Transcript Cardiopulmonary

Cardiopulmonary Resuscitation:
Basic and
Advanced Life Support
• Although the history of resuscitation can be traced to at least
biblical times,contemporary approaches to cardiopulmonary
resuscitation (CPR) date back to 1966, when a National Academy
of Sciences National Research Council conference generated
consensus standards for the performance of CPR.
• Since that time, successive conferences have reviewed the
practice of CPR in the light of available experimental and clinical
data and have prepared revisions of previous standards.
• The most recent recommendations, the “2005 American Heart
Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care” (Guidelines 2005), represent the
second internationally recognized resuscitation guidelines
developed by experts from the American Heart Association (AHA)
and the European Resuscitation Council; accordingly, these
guidelines represent a variety of countries, cultures, and medical
specialties.
Basic Life Support
• BLS involves early recognition of medical emergencies, activation of an
emergency response system (e.g., dialing 911 in the United States), and
interventions made in response to sudden cardiac arrest (SCA), heart
attack, stroke, and airway obstruction by a foreign body.
• Airway, breathing, and circulation are BLS assessments readily
performed without equipment.
• Rescue breathing, the Heimlich maneuver, CPR, and the application-use
of an automated external defibrillator (AED) are BLS interventions.
• All BLS interventions are time sensitive for preventing SCA, terminating
SCA, or supporting the circulation until restoration of spontaneous
circulation occurs after SCA.
• For those performing BLS interventions, particularly CPR, the
importance of prompt initiation and expert performance of these skills
cannot be overemphasized.
Cardiopulmonary Resuscitation
• SCA is a complex and dynamic process. Antegrade systemic
arterial blood flow continues after cardiac arrest until the
pressure gradient between the aorta and right heart structures
reach equilibrium. A similar process occurs during cardiac arrest
with antegrade pulmonary blood flow between the pulmonary
artery and the left atrium.
• As the arterial-venous pressure gradients dissipate, the left heart
becomes less filled, the right heart becomes more filled, and the
venous capacitance vessels become increasingly distended .
• When arterial and venous pressure equilibrates (approximately 5
minutes after cardiac arrest), coronary perfusion and cerebral
blood flow stop.
• In the absence of native cardiac function and systemic
circulation, CPR is performed until return of
spontaneous circulation occurs, the patient is
pronounced dead, or in some special circumstances,
the patient is placed on extracorporeal circulation and
membrane oxygenation (ECMO).
• Although CPR is far less efficient than the native
circulation, when properly performed, it can provide
coronary circulation and cerebral blood flow sufficient
to afford full recovery in many cases if return of
spontaneous circulation can be reestablished.
• “Push hard and push fast” are the recommendations for chest
compressions during CPR from the 2005 International Consensus
conference.
• Although there is insufficient evidence from human studies to identify
an ideal chest compression rate, chest compressions performed at a rate
of 100/min and with enough force to generate a palpable carotid or
femoral pulse are considered ideal.
• Chest compressions are frequently interrupted during resuscitation
attempts. These interruptions have a negative impact on coronary and
cerebral perfusion, as well as on return of spontaneous circulation.
• Current recommendations for CPR reflect these observations by placing
increased emphasis on limiting interruptions in chest compressions, even
for other resuscitative measures (i.e., rescue breaths, attempts at
defibrillation, tracheal intubation).
• During single- and two-person CPR, Guidelines 2005 recommends
compression-ventilation ratios of 30 : 2 in both scenarios with minimal
interruption in chest compressions for rescue breaths.
Physiologic Considerations
• Since the early 1960s, when CPR became a
widespread clinical technique, it has been assumed
that blood is ejected as a direct result of actual
compression of the heart between the sternum and
the vertebral column. This is commonly referred to as
the “cardiac pump mechanism.”
• Observations made with echocardiography during
CPR describe a reduction in left and right ventricular
volume, closure of the tricuspid and mitral valves
during chest compression, and ejection of blood into
the arterial system, all of which are consistent with
the cardiac pump mechanism
• Repeated, forceful coughing (cough CPR) can sustain
consciousness during ventricular fibrillation (VF) for as long as 100
seconds when the arrhythmia (or any arrhythmia capable of
rapidly compromising cardiac output) is immediately recognized
and the patient can respond to verbal prompts to cough.
• This observation suggests that mechanisms other than direct
cardiac compression may account for forward blood flow during
cardiac arrest.Vigorous coughing produces an arterial pressure
pulse associated with forward blood flow that opens the aortic
valve during the generation of pressure and flow.
• These findings support the proposal that increases in intrathoracic
pressure generate forward blood flow,which is commonly referred
to as the “thoracic pump mechanism”.
• The increasing intrathoracic pressure during
chest compression equalizes intravascular
pressure within the thorax. On the venous side,
valve and venous collapse at the thoracic inlet
limits the transmission of retrograde pressure or
flow. The arterial system, which is relatively
resistant to collapse, transmits pressure and
flow into the extrathoracic arterial tree.
• A peripheral arteriovenous pressure difference
is thus established that permits blood to flow
forward in the extrathoracic vascular system.
• Some studies suggest that during compression
or vigorous coughing the left side of the heart
may act as a passive conduit for transfer of
pulmonary venous blood out into the peripheral
arterial circulation. During compression, blood
flows from the lungs through the left ventricle
toward the periphery. The pulmonary valve is
closed and the mitral and aortic valves are open
during periods of high intrathoracic pressure
when the chest is compressed.
• There is evidence that both cardiac pump and thoracic pump
mechanisms exist at times during resuscitation attempts.
• Echocardiographic evidence clearly demonstrates findings
consistent with the cardiac pump theory. Cough CPR is effective in
maintaining consciousness, at least in the early period after the
onset of lethal arrhythmia, consistent with the thoracic pump
theory.
• Chest compressions during cardiac arrest may initially promote a
cardiac pump mechanism as a result of the presence of blood in
the left heart. As pressure gradients between the arterial and
venous systems equilibrate during prolonged resuscitation,
pulmonary blood volume increases and probably supports a
thoracic pump mechanism.
• Systemic, coronary, and cerebral blood flow during CPR is
dependent on effective chest compressions, as well as on
return of venous blood to the heart.
• At chest compression rates of 80 to 100/min, the
compression-relaxation ratio approaches 50 : 50. The time
available for return of blood to the thorax is limited.
• Venous blood returns to the thorax at very low pressure
during cardiac arrest. Modest increases in intrathoracic
pressure will impair return of venous blood and have a
negative impact on systemic, coronary, and cerebral
perfusion, in addition to reducing the chance of
spontaneous circulation
• Cardiac output during CPR with effective, uninterrupted chest
compression is 25% to 30% of the normal spontaneous circulation.
Systemic and pulmonary perfusion during CPR reflects the
decreased cardiac output as demonstrated by weak carotid pulses
with compression and low carbon dioxide excretion .
• In cardiac arrest without a hypoxic etiology (e.g., drowning,
suffocation), oxygen content in the lungs at the time of cardiac
arrest is usually sufficient for maintaining an acceptable arterial
oxygen content during the first several minutes of CPR. Rescue
breaths are less important than initiating chest compressions
immediately after the onset of SCA. Blood flow rather than
arterial oxygen content is the limiting factor for delivery of oxygen
to the coronary, cerebral, and systemic circulation during CPR.
• Multiple modifications to standard CPR exist,
as well as mechanical adjuncts to improve
circulation during CPR.
• A few will be reviewed here in light of
current understanding.
Interposed abdominal compression
(IAC)
• Interposed abdominal compression (IAC) is a form of CPR
in which the abdomen is compressed midway between
the xiphoid process and the umbilicus during the upstroke
of the chest compression phase in an attempt to sustain
aortic diastolic pressure and thus improve coronary
perfusion pressure, a critical determinant of successful
restoration of spontaneous circulation.
• Though accepted by the AHA as an satisfactory adjunct to
standard CPR, this intervention is rarely used despite
recognition of its benefits, minimal risk, and easy
application.
• When sufficient personnel trained in the technique are
available, AIC-CPR can be considered a reasonable
alternative to standard CPR.
Active compression-decompression
CPR (ACD-CPR)
• Active compression-decompression CPR (ACD-CPR) accomplishes
compression and active decompression of the thorax by means of a
device containing a suction header, bellows, and a compression area
within the bellows.
• Although these observations provided clinical support for experimental
studies indicating improved hemodynamic (and perhaps ventilatory)
function with ACD-CPR versus standard CPR, still lacking was evidence of
benefit on patient outcome.
• despite the earlier experimental and clinical evidence that ACD-CPR may
confer benefit to victims of cardiac arrest by virtue of enhanced
hemodynamic variables, no evidence supports the hypothesis that ACDCPR improves outcomes after cardiac arrest in humans when compared
with standard manual CPR.
• The ACD-CPR device may also expose patients to harm.Currently, no
ACD-CPR devices are approved by the Food and Drug Administration for
sale in the United States.
The impedance threshold device (ITD)
• The impedance threshold device (ITD) limits entry of air into the lungs
during the recoil phase after chest compression, thereby creating greater
negative intrathoracic pressure and drawing greater blood volume into
the chest than with standard CPR. What results appears to be greater
coronary blood flow (occurring during the diastole/chest recoil phase of
chest compressions), greater cerebral blood flow, and improved
hemodynamics in comparison to standard CPR.
• The results of animal and clinical studies endorse the benefits of this
device, which include improved resuscitation and short-term survival
when compared with standard CPR.
• Although this device is most effective with endotracheal tubes, if a
rescuer can maintain a good seal with a facemask, the ITD can be used.
• Even though long-term survival has not been documented after use of
the ITD during resuscitation, if the device is available, there are no
compelling reasons to not consider using this technology.
Circumferential compression of the chest
with a load-distributing band (LDB)
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Circumferential compression of the chest with a load-distributing band (LDB) has
been described as a mechanism for generating fluctuations in intrathoracic
pressure and thereby improving blood flow by exploiting the thoracic pump
mechanism beyond that possible with standard CPR.
This device wraps circumferentially around the patient's torso, is closed with
Velcro, and then automatically adjusts the length of the belt to fit snuggly around
the patient's chest. Repetitive shortening of the belt compresses the chest and
generates forward blood flow. Chest recoil occurs as the belt relaxes. As with the
other devices already mentioned, the LDB has been shown in a preliminary study
to increase both aortic and coronary perfusion pressure in animals, which has
resulted in improved survival and neurologic outcome.
However, a recent multicenter, randomized prehospital clinical trial to evaluate
the effectiveness of an LDB was halted early because of markedly reduced
neurologic recovery in cardiac arrest victims on whom the LDB was used when
compared with cardiac arrest victims who received standard CPR. The authors
speculate that application of the device probably delayed or interrupted CPR and
also noted that the time to first defibrillation in the LDB group occurred on
average 2.1 minutes after the standard CPR group.
• Although the devices mentioned here all
demonstrate improved circulation and blood
flow in comparison to standard CPR during
cardiac arrest in humans, none of the devices
demonstrate improved hospital discharge rates
after resuscitation from cardiac arrest.
• What is certain is that CPR, regardless of the
mechanism of blood flow and technique, is only
a temporizing procedure in need of rapid
supplementation with ACLS, most critically,
rapid defibrillation of the fibrillating heart.
Monitoring Performance of
Cardiopulmonary Resuscitation
• Until recently, palpation of the carotid or femoral pulse and
observation of pupillary size were the standard and very indirect
measures for assessing the apparent adequacy of CPR. Obviously,
a palpable large-artery pulse indicates only the transmission of a
pressure wave into the arterial tree during chest compression and
provides no objective evidence of the effectiveness of cardiac
output.
• Initial pupillary size and changes during CPR are of some
prognostic value. Pupils that are persistently contracted or initially
dilated but subsequently contracting are associated with a greater
likelihood of successful resuscitation and neurologic recovery than
persistently dilated or subsequently dilating pupils are
• Monitoring systemic arterial pressure directly, as
can usually be accomplished during in-hospital
CPR, is helpful in optimizing the rate and depth
of chest compressions.
• Aortic diastolic pressure in particular, an index
of coronary perfusion pressure, should be
monitored whenever possible and optimized
with appropriate changes in manual
compression technique and early and repeated
injection of epinephrine and vasopressin before
restoration of spontaneous circulation
• In 1978, Kalenda described the use of
capnography as a guide to the effectiveness of
external chest compressions. He demonstrated
the value of monitoring PETCO2 in three patients
in cardiac arrest and confirmed changes in
PETCO2 with restoration of spontaneous
circulation. Kalenda proposed that when
ventilation is constant, as during controlled
mechanical ventilation, “the expired CO2 is a
precise and continuous mirror of lung perfusion
and hence of cardiac output.”
• Evidence is increasing that PETCO2 measurements
obtained during cardiac arrest and CPR may
have predictive value relative to the likelihood
that spontaneous circulation will be restored.
• Although more such data are needed to
quantitate the predictive power of PETCO2, it
seems certain that PETCO2 measurements during
cardiac arrest and CPR will become an objective
index to predict the likelihood that persistent
resuscitative effort will result in restoration of
spontaneous circulation.
• PETCO2 reflects pulmonary blood flow and
therefore cardiac output.
• Monitoring of both systemic arterial pressure
by arterial catheter and PETCO2 with controlled
ventilation should provide optimal
hemodynamic assessment of the adequacy of
the resuscitative effort and response to
interventions such as changes in depth, rate,
and location of manual chest compressions, as
well as response to drugs such as epinephrine
and vasopressin.
• Compelling evidence confirms major deficiencies in the provision
of CPR, particularly by trained health care professionals, in both
out-of-hospital and in-hospital settings.
• Long pauses without chest compressions and compressions that
are suboptimal in both rate and depth are frequent in both
settings and result in decreased blood flow. Animal studies have
shown that inadequate blood flow from poorly performed CPR
during cardiac arrest has a negative impact on both restoration of
spontaneous circulation and survival.
• Clinical evidence also suggests that excessive ventilation occurs
during resuscitation attempts and likewise has a negative impact
on resuscitation outcomes.
• In light of these observations, the major focus in Guidelines 2005
simplified CPR for the purpose of prolonging uninterrupted chest
compression.
Airway Control and Ventilation
• Ventilation is critical for restoration of spontaneous circulation
and organ preservation during cardiac arrest. The AHA ACLS
training program has effectively conveyed this treatment priority.
• The techniques used for providing ventilation are obviously
dependent on the clinical situation. The head tilt–chin lift
maneuver is recommended for initial airway control.
• The epiglottis rather than the tongue is the major cause of upper
airway obstruction in unconscious humans.Because of its
ligamentous attachments to the hyoid bone, the epiglottis can be
lifted by manual maneuvers that displace the hyoid bone
anteriorly. These observations provide anatomic confirmation of
the efficacy of the head tilt–chin lift technique for opening an
obstructed airway. The head tilt–jaw thrust maneuver
accomplishes the same purpose in restoring airway patency.[
• When rescue breathing is indicated for a nontracheally
intubated cardiac arrest victim, two 1-second breaths are
delivered after the 30th compression during both oneand two-person CPR.
• Rescue breaths should provide only enough force and
volume to cause chest rise. Excessive ventilation force or
tidal volumes run the risk of overcoming esophageal
opening pressure and thereby contributing to gastric
inflation and its consequences.
• Once a tracheal tube is in place, ventilation can occur at a
rate of 8 to 10 breaths per minute independent of chest
compressions.
• Ventilation should minimally disrupt chest compressions.
• During the first few minutes after the onset of cardiac
arrest, chest compressions are more important than
rescue breathing (provided that the cardiac arrest is not
secondary to asphyxiation, as with drowning or
suffocation).
• Delivery of oxygen to tissues with CPR is limited more by
blood flow and low cardiac output than by arterial
content.The low cardiac output associated with CPR
results in low oxygen uptake from the lungs, which in turn
reduces the need to ventilate the patient during this lowflow state.
• In view of this information, uninterrupted chest
compressions must be given the highest priority early in
resuscitation efforts.
• Endotracheal intubation is the usual and expected standard of
airway control in the critical care setting. Alternative airways that
may be useful in gaining rapid control of the airway and
ventilation while reducing the risk of pulmonary aspiration of
gastric contents in situations in which tracheal intubation is not
possible include the laryngeal mask airway (LMA) and the
esophageal-tracheal Combitube . These devices are classified in
Guidelines 2005 as acceptable and possibly helpful, especially
when the rescuer is inexperienced in placing tracheal tubes.
• Although they may be helpful as temporizing devices,
endotracheal intubation remains the optimal technique for
controlling the airway and ventilating the lungs during CPR.
Regardless of the device used, once an advanced airway is
inserted and placement confirmed, ventilation can be provided at
a rate of 8 to 10/min without interruption of chest compressions.
Confirmation of proper placement of
an endotracheal tube
• Confirmation of proper placement of an
endotracheal tube can be difficult in a patient
who has undergone cardiac arrest.
Observation of the rise and fall of the thorax
and auscultation of lung fields in this
situation can be misleading. Likewise,
because of the very low pulmonary blood
flow during CPR, PETCO2 detection devices
may not readily distinguish tracheal from
esophageal intubation.
• For these reasons, esophageal detector devices based on
the description by Wee have been introduced and
advocated for use in emergency situations such as cardiac
arrest. Both a syringe and a self-inflating bulb have been
used.
• The efficacy of these devices in distinguishing esophageal
from tracheal intubation is based on the principle that the
trachea remains patent during aspiration of air whereas
the esophagus collapses because of its fibromuscular
structure.
• The effectiveness of the self-inflating bulb in
distinguishing esophageal from tracheal tube position and
in confirming proper position of the esophageal-tracheal
tube has been documented.
esophageal detector device
• In an emergency patient population, an
esophageal detector device as described by
Wee was observed to be more accurate than
detection of PETCO2 because of its greater
accuracy in patients in cardiorespiratory
arrest .
• False-negative results with the self-inflating bulb occur more
frequently in emergency intubations than in anesthetized patients
undergoing elective procedures. Causes include partial tube
obstruction with secretions, atelectasis, bronchospasm, and
endobronchial intubation. A high incidence of false-negative
results was observed in morbidly obese patients. In these
patients, reduced functional reserve capacity and large-airway
collapse secondary to invagination of the membranous posterior
tracheal wall after the application of subatmospheric pressure
with the self-inflating bulb were identified as the cause of the
false-negative results.
• With these limitations in mind, the self-inflating bulb or syringetype esophageal detector is useful in emergency situations such as
cardiac arrest, particularly when used in combination with PETCO2
detection.
LMA
• Despite extensive experience with the LMA in fasted patients undergoing
general anesthesia, its role during CPR remains somewhat controversial.
In anesthetized patients, positive-pressure ventilation with the LMA is
safe and effective, but concern was expressed that gastric inflation could
be a problem in the presence of increased inflation pressure.This
problem, of course, is common in patients who sustain cardiorespiratory
arrest because they typically have a full stomach and frequently require
high inflation pressure during ventilation.
• The LMA has been used successfully in arrested patients who have no
evidence of regurgitation or aspiration.
• In patients in whom endotracheal intubation is not possible, the LMA is
more secure than a facemask and offers an alternative to control the
airway and ventilate the patient.
• Importantly, placement of an LMA by an inexperienced provider cannot
result in unrecognized esophageal intubation in a patient requiring
emergency airway management.
The esophageal-tracheal
Combitube
• The esophageal-tracheal Combitube is an acceptable alternative
airway device for use in cardiac arrest. The Combitube is a doublelumen device with proximal pharyngeal and distal inflatable cuffs
that is introduced blindly into the airway. One lumen of the device
has a closed distal lumen and ventilation holes at the level of the
hypopharynx. The second lumen is open ended with a balloon cuff
at its distal end. Both lumens of the airway can accommodate
ventilation. Once inserted and followed by inflation of the
pharyngeal and distal cuffs, confirmation of the proper ventilation
port is mandatory. Auscultation and PETCO2 detection must
demonstrate that tracheal rather than esophageal ventilation has
been achieved.
• When the esophageal-tracheal Combitube is properly placed, the
airway is isolated and the risk for aspiration of gastric contents is
reduced.
• If these devices and techniques are unsuccessful
in securing an airway, immediate
cricothyroidotomy may be necessary. A 12-, 13or 14-gauge catheter-over-needle device can be
inserted quickly into the trachea through the
cricothyroid membrane. Equipment permitting
transtracheal jet ventilation from a 50-psi
oxygen source through such a catheter should
be available in the operating room and ICU.
• Increasingly, airway management and ventilation conducted in the
setting of resuscitation has come under scrutiny. Clinical studies
support the concept that circulation, not ventilation, has the
greatest impact on survivability after cardiac arrest. Yet chest
compressions are frequently interrupted for prolonged periods to
allow either ventilation or placement of an advanced airway in
both the in-hospital and prehospital environments.
• Ventilation during resuscitation, with or without the advanced
airway in place, is often excessive and associated with increased
intrathoracic pressure, lower coronary perfusion pressure,
impaired venous return, and ultimately, decreased survival.
• The team leader must be attentive to the rate and vigor of
ventilation performed during resuscitation attempts, in addition
to other components of therapy.
Automated External Defibrillators and
Manual Defibrillation
• The most frequent cardiac rhythm responsible for witnessed
cardiac arrest in adults is VF. CPR prolongs the duration of VF but
cannot convert the arrhythmia to an organized rhythm. Successful
termination of this arrhythmia requires prompt electrical
defibrillation, not medications. The most recent AHA guidelines
include early defibrillation with an AED as part of BLS training and
the concept of public-access defibrillation, which endorses the
policy of making defibrillation available to victims of cardiac arrest
through nonconventional providers (e.g., police, security guards,
and others). The AED, when applied to a patient, is capable of
analyzing cardiac rhythm, detecting VF and rapid ventricular
tachycardia (VT), and then delivering a defibrillatory shock. A
trained rescuer's role is to apply the defibrillator pads to the
patient's chest, activate the AED, and if the device indicates that a
shock is indicated, deliver the shock by pushing a button when
prompted to do so by the AED.
• Previous guidelines addressing AED use in
cardiac arrest recommended administering
up to three consecutive uninterrupted shocks
if needed to terminate VF.
• Chest compressions were not performed
during the shock sequence.
• Current experimental and clinical evidence
suggests that success in defibrillation and
survival are negatively influenced by frequent
or prolonged interruptions in chest
compressions during cardiac arrest.
• In light of this most recent information, Guidelines 2005
recommends a single shock from an AED followed immediately by
a 2-minute period of CPR, the equivalent of five cycles of 30 : 2
chest compression-ventilation, before reanalysis of the cardiac
rhythm.
• Chest compressions are continued until the AED is charged and
ready to deliver the shock.
• In most instances, the heart is at least transiently “stunned” by
defibrillation shocks and is benefited by a period of coronary
blood flow with chest compressions.
• For the exceptional patient with invasive monitoring present at
the time of cardiac arrest, if an organized cardiac rhythm with a
perfusing arterial waveform follows defibrillation, chest
compressions may not be indicated.
• VF is a highly metabolically active state of the
myocardium. In the presence of VF, myocardial stores
of oxygen and metabolic substrates are depleted
rapidly. Chest compressions deliver oxygen and
energy substrates to the myocardium, thus making
defibrillation more likely.
• Experimental animal and prehospital evidence from
Seattle and Oslo demonstrate increased defibrillatory
success when CPR is provided before defibrillation,
particularly if the cardiac arrest was unwitnessed or if
the time between cardiac arrest and arrival of
rescuers exceeds 4 minutes.
• Guidelines 2005 recommends 2 minutes of CPR
(five cycles of 30 : 2 compression-ventilation)
before the first rhythm analysis of the cardiac
arrest in the setting of unwitnessed cardiac
arrest or delays in initiation of CPR.
• In settings in which defibrillation technology
(manual defibrillator or AED) is immediately
available (i.e., <3 minutes), rescuers should
begin CPR and then defibrillate as soon as
possible.
• If a monophasic defibrillator is available, defibrillation energy should
begin at high energy (300 to 360 J). Prospective human clinical studies
have failed to identify the optimal biphasic energy levels for first or
subsequent defibrillation attempts. Although first-shock energies specific
to the defibrillation waveform have been recommended (150 to 200 J
with a biphasic truncated exponential waveform, 120 J with a rectilinear
biphasic waveform), a rescuer encountering an unfamiliar device should
choose an energy setting of 200 J for the first shock and may increase the
energy as needed for subsequent shocks when indicated.
• when biphasic waveform defibrillation is used, the body weight of the
patient does not influence the energy delivered because the waveforms
compensate for transthoracic impedance to allow uniform delivery of
energy and thus obviate the need to vary from the recommended
defibrillation energy.
• Time to the first shock remains the most important factor influencing
successful resuscitation
Advanced Cardiac Life Support
• It must be emphasized that CPR almost invariably necessitates
rapid interventional follow-up care with ACLS procedures.
Anesthesiologists should be capable of rendering such definitive
follow-up intervention, whether in the operating room, ICU,
emergency department, delivery room, or hospital ward.
• The somewhat reassuring observation that intraoperative cardiac
arrests are rare (1.1/10,000 and 1.4/10,000 in the two studies)
does not dismiss the need for anesthesiologists to be thoroughly
acquainted with ACLS equipment and interventions because when
these methods are needed, they must be executed skillfully and
decisively.
• Failure to intervene rapidly with ACLS pharmacologic therapy was
identified as a major cause of poor outcome in other reports of
intraoperative cardiac arrest.
• In a study using a computer program that simulates
critical patient incidents such as cardiac arrest, it was
observed that only 30% of participants, who consisted of
anesthesiology residents, faculty, and private
practitioners, managed a simulated cardiac arrest in
accordance with the AHA ACLS guidelines.
• Timing since the last ACLS training was noted to be an
important predictor of proper management of simulated
cardiac arrest.
• some form of periodic training and retraining in ACLS is
necessary for maintaining the level of knowledge and
skills essential for management of cardiorespiratory arrest
in accord with contemporary principles as incorporated in
the ACLS training program.
Monitoring and Recognition of
Arrhythmia
• Prompt recognition and treatment of
potentially life-threatening (pre-arrest)
cardiac arrhythmias are essential
components of ACLS.
• Early recognition and immediate
pharmacologic intervention necessitate the
full application of BLS and ACLS and can
frequently prevent the onset of fatal
arrhythmias.
Supraventricular Bradyarrhythmia
• Supraventricular bradyarrhythmias may be sinus or
junctional in origin, or they may be caused by second-degree
(types I and II) or third-degree atrioventricular (AV) block.
• Sinus (or junctional) bradycardia and type I (AV nodal)
second-degree block are usually manifestations of increased
vagal tone.
• Sinus bradycardia and type I second-degree AV block
(Wenckebach phenomenon) may be observed during highdose narcotic anesthesia.
• During spinal anesthesia, reduced venous return and
unopposed vagal tone may produce bradycardia and
hypotension of sufficient severity to progress to cardiac
arrest.
• Treatment is indicated whenever the
bradycardia, regardless of type, leads to a
significant decrease in systemic arterial
pressure, produces clinical signs of reduced
cardiac output (or a decrease in measured
output), or is accompanied by ventricular
ectopic depolarization.
• Any of these signs should be taken as evidence
of hemodynamic or electrophysiologic
deterioration with the propensity to progress to
lethal arrhythmias, either asystole or VF.
• Initial treatment is atropine, 0.5 to 1.0 mg
intravenously and repeated as needed at 3- to 5minute intervals up to 0.04 mg/kg.
• If such treatment is ineffective in producing an
increase in heart rate and hemodynamic
(increased systemic pressure, cardiac output, or
both) or electrophysiologic (elimination of
ventricular ectopy) improvement, alternatives
include external or transvenous pacing or,
during spinal anesthesia, low-dose (0.2 mg)
intravenous epinephrine.
• The availability of intraoperative cardiac pacing
equipment and techniques has diminished the need
for isoproterenol for the treatment of
bradyarrhythmias. The increase in myocardial oxygen
demand imposed by isoproterenol makes its use
potentially hazardous in the presence of acute
myocardial ischemia.
• If transvenous or transcutaneous pacing is not
available for treating atropine-refractory
bradyarrhythmias, an infusion of dopamine (5 to
20 µg/kg/min) or epinephrine (2 to 10 µg/min) would
be a better choice than isoproterenol.
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Pulmonary artery catheters that permit the insertion of atrial or ventricular
pacing probes are available. If such a catheter is in place, emergency pacing can
be instituted rapidly. Pacing probes can be advanced into position quickly to
permit rapid control of the cardiac rate by ventricular, atrial, or AV sequential
pacing. Atrial pacing wires require an intact AV nodal conduction system.
Ventricular pacing is indicated when AV nodal conduction is disrupted.
External transcutaneous pacing can be used to rapidly treat atropine-resistant
bradyarrhythmias. These devices have been described as safe and effective, and
intraoperative experience has been favorable. They should be readily available
for emergency use along with a defibrillator. External pacing is not beneficial in
bradyasystolic arrest.
Transesophageal atrial pacing has been effective in treating intraoperative
supraventricular bradyarrhythmias such as sinus or junctional bradycardia. In its
present configuration, however, it cannot be used to pace the ventricles and
therefore is not useful in the management of any form of bradycardia caused by
AV conduction disturbances.
Supraventricular Tachyarrhythmia
• Supraventricular tachyarrhythmias include atrial
flutter, atrial fibrillation, AV junctional tachycardia,
multifocal atrial tachycardia, paroxysmal reentrant
tachycardia, and other much less frequent
arrhythmias.
• Paroxysmal supraventricular tachycardia (PSVT),
atrial fibrillation (or flutter) with rapid ventricular
rates, and multifocal atrial tachycardia are discussed
here because not only can they produce
hemodynamic compromise, they can also present
diagnostic and therapeutic challenges.
Figure 97-4 A, A supraventricular tachycardia at a rate of 180 beats/min is
present; the origin of the tachycardia is not evident. B, After injection of
6 mg adenosine, atrial flutter waves are clearly visible.
If PSVT produces hemodynamic deterioration,
cardioversion is the treatment of choice.
The recommended initial dose for cardioversion of atrial
tachyarrhythmias is 100 to 200 J if a monophasic
defibrillator is used or 100 to 120 J with a biphasic device.
Energy can be increased as needed if the arrhythmia is
resistant to therapy.
If the patient is hemodynamically stable, vagal maneuvers
can be attempted (e.g., Valsalva maneuver in awake
patients) before initiating pharmacologic interventions.
Vagal maneuvers alone will terminate about 20% to 25%
of reentry supraventricular tachyarrhythmias.
• If vagal maneuvers are unsuccessful, adenosine is the drug of
choice for termination of organized rapid supraventricular
arrhythmias.
• Adenosine slows sinoatrial and AV nodal conduction and prolongs
refractoriness, which is very effective in terminating PSVT, the
most common cause of which is reentry within the AV node.
• The drug is of diagnostic usefulness in revealing the underlying
mechanism in tachyarrhythmias of uncertain origin (e.g., atrial
fibrillation, atrial flutter) by inducing transient block of AV nodal
conduction.
• Because of rapid cellular uptake and metabolism, adenosine must
be injected rapidly into a venous catheter proximal enough to the
heart to ensure delivery of a sufficient concentration of the drug
at the AV node to induce an AV nodal conduction block.
• Adenosine can be used initially in a dose of
6 mg, and if necessary, a second dose of 12 mg
can be given in 1 to 2 minutes. If a central
venous catheter is used, these doses can be
reduced to 3 and 6 mg, respectively.
• If the drug is injected more distally and slowly
(e.g., into a small-bore catheter in a dorsal hand
vein), not only may therapeutic failure result,
but transient acceleration of the
tachyarrhythmia may occur as well ( Fig. 97-5 ).
Figure 97-5 A, Atrial fibrillation with a ventricular response of
190 beats/min. B, After injection of 6 mg adenosine, the
ventricular response increased to 240 beats/min.
• This paradoxical acceleration of the rate is a
manifestation of the increase in sympathetic
nervous system traffic induced by adenosine
in the presence of inadequate AV nodal
blockade.
• Rate acceleration has also been observed after the
administration of adenosine to patients with atrial
fibrillation and preexcitation (Wolff-Parkinson-White
syndrome).
• As with verapamil in this setting, the acceleration in
rate is a result of the AV nodal block with diversion of
fibrillation wave fronts through the accessory
connection.
• Even though the short half-life of adenosine may
reduce this hazard, it seems prudent to avoid
adenosine, as well as other AV node–blocking drugs,
in patients with atrial fibrillation and preexcitation.
• Adenosine's very short half-life (<5 seconds) is both
advantageous and disadvantageous: side effects such
as flushing, dyspnea, and chest pain are short lived,
but the tachyarrhythmia may recur and necessitate
the use of another drug.
• The AV nodal–blocking action of adenosine is
antagonized by theophylline or related
methylxanthines and is potentiated by dipyridamole
and carbamazepine.
A suggested scheme for the use of adenosine,
including dosing adjustments, is presented in Table
97-2 .
Table 97-2
Administration of Adenosine *
• Peripheral :(antecubital) 6 mg, then 12 mg if
needed
• Central :3 mg, then 6 mg if needed
• If taking theophylline-containing drugs :9 mg
peripherally, 6 mg centrally
• If taking dipyridamole: 2 mg peripherally, 1 mg
centrally
* Use with caution in asthmatic patients and those
taking carbamazepine
• Bronchospasm has also been described after the injection of
adenosine, including intraoperatively. This complication has
occurred in patients with bronchial asthma or chronic obstructive
pulmonary disease (COPD). The mechanism is unknown, but the
bronchospasm may result from stimulation of bronchial smooth
muscle adenosine receptors or stimulation of mast cell–derived
mediators of bronchoconstriction.
• Aminophylline, an adenosine receptor antagonist, has been used
successfully intraoperatively to treat adenosine-induced
bronchospasm.
• In light of this experience, adenosine should not be used or
should be used with caution in patients with a history of bronchial
asthma or COPD with a bronchospastic component.
• If the PSVT does not respond to adenosine or if it recurs,
verapamil is the drug of choice. A dose of 5 mg produces a
more sustained block of AV nodal conduction. Verapamil
can also be used to slow the ventricular response in atrial
fibrillation or flutter. However, it should not be used in
patients with Wolff-Parkinson-White syndrome in whom
atrial fibrillation or flutter develops. In this setting,
verapamil-induced increases in conduction over the
accessory pathway may produce alarming acceleration of
the ventricular rate or VF.
• If atrial flutter or fibrillation results in hemodynamic
deterioration because of the rapid ventricular response,
cardioversion is the treatment of choice. Atrial flutter can
be terminated with low-energy synchronized shocks.
• Atrial flutter or fibrillation with a rapid ventricular
response can cause rate-related hemodynamic
compromise manifested perioperatively as hypotension,
decreased cardiac output, or both.
• In hemodynamically unstable patients, cardioversion
should be used. Recent-onset atrial flutter is typically very
sensitive to low-energy shocks (e.g., 50 J, monophasic or
biphasic waveforms).
• For atrial fibrillation, the initial dose for cardioversion is
100 to 200 J with monophasic waveforms or 100 J to 120 J
with biphasic waveforms. Escalation of energy doses for
the second and subsequent doses is indicated.
• In hemodynamically stable patients with rapid ventricular rates
secondary to atrial fibrillation or flutter, treatment is pharmacologic.
With acute onset of these tachyarrhythmias, ibutilide given
intravenously has the most rapid onset of effect in restoring sinus
rhythm. Ibutilide is a class III antiarrhythmic drug that prolongs the
action potential duration and effective refractory period without effects
on action potential upstroke. The dose is 1 mg given over a 10-minute
period. A second dose can be administered 10 minutes after the first, if
necessary. Conversion to sinus rhythm is more frequent with atrial
flutter than with atrial fibrillation (63% versus 31%) and more frequent
with atrial fibrillation of shorter duration.Prolongation of the QT interval
reflects the pharmacologic action of the drug; polymorphic ventricular
tachycardia (PVT) accompanied by increases in the QT interval has been
reported in 8.3% of patients receiving ibutilide, so clinicians should be
prepared to manage this arrhythmia
• Alternative options for the treatment of
supraventricular arrhythmias include
diltiazem, verapamil, β-blocking medications,
procainamide, and amiodarone. By slowing
conduction and increasing refractoriness in
the AV node, calcium channel–blocking
agents result in control of the ventricular rate
in patients with atrial flutter, atrial
fibrillation, and multifocal atrial tachycardia.
•
Diltiazem is given in an initial dose of 0.25 mg/kg over a 2-minute
period, followed, if needed, in 10 to 15 minutes by 0.35 mg/kg. An
infusion at a rate of 5 to 15 mg/hr can be used to maintain rate
control.
• If verapamil is used, 5 mg can be given initially and then 5 to
10 mg in 15 to 30 minutes if needed.
• β-Adrenergic–blocking drugs are helpful in controlling the
ventricular rate when no contraindications to use are present.
• Amiodarone is a complex agent with antiadrenergic effects in the
presence of supraventricular arrhythmias and tachycardias
resulting from accessory pathways or rapid AV node transmission
of atrial impulses and in situations in which other agents have
failed to control the heart rate. It is given as a 150-mg intravenous
bolus over a 10-minute period, followed by a 1-mg/min infusion
for 6 hours to a maximum daily dose of 2 g.
• Multifocal (multiform) atrial tachycardia is a quite common
tachyarrhythmia that is often misdiagnosed as atrial fibrillation.
Increased automaticity in multiple atrial foci results in a need for
therapy different from that for reentrant supraventricular
arrhythmias (atrial flutter, atrial fibrillation, PSVT).
• Multifocal atrial tachycardia is diagnosed by observing the
presence of at least three morphologically different P waves in the
same lead of a 12-lead electrocardiogram (ECG) and a ventricular
rate more rapid than 100/min ( Fig. 97-7 ).
• It is usually described as occurring in patients with COPD,
especially during exacerbations, and ICU management is
necessary. However, it occurs in other settings as well, such as
hypokalemia, catecholamine administration, and acute myocardial
ischemia.
• Treatment of underlying conditions probably
contributing to myocardial irritability is important.
Digitalization and cardioversion, sometimes helpful in
other supraventricular arrhythmias, are ineffective in
multifocal atrial tachycardia. Digitalis toxicity or
repeated and futile attempts at cardioversion can
follow misdiagnosis. Acceptable rate control
treatment in patients with preserved ventricular
function includes calcium channel blockers, βadrenergic blockers, and amiodarone. In the presence
of impaired ventricular function, diltiazem and
amiodarone may be useful.