dive before it flat lines
Non-shockable rhythm
pVT Pulseless ventricular tachycardia
VF/pVT Ventricular fibrillation/Ventricular tachycardia*
[doesn’t sustain very long]/[multiple QRS in EKG]
*Multiple QRS in EKG still some electrical activity but misfeeding
Shockable rhythm
Resuscitation Act of trying to restore circulation
CPR = cardiac pulmonary resuscitation
(mechanical intervention for resuscitation which attempts to restore blood flow)
Return of spontaneous circulation “full recovery”
(ROSC) Individual’s recovery from cardiac arrest

Major negative outcome of cardiac arrest  loss of neurologic function

May occur due to cardiac or non-cardiac origins
Asystole is the leading rhythm associated w/ cardiac arrest (contributing factors are bradycardia and/or apnea, pacemakers,
defibrillators, medication like BBs, or ACEI tat shorten durations of VF leading to asystole)
The leading cause in pediatrics is  respiratory failure or asphyxiation
Etiology Leading risk factor for adults is CAD occurring in ¾ of all pts (cardiac arrest is the first sign of CAD in most pts)
Other risk factors:
-cardiomyopathies
-vascular heart disease
-myocarditis
-cardiac hypertrophy
-1ry electrical heart disease
Leading risk factor for pediatrics is respiratory failure or shock
Pathophysiology Primary cardiac arrest (oxygenated blood flow @ the time of arrest for up to ~10 min) (w/in 10 minutes; O2 level low
before going into arrest)
Secondary cardiac arrest (existing hypoxemia  respiratory failure, hypotension)
In regard to CPR two theories are supported:
1.Cardiac pump theory: compression btw sternum & vertebrae results in forward blood flow (and out of the heart)
2.Thoracic pump theory: compression changes intrathoracic pressure & resulting blood flow (and into the body)
CPR restores blood flow to the heart & brain
-Prolongs the time VF is present preventing early asystole (you are helping move the blood out of the heart)
*every minute VF is not defibrillated results in survivability decreases
*CPR will NOT terminate VF (doesn’t have the electrical interruption needed; need a defibrillator; ONLY prolongs time)
Presentation Sudden cessation of circulation
-Leading up to event:
*anxiety
*crushing chest pain (elephant sitting on the chest)
*N/V
*diaphoresis (sweating)
-At time of event:
*apnea
*no pulse
*cyanosis
*cold, clammy skin (extremities)
Goals of Th Resurrection to minimize hypoxic damage to organs
-applicable only if a “do not resuscitate” order is placed
-note: “do not resuscitate” is not the same as “do not intubate”
Negative Outcomes Disability including coma and/or vegetative state (might not recover functionality)
Approach to Care “CAB”
-circulation (1st)
-airway
-breathing
Achieve optimal outcomes post arrest
-awake
-responsive
-spontaneous breathing
Process for Out-of- Recognition of cardiac arrest w/ activation of EMS (response) [call 911]
Hospital Cardiac Early High-Quality (good compressions) CPR
Arrest Rapid defibrillation for shockable rhythms
Effective advanced life support
Postcardiac arrest care (can they spontaneously breath or do they need a mechanical ventilator)
Cardiocerebral Alternative to ACLS that allows for continuous chest compressions as part of the community component in recognizing
Resuscitation (CCR) arrest
Three phases:
1.Electrical phase (0-5 min)  deliver defibrillation
2.Hemodynamic phase (5-15 min)  establish perfusion before/after defibrillation
3.Metabolic phase (>15 min)  tissue ischemia leads to accumulation of metabolic factors (buildup of metabolites) ;
very low survival; hypothermia care may be considered
Process for In- Systems in place to survey and prevent cardiac arrest
Hospital Cardiac Notification and response by multidisciplinary teams to cardiac arrest events
Arrest High-quality CPR (incorporate breathing w/in chest compressions)
Prompt defibrillation of shockable rhythms w/ advanced life support when applicable
Integrated, multi-disciplinary team postcardiac care
Management High-quality CPR:
-Leading intervention noted to have reduction in morbidity/mortality
-Must display adequate rate and depth of compressions
*Significant by:
1.full chest recoil w/ each compression
2.preventing excessive ventilation
3.minimization of interruption to compressions
*Optimal rate: 100-120 beats/min
-ACLS two-person delivery = 30 compressions to 2 breaths or 30 compressions to 1 ventilation every 6 sec
*Depth: 40-54 mm
*Fraction: 60% (of the time; hands on the chest; compression administration)
-proportion of time CPR is administered
*Mechanical devices deliver higher blood flow but DO NOT improve survivability
 BLS
Algorithm

ACLS
Algorithm
 Advanced Cardiac Life Support (Requires certification)
Noted addition of changes in breathing and/or airway
-Allows for delivery of breath Q6sec w/ continuous chest compressions (start two-man system)
*bag-mask-valve
No difference in outcomes
*advanced airway
-endotracheal tube
-supraglottic device
-Monitoring w/ end-trial CO2 (ETCO2)
*checks the concentration of carbon dioxide exhaled w/ each respiration
*ETCO2 decreases w/ lack of pulmonary circulation (ETCO2 used to predicting to stop CPR)
*ETCO < 10 mmHg in intubated pts during CPR = unlikely survivability
*decreasing ETCO2 during CPR = immediate re-evaluation of compression technique
Shockable Rhythm Non-Shockable Rhythm
If a shockable rhythm present (VF, pVT): If non-shockable rhythm present (PEA/Asystole):
1.Initiate CPR 1. Initiate CPR
2.Administer 1 defibrillation 2. Administer epinephrine w/ 1st cycle
3.Immediately follow w/ chest compressions again *continue compression while administering medications
4.Re-delivery 1 defibrillation Q2min if rhythm still present *repeat Q3-5min
5.Administer epinephrine after 2 cycles of ACLS 3. Assess for reversable causes
*continue compression while administering medications *”5 Hs & Ts”
(epinephrine DOES NOT change need for defibrillator or CPR) 4. Assess for ROSC
*repeat Q3-5min *if rhythm changes, Tx algorithm changes (VF/pVT)
6.Assess for ROSC *if ROSC unattainable, pt will pass away
*if rhythm changes, Tx algorithm changes (PEA/asystole) *DO NOT defibrillate in this pathway as it can reduce ROSC
*if ROSC unattainable, pt will pass away
VF and PVT Reversible causes in PEA/Asystole
Non-Pharmacological management: 5 Hs 5 Ts
-Defibrillation is the only way to restore cardiac function Hypovolemia Tension pneumothorax
*this is why an AED needs early implementation Hypoxia Tamponade (cardiac)
Hydrogen ion (acidosis) Toxins
*DO NOT check for a pulse after defibrillation continue chest
Hypo-/Hyper-kalemia Thrombosis (pulmonary)
compressions
Hypothermia Thrombosis (cardiac)
Pharmacotherapies: 5 Hs Indication Treatment
-Sympathomimetics Hypovolemia Flat neck veins IV fluid bolus (crystalloids)
*epinephrine is the preferred therapy Hypoxia Cyanosis, ABGs, airway loss Ventilation; Oxygenation
*associated w/ increase in ROSC but NOT survival Hydrogen ion Pre-existing acidosis Sodium bicarbonate
*no advantage w/ phenylephrine or norepinephrine (acidosis) Hyperventilation
Hypo-/Hyper- Hx of renal failure, DM, dialysis, Calcium chloride
compared to epinephrine
kalemia contributing meds Insulin/Dextrose
-Antiarrhythmics
Sodium bicarbonate
*amiodarone is the preferred agent SPS
Dialysis
Hypothermia Cold exposure Re-warm; warm IV fluids
*Hypoglycemia Hx of DM Dextrose
Access in Cardiac Arrest 5 Ts Indication Treatment
Central access takes more time Tension -Hx of asthma, mechanical ventilation, Needle decompression
-if already placed  it is preferred route of administration (IV) pneumothorax COPD, trauma
-Tracheal deviation
-allows for faster & higher peak of drug concentrations -No pulse w/ CPR
Alternative if no IV or IO option: Tamponade -Hx of trauma, renal failure, thoracic Pericardiocentesis
-endotracheal administration (advance temporary airway set (cardiac) malignancy
up) -No pulse w/ CPR
-Hypotension and/or bradycardia as
-only w/ the following medications: terminating event
*atropine, lidocaine, epinephrine, naloxone, vasopressin Toxins -Bradycardia Target antidote
-Low and delayed peak of drug concentrations -Hx of exposure Decontamination
*doses are 2-2.5x higher compared to IV/IO -Neuro exam (toxidromes)
Thrombosis -Hx of MI
*medications should be diluted into NS or SWFI (preferred) -EKG changes
(pulmonary)
Faster placement w/: -Cardiac enzyme elevation
-peripheral intravenous access (IV) Thrombosis -Hx of PE Thrombolytics
-intraosseous (IO) (cardiac) -No pulse w/ CPR Pulmonary arteriogram
*only when IV access cannot be obtained -Distended neck vein
*proximal tibia is preferred Trauma Hx/examination -Volume resuscitation
-Bleeding control
-ICP monitoring/intervention
 Drug Moa Use Dose Side effects
Epinephrine Vasoconstrictive properties Increases force of heart May be given IO  if IV High doses can lead to
Works on alpha & beta contraction not attainable catecholamine toxicity &
receptors Increases low coronary and Adults: 1 mg rapid IV/IO are not routinely
cerebral perfusion pressure when push (followed by NS recommended
added to chest compressions flush) Q3-5min -decreased cardiac indices
CPR alone restores ~25% of blood Needs to clear the line -left ventricular dysfunction
flow to brain & heart (w/ hands every time you -decreased oxygen delivery
on chest) administer something
Pediatrics: 0.01 mg rapid
IV/IO
Vasopressin Antidiuretic hormone Given when epinephrine alone is Combination of:
Noradrenergic not enough Vasopressin (20 units)
vasoconstrictor Advantages over epinephrine: +
Affects primarily the V1 -acidosis (metabolic Methylprednisolone (40 mg)
receptor complication) can diminish +
Endogenous release adrenergic responses Epinephrine (1 mg)
associated w/ a higher -lack of beta activity means no Higher rates of ROSC and
levels of ROSC increased myocardial oxygen survival w/ good
demands neurological function
-V2 effects may support renal NOT YET ADAPTED INTO
blood flow (not seen w/ THE GUIDELINES
splanchnic blood flow)
DOES NOT produce superior
clinical outcomes as a substitute
or in combination w/
epinephrine
Amiodarone Class III antiarrhythmic Role in therapy ONLY in Dose: 1st dose 300 mg
-actions do cover all four- shockable (VF or pVT) rhythms IV/IO push and 2nd dose
classification w/in Vaughn that are unresponsive to: 150 mg IV/IO push
Williams -CPR (can only go up to 450 mg
-defibrillation push)
-vasopressors Lidocaine (class 1b) used
Increases survival to hospital only when amiodarone
admission but not overall clinical not available (option
survival when C/I w/ amiodarone)
Additional Parmacotherapies
Magnesium No benefit to routine administration despite severe hypomagnesemia levels
Increased ROSC in pt w/ Torsades de Pointes
Thrombolytics Higher incidence of intracranial hemorrhage w/ Tenecteplase
Use restricted to underlying presence of pulmonary embolism
Atropine Antimuscarinic that decreases parasympathetic response
NOT RECOMMENDED outside of the setting of bradycardia (pulse < 50 in adults)
Dose: 0.5 mg IV/IO bolus Q3-5min w/ a max dose of 3 mg
Administered in a prefilled syringe that comes in 1mg  make sure to only push 0.5 mg
Sodium Bicarbonate NOT routinely used
If given  administered @ 50 mEq/50 mL IV/IO bolus
Reserved for hyperkalemia, tricyclic antidepressants overdose, aspirin toxicity
Post-resuscitative Care Implemented following ROSC
Four components:
1. Hypoxic brain injury (seizure, coma, brain death)
2. Myocardial dysfunction (cardiogenic shock, dysrhythmias)
3. Systemic ischemia-reperfusion response (hypotension, fever, hyperglycemia, infection,
multi-organ failure)
4. Precipitating pathophysiology (PE, toxic ingestion, electrolyte disturbances)
Benefits:
-reduces mortality through review of hemodynamics, addressing organ dysfunction, and
treating CNS injury
Most common reason for re-arrest is hypoxia
Rapid evaluation for MI should occur to provide PCI
 Post-resuscitative Care MAP goals should target > 80 mmHg due to cerebral hypoperfusion
(Continuation) -Avoid hypotension MAP < 65 mmHg or SBP < 90 mmHg
Implementation of hypothermia or target temperature management
Management of seizures
Achieve normoglycemia
Hypothermia (Target Following arrest free-radical production, mitochondrial damage, and excitatory amino acid
Temperature Management) release can lead to cerebral injury
Hypothermia can suppress these cerebral injury causes:
-reduces cerebral metabolism & oxygen consumption
-1 degree drop in body temperature decreases metabolism by ~10%
-may result in favorable neurological outcomes
-trial date not showing in-hospital benefits
-implemented in adults who remain comatose following ROSC
-Goal  32-36oC for @ least 24 hrs
-Methods: surface cooling, ice water immersion, invasive cooling via fluids, cooling catheters

Rapid sequence intubation (RSI)

Background Placement of a secure airway
Systematic approach to placing an advanced airway
RSI can aid in successful placement of an airway w/ reduced complications especially in precedingly
conscious pts
-assessment of airway
-assessment for difficult ventilation
-assessment for difficult intubation (reduced mouth opening, cervical injury, ect.)
RSI Pharmacotherapy Preinduction Goal: limit adverse responses w/ intubation
-W/ placement of endotracheal tube adverse response include:
*increased sympathetic release
*provoked bronchospasm
*hypertensive responses
-Therapies NOT routinely utilized
-Possible Th:
*opioids (fentanyl), and/or lidocaine can block hypertensive response
Induction Goal: facilitate intubation
-Medications routinely used
-Focus on sedation AND paralysis (in that order)

RSI Class/MOA/Benefits Drug Dose ADR

Sedation Nonbarbiturate hypnotic Etomidate 0.3 mg/kg IV push Inhibits cortisol production (can’t
(1st) Hemodynamically neutral (not offset Rapid onset & short repeat) & reduces adrenal
pulse) duration (6 min) responsiveness
Cerebral protective effects
Propofol 2 mg/kg IV push Hypotension (single administration
may be managed w/ IV fluid bolus)
Bronchodilation effect  good for Ketamine 2 mg/kg IV push Emergence phenomena (hallucinatory
respiratory arrest response  manage w/ benzos)
Barbiturate Sodium Thiopental Hypotension (similar to propofol)

Paralytics Depolarizing NMBs Succinylcholine 1.5 mg/kg IV push CI: malignant hyperthermia,
(2nd) Dimer of acetylcholine Rapid onset and short hyperkalemia, myopathy
duration (allow ventilation Precaution: renal insufficiency
to return in ~10 min)
Non-Depolarizing NMBs Rocuronium 1 mg/kg IV push
Beneficial if anticipated difficulty w/ Rapid onset and longer
intubation duration
Use when you can’t use the other
one