RACE – 2017

10 – 12 Feb, 2017
WORKSHOPS
Megacode Evaluation

CONTRIBUTORS

FACULTY
Dr. Jigi Divatia
Dr. Arun Kumar
Dr. Thamarai selvi
Dr. Renuka
Dr. Kamalakannan
Dr. Kalaiselvan
 CARDIO-PULMONARY RESUSCITATION.

Introduction:
Cardiopulmonary resuscitation (CPR) is a series of lifesaving actions that improve the chance
of survival following cardiac arrest1. Although the optimal approach to
CPR may vary, depending on the rescuer, the victim, and the available resources, the fundamental
challenge remains: how to achieve early and effective CPR. Given this challenge, recognition of arrest
and prompt action by the rescuer continue to be the priority.

Sudden cardiac arrest remains a leading cause of death in the United States. Seventy percent of out-
of-hospital cardiac arrests (OHCAs) occur in the home, and approximately 50% are unwitnessed.
Outcome from OHCA remains poor, i:e only 10.8% of adult patients with nontraumatic cardiac arrest
who have received resuscitative efforts from emergency medical services (EMS) survive to hospital
discharge2. In-hospital cardiac arrest (IHCA) has a better outcome, with 22.3% to 25.5% of adults
surviving to discharge3.When the links in the Chain of Survival are implemented in an effective way,
survival can approach 50% in EMS-treated
patients after witnessed out-of-hospital ventricular fibrillation(VF) arrest4,5.Unfortunately, survival
rates in many out-of hospital and in-hospital settings fall far short of this figure. For example, survival
rates after cardiac arrest due to VF vary from approximately 5% to 50% in both out-of-hospital and in
hospital settings.

The major changes in the 2015 ACLS guidelines include recommendations about prognostication
during CPR based on exhaled CO2 measurements, timing of epinephrine administration stratified by
shockable or non shockable rhythms, and the possibility of bundling treatment of steroids,
vasopressin, and epinephrine for treatment of in-hospital arrests. In addition, the administration of
vasopressin as the sole vasoactive drug during CPR has been removed from the algorithm6.

The science of CPR

One fact about CPR and other post–cardiac arrest treatments that is certain, is that no amount of
defibrillation will impact outcomes if there is no perfusion to the heart and brain. Re-establishing
blood flow to the vital organs is the single most important factor for successful resuscitation.
Coronary Perfusion Pressure

Coronary perfusion pressure is the difference between right arterial pressure (RAP) and aortic
pressure (AoP) during diastole. CPP has tremendous clinical significance, and Paradis, who measured
the coronary perfusion pressure of patients undergoing CPR in an ICU, demonstrated its importance7.

In Paradis' study, no patient achieved return of spontaneous circulation (ROSC) with coronary
perfusion pressures less than 15 mm Hg, while ROSC was achieved in 79% of those patients with a
CPP greater than 25 mm Hg7. (Fig-1).

Fig-1. Coronary perfusion pressure and the return of spontaneous circulation

The following show the progression of ventricular fibrillation (VF) over time and the impact of CPR
on reconstituting the waveform. Initially, VF is coarse and generally still shockable. Myocytes are
still contracting uniformly along a few wave fronts.(Fig 2).
Fig -2 Initial coarse VF which is shockable

After five minutes, myocyte contraction is more independent, more wave fronts develop, and the
ability of the heart to respond to a shock declines dramatically. This critical time can be observed by
the smoothing and decreasing amplitude of the waveform.(Fig 3).

Fig-3 VF which is morphologically different which is more smooth and less

amplitude.

Fig-4 Shown above is the waveform after three minutes of effective CPR. By
providing perfusion to the heart, CPR reconstitutes the VF into the shockable
coarse form.

Establishing circulation with CPR at a level fast enough and deep enough to achieve an effective
CPP is therefore the goal of CPR compressions. This was clearly the goal of the changes since 2010
AHA guidelines for CPR where more importance was given to compressions and early defibrillation
over ventilation.(Fig-5)
Fig-5.Aortic (Ao, dark band) and right atrial (RA, light band) pressures during standard CPR,
CC+RB, with a 15:2 compression:ventilation ratio. Aortic relaxation, or diastolic, pressure (lower
border of dark band) decreases during each set of 2 breaths, resulting in lower CPP during first several
compressions of next cycle. Right atrial relaxation, or diastolic, pressure is most inferior border.
Difference between Ao and RA relaxation pressures is CPP.
ADULT BLS SEQUENCE—UPDATED
Significant New and Updated Recommendations(BLS):

Many studies have documented that the most common errors of resuscitation are inadequate
compression rate and depth; both errors may reduce survival. New to this 2015 Guidelines Updateare
upper limits of recommended compression rate based on preliminarydata suggesting that excessive
rate may be associated with lower rate of return of spontaneous circulation (ROSC). In addition, an
upper limit of compression depth is introduced based on a report associating increased non–life-
threatening injuries with excessive compression depth.

 In adult victims of cardiac arrest, it is reasonable for rescuers to perform chest compressions at
a rate of 100 to 120/min (Class IIa, LOE C-LD). The addition of an upper limit of
compression rate is the result of 1 largeregistry study associating extremely rapid
compressionrates with inadequate compression depth

 During manual CPR, rescuers should perform chest compressions at a depth of at least 2
inches or 5 cm for an average adult, while avoiding excessive chest compression depths{(>2.4
inches (6 cm)}(ClassI, LOE C-LD).The addition of an upper limit of compressiondepth
followed review of 1 publication suggesting potential harm from excessive chest
compressiondepth (greater than 6 cm, or 2.4 inches).

 Total preshock and postshockpauses in chest compressions should be as short as

possiblebecause shorter pauses canbe associated with greater shock success, ROSC, and,
insome studies, higher survival to hospital discharge. The need to reduce such pauses has
received greater emphasis in 2015 Guidelines Update(Class I, LOE C-LD).

 In adult cardiac arrest with an unprotected airway, it maybe reasonable to perform CPR with
the goal of a chest compression fraction as high as possible, with a target of
at least 60% (Class IIb, LOE C-LD). The addition of thistarget compression fraction to the
2015 Guidelines Updateis intended to limit interruptions in compressions and tomaximize
coronary perfusion and blood flow during CPR.

 Routine use of passive ventilationtechniques during conventional CPR for adults,is not
recommended because the usefulness/effectiveness of these techniquesis unknown (Class IIb,
LOE C-EO). However, in EMSsystems that use bundles of care involving continuouschest
 compressions, the use of passive ventilation techniquesmay be considered as part of that
bundle (ClassIIb, LOE C-LD).

 It is reasonable for healthcare providers to provide chestcompressions and ventilation for all
adult patients in cardiacarrest, from either a cardiac or a noncardiac cause (ClassIIb, LOE C-
LD).

 When the victim has an advanced airwayin place during CPR, rescuers no longer deliver
cycles of30 compressions and 2 breaths (ie, they no longer interruptcompressions to deliver 2
breaths). Instead, it may be reasonablefor the provider to deliver 1 breath every 6 seconds (10
breaths per minute) while continuous chest compressionsare being performed (Class IIb, LOE
C-LD). This simple rate, rather than a range of breaths perminute, should be easier to learn,
remember, and perform.

 For patients with known or suspected opioid addictionwho have a definite pulse but no
normal breathingor only gasping (ie, a respiratory arrest), in addition toproviding standard
BLS care, it is reasonable for appropriatelytrained BLS providers to administer intramuscular
or intranasal naloxone (Class IIa, LOE C-LD).
Table 1 and 2 provides a summary of the components of high quality CPR
Table 1: Components of high quality CPR

Table 2: High quality CPR, Dos and Don’ts

ADULT ACLS SEQUENCE—UPDATED
The major changes in the 2015 ACLS guidelines include recommendations about
prognostication during CPR based on exhaled CO2 measurements, timing of epinephrine
administration stratified by shockable or nonshockable rhythms, and the possibility of bundling
treatment of steroids, vasopressin, and epinephrine for treatment of in-hospital arrests. In
addition, the administration of vasopressin as the solevasoactive drug during CPR has been
removed from the algorithm.

Highlights of the changes in ACLS 2015:

 Based on new data, the recommendation for use of the maximal feasible inspired oxygen
during CPR was strengthened. This recommendation applies only while CPR is ongoing and
does not apply to care after ROSC.(Class IIb, LOE C-EO).
 The new 2015 Guidelines Update continues to statethat physiologic monitoring during CPR
may be useful,but there has yet to be a clinical trial demonstratingthat goal-directed CPR
based on physiologic parameter improves outcomes(Class IIb, LOE C-EO).
 Ultrasound (cardiac or noncardiac) may be considered during the management of cardiac
arrest, although its usefulness has not been well established. The use of ultrasound should not
interfere with the standard cardiac arrest treatment protocol, if so ultrasound may be
considered as an adjunct tostandard patient evaluation (Class IIb, LOE C-EO).
 Either a bag-mask device or an advanced airway may be usedfor oxygenation and ventilation
during CPR in both the in-hospitaland out-of-hospital setting. For healthcare providers trained
in their use, either anSGA device or an ETT may be used as the initial advancedairway during
CPR (Class IIb, LOE C-LD).
 Continuous waveform capnography is recommended in additionto clinical assessment as the
most reliable method of confirmingand monitoring correct placement of an ETT (Class I,LOE
C-LD).If continuous waveform capnometry is not available, anonwaveform CO2 detector,
esophageal detector device, orultrasound used by an experienced operator is a
reasonablealternative (Class IIa, LOE C-LD).
 After placement of an advanced airway, it may be reasonablefor the provider to deliver 1
breath every 6 seconds (10breaths/min) while continuous chest compressions are
beingperformed (Class IIb, LOE C-LD).
 If using a manual defibrillator capable of escalating energies,higher energy for second and
subsequent shocks may beconsidered (Class IIb, LOE C-LD).A single-shock strategy (as
opposed to stacked shocks) is reasonablefor defibrillation (Class IIa, LOE B-NR).
 The role of antiarrhythmic drugs during and ImmediatelyAfter Cardiac Arrest is yet to be
shown to increase survival or neurologic outcome after cardiac arrest due to VF/pulseless VT.
Accordingly,
 1) Amiodarone may be considered for VF/pVT that is unresponsiveto CPR, defibrillation,
and a vasopressor therapy (ClassIIb, LOE B-R).
2) Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is
unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD).
3) The routine use of magnesium for VF/pVT is not recommendedin adult patients (Class
III: No Benefit, LOE B-R).
 There is inadequate evidence to support the routine use of lidocaine and β-blockers after
cardiac arrest. However, the initiation or continuation of lidocaine may be considered
immediately after ROSC from cardiac arrest due to VF/pVT (Class IIb, LOE C-LD).
 Standard-dose epinephrine (1 mg every 3 to 5 minutes) may bereasonable for patients in
cardiac arrest (Class IIb, LOE B-R).However high-dose epinephrine is not recommended for
routine use incardiac arrest (Class III: No Benefit, LOE B-R).
 Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest (Class IIb,
LOE B-R).Vasopressin in combination with epinephrine offers noadvantage as a substitute for
standard-dose epinephrine incardiac arrest (Class IIb, LOE B-R).The removal of vasopressin
has been noted in the AdultCardiac Arrest Algorithm of 2015.
 There is insufficient evidence to make a recommendationas to the optimal timing of
epinephrine administration. But it may be reasonable to administer epinephrine as soon as
feasible after the onset of cardiac arrest due to an initial nonshockable rhythm (Class IIb,
LOE C-LD).
 In IHCA, the combination of intra-arrest vasopressin,epinephrine, and methylprednisolone and
post-arrest hydrocortisonemay beconsidered; however, further studies are needed before
recommendingthe routine use of this therapeutic strategy (Class IIb,LOE C-LD).For patients
with OHCA, use of steroids during CPR is ofuncertain benefit (Class IIb, LOE C-LD).
 In intubated patients, failure to achieve an ETCO2 ofgreater than 10 mm Hg by waveform
capnography after 20minutes of CPR may be considered as one component of amultimodal
approach to decide when to end resuscitativeefforts, but it should not be used in isolation
(Class IIb,LOE C-LD).
 There is insufficient evidence to recommend the routine useof ECPR for patients with cardiac
arrest. In settings whereit can be rapidly implemented, ECPR may be considered forselect
cardiac arrest patients for whom the suspected etiologyof the cardiac arrest is potentially
reversible during a limitedperiod of mechanical cardiorespiratory support (Class IIb,LOE C-
LD).
POST CARDIAC ARREST CARE-UPDATED
POST CARDIAC ARREST CARE-UPDATED

The hypoxemia, ischemia, and reperfusion that occur during cardiac arrest and resuscitation may
cause damage to multiple organ systems.7 The severity of damage can vary widely among
patients and among organ systems within individual patients. Therefore, effective post–cardiac
arrest care consists of identification and treatment of the precipitating cause of cardiac
arrest combined with the assessment and mitigation of ischemia-reperfusion injury to
multiple organ systems. Care must be tailored to the particular disease and dysfunction that
affect each patient. Therefore, individual patients may require few, many, or all of the specific
interventions discussed in the remainder of this Part.
 Coronary angiography should be performed emergently(rather than later in the hospital stay or
not at all) for OHCApatients with suspected cardiac etiology of arrest and ST elevationon
ECG (Class I, LOE B-NR).
 Emergency coronary angiography is reasonable for select(eg, electrically or hemodynamically
unstable) adult patientswho are comatose after OHCA of suspected cardiac origin butwithout
ST elevation on ECG (Class IIa, LOE B-NR).
 Coronary angiography is reasonable in post–cardiac arrestpatients for whom coronary
angiography is indicated regardlessof whether the patient is comatose or awake (Class
IIa,LOE C-LD).
 Avoiding and immediately correcting hypotension (systolicblood pressure less than 90 mm
Hg, MAP less than 65 mm Hg)during postresuscitation care may be reasonable (Class
IIb,LOE C-LD).
 It is recommended that comatose (ie, lack of meaningful responseto verbal commands) adult
patients with ROSC after cardiacarrest to have TTM (Class I, LOE B-R for VF/pVT
OHCA;Class I, LOE C-EO for non-VF/pVT (ie, ―nonshockable‖) andin-hospital cardiac
arrest).
 It is recommend to select and maintain a constanttemperature between 32ºC and 36ºC during
TTM (Class I,LOE B-R) and it is reasonable that TTM be maintained for at least 24 hoursafter
achieving target temperature (Class IIa, LOE C-EO).It may be reasonable to actively prevent
fever in comatose patients after TTM (Class IIb, LOE C-LD).
 An EEG for the diagnosis of seizure should be promptlyperformed and interpreted, and then
should be monitoredfrequently or continuously in comatose patients after ROSC(Class I, LOE
C-LD).The same anticonvulsant regimens for the treatment of statusepilepticus caused by
other etiologies may be consideredafter cardiac arrest (Class IIb, LOE C-LD).
  Maintaining the Paco2 within a normal physiological range,taking into account any
temperature correction, may be reasonable(Class IIb, LOE B-NR).
 An EEG for the diagnosis of seizure should be promptlyperformed and interpreted, and then
should be monitoredfrequently or continuously in comatose patients after ROSC(Class I, LOE
C-LD).The same anticonvulsant regimens for the treatment of statusepilepticus caused by
other etiologies may be consideredafter cardiac arrest (Class IIb, LOE C-LD).
 Maintaining the Paco2 within a normal physiological range,taking into account any
temperature correction, may be reasonable(Class IIb, LOE B-NR).
 To avoid hypoxia in adults with ROSC after cardiac arrest, itis reasonable to use the highest
available oxygen concentrationuntil the arterial oxyhemoglobin saturation or the partial
pressureof arterial oxygen can be measured (Class IIa, LOE C-EO).
 When resources are available to titrate the Fio2 and to monitoroxyhemoglobin saturation, it is
reasonable to decreasethe Fio2 when oxyhemoglobin saturation is 100%, providedthe
oxyhemoglobin saturation can be maintained at 94% orgreater (Class IIa, LOE C-LD).
 The benefit of any specific target range of glucose managementis uncertain in adults with
ROSC after cardiac arrest(Class IIb, LOE B-R).

PROGNOSTICATION:

 The earliest time for prognostication using clinical examination in patients treated with TTM,
where sedation or paralysis could be a confounder, may be 72 hours after return to
normothermia (Class IIb, LOE C-EO).
 The recommended earliest time to prognosticate a poor neurologic outcome using clinical
examination in patients not treated with TTM is 72 hours after cardiac arrest (Class I, LOE B-
NR).
 In comatose patients who are not treated with TTM, theabsence of pupillary reflex to light at
72 hours or more aftercardiac arrest is a reasonable exam finding with which to predict poor
neurologic outcome(FPR, 0%; 95% CI, 0%–8%;Class IIa, LOE B-NR).
 In comatose patients who are treated with TTM, theabsence of pupillary reflex to light at 72
hours or more aftercardiac arrest is useful to predict poor neurologic outcome(FPR, 1%; 95%
CI, 0%–3%; Class I, LOE B-NR).
 In comatose patients it is recommend that, given their unacceptable (False Positive
Rates)FPRs, thefindings of either absent motor movements or extensor posturingshould not be
used alone for predicting a poor neurologicoutcome (FPR, 10%; 95% CI, 7%–15% to FPR,
15%; 95%CI, 5%–31%; Class III: Harm, LOE B-NR). The motor examinationmay be a
reasonable means to identify the population who need further prognostic testing to predict
poor outcome (Class IIb, LOE B-NR).
 We recommend that the presence of myoclonus, which isdistinct from status myoclonus,
should not be used to predictpoor neurologic outcomes because of the high FPR (FPR,
5%;95% CI, 3%–8% to FPR, 11%; 95% CI, 3%–26%; Class III:Harm, LOE B-NR).
 In combination with other diagnostic tests at 72 or morehours after cardiac arrest, the presence
of status myoclonusduring the first 72 to 120 hours after cardiac arrest is a reasonablefinding
to help predict poor neurologic outcomes (FPR,0%; 95% CI, 0%–4%; Class IIa, LOE B-NR).
 In comatose post–cardiac arrest patients who are treated withTTM, it may be reasonable to
consider persistent absence ofEEG reactivity to external stimuli at 72 hours after cardiacarrest,
and persistent burst suppression on EEG after rewarming,to predict a poor outcome (FPR, 0%;
95% CI, 0%–3%; Class IIb, LOE B-NR).
 Intractable and persistent (more than 72 hours) status epilepticusin the absence of EEG
reactivity to external stimulimay be reasonable to predict poor outcome (Class IIb, LOEB-
NR).
 In comatose post–cardiac arrest patients who are nottreated with TTM, it may be reasonable to
consider the presenceof burst suppression on EEG at 72 hours or more aftercardiac arrest, in
combination with other predictors, to predicta poor neurologic outcome (FPR, 0%; 95% CI,
0%–11%;Class IIb, LOE B-NR).
 In patients who are comatose after resuscitation from cardiacarrest regardless of treatment
with TTM, it is reasonable toconsider bilateral absence of the N20 SSEP wave 24 to 72hours
after cardiac arrest or after rewarming a predictor ofpoor outcome (FPR, 1%; 95% CI, 0%–
3%; Class IIa, LOEB-NR).
 In patients who are comatose after resuscitation from cardiacarrest and not treated with TTM,
it may be reasonable to usethe presence of a marked reduction of the GWR on brain
CTobtained within 2 hours after cardiac arrest to predict pooroutcome (Class IIb, LOE B-NR).
 It may be reasonable to consider extensive restriction ofdiffusion on brain MRI at 2 to 6 days
after cardiac arrest incombination with other established predictors to predict apoor neurologic
outcome (Class IIb, LOE B-NR).
 Given the possibility of high FPRs, blood levels of NSE andS-100B should not be used alone
to predict a poor neurologicoutcome (Class III: Harm, LOE C-LD).
 When performed with other prognostic tests at 72 hoursor more after cardiac arrest, it may be
reasonable to considerhigh serum values of NSE at 48 to 72 hours after cardiac arrestto
support the prognosis of a poor neurologic outcome (ClassIIb, LOE B-NR), especially if
repeated sampling reveals persistentlyhigh values (Class IIb, LOE C-LD).
Multiple System Approach to Post–Cardiac Arrest Care
Ventilation Hemodynamics Cardiovascular Neurological Metabolic

Capnography Frequent Continuous Serial Serial Lactate

Rationale: Blood Pressure Cardiac Neurological Rationale:

1)Confirm and Monitoring/Arteria Monitoring Exam
Confirm
secure Airway and lline
Titrate ventilation. Rationale: Rationale:
Rationale: adequate
2)Endotracheal 1)Detect recurrent 1)Serial examinations
1)Maintain perfusion
Tube when perfusion arrhythmia define coma, brain
injury,and prognosis.
Possible for And prevent 2)No
2)Response To verbal
Comatose patients Recurrent prophylactic
hypotension commands or physical
3)Petco ?35–40 antiarrhythmics
2)Meanarterial Stimulation
mm Hg 3)Treat
3)Pressure ?65mm 3)Pupillary Light and
4)Paco arrhythmias
Hg or Systolic corneal reflex,
?40–45 blood pressure ?90 as required
mm Hg spontaneous
mm Hg 4)Remove
eye movement
reversible
4)Gag, cough,
causes
spontaneous

breaths

Chest X-ray Treat 12-lead EEG Serum

Rationale: Hypotension ECG/Troponin Monitoring If Potassium

Confirm Rationale: Rationale: Comatose
Rationale:
Secure airway and 1)Maintain 1)Detect Acute Rationale:
detect causesor perfusion 1)Avoid
Coronary 1)Exclude
complications Fluid bolus if Syndrome/STEleva hypokalemia
tolerated tionMyocardial seizures
of arrest:
2)Anticonvulsants if which
2)Dopamine 5–10 Infarction;
pneumonitis, seizing promotes
mcg/kg per min 2)Assess QT
pneumonia, interval arrhythmias
3)Norepinephrine
pulmonaryedema 0.1–0.5 mcg/kg per 2)Replace
min
to maintain
4)Epinephrine 0.1–
0.5mcg/kgper min K >3.5

mEq/L

Pulse Treat Acute Core Urine Output,

Oximetry/ABG Coronary Temperature Serum

Rationale: Syndrome Measurement
Creatinine
1)Maintain 1)Aspirin/heparin If Comatose
Rationale:
adequate 2)Transfer to Rationale:
1)Detect
oxygenation Acute coronary 1)Minimize

and Treatment center brain injury and acute

minimize 3)Consider improve outcome kidney

Fio2 Emergent PCI or
injury
2)Prevent
2)Spo2 ?94% fibrinolysis
hyperpyrexia 2)Maintain
3)Pao2 ?100 mm Hg
>37.7°C euvolemia
4)Reduce
3)Induce therapeutic
Fio2as 3)Renal
hypothermia
tolerated Replacement
if no contraindications
5)Pao /Fio2 ratio to therapy
follow 4)Cold IV fluid
if
Acute lung Bolus 30 mL/kg if no
indicated
injury contraindication

5)Surface or
endovascular cooling

for 32°C–34°C×24

hours

6)After

24 hours, slow
 rewarming

0.25°C/hr

Mechanical Echocardiogram Consider Serum

Nonenhanced
Ventilation Rationale: Glucose
CT
Rationale: 1)Detect Rationale:
Scan
1)Minimize global 1)Detect
Rationale:
acute stunning, hyperglycemia
Exclude
lung wallmotion and
primary
injury, abnormalities, hypoglycemia
intracranial
potential structural 2)Treat
process
oxygen problems hypoglycemia

toxicity or (<80

2)Tidal cardiomyopathy mg/dL)

Volume with

6–8 dextrose

mL/kg 3)Treat

3)Titrate hyperglycemia

minute to

ventilation target

to P etco2 glucose

?35–40 144–180

Mm Hg mg/dL

Paco2 ?40–45 4)Local

mm Hg insulin

4)Reduce protocols

Fioas

tolerated

to keep
Spo2or Sao2

?94%

Treat Sedation/Muscle Avoid

Relaxation
Myocardial Hypotonic
Rationale:
Stunning Fluids
1)To
1)Fluids Rationale:
control
To optimize 1)May
shivering,
Volume status increase
agitation,
(requires clinical edema,
or
judgment) including
ventilator
2)Dobutamine cerebral
desynchrony
5–10 mcg/kg edema
as needed
per min

3)Mechanical

augmentation

(IABP)

Key changes in 2015 CPR guidelines summarized:

Parameters
that have been 2010 2015 Remarks
changed

BLS

Chest Chest compressions Chest compressions at The upper limit rate of 120/min has
compression at a rate of at least a rate of 100 to beenadded because 1large registry
rate 100/min. 120/min. data suggested that as the

compression rate increases to more

than 120/min, compression depth
decreases in a dose-dependent
manner. For ex,the proportion of
compressions of inadequate depth
 wasabout 35% for a compression
rate of 100 to 119/minbut increased
to inadequate depth in 50% of
compressionswhen the compression
rate was 120 to 139/min and to
inadequate depth in 70% of
compressions when compression rate
was more than 140/min.

Chest The adult sternum chest compressions to A recent very smallstudy suggests
Compression should be a depth of at least 2 potential injuries (none life
Depth depressed at least 2 inches (5 cm.) avoid threatening) fromexcessive chest
inches (5 cm.) excessive chest compression depth (greater than 2.4
compression depth inches[6 cm]).
(greater than 2.4
inches [6 cm.])

Chest Recoil Rescuers should Rescuers to avoid Chest wall recoil creates a relative
allow complete leaning on the chest in negativeintrathoracic pressure that
recoil of the chest between promotes venous return
after each compressions, to andcardiopulmonary blood flow.
compression, to allow full chest wall Leaning on the chest wallbetween
allow the heart to recoil for adults in compressions precludes full chest
fill completely cardiac arrest. wall recoil.
before the next
compression Incomplete recoil raises intrathoracic
pressure and reduces

venous return, coronary perfusion

pressure, and myocardial blood flow
and can influence resuscitation
outcomes.

Compression No emphasis on Goal ofa chest The addition of a target compression

fraction compression compression fraction fraction is intended to
fraction as high as possible, limitinterruptions in compressions
with a target of at least and to maximize coronaryperfusion
60% and blood flow during CPR.

Shock First When any rescuer For witnessed adult While numerous studies have
witnesses an out- cardiac arrest when an addressed the question of whether a
vs of-hospital arrest AED is immediately benefit is conferred by providing a
CPR First and an AED is available, it isspecified period (typically 1½ to 3
immediately reasonable minutes) of chest compressions
available on- before shock delivery, as compared
site,the rescuer that the defibrillator with
should start CPR be used as soon as
with chest possible. For adults delivering a shock as soon as the
compressions and with unmonitored AED can be readied, no difference in
 use the AED as cardiac arrest or for outcome has been shown. CPR
soon as possible. whom an AED should be provided while the AED
HCPs who treat pads are applied and until the AED
is not immediately is ready to analyze the rhythm.
cardiac arrest in available, it is
hospitals and other reasonable that CPR
facilities with on- be initiated while the
site AEDs or defibrillator
defibrillators equipment is being
should provide
immediate CPR retrieved and applied
and should use the and that defibrillation,
AED/defibrillator if indicated, be
as soon as it is attempted as soon as
available. the device is ready for
use

ACLS

Ventilation When an advanced It may be reasonable This simple single rate for adults,
During CPR airway is in place for the provider to children, andinfants—rather than a
With an during 2-person range of breaths per minute—
CPR, give 1 breath deliver 1 breath every shouldbe easier to learn, remember,
Advanced every 6 to 8 6 seconds (10 breaths and perform.
Airway seconds without per minute)
attempting to while continuous
synchronize breaths chest compressions
betweencompressio are being performed
ns(this will result in
delivery of 8 to 10 (ie, during CPR with
breaths per an advanced airway).
minute).

Vasopressin One dose of

Vasopressin in Review of the available evidence
vasopressin 40
combination with shows that efficacy of the 2 drugs is
units IV/IO may epinephrineoffers no similar and that there is no
replace either the advantage as a demonstrable benefitfrom
first or second dose
substitute for administering both epinephrine and
of standard-dose vasopressin as compared with
epinephrine alone. For
epinephrine in the epinephrine in cardiac simplicity,vasopressin has been
treatment of arrest. removed from the Adult
cardiac arrest.
Cardiac Arrest Algorithm.
Epinephrine No emphasis. It may be reasonable A very large observational study of
to administer cardiac arrest with
epinephrine as soon
as feasible after the Nonshockable rhythm compared
onset of cardiac arrest epinephrine given at 1 to
due to an 3 minutes with epinephrine given at
initialnonshockable 3 later time intervals (4
rhythm. to 6, 7 to 9, and greater than 9
minutes). The study found

an association between early

administration of epinephrine

and increased ROSC, survival to

hospital discharge, and

neurologically intact survival.

PROGNOSIS- No emphasis. In intubated patients, Failure to achieve an ETCO2 of 10

ETCO2 for failure to achieve an mm Hg bywaveform capnography
Prediction of after 20 minutes of resuscitation
ETCO2 of greater hasbeen associated with an
Failed
than 10 mm Hg by extremely poor chance of ROSC and
Resuscitation
waveform survival. However, the studies to
capnography date are limited in thatthey have
after 20 minutes of confounders and have included small
CPR may be numbers of patients, so it is not
considered as advisable to rely solely on ETCO2
onecomponent of a in determining when to terminate
multimodal approach resuscitation.
to decide when to
endresuscitative
efforts but should not
be used in isolation.

Extracorporeal No emphasis. ECPR may be Although no high-quality studies

CPR considered among have comparedECPR to
select cardiacarrestconventional CPR, a number of
patients who have not lower-quality studies suggest
responded to initial improved survival with good
conventional neurologicoutcome for select patient
populations. Because ECPR
CPR, in settings isresource intensive and costly, it
where it can be should be considered onlywhen the
rapidly implemented. patient has a reasonably high
likelihood of benefit— in cases
where the patient has a potentially
 reversible illnessor to support a
patient while waiting for a cardiac
transplant.

POST CARDIAC ARREST CARE

Coronary Primary PCI Coronaryangiography Multiple observational studies found

Angiography (PPCI) after ROSC should be performed positiveassociations between
in subjectswith emergency coronary
arrest of presumed emergently (rather revascularizationand both survival
ischemic cardiac than later in the and favorable functional
etiology may be hospital stay or not at outcome.Because the outcome of
all)for OHCA patients comamay be improved by correction
reasonable, even in with suspected cardiac of cardiac instability, and
the absence of a etiology of arrest theprognosis of coma cannot be
clearly defined reliably determined in the first
STEMI. and ST elevation on
ECG. Emergency few hours after cardiac arrest,
Appropriate coronaryangiography emergency treatment of post–
treatment of acute
coronary is reasonable for select cardiac arrest patients should follow
syndromes (ACS) (eg, electricallyor identical guidelines.
or STEMI, hemodynamicallyunst
including PCI or able) adult patients
fibrinolysis, should who are comatose
be initiated after OHCA of
suspected cardiac
regardless of coma. origin but without ST
elevation on ECG.
Coronary angiography
is reasonable in post–
cardiacarrest patients
for whom coronary
angiography is
indicated, regardless
of whether the patient
is comatose or awake.

Targeted Comatose (ie, All comatose (ie, A recent high-quality study

Temperature lacking of lacking meaningful compared temperature
Management meaningful
response response to verbal management at 36°C and at 33°C
commands) adult and found outcomes to be similar for
to verbal patients with ROSC both. Taken together, the initial
commands) adult studies suggest that TTM is
patients with after cardiac arrest beneficial, so the recommendation
ROSC after outof- should have TTM, remains to select a single target
 hospital VF cardiac with a target temperature and perform TTM.
arrest should be
cooled to 32°C to temperature between Given that 33°C is no better than
32°C and 36°C 36°C, clinicians can select
34°C for 12 to 24 selected and achieved,
hours. Induced then maintained from a wider range of target
hypothermia also constantly for at least temperature. The
may be considered 24 hours. selectedtemperature may be
for comatose adult determined by clinician orclinical
patients with factors.
ROSC after IHCA
of any initial
rhythm or after
OHCA with an
initial rhythm of
pulseless electrical
activity or asystole.

Continuing No emphasis. Actively preventing In some observational studies, fever

Temperature fever in comatose after rewarmingfrom TTM is
Management patients associated with worsened neurologic
Beyond injury,
after TTM is
24 Hours reasonable. although studies are conflicting.
Because preventing fever

after TTM is relatively benign and

fever may be associated with harm,
preventing fever is suggested.

Hemodynamic No emphasis. It may be reasonable Studies of patients after cardiac

Goals After to avoid and arrest have found that a
Resuscitation immediately
systolic blood pressure less than 90
correct hypotension mm Hg or a mean arterial pressure
(systolic blood of less than 65 mm Hg is associated
pressure less than 90 with higher mortality and
diminishedfunctional recovery,
mm Hg, mean arterial while systolic arterial pressures of
pressure less than 65 greater than 100 mm Hg are
mm Hg) during associated with better recovery.
post–cardiac arrest While higher pressures appear
care. superior, specific systolic or mean
arterial pressure targets could notbe
identified, because trials typically
studied a bundle of
manyinterventions, including
hemodynamic control. Also, because
baseline blood pressure varies from
 patient to patient, differentpatients
may have different requirements to
maintain optimal

organ perfusion.

Prognosticatio While times for 1)The earliest time to Clinical findings, electrophysiologic
n After usefulness of prognosticate a poor modalities, imagingmodalities, and
Cardiac Arrest specific tests were blood markers are all useful for
identified, no neurologic outcome predictingneurologic outcome in
specific overall using clinical comatose patients, but each
recommendation examination in finding,test, and marker is affected
was made about patients not treated differently by sedation
time to with TTM is 72 hours andneuromuscular blockade. In
prognostication. after cardiac arrest, addition, the comatose brain
but this time can be
even longer after may be more sensitive to
cardiac arrest if the medications, and medications
residual effect of maytake longer to metabolize after
sedation or paralysis is cardiac arrest.
suspected to confound
the clinical No single physical finding or test
examination. can predict neurologic

2) recovery after cardiac arrest with

100% certainty. Multiple

modalities of testing and

examination used together to

predict outcome after the effects of

hypothermia and

medications have been allowed to

resolve, are most likely to

provide accurate prediction of

outcome

List of commonly used drugs.

Table 1. IV Drugs Used for Tachycardia

Precautions or Special
Drug Characteristics Indication(s) Dosing Side Effects Considerations
Intravenous Drugs
Used to Treat
Supraventricular
Tachyarrhythmias
Adenosine Endogenous purine ● Stable, narrow-complex regular tachycardias 6 mg IV as a rapid IV push Hypotension, Contraindicated in
nucleoside; briefly ● Unstable narrow-complex regular tachycardias followed by a 20 mL saline flush; bronchospasm, patients with asthma;
depresses sinus while preparations are made for electrical repeat if required as 12 mg IV chest discomfort may precipitate atrial
node rate and AV cardioversion push fibrillation, which may be
node conduction; ● Stable, regular, monomorphic, wide complex very rapid in patients
vasodilator tachycardia as a therapeutic and diagnostic with WPW; thus a
maneuver defibrillator should be
readily available; reduce
dose in post–cardiac
transplant patients, those
taking dipyridamole or
carbamazepine and when
administered via a central
vein

Diltiazem, Non-dihydropyridine ● Stable, narrow-complex tachycardias if rhythm Diltiazem: Initial dose 15 to 20 Hypotension, Should only be given to
Verapamil calcium channel remains uncontrolled or unconverted by mg (0.25 mg/kg) IV over 2 bradycardia, patients with
blockers; slow AV adenosine or vagal maneuvers or if SVT is minutes; additional 20 to 25 mg precipitation of narrow-complex
node conduction and Recurrent (0.35 mg/kg) IV in 15 minutes if heart failure tachycardias (regular or
increase AV node ● Control ventricular rate in patients with atrial needed; 5 to 15 mg/h IV irregular). Avoid in
refractoriness; fibrillation or atrial flutter maintenance infusion (titrated to patients with heart
vasodilators, AF heart rate if given for rate failure and pre-excited
negative inotropes control) AF or flutter or rhythms
Verapamil: Initial dose 2.5 to 5 consistent with VT
mg IV given over 2 minutes; may
repeat as 5 to 10 mg every 15 to
30 minutes to total dose of 20 to
30 mg
Atenolol, b-Blockers; reduce ● Stable, narrow-complex tachycardias if rhythm Atenolol (b1 specific blocker) 5 Hypotension, Avoid in patients with
Esmolol, effects of circulating remains uncontrolled or unconverted by mg IV over 5 minutes; repeat 5 bradycardia, asthma, obstructive
Metoprolol, catecholamines; adenosine or vagal maneuvers or if SVT is mg in 10 minutes if arrhythmia precipitation of airway disease,
Propranolol reduce heart rate, Recurrent persists or recurs heart failure decompensated heart
AV node conduction ● Control ventricular rate in patients with atrial Esmolol (b1 specific blocker with failure and pre-excited
and blood pressure; fibrillation or atrial flutter 2- to 9-minute half-life) IV artrial fibrillation or
negative inotropes ● Certain forms of polymorphic VT (associated loading dose 500 mcg/kg (0.5 Flutter
with acute ischemia, familial LQTS, mg/kg) over 1 minute, followed
catecholaminergic) by an infusion of 50 mcg/kg per
minute (0.05 mg/kg per minute);
if response is inadequate, infuse
second loading bolus of 0.5
mg/kg over 1 minute and
increase maintenance infusion to
100 mcg/kg (0.1 mg/kg) per
minute; increment; increase in
this manner if required to
maximum infusion rate of 300
mcg/kg @0.3 mg/kg# per minute
Metoprolol (b1 specific blocker) 5
mg over 1 to 2 minutes repeated
as required every 5 minutes to
maximum dose of 15 mg
Propranolol (nonselective
b-blocker) 0.5 to 1 mg over 1
minute, repeated up to a total
dose of 0.1 mg/kg if required

(CONTINUED)
 Precautions or Special
Drug Characteristics Indication(s) Dosing Side Effects Considerations
Amiodarone Multichannel blocker ● Stable irregular narrow complex tachycardia 150 mg given over 10 minutes Bradycardia,
(sodium, potassium, (atrial fibrillation) and repeated if necessary, hypotension,
calcium channel, ● Stable regular narrow-complex tachycardia followed by a 1 mg/min infusion phlebitis
and noncompetitive ● To control rapid ventricular rate due to for 6 hours, followed by 0.5
a/b-blocker) accessory pathway conduction in pre-excited mg/min. Total dose over 24
atrial arrhythmias hours should not exceed 2.2 g.
Digoxin Cardiac glycoside ● Stable, narrow-complex regular tachycardias if 8 to 12 mcg/kg total loading Bradycardia Slow onset of action and
with positive rhythm remains uncontrolled or unconverted dose, half of which is relative low potency
inotropic effects; by adenosine or vagal maneuvers or if SVT is administered initially over 5 renders it less useful for
slows AV node Recurrent minutes, and remaining portion treatment of acute
conduction by ● Control ventricular rate in patients with atrial as 25% fractions at 4- to 8- hour arrhythmias
enhancing fibrillation or atrial flutter intervals
parasympathetic
tone; slow onset of
action
Intravenous Drugs
Used to Treat
Ventricular
Tachyarrhythmias
Procainamide Sodium and ● Hemodynamically stable monomorphic VT 20 to 50 mg/min until arrhythmia Bradycardia, Avoid in patients with QT
potassium channel suppressed, hypotension ensues, hypotension, prolongation and CHF
blocker or QRS prolonged by 50%, or torsades de
total cumulative dose of 17 pointes
mg/kg; or 100 mg every 5
minutes until arrhythmia is
controlled or other conditions
described above are met
Amiodarone Multichannel blocker ● Hemodynamically stable monomorphic VT
(sodium, potassium, ● Polymorphic VT with normal QT interval 150 mg given over 10 minutes Bradycardia,
calcium channel, and repeated if necessary, hypotension,
a- and noncompetitive followed by a 1 mg/min infusion phlebitis
b-blocker) for 6 hours, followed by 0.5
mg/min. Total dose over 24
hours should not exceed 2.2 g.
 Sotalol Potassium channel ● Hemodynamically stable monomorphic VT In clinical studies 1.5 mg/kg Bradycardia, Avoid in patients with QT
blocker and infused over 5 minutes; however, hypotension, prolongation and CHF
nonselective US package labeling recommends torsades de
b-blocker any dose of the drug should be Pointes
infused slowly over a period of 5
hours
Lidocaine Relatively weak ● Hemodynamically stable monomorphic VT Initial dose range from 1 to 1.5 Slurred speech,
sodium channel mg/kg IV; repeated if required at Altered
blocker 0.5 to 0.75 mg/kg IV every 5 to consciousness,
10 minutes up to maximum seizures,
cumulative dose of 3 mg/kg; 1 to Bradycardia
4 mg/min (30 to 50 mcg/kg per
minute) maintenance infusion
Magnesium Cofactor in variety of ● Polymorphic VT associated with QT 1 to 2 g IV over 15 minutes Hypotension, Follow magnesium levels
cell processes prolongation (torsades de pointes) CNS toxicity, if frequent or prolonged
including control of Respiratory dosing required,
sodium and Depression particularly in patients
potassium transport with impaired renal
Function

Atropine

Atropine remains the first-line drug for acute symptomatic bradycardia (Class IIa, LOE B).
Clinical trials in adults showed that IV atropine improved heart rate, symptoms, and signs
associated with bradycardia. Atropine sulfate reverses cholinergic-mediated decreases in heart
rate and should be considered a temporizing measure while awaiting a transcu-taneous or
transvenous pacemaker for patients with symp-tomatic sinus bradycardia, conduction block at
the level of the AV node, or sinus arrest.

The recommended atropine dose for bradycardia is 0.5 mg IV every 3 to 5 minutes to a

maximum total dose of 3 mg. Doses of atropine sulfate of, 0.5 mg may paradoxically result in
further slowing of the heart rate. Atropine admin-istration should not delay implementation of
external pacing for patients with poor perfusion.

Use atropine cautiously in the presence of acute coronary ischemia or MI; increased heart rate
may worsen ischemia or increase infarction size. Atropine will likely be ineffective in patients
who have undergone cardiac transplantation because the transplanted heart lacks vagal
innervation. One small uncontrolled study documented paradoxical slowing of the heart rate and
high-degree AV block when atropine was administered to patients after cardiac
transplantation.369
Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with
third-degree AV block with a new wide-QRS complex where the location of block is likely to be
in non-nodal tissue (such as in the bundle of His or more distal conduction system). These
bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and
are preferably treated with TCP or b-adrenergic support as temporizing measures while the
patient is prepared for trans-venous pacing.

Epinephrine

Epinephrine hydrochloride produces beneficial effects in patients during cardiac arrest, primarily
because of its a-adrenergic receptor-stimulating (ie, vasoconstrictor) properties. The a-adrenergic
effects of epinephrine can increase CPP and cerebral perfusion pressure during CPR. The value
and safety of the b-adrenergic effects of epinephrine are controversial because they may increase
myocardial work and reduce subendocardial perfusion.

There are no RCTs that adequately compare epinephrine with placebo in treatment of and
outcomes related to out-of-hospital cardiac arrest. A retrospective study compared epinephrine to
no epinephrine for sustained VF and PEA/ asystole and found improved ROSC with epinephrine
but no difference in survival between the treatment groups. A meta-analysis and other studies
have found improved ROSC, but none have demonstrated a survival benefit of high-dose
epinephrine versus standard-dose epinephrine in cardiac arrest.
It is reasonable to consider administering a 1 mg dose of IV/IO epinephrine every 3 to 5 minutes
during adult cardiac arrest (Class IIb, LOE A). Higher doses may be indicated to treat specific
problems, such as a b-blocker or calcium channel blocker overdose. Higher doses can also be
considered if guided by hemodynamic monitoring such as arterial relaxation ―diastolic‖ pressure
or CPP. If IV/IO access is delayed or cannot be established, epinephrine may be given
endotracheally at a dose of 2 to 2.5 mg.
CONCLUSION: High quality CPR comprising of early chest compressions with minimal
interruptions, early defibrillation and multidisciplinary post cardiac arrest is key to improve
survival and neurological outcome after cardiac arrest.
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