1. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 1
1 CARDIAC RESUSCITATION
Terry J. Mengert, M.D.
Approach to Cardiovascular Resuscitation
Out-of-hospital sudden cardiac arrest claims the lives of more than INITIATION OF CPR
300,000 persons in the United States each year, making it the leading While awaiting the arrival of a defibrillator and advanced help,
cause of death.1-4 In fact, approximately 50% of all cardiac deaths are the rescuer assesses the patient’s airway, breathing, and circulation
sudden deaths.5 In hospitals, a minimum of 370,000 patients also suf- [see The Primary Survey, below] and initiates CPR [see Table 1].
fer a cardiac arrest, followed by an attempted, but only sometimes When CPR is started within 4 minutes of collapse, the likelihood of
successful, resuscitation.6 Although most victims of sudden death patient survival at least doubles.17,18
have underlying coronary artery disease (70% to 80%), sudden death
is the first manifestation of the disease in half of these persons.2 Other INITIATION OF DEFIBRILLATION
causes and contributing factors include abnormalities of the my- When the AED or monitor-defibrillator arrives, attach it appro-
ocardium (i.e., chronic heart failure or hypertrophy from any cause), priately to the patient and analyze the patient’s rhythm; if the patient
electrophysiologic abnormalities, valvular heart disease, congenital is in VF or pulseless VT, a defibrillatory shock should be rapidly ap-
heart disease, and miscellaneous inflammatory and infiltrative disease plied [see Tables 2 and 3]. If required, two additional shocks may be
processes (e.g., myocarditis, sarcoidosis, and hemochromatosis).7-9 administered sequentially.The importance of rapid access to defib-
The pathophysiology that culminates in a sudden cardiac death rillation cannot be overemphasized. In a patient who is dying from a
is complex and poorly understood. It likely represents a mix of elec- shockable rhythm, the chance of survival declines by 7% to 10% for
trical abnormalities combined with acute functional triggers, such every minute that defibrillation is delayed.19
as myocardial ischemia, central and autonomic nervous system ef-
fects, electrolyte abnormalities, and even pharmacologic influ- INITIATION OF ADVANCED CARE
ences.1 Classically, most sudden deaths that occur in adults in the
If the patient remains pulseless despite the steps described above,
community are thought to be secondary to ventricular tachycardia
resume CPR; establish a definitive airway, confirm its correct place-
(VT) that quickly degenerates into ventricular fibrillation (VF). In a
ment, and then secure it; establish intravenous access; then adminis-
10-year study in the Seattle area, the different arrhythmias found in
ter appropriate medications as determined by the rhythm and the ar-
prehospital cardiac arrest patients presumed to have underlying car-
rest circumstances. If the patient is in VF or pulseless VT, repeated
diovascular disease were VF (45%), asystole (31%), pulseless elec-
attempts at defibrillation are interspersed with delivery of vasoactive
trical activity (PEA; 10%),VT (1%), and other arrhythmias (14%).3
and antiarrhythmic drugs [see Table 4].
Studies indicate that the out-of-hospital incidence of VF has de-
creased in recent years, probably because of the decrease in mortal- RESUSCITATION OUTCOME
ity from coronary artery disease.10
When every link in the chain of survival is quickly and sequen-
tially available, the patient is provided an optimal opportunity for
return of spontaneous circulation.19-22 In the United States, indi-
The Chain of Survival
vidual communities report survival rates of 4% to 40% or more in
The resuscitation of an adult victim of cases of sudden cardiac death.23-27 Prehospital victims of VF have
sudden cardiac arrest should follow an had survival rates to hospital discharge of greater than 50% when
orderly sequence, no matter where the an AED was expeditiously used.28 Many other factors also influ-
patient’s collapse occurs. This sequence ence patient survival, however; these include whether the patient’s
is called the chain of survival.11 It com- collapse was witnessed, the rapidity and effectiveness of bystander
prises four elements, all of which must be CPR, the rhythm associated with the cardiac arrest, and underly-
instituted as rapidly as possible: activa- ing comorbidities.29,30 With inpatient cardiac arrest, for example,
tion of the emergency medical service overall survival rates vary from 9% to 32%,31-37 but in one study,
network, cardiopulmonary resuscitation survival to hospital discharge was 30% for patients with primary
(CPR), early defibrillation, and provision heart disease, 15% for patients with infectious diseases, and only
of advanced care. 8% for patients with other end-stage diseases (e.g., cancer, lung
ACTIVATION OF EMERGENCY MEDICAL SERVICES disease, liver failure, or renal failure).38
Such statistics underline the importance of using cardiac resusci-
A person in cardiac arrest is unresponsive and pulseless, although tation appropriately and with discrimination. Cardiac resuscitation
agonal respirations may last for minutes. Confirm unresponsiveness provides rescuers with powerful tools that save the lives of thou-
by speaking loudly and gently shaking the patient. If the patient is sands of people every year.These techniques are capable of return-
truly unresponsive, immediately call for help by activating the emer- ing patients who would otherwise die to productive and meaningful
gency medical service in the community (in most locales, this
lives. However, cardiac resuscitation should not be employed to re-
means calling 911); or if the patient is already in the hospital, call a
verse timely and natural death. Under those circumstances, it has
code (e.g., code blue, code 199). If an automated external defibril-
the potential to lengthen the dying process and to increase human
lator (AED) is available, have it brought to the resuscitation scene.
suffering. All practitioners are well advised to remember that “death
AEDs are both easily used and lifesaving.12-16
is not the opposite of life, death is the opposite of birth. Both are as-

2. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 2
Patient is in cardiac arrest
Confirm unresponsiveness.
If out of hospital, call EMS.
If in hospital, activate appropriate code.
Approach to Call for a defibrillator.
Cardiovascular
Resuscitation Primary survey
Assess ABCs.
Begin CPR; when defibrillator arrives,
attach to patient and briefly withhold CPR.
Assess rhythm.
Pulseless VT or VF Pulseless electrical activity Asystole
Immediately administer shock, first at 200 J, Resume CPR. Resume CPR and confirm asystole.
then 200–300 J, then 360 J; if patient is already Ensure that patient is appropriately attached to
attached to a monitor-defibrillator, begin monitor-defibrillator, that ECG gain control on
resuscitation with immediate defibrillation. the defibrillator is at maximum, and that the
Resume CPR. rhythm is assessed in several leads.
Secondary survey
Endotracheally intubate, confirm tube placement, secure tube, establish I.V. access.
Concomitantly with preceding steps, identify and correct technical difficulties
hampering resuscitation [see Table 6]; initiate emergency therapy for conditions
contributing to cardiac arrest [see Table 7].
Pulseless VT or VF Pulseless electrical activity Asystole
Subsequent steps assume continuing VT or VF Subsequent steps assume continuing Subsequent steps assume continuing
despite interventions; do not interrupt CPR PEA despite interventions; do not asystole despite interventions; do not
except as required for rapid performance of interrupt CPR except as required for interrupt CPR except as required for rapid
lifesaving procedures. rapid performance of lifesaving performance of lifesaving procedures.
Administer vasoactive drugs with ongoing CPR: procedures. Attempt transcutaneous pacing, if
Epinephrine, 1 mg I.V. push, repeated every Administer epinephrine, 1 mg I.V. push, available (may be initiated simultaneously
3–5 min throughout CPR with ongoing CPR; repeat every 3–5 with above steps).
or min as long as CPR is required. Administer medications with ongoing CPR:
Vasopressin, 40 U I.V. push in a single dose; If heart rate as shown on monitor is Epinephrine, 1 mg I.V. push; repeat
if no response after 10 min, administer slow, administer atropine, 1 mg I.V. every 3–5 min for as long as patient
epinephrine as described above. push, with ongoing CPR; may repeat requires CPR (vasopressin, 40 U I.V.
every 3–5 min to a total dose of 3 mg. one time, is a reasonable alternative)
Follow medication delivery with a 20 ml and
saline bolus and elevation of the Atropine, 1 mg I.V. push; repeat every
Administer antiarrhythmic drugs with ongoing CPR: extremity containing the I.V. line. 3–5 min to a total dose of 3 mg
Amiodarone, 300 mg I.V. push; if a second dose is Follow medication delivery with a 20 ml
needed, 150 mg after 5 min saline bolus and elevation of the
or extremity containing the I.V. line.
Lidocaine, 1.0–1.5 mg/kg I.V. push; if a second
dose is needed, repeat initial dose in 3–5 min. End resuscitation attempt if patient remains
in confirmed asystole for > 10 min and
Hypomagnesemia or torsade de pointes is suspected: there is no technical problem preventing
Magnesium sulfate, 1–2 g I.V. push resuscitation, no imminently treatable
Intermittent or recurrent VT/VF after an initial cause, and no extenuating circumstance.
response to shocks:
Procainamide, 20–50 mg/min I.V. infusion to a
total dose of 17 mg/kg.
Follow medication delivery with a 20 ml saline
bolus; elevate extremity with I.V. line, and continue
CPR for 30–60 sec to circulate medication; then
administer shock (360 J for up to three shocks).

3. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 3
in the laboratory, an arterial pressure wave occurred.42 Further
Table 1 Initial Resuscitation Steps in the study and refinements led to the technique of closed-chest CPR,
the careful description of which was published in 1960.43 The first
Unresponsive Patient
report of the use of this technique in patients was in 1961.44 Since
Confirm unresponsiveness those early days, the fundamentals of closed-chest CPR have re-
Activate the emergency medical system mained relatively unchanged. Mouth-to-mouth, mouth-to-mask,
In most community locales, call 911 or bag-valve-mask ventilation oxygenates the blood. Chest com-
In the hospital, activate the appropriate code response pressions produce forward blood flow.This flow appears to result
Call for an automatic external defibrillator (AED) from a combination of direct compression of the heart and in-
Begin basic life support (CPR) trathoracic pressure changes.45,46
Open airway CPR in isolation does not defibrillate the heart. Its main benefit
Check breathing; if not breathing, deliver two initial breaths
is to extend patient viability until a defibrillator and advanced inter-
Check for a carotid pulse; if pulseless, do the following:
ventions become available and, one hopes, succeed in restoring
Begin chest compressions at the rate of 100 compressions/min, de-
pressing the sternum 4–5 cm per compression in patients older than spontaneous circulation in the patient. CPR is not nearly as effec-
8 yr tive as a contracting heart; systolic arterial pressure peaks of 60 to
Intersperse ventilations with chest compressions: in nonintubated pa- 80 mm Hg may be generated, but diastolic blood pressure remains
tients, deliver 15 compressions, pause for two breaths, then repeat;
in intubated patients, deliver one breath every 5 sec, with no pause low, and a cardiac output of only 25% to 30% of normal can be
in compressions achieved even under optimal conditions.47 Still, effective CPR is
Reassess for return of spontaneous circulation every 1–3 min critical to keeping the patient alive. It is worth remembering that
When defibrillator arrives, immediately analyze and treat arrhythmia the most important rescuers at a cardiac resuscitation are those
Attach patient to AED [see Table 2] or the monitor-defibrillator who are performing expert CPR, because it is only through their ef-
[see Table 3]
Analyze arrhythmia and treat as appropriate
forts that the patient’s heart and brain are kept viable until defibril-
lation and other advanced interventions can restore spontaneous
circulation.
After unresponsiveness is confirmed, the emergency medical
pects of life.”39 It is untimely death that requires immediate inter- system is activated and an AED is called for; the primary survey
vention with cardiac resuscitation. (A, B, C, and D) proceeds as described (see below) until the
AED arrives.
The Primary and Secondary Surveys of Cardiac Airway Optimization
Resuscitation
Open the patient’s mouth and optimize the airway in the non-
A cardiac resuscitation is a stressful event for everyone involved. trauma patient by use of the head-tilt and chin-lift maneuver. A
Too often, clinic and inpatient cardiac arrests and their manage- jaw-thrust maneuver should be used instead of the head-tilt tech-
ment are episodes of chaos in the busy lives of resident and attend- nique if cervical spine injury is suspected. In patients with suspect-
ing physicians.Yet, it has been eloquently stated that a good resusci- ed spine injury, proper spine alignment must be maintained
tation team should function like a fine symphony orchestra.40 Such throughout all phases of the resuscitation. In such circumstances, as
skill levels require dedicated individual and team practice and care-
ful code-team organization. Mastery in cardiac resuscitation is in
fact a lifelong pursuit that requires training and retraining in ad-
vanced cardiac life support (ACLS); regular practice and review;
and leadership and team skill development. Its key elements in- Table 2 Using an Automatic External
clude not only the resuscitation itself but the response to the an- Defibrillator in Patients Older than 8 Years
nouncement of a code, postresuscitation stabilization of the patient,
notification of the family and primary care provider, and code cri- Automatic external defibrillator (AED) arrives (CPR is in progress)
Place AED beside patient.
tique and debriefing.To help practitioners learn and apply some of
Turn on the AED.
the most essential techniques used in cardiac resuscitation more
Attach the electrodes to the AED (they may be preattached).
easily and effectively, the American Heart Association (AHA) has Attach the electrode pads to the patient (as diagrammed on the pads).
developed the concepts of primary and secondary surveys of a pa- AED analyzes patient’s rhythm
tient in atraumatic cardiac arrest.41 Stop CPR (and ensure no one is touching the patient).
Press the Analyze button on the AED (some devices analyze the rhythm
THE PRIMARY SURVEY automatically as soon as the pads are placed on the patient).
The primary survey for the victim of AED instructs rescuers (via an audible voice prompt and/or on-screen
instructions)
sudden cardiac arrest consists of the ap- Shock is indicated: clear the patient (ensure no one is touching the
propriate assessment of the patient’s air- patient) and push the Shock button.
way (A), breathing (B), and circulation After delivering shock, press the Analyze button again; the sequence of
(C) and the simultaneous application of analysis followed by shock (if so indicated) may be performed a total
of three times.
expert CPR until defibrillation (D) be- or
comes possible (assuming the patient is Shock not indicated: reassess the patient for signs of circulation; if pres-
in VF or pulseless VT).Thus, the primary ent, assess the adequacy of breathing; if there are no signs of circula-
survey includes the second and third tion, resume CPR for 1–2 min. After 1 min of CPR, assess the patient
again for signs of circulation; if present, assess the adequacy of
links in the chain of survival (see above). breathing. If the patient is still pulseless, repeat analysis, followed
In 1958, Kouwenhoven noted that when his research fellow (if indicated) by shock steps.
forcefully applied external defibrillating electrodes on a dog’s chest

4. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 4
nal thrusts are then applied, followed by a finger sweep of the
52,89 oropharynx to relieve suspected obstruction, and then ventilation
Table 3 Using a Manual Defibrillator attempts are repeated. Definitive intervention for an obstructed air-
Defibrillator arrives (CPR is in progress)
way in the hospital setting may involve laryngoscopic visualization
Place defibrillator beside patient. of the cause of obstruction and foreign-body removal. If an ade-
Turn defibrillator on (initial energy level setting is typically 200 J).* quate airway cannot be established by less invasive means, cricothy-
Set Lead Select switch to Paddles. Alternatively, if patient is already at- rotomy may be required.
tached to monitor leads, set Lead Select switch to lead I, II, or III; en-
sure all three leads are correctly attached to the patient and the defib- CPR Initiation
rillator: white to right shoulder, black to left shoulder, red to ribs on left
side. The health care rescuer next checks for a carotid pulse in the un-
Apply gel to paddles or place conductor pads on patient’s chest. Some responsive patient but should allow no more than 10 seconds to do
devices use disposable electrode patches that are prepasted with a
conducting gel. In either case, the appropriate positions of the pad-
so. (The AHA no longer recommends pulse checks for rescuers who
dles with applied gel, conductor pads, or disposable paddles are as are not health care providers.49 Instead, lay rescuers should initiate
follows: sternal paddle is placed to the right of the sternum, just below chest compressions if the patient is not breathing, coughing, or mov-
the right clavicle; apex paddle is placed to the left of the left breast,
centered in the left midaxillary line at the fifth intercostal space. ing after the initial two breaths.) If the patient has no carotid pulse,
Analyze rhythm begin chest compressions.The patient should be on a firm surface,
Briefly withhold CPR and the heel of the rescuer’s hand should be in the center of the infe-
If using paddles to assess rhythm, apply paddles as described with firm rior half of the patient’s sternum (but cephalad to the xiphoid
pressure (25 lb of pressure to each paddle) and visually assess rhythm
on monitor (if using leads, briefly withhold CPR and assess rhythm in
process). The rescuer’s other hand is placed on top of the lower
leads I, II, or III). If rhythm is either pulseless VT or VF, proceed as fol- hand, with the fingers interlocked.
lows: The rescuer’s arms are held straight, with the force of each com-
Defibrillate, then reassess pression coming from the rescuer’s trunk. In patients older than 8
Announce to resuscitation team, “Charging defibrillator, stand clear!”
and press Charge button on either paddles or defibrillator (initial
years, the sternum is smoothly compressed by 1.5 to 2.0 inches,
energy, 200 J, not synchronized).* then released.The duration of the compression-release cycle is di-
Warn resuscitation team that a defibrillatory shock is coming: vided equally between compression and release. The rate of chest
“I am going to shock on three! ONE, I’m clear; TWO, you’re clear, compression is 100 compressions/min in patients older than 8
THREE, everybody’s CLEAR!” Simultaneously with these statements,
visually ensure that no resuscitation team member is in contact with years.The chest should be allowed to rebound to its precompres-
patient. sion dimensions between compressions, but the resuscitator’s palm
Press the Discharge buttons on both paddles simultaneously to deliver a closest to the patient should remain in contact with the sternum.
defibrillatory shock.
Reassess rhythm on monitor; if patient is still in VT or VF, recharge defib-
In nonintubated patients, chest compressions are regularly inter-
rillator (now 300 J)* and repeat process of loudly informing team mem- rupted for the delivery of ventilations.The sequence is the same, re-
bers by giving the warning statements as above, and then apply defib- gardless of whether one-rescuer or two-rescuer CPR is being per-
rillatory shock.
formed: the rescuer delivers 15 compressions, pauses for two
Reassess rhythm on monitor; if patient is still in VT or VF, recharge defib-
rillator (now 360 J)* and repeat process of loudly informing team mem- breaths (each given over 2 seconds), then resumes compressions. In
bers by giving the warning statements as above, and then apply defib- endotracheally intubated patients, no pause for ventilation is neces-
rillatory shock.
sary; every 5 seconds, one ventilation is delivered over a period of 1
Reassess rhythm on monitor; if patient is still in VT or VF, resume CPR
and continue with resuscitation sequence. to 2 seconds, while compressions continue.18
The optimal timing and ratio of ventilations to compressions in
*Note: if using a biphasic defibrillator, a lower initial defibrillatory energy level (< 200 J) CPR is an ongoing area of research, which may lead to changes in
without energy escalation on subsequent shocks is acceptable.
VF—ventricular fibrillation VT—ventricular tachycardia
the current recommendations. In the porcine model, for example,
optimal neurologic outcome was achieved with the use of only com-
pressions for the first 4 minutes, followed by a compression-ventila-
tion ratio of 100:2.50 In the prehospital setting, when rapid advanced
equipment becomes available, the patient’s spine requires immobi- care is available within minutes, bystander-initiated mouth-to-
lization with a padded backboard, hard cervical collar, appropriate mouth ventilation combined with chest compressions offers no ad-
bolstering around the patient’s head to prevent movement, and vantage over chest compressions alone.51
strapping of the patient to the backboard.48 Good technique is critical throughout CPR delivery.The patient
should have carotid pulses with chest compressions and should
Breathing Assessment have appropriate breath sounds and chest movement with ventila-
To assess breathing, the rescuer places his or her cheek close to tions. Interestingly, femoral pulsations with CPR do not necessarily
the patient’s mouth and looks, listens, and feels for patient respira- indicate effective CPR; these pulsations often are venous rather
tions. If the respirations are agonal or the patient is apneic, the res- than arterial. Quantitative end-tidal carbon dioxide levels can be
cuer then delivers two initial breaths. Each breath is delivered over monitored, if practical. Higher levels correlate with more effective
1.5 to 2.0 seconds.The patient’s chest should rise with each deliv- CPR and increased survival.52 The patient should be reassessed for
ered breath, and exhalation is allowed for between breaths. Breaths return of spontaneous circulation every 1 to 3 minutes [see Table 1].
may be delivered using the mouth-to-mouth technique with appro-
priate barrier precautions (the patient’s nose should be pinched if Defibrillation
the mouth-to-mouth technique is used) or mouth-to-mask tech- When the monitor-defibrillator or AED arrives, it is attached to
nique.The ideal device, if available, is a bag-valve-mask device at- the patient; the rhythm is analyzed, and if the patient is in VF or
tached to high-flow oxygen; this allows the delivery of a substantial- pulseless VT, defibrillation is provided [see Tables 2 and 3].
ly higher oxygen concentration to the patient. If the patient cannot Defibrillation is thought to work by simultaneously depolarizing a
be ventilated, the rescuer repositions the airway and attempts the sufficient mass of cardiac myocytes to make the cardiac tissue ahead
technique again. If the airway is still obstructed, up to five abdomi- of the VT or VF wavefronts refractory to electrical conduction. Subse-

5. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 5
Table 4 Drugs Useful in Cardiac Arrest3,90
Drug and Doses Indications in
Category Adult Dosage Comments
Supplied Cardiac Arrest
I.V. boluses of epinephrine (1 mg) are appropriate only in
1 mg I.V. push; may repeat every 3–5 min pulseless cardiac arrest patients; if continued epinephrine
Epinephrine, 1 mg in 10 ml Pulseless VT or VF unre-
for as long as patient is pulseless; can is required after resuscitation, a continuous infusion should
emergency syringe; sponsive to initial de-
Vasopressors also be given via the endotracheal route: be started (1–10 µg/min).
1 mg/ml (1 ml and 30 ml fibrillatory shocks; PEA;
2–2.5 mg diluted with normal saline (NS) High-dose epinephrine (up to 0.2 mg/kg I.V. per dose) does
vials) asystole
to 10 ml total volume not improve survival to hospital discharge in cardiac arrest
patients and is no longer recommended in adults.
Vasopressin, Pulseless VT or VF unre- 40 IU I.V. push, single dose only; can also be
If no response after 10 min of continued resuscitation, ad-
20 IU/ml (1 ml vial) sponsive to initial de- given via endotracheal tube: same dose,
minister epinephrine, as above.
fibrillatory shocks diluted with NS to 10 ml total volume
Pulseless VT or VF unre- VT/VF: 300 mg diluted in 20–30 ml; NS or
sponsive to initial de- D5W rapid I.V. push; a repeat dose of
Amiodarone, Side effects may include hypotension and bradycardia in the
fibrillatory shocks and 150 mg may be given if required in 5
50 mg/ml (3 ml vial) postresuscitation phase.
epinephrine plus min; maximum dose in 24 hr should not
shock(s) exceed 2,200 mg
Initial dose: 1–1.5 mg/kg I.V.; for refractory If lidocaine is effective, initiate continuous I.V. infusion at 2–4
Lidocaine, 50 mg or Pulseless VT or VF unre- VF or unstable VT, may repeat 1–1.5 mg/min when patient has return of a perfusing rhythm (but
100 mg in 5 ml emer- sponsive to initial de- mg/kg I.V. in 3–5 min; maximum dose, do not use if this rhythm is an idioventricular rhythm or
gency syringes; pre- fibrillatory shocks and 3 mg/kg third-degree heart block with an idioventricular escape
mixed bag, 1 g/250 ml epinephrine plus May also be given endotracheally: rhythm).
or 2 g/250 ml shock(s) 2–4 mg/kg diluted with NS to 10 ml total Continuous infusion should begin at 1 mg/min in congestive
volume heart failure or chronic liver disease or in elderly patients.
Antiarrhythmics Pulseless VT or VF un- Administer 1–2 g diluted in 100 ml D5W Measured magnesium levels correlate only approximately
responsive to initial de- I.V. over 1–2 min
Magnesium sulfate, with the actual level of deficiency.
fibrillatory shocks and Total body magnesium deficits should be
500 mg/ml (2 ml and Patients with renal insufficiency are at risk for dangerous
epinephrine plus replaced gradually after initial therapy
10 ml vials), or 10 ml hypermagnesemia; use appropriate caution.
shock(s) if suspected has stabilized the emergency: adminis-
emergency syringe
hypomagnesemic ter 0.5–1 g/hr for 3–6 hr, then reassess Side effects may include bradycardia, hypotension, generalized
state continued need weakness, and temporary loss of reflexes.
20–30 mg/min I.V. (up to 50 mg/min if sit-
uation is critical); maximum dose is 17 Administer procainamide during a perfusing rhythm.
Procainamide, 100 mg/ml
Recurrent or intermittent mg/kg over time (but maximum dose is Stop procainamide administration when arrhythmia is ade-
(10 ml injection);
pulseless VT or VF reduced to 12 mg/kg in setting of car- quately suppressed, hypotension occurs, QRS widens to
500 mg/ml (2 ml vial)
diac or renal dysfunction) > 50% of original duration, or maximum dose is administered.
Maintenance infusion is 1–4 mg/min
For asystole or PEA: 1 mg I.V. every 3–5
Atropine, 1 mg in 10 ml Asystole or PEA (if rate of min up to 3 mg Minimal adult dose is 0.5 mg.
Anticholinergic Avoid use in type II second-degree heart block or third-
emergency syringe rhythm is slow) May be given via ET tube: 2–3 mg diluted
with NS to 10 ml degree heart block.
Significant hyperkalemia
In non–dialysis-dependent hyperkalemic patients, bicarbon-
Significant metabolic aci- Hyperkalemia therapy: 50 mEq I.V.
ate is most useful if metabolic acidosis is also present; bi-
dosis unresponsive to Metabolic acidosis: 1 mEq/kg slow I.V. carbonate is less effective in dialysis-dependent renal fail-
Bicarbonate, 50 mEq optimal CPR, oxygena- push; may repeat half initial dose in 10
in 50 ml emergency ure patients. The use of bicarbonate in metabolic acidosis
tion, and ventilation min; ideally, ABGs should help guide fur- management in cardiac arrest patients is controversial.
syringe ther therapy
Certain drug overdoses, in- Side effects may include sodium overload, hypokalemia, and
Miscellaneous cluding tricyclic anti- Use in overdose: discuss with toxicologist metabolic alkalosis.
depressants and aspirin
Significant hyperkalemia Do not use if suspected cause of hyperkalemia is acute
In hyperkalemia: 5–10 ml slow I.V. push;
Calcium chloride, Calcium channel blocker digoxin poisoning.
may repeat if required
100 mg/ml in 10 ml drug overdose Do not combine in same I.V. with sodium bicarbonate.
prefilled syringe In calcium channel blocker overdose: dis-
Profound hypocalcemia of cuss with toxicologist Calcium chloride is not a routine medication in cardiac
other causes arrest.
Note: All medications used during cardiac arrest, when given via a peripheral venous site in an extremity, should be followed by a 20 ml I.V. saline bolus and elevation of the extremity for
10 to 20 sec.
ABG—arterial blood gases D5W—5% dextrose in water ET—endotracheal PEA—pulseless electrical activity VF—ventricular fibrillation VT—ventricular tachycardia
quently, the sinus node or another appropriate pacemaker region of charge was 74% for patients who received their first defibrillation no
the heart with inherent automaticity can resume orderly depolariza- later than 3 minutes after a witnessed collapse.28 In this study, defib-
tion-repolarization, with return of a perfusing rhythm.15,53 The sooner rillation was delivered via an AED operated by casino security officers.
defibrillation occurs, the higher the likelihood of resuscitation.When Early defibrillation is so critical that if a defibrillator is immediately
defibrillation is provided immediately after the onset of VF, its suc- available, its use traditionally takes precedence over CPR for patients
cess rate is extremely high.54 In a study of sudden cardiac arrest pa- in VF or pulseless VT of recent onset. If CPR is already in progress, it
tients in Nevada gambling casinos, the survival rate to hospital dis- should of course be halted while defibrillation takes place. Newer de-

6. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 6
fibrillators can compensate for thoracic impedance, ensuring that the
selected energy level is in fact the energy that is delivered to the my- Table 5 Confirmation of Endotracheal
ocardial tissue. In addition, defibrillators that deliver biphasic defibril-
Tube Placement
lation waveforms instead of the standard monophasic damped sinu-
soidal waveforms allow effective defibrillation at lower energy levels Intubation process
(< 200 joules) and without the need for energy-level escalation during Vocal cords are visualized by intubator
subsequent shocks.15,55-58 In the Optimized Response to Cardiac Ar- Tip of ET tube is seen passing between the cords
rest (ORCA) study, which involved 115 patients with prehospital VF, Cuff of ET tube also passes cords by 1 cm
the 150-joule biphasic-shock AED was more effective than the tradi- Postintubation checks
tional high-energy monophasic-shock AED in four respects: it was Esophageal detector device or end-tidal CO2 detector confirms ET tube
placement in trachea
more successful in producing defibrillation with the first shock (96%
Breath sounds are symmetrical (auscultate over lateral anterior chest
versus 59%); it led to a higher rate of ultimate success with defibrilla- and in midaxillary line bilaterally)
tion (100% versus 84%); it had a better rate of return of spontaneous No gurgling with auscultation over epigastrium
circulation (76% versus 54%); and its use was associated with a high- Patient’s chest rises and falls appropriately with ventilation
er rate of good cerebral performance in the survivors (87% versus ET tube depth is appropriate: 21 cm at the corner of the mouth in
women, 23 cm in men
53%).59 There were no differences, however, in terms of survival to
Secure the ET tube to prevent dislodgment
hospital admission or discharge, and replication of the ORCA find-
Reassess the adequacy of oxygenation and ventilation throughout the re-
ings is lacking at this time. Current AHA guidelines state that lower- suscitation (bedside patient assessment; also obtain ABGs when feasible)
energy biphasic waveform defibrillators are safe and have equivalent After resuscitation, obtain a portable chest radiograph
or higher efficacy for termination of VF, as compared with the stan-
dard monophasic waveform defibrillator.15,49 ABG—arterial blood gas ET—endotracheal
Ongoing research suggests that the duration of VF is a consider-
ation in deciding whether to defibrillate immediately and as soon as
a defibrillator is available or to perform CPR for a brief period first
to “prime the pump” before proceeding to defibrillation. In the theless, oral endotracheal intubation is generally the preferred ad-
porcine model in the setting of prolonged VF (> 10 minutes), CPR vanced airway technique for cardiac resuscitation, especially in the
before countershock provides several physiologic benefits.60 Studies hospital setting, where experienced intubators are generally present;
have found that patients with VF of longer than 5 minutes’ duration in the prehospital setting, the evidence supporting endotracheal in-
had better return of spontaneous circulation, survival to hospital tubation remains inconsistent. Endotracheal intubation isolates the
discharge, and 1-year survival if ambulance personnel provided 3 airway, maintains airway patency, helps protect the trachea from the
minutes of CPR before performing defibrillation than if ambulance ever-present risk of aspiration, helps permit optimal oxygenation
personnel performed defibrillation immediately after arriving at the and ventilation of the patient, allows for tracheal suctioning, and
scene; however, some experts question the validity of these results, even provides a route for delivery of some medications to the sys-
on the basis of study design.61,62 temic circulation (via the pulmonary circulation) if intravenous ac-
cess is unobtainable or lost.63
THE SECONDARY SURVEY
The secondary survey for a victim of Optimization of Breathing and Ventilation
persistent cardiac arrest takes place after When a cardiac arrest patient undergoes endotracheal intuba-
completion of the primary survey. Like tion, correct positioning of the ET tube must be immediately con-
the primary survey, the secondary survey firmed and regularly reconfirmed during and after the resuscitation
follows an ABCD format, which in this [see Table 5]. Routine use of an esophageal detector device or end-
case consists of advanced airway inter- tidal CO2 detector is recommended, along with careful patient ex-
ventions (A); optimized oxygenation and amination. Caution is necessary with qualitative colorimetric end-
ventilation by confirmation of endotra- tidal CO2 detectors because both false positive and false negative
cheal (ET) tube placement and repeated results have been documented during cardiac arrests.65 Breath
reassessment of the adequacy of deliv- sounds should be present during auscultation over the anterior and
ered breaths (B); intravenous access and appropriate medication lateral chest walls, and the patient’s chest should rise and fall with
delivery to the patient’s circulation (C); and definitive therapy (D), delivered ventilations. No gurgling should be heard when the epi-
based on a differential diagnosis that considers the specific disease gastrium is auscultated.The ET tube should be inserted to the ap-
processes thought to be responsible for, or contributing to, the car- propriate depth marking: for average-sized adults, this is 21 cm at
diac arrest. The secondary survey includes the fourth link in the the corner of the mouth in a woman and 23 cm in a man.The pa-
chain of survival, rapid advanced care (see above). tient’s skin color should be reasonable (i.e., not dusky or cyanotic),
provided that the patient’s pigmentation allows such assessment.
Placement of an Advanced Airway Once correct positioning is confirmed, the ET tube is then appro-
Patients who remain in cardiac arrest after completion of the pri- priately secured to prevent its dislodgment.When feasible, an arteri-
mary survey require placement of an advanced airway. Depending al blood gas (ABG) measurement will help further confirm the ade-
on the setting and the experience of the rescuers, this advanced air- quacy of oxygenation and ventilation as the resuscitation proceeds.
way may be a laryngeal mask airway, an esophageal-tracheal Com-
bitube (a tracheal tube bonded side by side with an esophageal ob- Establishment of Circulation Access
turator), or an ET tube.36,63,64 The laryngeal mask airway and the Access to the patient’s venous circulation is mandatory; such ac-
Combitube can be placed by personnel with less training than that cess may be achieved by a code-team member or members simulta-
required for endotracheal intubation, and they do not require addi- neously while other resuscitators pursue steps A and B of the sec-
tional special equipment or visualization of the vocal cords. Never- ondary survey. Ideally, a large intravenous cannula is placed in a

7. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 7
Table 6 Technical Problems That May Prevent a Successful Resuscitation
Problem Patients at Risk Recommendations
Ensure technically perfect CPR.
Confirm carotid pulses with CPR.
Ineffective CPR All cardiac arrest
If arterial line was in place before cardiac arrest, confirm adequate arterial waveform with CPR on arterial line monitor.
patients
Monitor end-tidal CO2 if available (higher levels correlate with better CPR and improved patient survival).
Confirm adequate oxygenation with an ABG when feasible.
Ensure optimal airway positioning and control.
Have suction immediately available to manage pharyngeal and airway secretions.
Ensure use of properly fitting, tightly sealed face mask for bag-valve mask (BVM) ventilation until a definitive airway is
established.
Inadequate Apply cricoid pressure to prevent gastric distention during BVM ventilation until a definitive airway is established.
oxygenation All cardiac arrest Ensure that supplemental oxygen is flowing to BVM at 15 L/min.
and ventilation patients
Deliver an appropriate tidal volume per breath (6–7 ml/kg if oxygen is available) at the rate of 12–15 breaths/min.
Confirm bilateral and equal breath sounds with ventilation.
Confirm that patient’s chest rises with each ventilation.
Allow adequate time for exhalation between breaths.
Confirm optimal oxygenation and ventilation with an ABG when feasible.
Allow ≤ 20–30 sec/intubation attempt.
Intubator should see tip of ET tube and cuff pass between vocal cords at time of intubation.
All patients intubated After intubation, immediately confirm correct ET tube placement; regularly reconfirm ET tube placement throughout
ET tube difficulties resuscitation.
with ET tube
Confirm adequacy of oxygenation and ventilation with an ABG.
After intubation, consider nasogastric tube placement to decompress stomach and optimize diaphragmatic excur-
sions with ventilation.
Place one or more 18-gauge or larger I.V. cannulas in an antecubital or external jugular vein site.
Check for I.V. infiltration regularly throughout the resuscitation.
Follow all medications administered through a peripheral I.V. site with a 20 ml saline bolus and elevation of the
extremity containing the I.V. for 10–15 sec (if possible).
Consider central line placement if the resuscitation is prolonged.
Intravenous line All cardiac arrest Be aware of all I.V. infusions the patient is receiving.
difficulties patients
Stop all nonessential medications that had been started before the cardiac arrest.
During the resuscitation, the only infusions the patient should receive are normal saline, blood products (if clinically
indicated), and pertinent medications necessary to assist with return of spontaneous circulation.
Pulmonary artery catheters and central lines occasionally act as an arrhythmogenic focus within the right ventricle. If
applicable, deflate all relevant balloons on the catheter and withdraw the catheter to a superior vena cava position.
Make sure Synchronization Mode button is in the off position when defibrillating patients in pulseless VT or VF.
Make sure electricity is not arcing over the patient’s chest because of perspiration or smeared conducting gel; dry
patient’s chest with a towel except for areas directly beneath pads or paddles.
Do not administer shock through nitroglycerin paste or patches.
If the patient has an internal cardioverter-defibrillator (ICD) or a pacemaker, the patient may still be manually defibrillat-
Monitor defibrillator All cardiac arrest ed, but do not shock directly over the internal device. Under these circumstances, place the pads or paddles at
difficulties patients least 2.5 cm away from the patient’s internal device. If the ICD is intermittently firing but not defibrillating the patient
and if the ICD is thought to be compromising the resuscitation, turn the device off with a magnet so that manual
defibrillation may take place without interference.
Maximize the gain or electrocardiography “size” and check the rhythm in several leads (or change the axes of the
paddles if reading the rhythm in Paddles mode) to confirm asystole when the initial rhythm appears to be asystole.
ABG—arterial blood gas ET—endotracheal VF—ventricular fibrillation VT—ventricular tachycardia
prominent upper-extremity vein or the external jugular vein to opti- the arrest arrhythmia is asystole or PEA is slow), and miscellaneous
mize delivery of needed medications. If a peripheral line is not drugs used to treat specific problems contributing to the arrest
achievable, additional access possibilities include central line place- state, such as sodium bicarbonate (for severe metabolic acidosis, hy-
ment via the internal jugular, subclavian (via the supraclavicular ap- perkalemia, and certain drug overdoses), and calcium chloride (for
proach), or, less ideally, femoral vein; even intraosseous access is pos- hyperkalemia, calcium channel blocker drug overdose, or severe
sible (intraosseous access is a common emergency vascular access hypocalcemia) [see Table 4].
site in pediatric patients, but it is an unusual route of access in adults). Persons in cardiac arrest (which can result from pulseless VT,VF,
It is useful to remember, as already noted, that some important re- PEA, or asystole) require a vasopressor for as long as they remain
suscitation medications can be delivered via the ET tube in cases of pulseless.Typically, this consists of 1 mg of epinephrine intravenously
failed intravenous access; such medications include naloxone, atropine, every 3 to 5 minutes. Epinephrine stimulates adrenergic receptors,
vasopressin, epinephrine, and lidocaine (mnemonic: NAVEL). which leads to vasoconstriction and optimization of CPR-generated
The commonly used medications in cardiac resuscitation may be blood flow to the heart and brain.Vasopressin (40 units I.V. once only)
grouped into the following general categories: vasopressors (epi- is a reasonable alternative to epinephrine, at least initially.Vasopressin
nephrine or vasopressin), antiarrhythmics (amiodarone, lidocaine, in the recommended dose is a potent vasoconstrictor. It also has the
magnesium, and procainamide), anticholinergic agents (atropine, if theoretical advantage over epinephrine of not increasing myocardial

8. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 8
Table 7 Potentially Treatable Conditions That May Cause or Contribute to Cardiac Arrest3
Condition Clinical Setting Diagnostic and Corrective Actions
Obtain stat ABG.
Preexisting acidosis, diabetes, Reassess technical quality of CPR, oxygenation, and ventilation.
Acidosis diarrhea, drugs, toxins, prolonged Confirm correct endotracheal tube placement.
resuscitation, renal disease, shock Hyperventilate patient (PaCO2 of 30–35 mm Hg) to partially compensate for metabolic acidosis.
If pH < 7.20 despite above interventions, consider I.V. sodium bicarbonate, 1 mEq/kg I.V. slow push.
Initiate large-volume I.V. crystalloid resuscitation.
Hemorrhagic diathesis, malignancy, Confirm diagnosis with emergency bedside echocardiogram, if available.
Cardiac tamponade pericarditis, post cardiac surgery, Perform pericardiocentesis.
post myocardial infarction, trauma Immediate surgical intervention is appropriate if pericardiocentesis is unhelpful but cardiac tamponade is known or
highly suspected clinically.
Adrenal insufficiency, alcohol abuse, Consider clinical setting and obtain finger-stick glucose or stat blood glucose measurements (may be obtained on
aspirin overdose, diabetes, drugs, ABG specimen).
Hypoglycemia
toxins, liver disease, renal disease,
sepsis, certain tumors If glucose < 60 mg/dl, treat: 50 ml = 25 g of D50W I.V. Follow glucose levels closely post treatment.*
Alcohol abuse, burns, diabetic
ketoacidosis, severe diarrhea, Obtain stat serum magnesium level.
diuretics, drugs (e.g., cisplatin,
Hypomagnesemia Treat: 1–2 g magnesium sulfate I.V. over 2 min.
cyclosporine, pentamidine),
malabsorption, poor intake, Follow magnesium levels over time, because blood levels correlate poorly with total body deficit.
thyrotoxicosis
Alcohol abuse, burns, central ner-
vous system disease, debilitated Obtain core body temperature.
and elderly patients, drowning, If severe hypothermia (< 30° C), limit initial shocks for pulseless VT/VF to three, initiate active internal rewarming and
†
Hypothermia drugs, toxins, endocrine disease, cardiopulmonary support, and hold further resuscitation medications or shocks until core temperature > 30° C .
exposure history, homelessness, If moderate hypothermia (30°–34° C), proceed with resuscitation (space medications at intervals greater than usual),
poverty, extensive skin disease, passively rewarm, and actively rewarm truncal body areas.
spinal cord disease, trauma
Initiate large-volume I.V. crystalloid resuscitation.
Obtain stat hemoglobin level on ABG specimen.
Major burns, diabetes, gastrointesti- Emergently transfuse packed red blood cells (O negative if type-specific blood not available) if hemorrhage or pro-
Hypovolemia, hemor- nal losses, hemorrhage, hemor- found anemia is contributing to arrest.
rhage, anemia rhagic diathesis, malignancy, preg-
nancy, shock, trauma Emergently consult necessary specialty for definitive care.
Emergency thoracotomy with open cardiac massage is a consideration if experienced providers are available for the
patient with penetrating trauma and cardiac arrest.
Reassess technical quality of CPR, oxygenation, and ventilation.
Hypoxia All cardiac arrest patients are at risk Confirm correct ET tube placement.
Obtain stat ABG to confirm adequate oxygenation and ventilation.
Consider in all cardiac arrest patients,
especially those with risk factors Review prearrest clinical presentation and ECG.
Myocardial for coronary artery disease, a his- Continue resuscitation algorithm; proceed with definitive care as appropriate for the immediate circumstances (e.g.,
infarction tory of ischemic heart disease, or thrombolytic therapy, cardiac catheterization/coronary artery reperfusion, circulatory assist device, emergency
prearrest picture consistent with cardiopulmonary bypass).
an acute coronary syndrome
(continued)
oxygen consumption or lactate production in the arrested heart.66 De- quired when spontaneous circulation does not return despite appro-
spite its potential advantages, however, in a study of 200 inpatient car- priate initial interventions.This situation poses a critical question to
diac arrest patients, vasopressin did not provide a better survival rate the resuscitators:Why is this patient dying right now? The intellectu-
than epinephrine.67 Vasopressin was also found to be comparable to al challenge of that question, which the resuscitators must try to an-
epinephrine in out-of-hospital cardiac arrests when the rhythm was VF swer expeditiously and at the bedside, is compounded by the emo-
or PEA but superior to epinephrine for patients in asystole.68,69 tional intensity that pervades most cardiac resuscitations.
During resuscitation with ongoing CPR, medication delivery The solvable problems that may interfere with resuscitation can
through an intravenous cannula needs to be followed by a 20 ml be grouped into three broad categories: technical [see Table 6], phys-
saline bolus; if the cannula is in a peripheral vein, the extremity con- iologic, and anatomic [see Table 7]. Technical problems consist of
taining the cannula should then be elevated for 10 to 15 seconds to difficulties with the resuscitators’ equipment or skills; such difficul-
augment delivery of the medication to the central circulation.This is ties include ineffective CPR, inadequate oxygenation and ventila-
especially important because of the low-flow circulatory state with tion, ET tube complications, intravenous access difficulties, and
closed-chest CPR. monitor-defibrillator malfunction or misuse. The physiologic and
anatomic problems consist of life-threatening but potentially treat-
Differential Diagnosis and Definitive Care able conditions that may have led to the cardiac arrest in the first
The most challenging part of the secondary survey, as well as car- place.This differentiation between physiology and anatomy is ad-
diac resuscitation management in general, is the problem-solving re- mittedly artificial, given that physiology is always involved in a car-

9. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 9
Table 7 (continued)
Condition Clinical Setting Diagnostic and Corrective Actions
Alcohol abuse, bizarre or puzzling be- Consider clinical setting and presentation; provide meticulous supportive care.
havioral or metabolic presentation,
Emergently consult toxicologist (through regional poison center) for resuscitative and definitive care advice, in-
classic toxic syndrome, occupational
Poisoning cluding appropriate antidote use.
or industrial exposures, history of in-
gestion, polysubstance abuse, psychi- Prolonged resuscitation efforts are appropriate. If available, immediate cardiopulmonary bypass should be
atric disease considered.
Metabolic acidosis, excessive administra- Obtain stat serum potassium level on ABG specimen.
tion, drugs and toxins, vigorous exercise,
hemolysis, renal disease, rhabdomyoly- Treatment: calcium chloride 10% (5–10 ml I.V. slow push [do not use if hyperkalemia is secondary to digitalis
Hyperkalemia
sis, tumor lysis syndrome, significant tis- poisoning]), followed by glucose and insulin (50 ml of D50W and 10 U regular insulin I.V.); sodium bicarbonate
sue injury (50 mEq I.V.); albuterol (15–20 mg nebulized or 0.5 mg I.V. infusion).‡
Alcohol abuse, diabetes, diuretic use,
drugs and toxins, profound gastroin- Obtain stat serum potassium level on ABG specimen.
Hypokalemia testinal losses, hypomagnesemia, ex- If profound hypokalemia (K+ < 2–2.5 mEq/L) is contributing to cardiac arrest, initiate urgent I.V. replacement
cess mineralocorticoid states, meta- (2 mEq/min I.V. for 10–15 mEq) then reassess.§
bolic alkalosis
Hospitalized patients, recent surgical pro- Review prearrest clinical presentation; initiate appropriate volume resuscitation with I.V. crystalloid and augment
cedure, peripartum, known risk factors with vasopressors as necessary.
for venous thromboembolism (VTE), Attempt emergency confirmation of diagnosis, depending on availability and clinical circumstances; consider
Pulmonary history of VTE, prearrest presentation emergency cardiopulmonary bypass to maintain patient viability.
embolism consistent with acute pulmonary Continue resuscitation algorithm; proceed with definitive care (thrombolytic therapy, embolectomy via interven-
embolism tional radiology, or surgical thrombectomy) as appropriate for immediate circumstances and availability.
Post central line placement, mechanical
Tension ventilation, pulmonary disease (includ- Consider risks and clinical presentation (prearrest history, breath sounds, neck veins, tracheal deviation).
pneumothorax ing asthma, COPD, necrotizing pneu- Proceed with emergency needle decompression, followed by chest tube insertion.
monia), post thoracentesis, trauma
*Unrecognized hypoglycemia can cause significant neurologic injury and can be life threatening, but caution with I.V. glucose is appropriate in the setting of cardiac arrest. Available evidence
indicates that hyperglycemia may contribute to impaired neurologic recovery in cardiac arrest survivors.
†Active internal or core rewarming includes warm (42˚–46˚ C) humidified oxygen delivered through the endotracheal tube; warm I.V. fluids; peritoneal lavage; esophageal rewarming tubes;
bladder lavage; and extracorporeal rewarming if immediately available. Active external rewarming includes warming beds, hot-water bottles, heating pads, and radiant heat sources applied
externally to the patient.
‡Glucose is not necessary initially if patient is already hyperglycemic, but glucose levels should be followed closely after administration of I.V. insulin because of the risk of hypoglycemia
(especially in patients with renal failure, because of the long duration of action of I.V. insulin in such patients). Sodium bicarbonate is most helpful in patients with concomitant metabolic aci-
dosis; it is less effective in lowering serum potassium in dialysis-dependent renal failure patients. High-dose nebulized albuterol should lower serum potassium by 0.5 to 1.5 mEq/L within 30
to 60 min, but administration during cardiac arrest may be difficult.
§In a non–cardiac arrest situation, usual I.V. potassium replacement guidelines for patients requiring parenteral therapy are generally 10 to 20 mEq/hr with continuous electrocardiographic
monitoring. If profound hypokalemia is contributing to cardiac arrest, however, these usual replacement rates are not timely enough, given the critical nature of the situation. Under these
circumstances, potassium chloride, 2 mEq/min I.V. for 10 to 15 mEq, is reasonable, but reassessment and careful attention to changing levels, redistribution, and ongoing clinical circum-
stances are essential to prevent life-threatening hyperkalemia from developing.
ABG—arterial blood gas COPD—chronic obstructive pulmonary disease D50W—50% dextrose in water ET—endotracheal VF—ventricular fibrillation VT—ventricular tachycardia
diac arrest, but it has some usefulness as a teaching and problem- ECG showed prominent ST segment elevation in leads V1 through
solving tool. Physiologic problems classically include hypoxia, aci- V4 consistent with a large anterior myocardial infarction, if the pa-
dosis, hyperkalemia, severe hypokalemia, hypothermia, hypoglycemia, tient’s resuscitation is failing despite appropriate interventions, and
and drug overdose. Anatomic problems are hypovolemia/hemor- if there appear to be no technical problems hampering the resusci-
rhage, tension pneumothorax, cardiac tamponade, myocardial in- tation, a working diagnosis of massive myocardial infarction can be
farction, and pulmonary embolism.41 made; intravenous thrombolytic therapy may then be a reasonable
Whenever possible, the patient’s medical and surgical history and and needed step in such a resuscitation.70
the circumstances and symptoms immediately before the cardiac Thoughtful consideration of the possible reasons why a resuscita-
arrest should be sought from family members, bystanders, or hospi- tion is failing will regularly push the code-team captain’s and resus-
tal staff as the resuscitation proceeds.This information may contain citation team’s expertise and clinical skills to the limits. Neverthe-
important clues to the principal arrest problem and how it may be less, the failure to consider these formidable issues will deprive the
expeditiously treated. For example, a patient who presents to an patient of an optimal opportunity to survive the cardiac arrest.
emergency department with chest pain and then suffers a VF car-
diac arrest is probably dying of a massive myocardial infarction, pul-
monary embolism, or aortic dissection, with tension pneumothorax Cardiac Resuscitation Based on Rhythm Findings
or cardiac tamponade also being possibilities. When a monitor-defibrillator arrives at the scene of a cardiac ar-
Specific questions to consider include the following: Does the pa- rest, the patient’s rhythm is immediately analyzed.This step consti-
tient have risk factors for heart disease, pulmonary embolism, or tutes the beginning part of the defibrillation stage, or step D, of the
aortic disease? What was the quality of the patient’s pain and its ra- AHA’s primary survey.There are four rhythm possibilities [see Figure
diation before the cardiac arrest? What were the prearrest vital signs 1]: (1) pulseless VT; (2) VF; (3) organized or semiorganized electrical
and physical examination findings? What did the prearrest ECG activity despite the absence of a palpable carotid pulse, which defines
show (if available)? Can any of this information be used now, at the PEA; and (4) asystole.The detailed management of these different
bedside, to dictate the needed resuscitation interventions during the cardiac resuscitation scenarios is based on the recommendations of
D phase of the secondary survey? For example, if the prearrest the AHA49 and the International Liaison Committee on Resuscita-

10. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 1 Cardiac Resuscitation — 10
tion.71 In following these guidelines, the clinician should remember volved, it is exceptionally difficult to perform high-quality research
that, with the exception of early CPR and early defibrillation for VF in cardiac resuscitation.
and pulseless VT, many of the recommendations that form the
foundation of modern resuscitation are evidence supported or con-
PULSELESS VENTRICULAR TACHYCAR-
sensus based (rather than evidence based, as would be ideal). Be-
DIA OR VENTRICULAR FIBRILLATION
cause of the nature of cardiac arrest and the multiple variables in-
The appearance of either VF or
pulseless VT on the rhythm monitor in
a a patient with ongoing CPR is a rela-
tively favorable finding, because there is
reasonable hope for a successful out-
come with these rhythms. In addition,
the interventions and medications se-
quentially used in the resuscitation are
plainly delineated, and the initial course
b of action is clear.VF and pulseless VT are managed identically.
Initiation of Defibrillation
Defibrillation with 200 joules should be attempted immediately.
However, if the time from onset of arrest to CPR to the availability
of defibrillation is estimated to be longer than 5 minutes, it may be
reasonable to continue CPR for another 3 minutes before initiating
c defibrillation [see Defibrillation, above]. If the VF or VT persists after
the initial shock, subsequent attempts should be made with 200 to
300 joules and then 360 joules.
A lower, nonescalating equivalent biphasic energy level is accept-
able, if the defibrillator offers this option. Manually checking the
patient’s carotid pulse between shocks is no longer recommended,
but the displayed rhythm on the monitor must be carefully assessed
after each defibrillation attempt. If there are any doubts concerning
d the rhythm or if there is suspicion of a dysfunctional lead or paddle
cable, then a manual pulse check would be appropriate. If VF or
pulseless VT persists, CPR is resumed, the patient endotracheally
intubated, correct ET tube placement confirmed, and the tube se-
cured. Simultaneously, intravenous access should be established.
Initiation of Drug Therapy
e In patients with ongoing VF, drug therapy begins with the ad-
ministration of a vasoconstrictor (either epinephrine or vaso-
pressin) [see Table 4]. If there is no intravenous access, the drug can
be given endotracheally. After each intravenous dose, drug delivery
is followed by a 20 ml saline bolus and the extremity containing the
I.V. line is elevated. Rescuers continue CPR for 30 to 60 seconds to
allow the drug to reach the heart, then attempt defibrillation again
f with one to three shocks at 360 joules each. As long as the patient
remains pulseless, epinephrine is administered every 3 to 5 min-
utes, with each dose followed by one to three attempts at defibrilla-
tion.When vasopressin is the chosen initial drug, only a single dose
is given; if the resuscitation continues 10 minutes or longer after vaso-
pressin is administered, epinephrine should be substituted for vaso-
pressin for the remainder of the code. If VF or pulseless VT persists
g despite the initial administration of a vasoconstrictor and repeated
defibrillation attempts, parenteral antiarrhythmic drug therapy is
added; amiodarone or lidocaine is an appropriate agent [see Choice
of Antiarrhythmic Drugs, below].Throughout all of these steps, the
code-team leader is also actively looking for and correcting any
technical and physiologic or anatomic problems that may be pre-
venting a successful resuscitation [see Tables 6 and 7].
Figure 1 The sudden cardiac arrest arrhythmias. (a) Ventricular tachy- Emergency Laboratory Tests
cardia. (b) Ventricular fibrillation. Pulseless electrical activity encompasses
any of several forms of organized electrical activity in the pulseless patient; If spontaneous circulation does not return after the first round of
these include (c) normal sinus rhythm, (d) junctional rhythm, (e) bradycardic antiarrhythmic drug therapy, the resuscitation team must also en-
junctional rhythm, and (f) idioventricular rhythm. (g) Asystole. deavor to identify and treat the clinically relevant conditions causing