Ebook Critical care medicine the essentials: Part 2

Chapter 20
Cardiopulmonary Arrest
• Key Points
1. The success (hospital discharge without neurological impairment) of cardiopulmonary resuscitation is
highly variable among patient populations. Cardiopulmonary resuscitation is very effective when applied
promptly to patients with sudden cardiac death because of electrical instability, but is quite ineffective
when applied in chronically debilitated patients and those suffering arrest as part of the natural
progression of multiple organ failure.
2. The goal of resuscitation is to preserve neurological function by rapidly restoring oxygenation, ventilation,
and circulation to patients with arrested circulation.
3. The resuscitation status of every patient admitted to the ICU should be considered at admission. When a
clear determination regarding resuscitation status cannot be made quickly, the physician generally should
err on the side of promptly initiating resuscitation efforts. Obvious exceptions to this recommendation
apply when cardiopulmonary resuscitation is prohibited by patient mandate or not indicated because it
cannot produce successful results.
4. Most successful resuscitations require only 2 to 3 minutes. In these, establishing a patent airway and
promptly applying direct current shocks to reestablish a perfusing rhythm are the key actions necessary.
It is quite uncommon to successfully resuscitate a patient after more than 20 to 30 minutes of effort. A
notable exception to this rule occurs in patients with hypothermia who are occasionally resuscitated after
hours of effort.
5. Although widely published guidelines provide a framework for resuscitation, cardiopulmonary arrest in a
hospitalized patient often has a specific cause; therefore, resuscitative efforts should be individualized.
Common situations are outlined in Table 20-1.
6. In most cases, reestablishing an effective rhythm involves either the application of direct current shocks
to terminate ventricular fibrillation or tachyarrhythmia or the acceleration of bradyarrhythmias.
7. Although the systemic acidosis seen in patients with circulatory arrest can be buffered with NaHCO3, a
better strategy is to optimize ventilation and circulation. NaHCO3 should not be used routinely but retains
a role for specific arrest circumstances such as tricyclic antidepressant overdose, hyperkalemia, and
extreme acidosis.

By necessity, most recommendations for treating cardiopulmonary arrest are not derived from highquality

randomized human studies but rather from retrospective series, animal experiments, and expert opinion.
Treatment recommendations traditionally have been most applicable to patients who sustained sudden cardiac
catastrophes, especially those occurring outside the hospital. Because the focus of this book is on the
hospitalized critically ill patient, some of the discussion that follows will naturally differ from widely disseminated
recommendations. Most arrests among patients with ischemic heart disease are due to ventricular tachycardia
(VT) and ventricular fibrillation (VF). As a corollary, because pulseless VT or VF is so likely to be the cause of
death in the cardiac ICU, such patients should almost always be treated immediately with unsynchronized
cardioversion. By contrast, a respiratory event (aspiration, excessive sedation, pulmonary embolism,
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airway obstruction) is much more likely to occur at other sites in the hospital. It follows that arrests on a hospital
ward or noncardiac ICU are more likely to respond to a directed intervention beyond a cardiac rhythm change,
often one involving the lungs.

Table 20-1. Common Clinical Scenarios of Cardiopulmonary Arrest
Setting

Likely Etiology

Appropriate Intervention

During mechanical ventilation

Misplaced ET tube
Tension pneumothorax
Hypovolemia
Auto-PEEP
Hypoxemia

Mucus plugging

Confirm proper location by visualization
and auscultation, CO2 detector
Physical examination, chest tube
placement
Fluid bolus
Reduce minute ventilation, increase
expiratory time, bronchodilator, suction
airway
Check ET tube placement, oximeter
saturation; administer 100% O2
Suction airway

Postcentral line
placement/attempt

Tension pneumothorax
Tachyarrhythmia
Bradycardia/heart block

Physical examination, chest tube
placement
Withdraw intracardiac wires or
catheters; consider
cardioversion/antiarrhythmic
Withdraw intracardiac wires or
catheters, consider chronotropic drugs,
temporary pacing

During dialysis or
plasmapheresis

Hypovolemia
Transfusion reaction
IgA deficiency: allergic
reaction
Hyperkalemia

Fluid therapy
Stop transfusion; treat anaphylaxis
Stop transfusion; treat anaphylaxis

During transport

Displaced ET tube
Interruption of vasoactive
drugs

Early identification using end-tidal CO2
Restart IV access

Acute head injury

Increased intracranial
pressure (especially with
bradycardia)
Diabetes insipidus:
hypovolemia (especially
with tachycardia)

Lower intracranial pressure (ICP):
hyperventilation, mannitol, 3% NaCl
Administer fluid

Check K+; treat empirically if ECG
suggests hyperkalemia


After starting a new medicine

Anaphylaxis (antibiotics)
Angioedema (ACE
inhibitors)
Hypotension/volume
depletion (ACE inhibitors)
Methemoglobinemia

Stop drug; administer fluid,
epinephrine, corticosteroids
Volume expansion
Methylene blue

Toxin/drug overdose cyclic
antidepressants β-

Seizures/tachyarrhythmias
Severe bradycardia
Severe bradycardia

Sodium bicarbonate
Chronotropes, pacing, glucagon, insulin
+ glucose
Decontamination, atropine, pralidoxime

After myocardial infarction

Tachyarrhythmia/VF
Torsades de pointes
Tamponade, cardiac
rupture
Bradycardia, AV block

DC countershock, lidocaine
Cardioversion, Mg, pacing,
isoproterenol, stop potential drug
causes
Pericardiocentesis, fluid, surgical repair
Chronotropic drugs, temporary pacing

After trauma

Exsanguination
Tension pneumothorax
Tamponade
Abdominal compartment
syndrome

Fluid/blood administration, consider
laparotomy-thoracotomy

Physical examination, chest tube
placement
Pericardiocentesis/thoracotomy
Measure bladder pressure;
decompress abdomen

Burns

Airway obstruction
Hypovolemia
Carbon monoxide
Cyanide

Intubate
Fluid administration
100% O2
Hydroxocobalamin

blocker/Ca2+ blocker
Organophosphates
Carbamates

ABG, arterial blood gases; ACE, angiotensin-converting enzyme; AV, atrioventricular; DC, direct current;
ECG, electrocardiogram; ET, endotracheal; PEEP, positive end-expiratory pressure; VF, ventricular
fibrillation.

PRIMARY PULMONARY EVENTS (RESPIRATORY ARREST AND SECONDARY
CARDIAC ARREST)
Patients found unresponsive without respirations but with an effective pulse have suffered a respiratory arrest.
Failure to rapidly restore ventilation results in hypoxemia and progressive acidosis that culminates in reduced

contractility, hypotension, and eventual circulatory collapse. Although the etiology of many respiratory arrests
remains uncertain even after thorough investigation, the cause often can be traced to respiratory center
depression (e.g., sedation, coma, stroke, high intracranial pressure) or to failure of the respiratory muscle pump
(e.g., excessive workload, impaired mechanical efficiency, small or large airway obstruction, or muscle
weakness). Tachypnea usually is the first response to stress, but as the burden becomes overwhelming, the


respiratory rhythm disorganizes, slows, and eventually ceases. Initially, mild hypoxemia enhances the peripheral
chemical drive to breathe and stimulates heart rate. Profound hypoxemia, however, depresses neural function
and produces bradycardia refractory to autonomic influence. At this point, cardiovascular function usually is
severely disordered, both because cardiac and vascular smooth muscle function poorly under conditions of
hypoxia and acidosis and because cardiac output falls as heart rate declines. The observation that nearly one
half of hospitalized cardiopulmonary arrest victims exhibit an initial bradycardic rhythm underscores the role of
respiratory causes of circulatory arrest.

FIGURE 20-1. Change in arterial partial pressure of oxygen and carbon dioxide after respiratory arrest
(normal lungs). Oxygen concentration falls precipitously to dangerously low levels within minutes. By contrast,
the rise in carbon dioxide tension is much slower, requiring 15 to 20 minutes to reach levels sufficient to produce
life-threatening acidosis.
In many critically ill patients, the arterial partial pressure of oxygen (PaO2) plummets shortly after ventilation
ceases because limited O2 stores are rapidly consumed. Reserves are diminished by diseases that reduce
baseline saturation (e.g., chronic obstructive pulmonary disease [COPD], pulmonary embolism), lower functional
residual capacity (e.g., morbid obesity, pregnancy), or both (e.g., pneumonia, pulmonary fibrosis, congestive
heart failure). Ambulatory patients who suffer sudden cardiac arrest usually draw upon substantially greater O2
reserves because they typically do not have diseases causing significant desaturation or thoracic restriction at
baseline. For this reason, attention to oxygenation is much more important in the hospitalized respiratory arrest
victim, whereas establishing artificial circulation and prompt rhythm correction are priorities for the “cardiac”
death patient. Unlike O2, CO2 has a huge storage pool and an efficient buffering system. Therefore, PaCO2
initially builds rather slowly, at a rate of 6 to 9 mm Hg in the first apneic minute and 3 to 6 mm Hg/min thereafter
(Fig. 20-1). However, as the apneic patient develops metabolic acidosis from tissue hypoxia, H+ combines with

to dramatically increase the rate of CO2 production. The net effect of these events is that life-threatening
hypoxemia occurs long before respiratory acidosis itself presents a major problem.
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PRIMARY CARDIOVASCULAR EVENTS (CARDIOPULMONARY ARREST)
The heart may abruptly fail to produce an effective output because of arrhythmia or suddenly impaired pump
function resulting from diminished preload, excessive afterload, or decreased contractility. The normal heart
compensates for changes in heart rate over a wide range through the Starling mechanism. Thus, cardiac output
usually is maintained by compensatory chamber dilation and increased stroke volume despite significant slowing
of rate. Children and adults with dilated or noncompliant hearts have less reserve and are highly sensitive to
bradycardia.
Decreases in left ventricular preload sufficient to cause cardiovascular collapse usually are the result of
venodilation, hemorrhage, pericardial tamponade, or tension pneumothorax. In contrast to the left ventricle, which
is continually adapting to afterload that changes over a wide range, the right ventricle does not readily
compensate for increased impedance to ejection. Therefore, abrupt increases in right ventricular afterload (e.g.,
air or thromboembolism) are likely to cause catastrophic cardiovascular collapse. Acute dysfunction of cardiac
muscle can result from tissue hypoxia, severe sepsis, acidosis, electrolyte disturbance (e.g., hypokalemia), or
drug intoxication (e.g., β-blockers). Regardless of the precipitating event, patients with narrowed coronary
arteries are particularly susceptible to the adverse effects of a reduced perfusion pressure.
Neural tissue is disproportionately sensitive to reduced blood flow. Circulatory arrest always produces
unconsciousness within seconds, and respiratory rhythm ceases rapidly thereafter. Thus, ongoing respiratory
efforts indicate very recent circulatory collapse or the continuation of some blood flow, even if below the palpable
pulse threshold. (In a person of normal body habitus, a systolic pressure of approximately 80, 70, or 60 mm Hg
must be present for a pulse to be consistently detected at radial, femoral, or carotid sites, respectively.)

CARDIOPULMONARY RESUSCITATION
Cardiopulmonary resuscitation (CPR) was conceived as a temporary circulatory support procedure for otherwise
healthy patients suffering sudden cardiac death. In most cases, coronary ischemia or primary arrhythmia is the

inciting event. Since its inception, however, CPR use has been expanded to nearly all types of patients who
suffer an arrest. A general approach currently recommended by the American Heart Associated is presented in
Figure 20-2. Note that although this approach presents a general overview of intervention for cardiac arrest,
specific interventions and situations encountered in the ICU as described in Table 20-1 must be considered. The
intensivist is frequently consulted for cardiac arrest occurring on the medical/surgical unit or in clinic spaces of
the hospital where this initial approach is applicable. Currently, less than one half of all patients undergoing CPR
will be successfully resuscitated initially, and less than one half of these initial survivors live to hospital
discharge. Even more discouraging, at least one half of the discharged patients suffer neurological damage
severe enough to prohibit independent living. Despite the success portrayed on television, a small number of
CPR recipients enjoy even a near-normal postarrest life. In addition, pharmacoeconomic analyses suggest that
in-hospital resuscitation may be the least cost-effective treatment delivered with any regularity. The likelihood of
successful CPR (discharge without neurological damage) depends on the population to whom the procedure is
applied and the time until circulation is restored. Brief periods of promptly instituted CPR are highly successful
when applied to patients with sudden cardiac death, but when CPR takes place in the setting of progressive
multiple organ failure, the likelihood of benefit approaches zero.

Principles of Resuscitation
This chapter emphasizes enduring principles of resuscitation and intentionally omits details that are not based on


convincing evidence or are likely to change. Current expert recommendations for resuscitation are much simpler
than those in the past and stress the importance of effective circulatory support and prompt shock of pulseless
VT and VF while de-emphasizing respiratory support. Although that advice makes sense for most out of hospital
events, in the hospital, the resuscitation team must quickly consider the specific circumstances of each arrest to
determine the best course of action (Table 20-1). For example, a mechanically ventilated patient found in VF will
not be saved by
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a formulaic approach to arrhythmia treatment if it is not recognized that the cause of the event is a tension
pneumothorax or major airway obstruction. Because survival declines exponentially with time after arrest (Fig.

20-3), most successfully resuscitated patients are revived in less than 10 minutes. To this end, first responders
should summon help and begin effective chest compression. If the cardiac rhythm can be monitored and is
pulseless VT or VF, unsynchronized direct current (DC) cardioversion using maximal energy should be delivered
as quickly as possible. If these initial actions are unsuccessful, more prolonged, “advanced” resuscitation
measures may be indicated.


FIGURE 20-2. General overview of approach to cardiac arrest. This strategy may be modified based on
presenting considerations as listed in Table 20-1. CPR, cardiopulmonary resuscitation; IO, intraosseous; IV,
intravenous; PEA, pulseless electrical activity; PETCO2, end tidal PCO2; PVT, pulseless ventricular tachycardia;
ROSC, return of spontaneous circulation; VF, ventricular fibrillation. (Numbers guide progress through this
algorithm.)

FIGURE 20-3. Probability of successful initial resuscitation after cardiopulmonary arrest. Exponential
declines in survival result in low success rates after 6 to 10 minutes of full arrest conditions.
The primary activities of resuscitation include (1) team direction, (2) circulatory support, (3)
cardioversion/defibrillation, (4) airway management and ventilation, (5) establishing intravenous access, (6)
administering drugs, (7) performance of specialized procedures (e.g., pacemaker and chest tube placement), and
(8) database access and recording. Managing a cardiopulmonary arrest usually requires several persons to
directly execute procedures. Additional personnel are needed for nonprocedural tasks such as documentation,
chart review, and communication with the laboratory or other physicians, but limiting the number of people
involved to the minimum required avoids confusion.
Principle 1: Define the Team Leader
A single person must direct the resuscitation team because chaos often surrounds the initial response. This
person should attempt to determine the cause of the arrest, confirm the appropriateness of resuscitation,


establish treatment priorities, and coordinate the steps of ACLS protocol. The leader should also monitor the
electrocardiogram (ECG), order medications, and direct the actions of the team members but must avoid
distraction from the command role by performing other functions.

Principle 2: Establish Effective Artificial Circulation
Blood flow during closed-chest CPR likely occurs by two complementary mechanisms: direct cardiac
compression and thoracic pumping. First, compressions generate positive intracardiac pressures, simulating
cardiac chamber contraction with the unidirectional heart valves helping to ensure forward flow. In addition, as
the chest is compressed, a positive gradient is established between intrathoracic relative to extrathoracic arterial
pressures, propelling flow forward. Retrograde venous flow is prevented by jugular venous valves and functional
compression of the inferior vena cava at the diaphragmatic hiatus. On relaxation of chest compression, falling
intrathoracic pressures promote blood return into the right heart chambers and pulmonary arteries, filling these
structures for the next compression. Automated systems are available to provide CPR as other cares or patient
transfer occurs (Fig. 20-4).
Regardless of mechanism, even ideally performed closed-chest compression provides only one third of the usual
output of the beating heart. Thus, when CPR is performed for more than 10 to 15 minutes, hypoperfusion
predictably results in tissue acidosis. If performed improperly, CPR is not only ineffective
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but potentially injurious. Several points of technique deserve emphasis. Maximal flow occurs with a compression
rate of 100 to 120 beats/min. Current recommendations have increased the ratio of compressions to breaths in
an attempt to maximize flow. For the same reason, current protocols suggest continuing CPR for several minutes
after electrical shock attempts. To optimize cardiac output, it is important to adequately compress the chest.
Ideally, the anterior chest is depressed by at least 2 in. in the adult. Timing of the stroke is important: shortduration “stabbing” chest compressions simulate the low stroke volume of heart failure, whereas failure to fully
release compression simulates pericardial tamponade or excessive levels of positive end-expiratory pressure
(PEEP). Openchest cardiac compression may provide double the cardiac output of the closed-chest technique
but presents obvious logistical problems and has not been demonstrated to improve survival.


FIGURE 20-4. Mechanical system for performance of chest compressions in CPR.
During CPR, it is difficult to determine whether blood flow is adequate, because pulse amplitude, an index of
pressure, does not directly parallel flow and organs vary with regard to the flow they receive at a given pressure.
For example, brain flow relates to differences between mean aortic pressure and right atrial pressure, assuming
normal intracranial pressure. Therefore, increasing right atrial pressure will decrease brain blood flow when
mean arterial pressure is held constant. Coronary blood flow, on the other hand, is best reflected by the diastolic

aortic to right atrial pressure gradient. For both, vasoconstrictive drugs (i.e., epinephrine) are recommended to
raise the mean aortic pressure.
Principle 3: Establish Effective Oxygenation and Ventilation
Establishing a secure airway and provision of supplemental oxygen are essential if the primary problem was
respiratory in origin, or whenever resuscitative efforts continue for more than a few minutes. Except in unusual
circumstances, ventilation can be quickly accomplished in the nonintubated patient with mouth-to-airway or bagmask ventilation. Because position, body habitus, and limitations of available equipment often compromise either
upper airway patency or the seal between the mask and face, effective use of bag-mask ventilation often
requires two people. When the airway is patent, the chest should rise smoothly with each inflation. Gastric
distension and vomiting may occur if inflation pressures are excessive. Inflation pressures generated by bagmask ventilation are sufficient to cause barotrauma and impede venous return; to minimize these risks, breaths
should be delivered slowly, avoiding excessive inflation pressures and allowing complete lung deflation between
breaths.
In cardiopulmonary arrest, the most common cause of airway compromise is obstruction of the upper airway by
the tongue and other soft tissues. Thus, in most cases after effective chest compression and ventilation have
been achieved, an experienced person should intubate the airway (see Chapter 6). As a rule, intubation attempts
should not interrupt ventilation or chest compression for longer than 30 seconds. Therefore, all materials,


including laryngoscope, endotracheal (ET) tube, and suction equipment, should be assembled and tested before
any attempt at intubation. Inability to establish effective oral or bag-mask ventilation signals airway obstruction
and should prompt an immediate intubation attempt. When neither intubation nor effective bag-mask ventilation
can be accomplished because of abnormalities of the upper airway or restricted cervical motion, temporizing
measures should be undertaken while preparations are made to create a surgical airway. The laryngeal mask
airway (LMA) is an easily inserted, highly effective temporizing device. It is important to have an LMA, which is
appropriately sized for the patient. If the LMA is too large, it may obstruct the larynx or cause trauma to laryngeal
structures. An LMA that is too small or inserted improperly may push the base of the tongue posteriorly and
obstruct the airway. The LMA should only be used in an unresponsive patient with no cough or gag reflex. If the
patient has a cough or gag reflex, the LMA may stimulate vomiting and/or laryngospasm. In unusually difficult
circumstances, insufflation of oxygen (1 to 2 L/min) via a large-bore (14- to 16-gauge) needle puncture of the
cricothyroid membrane can temporarily maintain oxygenation. Phasic delivery of higher flows of oxygen by the
transtracheal route also can promote CO2 clearance, but CO2 removal is of much lower priority.

In the arrest setting, direct visualization of the tube entering the trachea, symmetric chest expansion, and
auscultation of airflow distributed equally across the chest (without epigastric sounds) are the most reliable
clinical indicators of successful intubation. Colorimetric CO2 detectors attached to the ET tube may support
impressions of proper tracheal
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tube placement; however, because circulation and CO2 delivery to the lungs are both severely compromised
during CPR, detectors may fail to change color on many properly placed tubes. For the same reason, attempts to
eliminate CO2 by ventilation are relatively ineffective.
During CPR, ventilation should attempt to restore arterial pH to near-normal levels and provide adequate
oxygenation. Unfortunately, the adequacy of ventilation and oxygenation is difficult to judge because blood gas
data are rarely available in a timely fashion. Furthermore, blood gases alone are poor predictors of the outcome
of CPR, making their use in decisions to terminate resuscitation of questionable value. The cornerstone of pH
correction is adequate ventilation after effective circulation has been achieved—not NaHCO3 administration.
CO2 in mixed venous blood returned to the lung during CPR freely diffuses into the airway for elimination;
however, reductions in pulmonary blood flow profoundly limit the capacity for CO2 excretion. Consequently,
hypocapnia seldom is produced at the tissue level during ongoing CPR. Conversely, excessive NaHCO3
administration can produce hyperosmolality and paradoxical cellular acidosis. Because exhaled CO2
measurements reflect the effectiveness of the circulation during CPR, they predict efficiency of compressions as
well as outcome. Higher endtidal levels of CO2 (>10 mm Hg) indicate improved perfusion and portend a better
prognosis, whereas persistently low end-tidal CO2 concentrations (<10 mm Hg) portend a poor prognosis.
Failure of a colorimetric CO2 detector to change color during CPR carries a similarly poor prognosis.
Principle 4: Establish a Route for Medication Administration
Access to the circulation must be established rapidly during CPR. Existing peripheral IV catheters are perfectly
acceptable for medication administration. When medications are given through peripheral IV lines, they should be
followed by at least 20 mL of fluid to facilitate drug entry into the circulation and to prevent mixing incompatible
drugs. Central venous catheters (CVCs) reliably deliver drugs directly to the heart, but valuable time should not
be wasted inserting a CVC if functioning peripheral venous access exists. (There is also a theoretical concern of
delivering very high drug concentrations close to the heart when using a CVC.) Femoral access is less desirable
than a jugular or subclavian route because of the higher risk of infection, but is certainly easier to establish
without interrupting CPR.

A large intraosseous (IO) needle can be placed very rapidly into the marrow of a long bone, typically the proximal
tibia. This IO access is an effective route for drug administration in those patients who do not have a functioning
IV. The luxuriant venous plexus of bone provides an efficient conduit to the circulation. There are currently
several commercially available stylet/needle devices to rapidly achieve IO access. Typically, the needle
penetrates the cortex using a screwing motion until resistance fades. After removal of the stylet, IO positioning is
confirmed by aspiration of a small amount of marrow and the ability to gravity-infuse fluid at a slow rate. Major
advantages of the IO route include a high success rate for cannulation (>80%), quick insertion (<2 minutes),
avoidance of CVC-related complications, and rapid delivery of drug to the circulation. (In experimental models,
IO-administered drugs reach the heart in <30 seconds.) Risks are uncommon and predictable. These include
nerve or vessel injury, extravasation of drug into soft tissue with necrosis, compartment syndrome, and
osteomyelitis.
The intratracheal (IT) route may be used to produce therapeutic drug levels rapidly during resuscitation. Drugs
given via the IT route must be delivered with at least 20 mL of fluid to permit most of the dose to access the
alveolar compartment, where absorption occurs. The doses of all drugs given by the IT route should be
increased at least 2 to 2.5 times than used with IV dosing. The IT route has been demonstrated to be effective
for administration of naloxone, atropine, vasopressin, epinephrine, and lidocaine, easily remembered as by
mnemonic “NAVEL.” Some commonly used drugs (e.g., norepinephrine, CaCl2, NaHCO3) should not be given
via the IT route. The first two agents may cause lung necrosis and the third inactivates surfactant.
Intracardiac injections, although dramatic, are rarely necessary, often unsuccessful, and offer no greater
likelihood of successful resuscitation. In addition, intracardiac injections are fraught with complications including
coronary laceration, pneumothorax, and tamponade. Intramural drug injection may expose the myocardium to
massive concentrations of vasoactive drugs, provoking intractable ventricular arrhythmias.
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Principle 5: Create an Effective Cardiac Rhythm
As a conceptual guide to treatment, cardiac electrical activity during the arrest can be thought of in two broad
categories. The first is the combination of pulseless ventricular tachycardia and ventricular fibrillation (VT/VF),
and the second group consists of asystole and pulseless electrical activity (PEA).
Ventricular Tachycardias and Ventricular Fibrillation

VT and VF are the most commonly discovered rhythms in victims of sudden cardiac death. Although VF may be
the original arrhythmia, in many cases, the first dysfunctional rhythm is VT, which deteriorates to VF as the heart
becomes progressively hypoxic. VT is described as either pulseless or pulse generating. VT without a pulse is
treated as VF. VT has been further subclassified as being either monomorphic or polymorphic because there are
potential treatment implications for the polymorphic variety. Monomorphic VT is typically a monotonous
appearing wide complex tachycardia with a constant axis. Torsades de pointes is the name given to a unique
appearing form of polymorphic VT that is frequently associated with baseline prolongation of the QT interval.
Torsades is characterized by a constantly changing QRS axis that produces an apparent “twisting of points”
about the isoelectric axis (see Chapter 4). Many reversible precipitating factors have been identified, including
hypomagnesemia and the use of tricyclic antidepressants, haloperidol, droperidol, type Ia antiarrhythmics (e.g.,
quinidine, procainamide, and disopyramide), and quinolone antibiotics (see Chapter 4).
When VT/VF is encountered, the American Heart Association recommends consideration of a standard list of
reversible causes including hypovolemia, hypoxia, acidosis, hypokalemia, hyperkalemia, and hypothermia (the
“Hs”) to go along with the (“Ts”) tension pneumothorax, cardiac tamponade, toxins, pulmonary thrombosis, and
coronary thrombosis. Both VT and VF potentially can be converted with electrical shock, but VF tends to be more


resistant. With VF, the success of cardioversion is influenced by the amplitude of the electrical signal, which
correlates inversely with the duration of fibrillation. Success rates vary from less than 5% when low-amplitude VF
is the initial rhythm to greater than 30% when coarse VF is the rhythm. When fine VF is shocked, the most likely
resulting rhythm is asystole, whereas coarse VF is more likely to be converted to a supraventricular tachycardia
or sinus rhythm. Epinephrine is sometimes successful in coarsening a fine VF waveform prior to the attempted
shock.
Regardless of whether the initial rhythm is VF, or monomorphic or polymorphic VT, maximal intensity (360 J)
unsynchronized monophasic shock should be administered as quickly as possible for all patients in VF and
pulseless VT. (Equivalent lower-intensity biphasic [200 J] shocks are equally effective.) For patients receiving
open-chest defibrillation, epicardial shocks of 10 to 20 J are almost always sufficient. The goal of delivery for DC
countershocks is to abolish all chaotic ventricular activity, allowing an intrinsic pacemaker to emerge. Many
defibrillators allow a “quick look” at the rhythm before shock is attempted, but careful inspection of the rhythm is
not mandatory before proceeding. Blind cardioversion will not harm adult patients with agonal bradyarrhythmias

or asystole and should benefit those with pulseless tachycardias or VF. Previous guidelines recommended a
series of rapidly delivered, incremental intensity shocks based upon the observations that thoracic impedance
declines (but only slightly) with multiple defibrillations and that using a lower electrical dose might reduce
defibrillation-induced cardiac damage. Current guidelines recommend simple administration of single shocks.
Although all of these approaches have merit, it is clearly more important to restore a circulating rhythm rapidly
than to be concerned about potential cardiac electrical injury.
Defibrillators are typically calibrated to discharge through impedance less than that of the adult chest. Therefore,
the delivered energy usually is lower than is indicated by the nominal machine settings. This is particularly true
in situations, which increase the distance between the paddles and the heart, like morbid obesity and conditions
producing high lung volumes (e.g., COPD, large tidal volumes, high PEEP). Improper paddle positioning also
dissipates energy and reduces the rate of successful defibrillation. Using the anterolateral technique, paddles
are placed at the cardiac apex and just below the clavicle to the right of the sternum. Because bone and cartilage
are poor conductors of electricity, paddles should not be located over the sternum. Defibrillator paddles should
not be placed over ECG monitor leads, implanted pacemakers or defibrillators, or transcutaneous drug patches,
because of the possibility of electrical arcing and equipment damage. Contact between the
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defibrillator and chest wall should be maximized by use of conducting gels or pads. (Note: Ultrasound gel is a
poor electrical conductor.) Standard-sized (8 to 13 cm diameter) paddles on adult defibrillators provide optimal
impedance matching between machine and chest wall. If for some reason the defibrillator fails to discharge,
ensure that the defibrillator is energized, connected, and correctly set. One rather common reason for failure to
discharge during VF is for the machine to be set in the synchronized cardioversion mode. (In the absence of a
QRS complex, there is no signal to trigger a “synchronized” discharge of the defibrillator.)
The availability of AEDs has changed defibrillation from an often delayed procedure performed by an expert in a
hospital or ambulance to one rapidly accomplished by a novice in a public location. Fortunately, considerable
standardization of AEDs has occurred so that regardless of manufacturer, the same basic steps are always used:
power on the defibrillator, attach the pads and connect the cables using the illustrations provided, wait for the
device to analyze the rhythm and charge, make sure all people are clear of the patient, and then discharge the
device if the machine advises to do so.
Pulseless VT or VF that remains resistant to cardioversion after several minutes of effective CPR portends a
poor outcome. If initial attempts at defibrillation prove unsuccessful, “coarsening” the rhythm and increasing the

vascular tone with epinephrine (1 mg IV, every 3 to 5 minutes) may be helpful. All the while, effective ventilation
and chest compression should be maintained. After epinephrine is given, maximum energy defibrillation should


be repeated. When the preceding measures fail, a trial of the antiarrhythmic amiodarone (300 mg IV) may help
convert the rhythm when followed by additional shocks.
The small subgroup of patients with torsades deserves special mention. Although torsades is not particularly
resistant to cardioversion, the arrhythmia frequently recurs within a short time. For long-term control,
discontinuation of potentially precipitating drugs and correction of electrolyte abnormalities are indicated. For
patients with a previously normal QT interval, coronary ischemia is a common precipitant amenable to standard
treatment. β-Blockers, lidocaine, and amiodarone have all been tried for refractory torsades without any one
emerging as a clearly superior agent. For patients known to have prolonged baseline QT interval, MgSO4 may
be helpful, but the most effective measure is to shorten the QT interval, usually by increasing the heart rate (i.e.,
pacing or catecholamine infusion). In patients with QT prolongation, phenytoin and lidocaine may be tried if the
rhythm is refractory to magnesium and cardioacceleration.
Regardless of the initial rhythm, if cardioversion consistently produces any bradycardic rhythm that degenerates
to VF, increasing the heart rate with epinephrine, atropine, or pacing can prove useful. (In this situation,
overdose of digitalis, calcium channel blockers, or a β-blocker should also be considered.) If countershock
produces any tachycardia that repeatedly degenerates to VF or VT, consider the possibility of excessive
catecholamine stimulation and decrease infusion rates of adrenergic agents, and/or try administering
antiarrhythmics (amiodarone 300 mg IV bolus, procainamide 20 to 50 mg/min IV infusion [with maximum 17 mg/kg
or until the QRS duration increases >50%], lidocaine 1 to 1.5 mg/kg IV bolus). Hypokalemia, a frequent
contributor to refractory or recurrent VT/VF, is found in approximately one third of all patients suffering sudden
death. In this desperate setting, potassium repletion may be considered. Up to 40 mEq of potassium may be
administered rapidly. In some cases, the low toxicity compound MgSO4 may help stabilize refractory VT/VF, but
Mg3+ levels are unlikely to be measured during the time span of a resuscitative effort and do not correlate well
with effects. Thus, it is reasonable to administer MgSO4 empirically (1 to 2 g over several minutes).
Asystole and Pulseless Electrical Activity
For purposes of resuscitation, asystole and PEA are grouped together. Almost any rhythm is preferable to
asystole, the complete absence of electrical activity (a flat ECG), but some rhythms (i.e., pulseless slow

bradycardia or ventricular escape beats) are not much better. Therefore, a key aim in asystole is to stimulate
some electrical activity and then modify that activity to a rhythm with a pulse. Because asystole usually indicates
extended interruption of perfusion and carries a grave prognosis, its discovery should prompt serious
consideration of whether resuscitative efforts should even begin. It makes no sense to countershock the truly
asystolic patient because there is no “rhythm” to modify. However, low-amplitude VF may go unrecognized
unless sought using several leads. VF is best detected in leads II and III. Epinephrine (1 mg IV, every 3 to 5 min)
given during effective CPR may
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restore a vestige of electrical activity. Manipulation of electrolyte balance (Ca2+, K+) also may be useful in
specific cases. NaHCO3 may be useful if severe acidosis, hyperkalemia, or tricyclic antidepressant overdose is
the cause of asystole.
PEA, also known as electromechanical dissociation (EMD), is characterized by the inability to detect a pulse
despite coordinated ECG complexes. The more common causes of PEA can be easily recalled as a list of
conditions beginning with the letters “H” and “T” (Table 20-2). When cardiac in origin, PEA carries a dismal
prognosis because it usually is a sign of critical pump failure such as major infarction. A hint to the origin of the
problem (cardiac vs. noncardiac) can be gleaned from the width of the QRS complex. Narrow complexes are
more likely the result of a noncardiac cause. Mechanical obstruction to the normal transit of blood through the


heart may also cause PEA. Hence, atrial myxoma, mitral stenosis, and critical aortic stenosis may be potential
causes. Other reversible conditions that can produce this syndrome include (1) hypovolemia, particularly from
acute blood loss (vasopressors lose effectiveness); (2) pericardial tamponade, suspected on the basis of venous
engorgement, a history of chest trauma, or preexisting pericardial disease; (3) tension pneumothorax; (4)
dynamic hyperinflation (auto-PEEP) from overly zealous ventilation; (5) massive pulmonary embolism by clot or
air (thromboembolism may fragment and migrate during CPR, opening the central pulmonary artery and
reestablishing effective output; air embolism can be treated by positioning the patient (left side down,
Trendelenburg position) and/or transvenously aspirating air from the right heart); (6) hyperkalemia; and/or (7)
metabolic acidosis.
As adequate intravascular volume is assured or addressed, epinephrine is given in doses identical to those used
for asystole. On the rare occasion when a toxic overdose has resulted in PEA, specific therapy may be available

(see Chapter 33). Even though it is becoming much less common, digitalis toxicity deserves mention. A wide
variety of arrhythmias are associated with digitalis toxicity including high-grade AV block with bradycardia,
junctional tachycardias, and even asystole. Treatment begins by stopping the drug and correcting hyperkalemia
and hypomagnesemia. Ca2+ exacerbates the toxicity and should be avoided. Cardioversion (with the lowest
effective energy) is indicated if ventricular arrhythmias cause symptomatic hypotension. Phenytoin, lidocaine,
and procainamide are useful. Pacing usually is required for high-grade AV block. Use of specific digitalis
neutralizing Fab antibody fragment preparations is safe and highly effective if renal function is maintained.
Because the Fab-digitalis complex is cleared by the kidney, dialysis may be needed for the patient with renal
insufficiency (see Chapter 33).

Table 20-2. Causes of PEA
Hypovolemia

Tamponade

Hypoxemia

Tension pneumothorax

Hydrogen ions (severe acidosis)

Thrombosis (pulmonary, coronary)

Hyperkalemia or hypokalemia

Trauma
Toxic overdose

Hypoglycemia

Digitalis

Hypothermia

β-Blockers

Hyperinflation (auto-PEEP)

Calcium channel blockers
Tricyclic antidepressants

Bradycardias
Bradyarrhythmias that cause sudden death have a poor prognosis. In adults, these rhythms are often a


manifestation of prolonged hypoxemic, hypercarbic respiratory failure and portend asystole (Table 20-3). Indeed,
the most important measure to undertake first in treating a patient with hypotensive bradycardia is ensuring
adequate oxygenation—not administering sympathomimetic or vagolytic drugs. In general, the slower the rate
and the wider the ventricular complex, the less effective the myocardial contraction. The vagolytic action of
atropine is most useful in narrow complex bradycardias resulting from sinoatrial node failure or type II or III AV
block. Doses of at least 0.5 mg of atropine should be administered and can be repeated up to a total dose of 3
mg. Epinephrine (2 to 10 μg/m) or dopamine
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(2 to 20 μg/kg/m) may be helpful for their chronotropic actions. If available, transthoracic pacing can sometimes
provide temporary support until definitive transvenous pacing is established or pharmacologic cardioacceleration
is achieved. Although useful for symptomatic bradycardia, transvenous ventricular pacing is difficult to achieve in
the acute resuscitation situation.

Table 20-3. Causes of Bradycardia
Hypoxemia

Intense vagal stimulation
β-Blockade
Sinus/atrioventricular node ischemia
Calcium channel blocker use
Drug overdosage (cholinergic effects)
Digitalis
Increased intracranial pressure
Sedative agents (e.g., propofol, dexmedetomidine)

Tachycardias
Pathologic tachycardia is typically defined as a heart rate greater than or equal to 150 bpm. Absence of a pulse
is treated as PEA. The airway should be protected and oxygen provided. End-tidal CO2 monitoring contributes to
evaluation of effectiveness of the rhythm in maintaining perfusion. Symptomatic patients are typically hypotensive
with altered mental status, signs of end-organ hypoperfusion, chest discomfort, or heart failure. These individuals
should receive synchronized cardioversion. On occasion, adenosine may be therapeutic as well as diagnostic.
The first dose of adenosine is 6 mg IV by rapid push with a second dose of 12 mg given later, if required. If the
patient has a wide QRS complex (≥0.12 seconds) and is not symptomatic, adenosine may be considered if the
rhythm is regular and QRS monomorphic or another antiarrhythmic agent given, such as procainamide,
amiodarone, or sotalol. In the patient with a narrow complex QRS, vagal maneuvers and administration of
adenosine are appropriate. These patients may also be considered for beta-blockade or a calcium channel
blocker.
Principle 6: Evacuate the Patient to the ICU as Soon as Practical
When cardiac arrests occur outside an ICU, facilities, equipment, and personnel for resuscitation are less than
ideal. On general wards and in public hospital areas, it is often difficult to access the patient, especially if they
have fallen alongside a bed or are in a bathroom or elevator. Simply getting emergency equipment to the
patient's side can be a challenge in cramped quarters. There is often a crush of unhelpful bystanders and
distraught family members, and even the patient's primary caregiver's effectiveness is hindered by their shock
from an unexpected arrest. Electrical access and suction capabilities are commonly limited and specialized

equipment, especially for airway management, is not always available. However, the most important limitation of
performing resuscitation outside the ICU, especially in a remote part of the hospital (e.g., CT scanner), is that
many of the personnel available to help have little experience performing real resuscitations. Preparation of
emergency medications and assistance with procedures that are second nature for ICU personnel are often
unfamiliar to non-ICU workers. For all these reasons it makes sense to do the absolute minimum required to
establish ventilation and a rhythm that produces a pulse, then transport the patient to the ICU.
Principle 7: Reevaluate and Stabilize
After arriving in the ICU with a perfusing rhythm with adequate oxygenation and ventilation, it is important to
rethink the cause of the arrest, to take measures to prevent recurrence, and to search for resuscitation
complications. Tubes and catheters inserted during resuscitative efforts are often suboptimally positioned or are
inserted with less than ideal sterile technique. Any intravenous catheter not known to be inserted in a sterile
manner should be removed altogether or, if still needed, replaced at a new site using sterile technique. It may be
wise to administer a single dose of antibiotic that provides coverage of commonly encountered skin flora (e.g.,
cefazolin) even though this practice is not evidence based. The position of the ET tube and any chest tubes or
CVCs should be confirmed radiographically. (It is extremely common that emergently inserted ET tubes have
been advanced into the right main bronchus.) The chest radiograph should also be examined for evidence of
resuscitation or procedural injury (e.g., hemothorax or pneumothorax or rib or sternal fractures) and for clues to
the cause of the original arrest (mediastinal widening of aortic injury, enlarged cardiac silhouette of pericardial
tamponade, pneumothorax) (Table 20-4). The chest film should also be evaluated for the presence of aspiration
or pneumonia that may have precipitated the arrest or resulted from it. If there is a suspicion of hemothorax, or
hemoperitoneum, or
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retroperitoneal hematoma, chest and abdominal CT scans are usually diagnostic. However, careful consideration
should be given to transporting a recently resuscitated patient outside the ICU; potential benefits should clearly
outweigh the risks. If there is suspicion that the arrest may have been precipitated by a neurological event (e.g.,
ischemic stroke, hemorrhage, tumor, new seizure), it is prudent to obtain a noncontrast head CT scan with the
same caveats regarding transport safety. For patients who are not fully awake after resuscitation, the prospect of
ongoing seizures should be considered. If a seizure is a reasonable possibility, an electroencephalogram (EEG)
should be obtained.

Table 20-4. Complications of CPR
Rib fractures and cartilage separation
Bone marrow emboli
Fractured sternum
Mediastinal bleeding
Liver laceration
Subcutaneous emphysema
Mediastinal emphysema

Acid-base and electrolyte abnormalities are so common after resuscitation that it makes sense to evaluate a full
panel of electrolytes, especially Na+, K+, Ca2+, Mg3+, and an arterial blood gas. Because hypoglycemia can
cause cardiac arrest, and postarrest hypoglycemia and hyperglycemia can cause or exacerbate brain injury, a


rapid determination of blood glucose should be done. If there is suspicion that the cause of the arrest could be
medication or toxin ingestion, obtaining a urine or plasma drug screen and specific drug levels (e.g., digitalis,
lidocaine, phenytoin) may be enlightening. Although troponin and creatine phosphokinase (CPK) levels are
frequently modestly elevated, they rarely provide a definitive diagnosis. Noteworthy elevation of the myocardial
band (MB) isoenzyme of CPK is unusual unless repeated high-energy electrical shocks have been delivered.
Similarly, after resuscitation, impressive elevation of hepatic (and/or skeletal muscle) enzymes is common but of
uncertain significance because frank ischemic necrosis and failure of the liver rarely occur. It is smart to obtain a
hemoglobin concentration to search for occult bleeding (e.g., hemothorax from rib fractures or arterial injury,
hemoperitoneum from liver or spleen laceration) and to detect anemia that might warrant transfusion. Although
elevations of white blood cell counts are routine, they are nonspecific and by themselves should not drive
antibiotic use. A decision to obtain lung, blood, or urine cultures should be made on an individual basis,
depending on the level of suspicion the role of infection played in the arrest.
It is prudent to obtain a 12-lead ECG in all patients after stabilization to evaluate the rhythm and to look for signs
of infarction, ischemia, and electrolyte abnormalities, conduction defects, and preexcitation pathways. The use of
antiarrhythmic therapy should be based on an evaluation of the current rhythm and the likelihood of stability (see
Chapter 4). If there are questions about valvular competence or stenosis, pericardial fluid, or wall motion

abnormalities, an echocardiogram is quite helpful.
Several general recommendations can be made. Finger oximetry should be utilized to maintain oxygen saturation
at 94% to 96%. In general, patients should not be hyperventilated and hyperoxia must be avoided. Isotonic fluid
should be given judiciously to treat hypotension, defined as systolic blood pressure less than 90 mm Hg. Typical
fluids used in this setting are normal saline or lactated Ringers. Vasoactive drugs for the patient requiring
catecholamine support are norepinephrine, epinephrine, and dopamine. The patient who is alert and able to
follow commands should be monitored closely and further evaluated as described. Where patients cannot follow
commands, careful temperature regulation as described below should be emphasized.
Although the primary focus must be on caring for the patient, it is important not to ignore the family and visitors,
especially if they witnessed the arrest. Dispatching any free staff member to update the family during the
resuscitation and postresuscitation processes can be very effective in allaying fears. In recent years, there has
been substantial discussion regarding having family present during resuscitative efforts. This is a very
complicated topic, but it is clear that this practice should neither have a blanket prohibition nor absolute
requirement. Some family members derive comfort from knowing, by seeing, that all that could be done for their
loved one was tried. Other family members suffer terror and revulsion seeing the resuscitation process, which is
often unavoidably undignified, unlike stylized popular media portrayals. For these families, a lasting memory of a
violent death endures. Unfortunately, there is no reliable way to know how any particular person will react.
Because the adverse risk usually outweighs the potential benefit, we do not encourage or advise their direct
observation unless asked.
Principle 8: Preserve the Brain
Because neurological outcomes in survivors of cardiopulmonary arrest are poor, there has long been interest in
methods for cerebral preservation. It should go without saying that maintaining
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a reasonable perfusion pressure and hemoglobin concentration and saturation are prerequisites for optimal
cognitive recovery. The association of worse outcomes associated with hypoglycemia and hyperglycemia
suggests that maintaining a normal range of glucose is helpful. There is no evidence to support the routine
administration of anticonvulsants, anticoagulants, barbiturates, benzodiazepines, or neuromuscular blockers.
Although unproven for this purpose, prevention of excessive cerebral metabolic demand (e.g., suppression of

fever, seizures) makes sense and, particularly with respect to temperature control, is safe and inexpensive. The
patient who remains comatose after cardiac arrest should have a temperature maintained in the range of 34°C to
36°C. Perhaps, even more important, is the avoidance of fever. Potential candidates for this targeted
temperature management approach should not have active bleeding or significant bradycardia because
hypothermia may exacerbate both, as well as cause other complications (see Chapter 28). Therapeutic
hypothermia is difficult if not impossible to achieve in waking patients without deep sedation and usually
therapeutic neuromuscular blockade to prevent the inevitable, heat-generating shivering. Interestingly, external
skin warming (e.g., by air blanket) may effectively block the shiver response as body temperature falls. Servoregulated intravenous cooling catheters have emerged as the current standard of practice. Regardless of
method, the target is a core temperature of 36°C for 12 to 24 hours, with subsequent slow rewarming over 6 to 8
hours.

Controversies in Resuscitation
Over the years, advocacy of NaHCO3 and calcium in the resuscitation of arrest victims has waxed and waned;
currently, both are assigned low importance. Despite effective artificial support measures, progressive acidosis is
an inevitable result of prolonged CPR. When severe, acidosis can render the heart more resistant to
defibrillation. However, ventilation is key to pH correction. NaHCO3 is rarely necessary if circulation and
ventilation are restored promptly, and no data support its early routine use to improve defibrillation or survival
rates. The inability to restore pH toward normal is an ominous sign indicating some combination of failed
ventilation and circulatory support. When used, NaHCO3 should be administered cautiously, guided by point-ofcare blood gas analysis. An arterial pH ≥ 7.00 usually is adequate for cardiovascular function. However, the
appropriate pH target for the arrested circulation is highly controversial. Previously recommended doses of
NaHCO3 (1 mg/kg) may produce unwanted side effects, including (1) arrhythmogenic alkalemia, (2) increased
CO2 generation, (3) hyperosmolarity, (4) hypokalemia, (5) paradoxical intracellular acidosis of central nervous
system (CNS) and myocardium, and (6) a leftward shift in the oxyhemoglobin dissociation curve, limiting delivery
of O2 to tissues. Even though the use of NaHCO3 has fallen out of favor, in specific settings (e.g., hyperkalemia
with metabolic acidosis, tricyclic antidepressant or aspirin overdose) it can be a useful medication.
Because excessive calcium exacerbates digitalis toxicity and the arrhythmic tendency of unstable ischemic
myocardium, enhances coronary artery spasm, impairs cardiac relaxation, and may hasten cellular death, its use
should be restricted to patients with known hypocalcemia, calcium channel blocker or β-blocker overdose, and
hyperkalemia. Calcium forms insoluble precipitates when administered with NaHCO3; hence, the two compounds
should not be commingled.

DECIDING WHEN TO FORGO OR TERMINATE RESUSCITATION
Certain clinical disorders are associated with a virtually hopeless short-term prognosis (e.g., refractory widely
metastatic carcinoma, unremitting multiple organ failure, or severe sepsis), and in such cases, it often is
appropriate to decline CPR. Each case must be considered individually with regard to the physical condition of
the patient, the wishes of the patient and family (if known), and the likelihood that resuscitation can succeed if
performed. CPR is rarely successful if cardiac arrest ensues as the final manifestation of days or weeks of
multiple organ failure. The importance of clarifying the “code status” of all seriously ill patients early in the course
of an illness should be emphasized. Ideally, the code status is included as part of the admission order set to the
ICU. When doubt exists regarding the propriety of resuscitative efforts, CPR should be initiated. A single set of
guidelines regarding termination of effort cannot be applied to all clinical situations.
During CPR, neurologic signs and arterial blood gases are unreliable predictors of outcome and should not be
used in the decision to terminate


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resuscitative efforts. With that caveat, however, resuscitation seldom is successful when more than 20 minutes is
required to establish coordinated ventricular activity. With rare exceptions, failure to respond to 30 minutes of
advanced life support predictably results in death. Best results occur when sudden electrical events are
corrected promptly with cardioversion. Prolonged resuscitation with a good neurologic outcome may occur,
however, when hypothermia or profound pharmacologic CNS depression (e.g., barbiturates) precipitates the
arrest.

PROGNOSTICATION
CPR frequently fails to deliver the desired result of “discharge alive with normal neurological function.”
Resuscitation initially returns circulatory function in approximately 50% of patients to whom it is applied. (The
fraction is lower in out-of-hospital cardiac arrests and higher in hospitalized patients, especially those who suffer
arrest in the ICU.) Of these early “successes,” approximately 50% survive for 24 hours, but at best, only 25% to
50% of these 24-hour survivors live to hospital discharge. Many survivors suffer neurologic impairment.
Downtime greater than 4 minutes before beginning resuscitation, initial rhythms of asystole or bradycardia,

prolonged resuscitative efforts, a low exhaled CO2 concentration, and the need for vasopressor support after
resuscitation all are adverse prognostic factors. Likewise, poor prearrest health (e.g., severe sepsis, CHF, renal
failure), out-of-hospital arrest, and presence of hyperglycemia all are associated with a poor outcome.
Interestingly, age alone is not a good predictor of the success of CPR. Long-term survival of severe anoxia is
unusual in patients with underlying vital organ dysfunction, perhaps because further organ injury occurs or
because neural centers critical to autonomic control and maintenance of protective reflexes are damaged by the
event.
The probability of awakening after cardiac arrest is greatest in the first day after resuscitation and declines
exponentially thereafter to a very low stable level. (Almost all awakening occurs within 96 hours of resuscitation.
Nonetheless, recovery from comatose or vegetative states has been reported after 100 days.) Targeted
temperature management also appears to prolong the interval of observation necessary to confidently assign
prognosis. Surprisingly, the clinical examination is a better predictor of neurologic recovery than any imaging or
laboratory test. Absence of pupillary and corneal responses at or beyond 72 hours, especially if there is no motor
response or extensor posturing, is a powerful predictor of a poor outcome. Similarly, myoclonus or status
epilepticus within the first day following arrest predicts poor outcomes. Although an EEG is very useful for care if
it demonstrates seizures, EEG activity is suppressed by sedatives, anticonvulsants, and hypothermia making the
test an insensitive predictor of outcome. CT or MRI of the head may show perfusion-related abnormalities or
cerebral edema following CPR that may support the clinical assessment. However, unless such abnormalities
are profound, used alone they are unreliable predictors of eventual outcome.

SUGGESTED READINGS
Callaway CW, Donnino MW, Fink EL, et al. Part 8: Postcardiac arrest care. 2015 American Heart Association
Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation.
2015;132 (suppl 2):S465-S482.
Callaway CW, Soar J, Aibiki M, et al. Part 4: Advanced life support. 2015 International Consensus on
cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations.
Circulation. 2015;132(suppl 1):S84-S145.
Hazinski MF, Nolan JP, Aickin R, et al. Part 1: Executive summary. 2015 International Consensus on

cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations.
Circulation. 2015;132(suppl 1):S2-S39.
Lavonas EJ, Drennan IR, Gabrielli A, et al. Part 10: Special circumstances of resuscitation: 2015 American
Heart Association Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care.
Circulation. 2015;132(suppl 2):S501-S518.
Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult advanced cardiovascular life support: 2015
American Heart Association Guidelines update for cardiopulmonary resuscitation and emergency
cardiovascular care. Circulation. 2015;132(suppl 2):S444-S464.
Neumar RW, Shuster M, Callaway CW, et al. Part 1: Executive summary: 2015 American Heart Association
Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation.
2015;132 (suppl 2):S315-S367.


Chapter 21
Acute Coronary Syndromes
• Key Points
1. In ischemic heart disease, survival and ventricular function are maximized by rapidly reestablishing
sufficient myocardial blood flow to prevent myocardial necrosis. Percutaneous coronary intervention is
the reperfusion modality of choice, but if there are substantial delays in transfer to the cath suite, then
fibrinolytic therapy should be used in lytic-eligible patients. The door-to-balloon time should be less than
90 minutes.
2. Reducing myocardial oxygen consumption by limiting heart rate (avoidance of exercise and judicious use
of β-blockade), reducing afterload (controlling hypertension and normalizing ventricular filling pressures),
and alleviating excessive catecholamine stimulation are important steps to optimize myocardial supply
and demand.
3. Myocardial oxygen supply can be quickly and simply boosted with nitrates, restoring normal oxygen
saturation and optimization of hemoglobin concentration.
4. Most patients should receive agents to interrupt the clotting cascade, as well as oxygen (when needed),
pain relievers, and β-blockers in those without signs of ventricular insufficiency. All suitable candidates
should be considered for immediate interventional procedures (angioplasty/stent) or for antithrombotic

therapy. The presence of ST segment elevation and the duration of chest pain prior to arrival have a
direct bearing on the value of thrombolytics and interventional catheterization.
5. After stabilization has been achieved, an angiotensin-converting enzyme inhibitor and high-dose statin
should be considered to minimize the risk of lasting ventricular dysfunction.

NON-ST ELEVATION ACUTE CORONARY SYNDROMES: UNSTABLE ANGINA
AND NON-ST ELEVATION MYOCARDIAL INFARCTION
Definitions and Pathophysiology of Acute Coronary Syndrome
Unstable angina (UA) and non-ST segment elevation myocardial infarction (NSTEMI) are now grouped under the
heading of non-ST elevation acute coronary syndromes (NSTE-ACSs). Because they share a common
underlying pathophysiology, the management of these two conditions is quite similar. UA is synonymous with the
terms preinfarction angina, crescendo angina, intermediate coronary syndrome, and acute coronary
insufficiency. NSTEMI implies non-Q wave myocardial injury. The main difference between UA and NSTEMI is
that biomarkers of myocardial necrosis are elevated in the latter (e.g., creatine kinase-myocardial band [CK-MB],
troponin-I, troponin T).
Myocardial ischemia results from an imbalance between oxygen supply and demand. Anginal chest pain is the
clinical expression of this imbalance. Because the left ventricle (LV) comprises most of the cardiac muscle mass
and faces the greater afterload, it is at higher risk for ischemia. Myocardial oxygen delivery may be limited by (1)
coronary atherosclerosis, (2) plaque rupture with thrombosis, (3) coronary artery spasm, (4) anemia, (5)
hypoxemia, (6) limited diastolic filling time (tachycardia), and (7) hypotension.
Four major factors increase cardiac oxygen demand: (1) tachycardia and/or increased systemic
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metabolic demands for cardiac output, (2) heightened LV afterload causing increased transmural wall tension
(e.g., hypertension, LV cavity dilation, aortic stenosis), (3) increased LV mass (hypertrophy), and (4) increased
contractility. Despite the predisposition of the LV to ischemia, conditions that cause hypertrophy, dilation, or
increased afterloading of the right ventricle (RV) also can put its muscle mass at risk. For example, pulmonary
embolism may precipitate RV ischemia—a phenomenon that is most common in patients with underlying right
coronary artery (RCA) narrowing or cor pulmonale.

Instability of a coronary atherosclerotic plaque is the key to the pathophysiology of ACS and infarction. Degree of
coronary narrowing plays a secondary role. Histologic studies of coronary vessels have shown that
atherosclerotic plaques are intimomedial in location. In general, there are two types of coronary plaques: (1)
stable plaque with small lipid core and thick fibrous cap and (2) unstable plaque with large lipid core and thin
cap. The former generally causes stable angina pectoris if it causes significant obstruction of the vessel (>50%
to 70% of the vessel lumen diameter). Soft, lipid-laden plaques with thin caps are more prone to rupture, promote
local clotting, and provoke ACS. Many of these plaques do not cause significant obstruction of the lumen of
coronary vessels before the onset of the ACS. Hence, the patient may not have experienced any cardiac
symptoms prior to the onset of ACS even with exercise, and stress tests may be negative.
Acute instability and rupture of one or more coronary plaques with superimposed thrombosis are central to the
pathophysiology of ACS. This clot, composed of platelets and thrombin, not only produces a fixed vessel
occlusion but also stimulates reversible vasoconstriction. The resulting sudden coronary artery occlusion, which
may be total or subtotal, causes acute myocardial ischemia or infarction. UA represents a high-risk transition
period during which most patients undergo accelerated myocardial ischemia. If unchecked, this transition
culminates in acute myocardial infarction (AMI) or sudden cardiac death (SCD) in up to 15% of patients within
just a few weeks. Coronary angiography in many of these patients demonstrates complex coronary plaque
lesions with varying degrees of superimposed thrombosis. Intravascular ultrasonic examination of coronary
vessels (IVUS) is another useful tool that has helped shed considerable light, not only on the pathophysiology
but also on the management of coronary artery disease (CAD), particularly in the setting of ACS.
The key role of platelets in the pathophysiology of ACS has undergone considerable review in the past decades.
Platelet activation and aggregation encourage formation and propagation of a plateletrich or “white” clot over a
ruptured atherosclerotic plaque in patients with UA and NSTEMI. This contrasts with the fibrin-rich or “red” clot
seen in the coronaries of patients with STEMI. The current recommendations on the use of antithrombin and
antiplatelet therapies in NSTEMI and that of fibrinolytic therapy in patients with STEMI derive not only from the
pathophysiology of these conditions but also from the results of informative clinical trials performed within the last
two decades.

Diagnosis
History and Physical Examination
The term UA denotes new pain or a departure from a previous anginal pattern. UA occurs at rest or

with less provocation than stable angina. Pain lasting longer than 15 minutes also suggests UA.
Angina occurring in the early post-MI period or within weeks of an interventional coronary procedure
also is best termed “unstable.” Commonly, the pain is described as a “tightness,” “heaviness,” or
“squeezing” in the substernal region. UA may awaken patients from sleep or present as pain at a new
site such as the jaw or arm. Elderly, female, and diabetic patients are more likely to experience atypical
symptoms, pain intensity, and distribution. Although the classical description is one of heavy central
chest pressure radiating to the jaw and left arm, it is rational to raise suspicion of UA or evolving MI in
patients reporting acute pain from “nose to navel.” Autonomic manifestations (nausea, vomiting,


tachycardia, or sweating) also favor “instability.” Blood pressure frequently rises before the onset of
pain, even in resting patients. Rising blood pressure boosts afterload, increasing wall tension and
myocardial O2 consumption. Less commonly, the abrupt onset of dyspnea and congestive heart failure
(CHF) may be the only manifestation of UA.

Data Profile
Electrocardiographic Changes
Electrocardiographic patterns are invaluable in determining the presence of coronary occlusion and in
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guiding the nature and urgency of therapeutic intervention. During episodes of ischemic chest pain,
electrocardiogram (ECG) features may include (1) ST segment elevation or depression, (2) T wave
flattening or inversion, (3) premature ventricular contractions (PVCs), or (4) conduction disturbances,
including bundle-branch block (Fig. 21-1). Q waves often but not invariably indicate completed infarction.
ST segment elevation strongly correlates with fresh coronary occlusion (STEMI), whereas ST depression in
association with or without T wave inversion indicates ischemia without acute coronary luminal occlusion
(non-STEMI or NSTEMI). Perhaps only 20% to 25% of ACS syndromes are STEMIs.
Reversible ST depression or T wave inversion is detectable in most affected patients if continuous ECG
monitoring is used, a finding that may not emerge during a single 12-lead ECG. Even with intensive
monitoring, ECG findings are absent in up to 15% of symptomatic patients with UA. Therefore, a normal
ECG does not exclude a diagnosis of UA or MI. Conversely, it has been estimated that up to 70% of all

ECG-documented episodes of ischemia are clinically silent.
Cardiac Enzyme Markers
Elevated total CK (including the CK-MB fraction) and cardiac troponins (I and T) are markers of myocardial
necrosis and indicate an MI, even in the absence of convincing ST segment-T wave changes. Troponins
(I/T) are more sensitive and specific in making the diagnosis of an AMI than is CK-MB. Their rise may be
delayed 1 to 3 hours after onset, so that their absence at a very early stage does not exclude an ongoing
AMI. Once present, elevations are often detected for 10 days or longer, especially in patients with renal
insufficiency. Troponin elevation in NSTE-ACS correlates with adverse prognosis. These are also patients
who are likely to benefit from aggressive antiplatelet regimens and from early coronary angiography and
revascularization. Highly sensitive C-reactive protein (hs-CRP) levels are also increased in patients with
ACS. ACS patients with the highest levels of hs-CRP and troponins have the worst prognosis.

FIGURE 21-1. Electrocardiographic evolution of AMI. SEMI, subendocardial (nontransmural) MI.


Prognostic Factors
Patients with UA have a lower short-term mortality rate (2% to 3% at 30 days) compared to those with acute
NSTEMI (5% to 7% at 30 days). The in-hospital or short-term mortality of patients with STEMI is higher
compared with those with NSTEMI (6% to 9% vs. 5% to 7% at 30 days). However, the longterm mortality in
NSTEMI (10% to 12%) is similar to or greater than that associated with STEMI (9% to 11%), likely because of
their greater incidence of multivessel CAD.
Thrombolysis in Myocardial Infarction Risk Score
Several risk variables have been identified in patients with NSTE-ACS. A value of 1 has been assigned to each
risk variable, and the total score has been shown to bear a linear relationship with risk of adverse events (death,
MI, recurrent ischemia, and need for urgent revascularization) in the short term. The variables are (1) age greater
than or equal to 65 years, (2) prior coronary stenosis greater than or equal to 50%, (3) presence of greater than
or equal to three coronary risk factors, (4) ST segment deviation on admission ECG, (5) elevated cardiac
biomarkers, (6) greater than or equal to two anginal episodes in the last 24 hours, and (7) prior use of aspirin
(marker for vascular disease). The adverse event rate is 4% to 5% for thrombolysis in myocardial infarction
(TIMI) risk score of 0 to 1 but approaches 40% for those with score of 6 to 7. Elevated levels of hs-CRP indicate

a worse prognosis in each TIMI scoring category.

Management of NSTE-ACS
Patients with NSTE-ACS should be monitored closely and should receive aggressive antithrombotic,
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antiplatelet, and antianginal treatments (Fig. 21-2). Most patients with UA can be stabilized with appropriate
medical therapy. Although the immediate urgency of STEMI-ACS is attenuated, coronary angiography and
revascularization procedures have become increasingly popular in the treatment of these patients over the
course of the last decades. Emergent coronary angiography and revascularization procedures are uncommon for
NSTE-ACS patients, but most are advised to undergo coronary angiography and possible revascularization
within a few days of admission to the hospital. Coronary revascularization procedures include either
percutaneous coronary interventions (PCIs) (PTCA and stenting) (Fig. 21-3) or coronary artery bypass graft
(CABG) surgery. Essentially, only patients with contraindications for invasive cardiac procedures are treated by
noninvasive medical management alone. Thrombolytics are not advisable in most (nonocclusive) NSTE-ACS
because “red thrombus” is not present and because thrombolytics have procoagulant properties. Apart from
considerations relating to coronary patency, the two basic principles in the treatment of UA are to reduce
myocardial O2 demand and improve O2 supply.


FIGURE 21-2. Non-ST elevation MI (NSTEMI) management algorithm. ECG, electrocardiogram.
Reducing Myocardial Oxygen Consumption
The principal measures to decrease myocardial oxygen consumption are to limit heart rate and afterload. These
goals are immediately accomplished by curtailing physical activity with bed rest. Exercise stress tests are
contraindicated in unstable patients because frank infarction may ensue. Arrhythmias like atrial fibrillation (AF)
and sinus tachycardia should be controlled, both to reduce O2 consumption and to optimize diastolic filling time,
thereby maximizing the sufficiency of coronary perfusion. Controlling hypertension and CHF decreases
myocardial wall tension and therefore facilitates perfusion (see Chapter 22). Situations that increase heart rate
(anxiety, use of short-acting nifedipine) or both heart rate and total body oxygen consumption (e.g.,
thyrotoxicosis, alcohol withdrawal, stimulant drug intoxication, anxiety, agitation, infections, etc.) should be
promptly recognized and corrected. β-Blockers effectively reduce myocardial oxygen consumption by decreasing

heart rate and cardiac contractility and improve O2 supply by lengthening diastolic filling time. β-Blocking drugs
are particularly useful in reducing oxygen consumption in the tachycardic and hypertensive patient with UA and
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ACS but are contraindicated in acute heart failure, coronary artery spasm, or severe bronchospasm. Selective βblocking agents such as carvedilol may be used cautiously in patients with modestly impaired ejection fractions
and tachycardia, but, in general, should be withheld until stability is achieved.