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Issue 1, March 2003
Biological & Biomedical Sciences
Review
Article: Cardiac
Resuscitation in Pre-Hospital and Hospital Settings: Treatments for
Ventricular Fibrillation and Cardiac Arrest
Holly Cummings
University of Maryland - College Park
Abstract
This review was performed with the intent of determining the most
effective treatment for ventricular fibrillation (VF) leading to
cardiac arrest (CA). Emphasis was placed on pre-hospital care, in-hospital
care, and electrical defibrillation separately. Computerized databases
covering topics of health and medicine, including Medline, were
accessed between March 28 and May 12, 2002 and searched for the
following terms: cardiac arrest, ventricular fibrillation, defibrillation,
cardiopulmonary resuscitation (CPR), and drug treatment. Certain
information pertinent to cardiac physiology was obtained from a
college-level physiology textbook, and a number of sources were
found from the bibliographic references of other studies. All sources,
with the exception of a few articles considered to be landmark cases
in the history of cardiac care, or ones used to reference other
sources, were from no earlier than 1995. All sources dealing with
CA treatment obtainable through Internet or library access were
utilized for this review. The final study selection included multiple
types of studies, including prospective, retrospective, and blind
studies. Pre-hospital CA should be treated with continuous chest
compression CPR (CCC-CPR), especially when only a single lay rescuer
is available. The best in-hospital CPR treatment has yet to be determined,
although minimally invasive direct cardiac massage (MID-CM) has
been shown effective. Drug therapies vary in dosage and drug combination,
and much more extensive research is necessary. Electrical defibrillation
provides the best survival rates from VF/CA, but automated external
defibrillation (AED) devices requiring extensive amounts of time
to diagnose VF before shock delivery are detrimental to survival
rates.
Introduction
Cardiac arrest (CA), once thought to be due to a spontaneous cessation
of the heart during diastole, is now known to be due to ventricular
fibrillation (VF) (Sternbach et al 2000). While the first resuscitation
treatments were recorded as early as biblical times (Paraskos 1992),
and modified throughout previous centuries (Chameides 1998), it
was not until 1960 that cardiopulmonary resuscitation (CPR) was
"rediscovered" and then standardized (Bains 1998; Kouwenhoven et
al 1960). Since then, recommendations for the best treatment for
CA have been under continuous scrutiny since none has provided absolute
success. Survival rates for patients suffering from CA are extremely
poor; the best reported survival rates are 25% to 30%, but the average
rate is only 2% to 5% (Berg et al 2001; Xu et al 2002). Survival
after CA is dependent upon time - the chance of survival decreases
7% to 10% each minute with no-flow after CA (Xu et al 2002; Eynon
2000; Larsen 1993).
Because CA requires the most emergent care of any medical condition,
and because available treatments vary widely in their effectiveness
and ease of application, the best treatment for CA has not yet been
conclusively established. This article reviews the current CPR,
surgical, drug, and electrical therapies available for CA treatment
and their use in both a pre-hospital and in-hospital setting.
Physiology of VF
VF occurs when multiple sites of independent action potential conduction
and myocyte contraction occur after loss of sino-atrial (SA) node
pacemaker capability (Eynon 20002; Silverthorn 2001). VF is characterized
by rapid fluttering contractions that fail to eject blood into pulmonary
and systemic circulation, causing a severe decrease in perfusion.
Decreased blood flow and oxygen transport have critical implications
for cerebellar function. As uncoordinated ventricular contractions
continue, the increased frequency of contraction places higher metabolic
demands on the system that will become increasingly impossible to
meet (Eynon 2000; Eichhorn 1998). Consequently, the pumping capability
of the heart will become increasingly decreased and the organ will
fail completely (Eichhorn 1998).
The most common cause of primary CA is VF due to myocardial ischemia
(Fabbri et all 2001). About 70% of patients in pre-hospital CA are
in VF when emergency medical system (EMS) personnel arrive (Truong
and Rosen 1997), and time is the most critical element when treating
VF. Severe, irreversible effects, including cardiac and cerebral
reperfusion injuries, may be sustained if VF continues for more
than four minutes (Eynon 2000; Truong and Rosen 1997; Panzer et
al 1996). Without immediate treatment, and even with the incorrect
or inefficient treatment, VF will quickly deteriorate into asystole,
followed by death (Truong and Rosen 1997; Achletiner et al 2001;
Monsieurs et al 1998).
Emergency treatment for CA is dependent upon a multiple-link chain
of response. Bystander response is the first, and one of the most
important, links (Kern et al 2002; AHA 2000), since bystanders are
depended upon to alert emergency personnel and begin care.
CA Treatment in a Pre-Hospital Setting
CA occurring in a pre-hospital setting is particularly dependent
on quick, early response efforts, and bystander recognition and
care of CA patients is quite important. The standard of care for
CA patients is CPR, and a number of variations on the American Heart
Association (AHA) guidelines for CPR (AHA 2000) have recently come
under study, including active compression-decompression CPR (ACD-CPR),
phased thoracic-abdominal active compression-decompression CPR (PTACD-CPR)
and continuous chest compression CPR (CCC-CPR).
Standard CPR
Standard CPR (S-CPR) has been defined by the AHA to consist of chest
compressions performed at a rate of 100/min, in accordance with
studies showing optimal compression rates of >80/min and 120/min
(AHA 2000; Sunde et al 1998). Rescue breathing is performed after
every 15th chest compression, with each of two breaths lasting no
more than two seconds each (AHA 2000). Although S-CPR has been taught
to laypeople since 1974, evaluation of post-course performance of
those trained in it has found layperson CPR to be ineffective. New
guidelines have attempted to address some of these issues, including
the fact that lay rescuers cannot be relied upon to effectively
determine whether a patient has a pulse or not (AHA 2000), and the
fact that many show what may be irrational or uninformed reluctance
to perform rescue breathing due to a fear of infectious disease
transmission (Berg et al 2001; Kern et al 2002; AHA 2000; Kern et
al 2001).
CPR works by increasing perfusion to vital organs and enhancing
the viability of myocardial cells (Truong and Rosen 1997). It can
prevent VF from deteriorating into asystole and improves the chances
of survival, but only if performed correctly, and at optimal rates
of about 100 compressions/min (AHA 2000; Sunde et al 1998). This
rate significantly increases cardiac output (CO), coronary perfusion
pressure (CPP), and coronary blood flow velocity (Sunde et al 1998).
Layperson CPR is often performed inadequately, and Xu et al (2002)
determined this might be detrimental enough to cerebral blood flow
that it should be bypassed if more effect resuscitation is en route.
The benefit of waiting for better-trained personnel outweighs the
risk of performing less-than-optimal CPR (Xu et al 2002).
ACD-CPR
ACD-CPR utilizes a hand-held device equipped with a suction cup
to actively lift the chest during the decompression phase of CPR,
thereby decreasing intrathoracic pressure (Figure 1). Studies have
shown varying success with this type of CPR. A 1996 retrospective
study conducted in Gšttingen, Germany (Panzer et al 1996) showed
no overall difference in survivability between S-CPR and ACD-CPR,
although it did show increased survival rates if the rhythm found
at onset of CPR was asystole. Additionally, ACD-CPR was shown to
increase survivability to the initial endpoint, return of spontaneous
circulation (ROSC) (Panzer et al 1996). Other studies have shown
superior mean arterial pressure (MAP) and organ perfusion (AHA 2000),
and a 1998 study performed on pigs found cerebral blood flow, CPP,
and mean aortic pressure all increased with an ACD-CPR rate of 90/min
versus 60/min (Sunde et al 1998). The only overall improved survivability
rates with ACD-CPR are from a study in France that showed one-year
patient survivability increased from 2% to 5% (Plaisance et al 1999).
PTACD-CPR
PTACD-CPR merges the concepts behind ACD-CPR and interposed abdominal
compression CPR (IAC-CPR) (AHA 2000). Two rescuers are needed to
perform the compression components of IAC-CPR: one to perform chest
compressions, and one to perform abdominal compressions (Figure
2). The aim of these compressions is to increase organ perfusion,
and while two studies have shown increased ROSC and 24-hour survival
rates with IAC-CPR, these results only apply to in-hospital treatment
(AHA 2000). PTACD-CPR is performed with a handheld device on which
two suction cups are attached, one of which is placed over the sternum
and the other of which is placed over the epigastrium (Arntz et
al 2001). The two cups are attached with a rigid handle so that
when one is compressed, the other is actively decompressed, and
vice versa (Figure 3). When Arntz et al (2001) tested one such device,
the Lifestick, with the help of the Berlin EMS, they found implementation
of PTACD-CPR resulted in a higher rate of ROSC versus S-CPR if the
presenting rhythm was asystole (33% vs. none) (Arntz et al 2001).
However, if the presenting rhythm was VF, S-CPR was superior in
attaining ROSC (68% vs. 44%), and overall, S-CPR resulted in 50%
ROSC versus 38% with PTACD-CPR. As for survival beyond ROSC, implementation
of S-CPR resulted in a greater chance of survival to hospital admission
(46% vs. 29%) and to hospital discharge (58% vs. none), with 86%
of those surviving to hospital discharge attaining long-term survival
greater than six months (Table 1). Despite these poor results with
PTACD-CPR, the researchers found the overall practicability of use
of the Lifestick device was better than that of ACD-CPR devices,
which cause strain on rescuers due to the force needed to produce
active chest decompressions. Additionally, PTACD-CPR resulted in
fewer sternum or rib fractures compared to S-CPR (Arntz et al 2001).
The Lifestick also eliminates the need for a second rescuer to perform
abdominal compressions, making it better suited for pre-hospital
care, in which multiple rescuers may not be present.
CCC-CPR
It has been well established that layperson CPR is not as effective
as CPR performed by professional emergency care providers (Xu et
al 2002; Kern et al 2002). Many lay rescuers, in addition to being
unable to adequately find a pulse, take much longer than the recommended
four seconds to deliver the two rescue breaths. Instead, some research
has shown a more realistic time for layperson rescue breathing to
be about 16 seconds (Kern et al 2002) - quadruple the recommended
time - and this decreases the effectiveness of the ensuing chest
compressions (AHA 2000). A factor compounding this problem is the
fact that many laypeople trained in CPR show reluctance to performing
mouth-to-mouth rescue breathing on people unrelated to them (Berg
et al 2001; Kern et al 2002; AHA 2000; Kern et al 2001). CCC-CPR
eliminates the rescue-breathing component of S-CPR, making it easy
to administer with promising research results.
Two studies of the effects of CCC-CPR as compared to S-CPR found
CCC-CPR resulted in better outcome after treatment (Berg et al 2001;
Kern et al 2002). Berg et al determined the interruption of chest
compressions for rescue breathing resulted in a lower number of
chest compressions administered, lower CPP, and left ventricular
myocardial blood flow throughout treatment on pigs (Berg et al 2001).
While arterial oxygen saturation and pH were higher, and Pco2 lower,
in the standard CPR trials, the left ventricular myocardial oxygen
delivery and CO were not different from those of the CCC-CPR trials.
Thus, the increased oxygenation benefits afforded by rescue breathing
are negated by the poor hemodynamic effects of stopping compressions.
This study found no significant difference in neurological outcome
between the two trial groups (Berg et al 2001).
Kern et al, in their study, showed CCC-CPR provided a better outcome
than S-CPR. A higher percentage of pigs in the CCC-CPR trials reached
ROSC, all-endpoint survival, and neurological function retention/non-impairment
than those in the standard CPR trials (Table 2) (Kern et al 2002).
They, too, found the decreased number of chest compressions, along
with the frequent, extended interruptions for rescue breathing,
were detrimental to the effectiveness of standard CPR (Kern et al
2002).
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CA Treatment in a Hospital Setting
Although all of the pre-hospital CA treatments are available for
in-hospital use as well, the same is not true of all hospital treatments
for pre-hospital rescuers. Surgical procedures and certain drug
therapies must be administered by physicians, limiting their use
to a hospital setting.
Minimally invasive direct cardiac massage
Closed-chest compressions, which are used in S-, ACD-, PTACD-, and
CCC-CPR, are not as effective in creating coronary and cerebral
perfusions as open-chest cardiac massage (OC-CM). OC-CM was the
standard for cardiac resuscitation before the 1960s, when closed-chest
compressions proved successful and current CPR techniques were developed
(Bains 1998; Kouwenhoven 1960). It requires open-chest surgery,
making it even more unfavorable in an emergent setting. However,
because direct cardiac massage produces better coronary perfusion,
recent studies have looked at methods to minimize the invasiveness
of surgery. Minimally invasive direct cardiac massage (MID-CM) utilizes
a small device inserted through a small incision in the chest to
compress the heart internally. MID-CM was shown in 1995 to be technically
feasible and equivalent to traditional OC-CM in maintaining aortic,
pulmonary artery, and pulmonary pressures, and differences from
baseline measurements in arterial pH and arterio-venous Pco2 were
similar (Buckman et al 1995). A 2000 report found MID-CM to provide
better resuscitation results than S-CPR, with ROSC occurring in
7/10 MID-CM animals versus 2/10 S-CPR animals. One-hour survival
was also better for the MID-CPR trial animals (5/10 vs. 1/10) (Eynon
2000).
Paiva et al found that although ROSC rates were significantly higher
for pigs treated with MID-CM as compared to those that received
S-CPR (7/10 vs. 2/10), there was no significant difference in the
increased rate of survival to one hour or 24 hours (Paiva et al
2000). The group found CPP levels to be similar in the two groups,
and concluded the lack of significant difference between the MID-CM
and S-CPR groups for the majority of comparisons to be due to the
small study groups, suggesting further studies are in order (Paiva
et al 2000).
Drug treatment for VF
Yet another variable in the equation for treating VF-induced CA
is the availability of drugs. Epinephrine is used for its vasoconstriction
properties (AHA 2000), but its effectiveness has been challenged.
Two studies designed to test the efficacy of epinephrine versus
vasopressin found conflicting results. Achleitner et al (2000) found
vasopressin to be superior to epinephrine in maintaining myocardial
function above a threshold necessary to achieve successful defibrillation,
as well as one-hour survival (10/10 vs. 0/11), in pigs. CPP was
also higher for the animals in the vasopressin group (Achleitner
et al 2000). In contrast, Voelckel et al (2000) found that administration
of epinephrine, either by itself or in combination with vasopressin,
increased left ventricular myocardial blood flow, and that ROSC
rates were significantly higher in epinephrine-treated pigs than
in animals treated with vasopressin alone.
Other studies have focused on a variety of other drugs, or combinations
of drugs, for use in cardiac resuscitation. Sun et al (2001) studied
_-methylnorepinephrine (_MNE), a selective _2-adrenergic agonist,
and its effects compared to epinephrine. Twenty rats were induced
into VF, then treated with either _MNE or epinephrine. The two control
groups consisted of a saline placebo group and a group treated with
yohimbine, an _2-receptor blocker, before injection of _MNE. All
the animals were successfully resuscitated after eight minutes of
untreated VF, mechanical ventilation, precordial compression, and
injection of the appropriate drug. However, those treated with _MNE
showed better post-resuscitation myocardial function and survival,
and these results were negated with pretreatment with yohimbine
(Sun et al 2001). Seaberg et al have performed previous studies
relating improved resuscitation rates with various drug combinations
(Menegazzi et al 1993; Menegazzi et al 2000), and continued their
research by testing the efficacy of magnesium. They found 100% ROSC
and survival to one hour in pigs treated with a combination of epinephrine,
lidocaine, bretylium, propranolol, magnesium, and U-74389G. ROSC
and one-hour survival rates were no greater than 38% in control
groups (Table 3) (Seaberg et al 2001).
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Electrical Defibrillation
The first reported use of current-terminated VF was by the French
physiologists Prevost and Battelli in 1899 (Sternbach et al 2000).
Since then, the method has been refined and electrical defibrillation
is now considered to be the most important link in the CA chain
of survival (AHA 2000). The AHA states early defibrillation, defined
as shock delivery within five minutes of EMS notification, to be
a high-priority goal (AHA 2000; Kern et al 2001). In a hospital
setting, this is often possible, but such quick EMS response to
out-of-hospital CAs is not always possible. In instances when VF
has continued untreated for longer periods of time, immediate defibrillation
has been shown to be detrimental, oftentimes causing VF to deteriorate
into asystole (Achletiner et al 2001; Cobb et al 1999; Leng et al
2001). Leng et al (2001) showed CPR and epinephrine provided better
rates of survival after prolonged (>12 minute) VF. They postulate
that the improved results are due to the better myocardial perfusion
afforded by the CPR, making defibrillation more likely to succeed.
The importance of improved perfusion is therefore of primary importance
over the presence of a dysrhythmia (Leng et al 2001).
Niemann et al (2000) attempted to find the lower limit of VF duration
at which point pre-defibrillation CPR was no longer beneficial.
They compared two groups of pigs, one of which received immediate
defibrillation after five minutes of VF, and one of which received
90 seconds of CPR before defibrillation. They found pre-shock CPR
did not improve the response to first shock, decrease the incidence
of post-shock deterioration to asystole, or increase the rate of
ROSC. In fact, they found pre-shock CPR resulted in a significantly
lower cardiac resuscitation rate (Niemann et al 2000). Two other
studies have shown contrasting results (Achleitner et al 2001; Cobb
et al 1999). In a review of 1117 patients in VF upon paramedic arrival,
639 of who received immediate defibrillation and 478 of who received
90 seconds of CPR prior to defibrillation, Cobb et al (1999) found
higher rates of survival to all endpoints in the group treated with
pre-shock CPR. Significantly higher differences in favor of pre-shock
CPR were shown in all subsets of data for patients in VF for longer
than four minutes before paramedic arrival (Cobb et al 1999). Achleitner
et al (2001) evaluated the hemodynamics of patients treated with
90 seconds of pre-shock CPR and found this treatment provided increased
CPP and MAP when VF endured for more than four minutes.
Automated external defibrillators (AEDs) have come into favor for
their ease of use and increasingly lower cost (Xavier et al 2002;
Yu et al 2001). Their availability also means AHA goals of providing
quick defibrillation can be met (AHA 2000). However, in situations
of prolonged untreated VF, AEDs have been shown to be less effective
than immediate manual defibrillation with traditional defibrillators.
Xavier et al (2002) examined the one-hour survival, 24-hour survival,
and neurological outcome of patients treated with either immediate
defibrillation following eight minutes of untreated VF or AED. AED
use resulted in a 60-second delay of defibrillation, caused by the
time the AED device requires to register and diagnose VF before
delivering the shock. This 60-second delay caused decreased survival
in all three categories when compared to the survival rates for
immediate defibrillation (Table 4) (Xavier et al 2002).
Similarly, Yu et al (2001) found the rate of ROSC decreased as the
delay before shock increased from three to 20 seconds, following
seven minutes of untreated VF in pigs (Figure 4). They also found
MAP decreased in a similar manner. These delay times are typical
of the time it takes for AEDs to register and diagnose VF, and are
indicative of the time periods in which CPR would have to be interrupted
in order for the AED device to work (Yu et al 2001). They also mimic
the delay times encountered when lay rescuers perform rescue breathing
during CPR, which has been found detrimental in numerous studies
mentioned earlier (Berg et al 2001; Kern et al 2002; AHA 2000).
Conclusion
Because there are many factors affecting the availability of various
treatments for CA, a number of considerations must be taken into
account when deciding which is most effective. Specialized devices
are necessary to perform ACD- and PTACD-CPR, which are not always
readily available to the lay rescuer who witnesses CA, and S-CPR
performed by laypeople has been proven inefficient due to an inability
to provide rescue breathing quickly enough when they are even willing
to attempt rescue breathing in the first place. CCC-CPR is easier
for the layperson to perform, especially in a single-rescuer scenario,
while providing greater rates of multiple-endpoint survivability
and good neurological outcome. Therefore, the AHA should consider
revising its recommendations to instruct lay rescuers in a pre-hospital
setting to perform CCC-CPR after notifying EMS of the need for more
advanced care. Although some may question the practice of ignoring
ventilation in favor of chest compressions only, enough evidence
has shown lay rescuers, and especially lay rescuers acting alone,
to be unable to provide adequate treatment to patients suffering
from VF/CA if they must provide airway management in addition to
chest compressions.
In a hospital setting, surgical techniques and drug therapies are
more readily available. Because MID-CM has been shown to be technically
feasible with minimal invasiveness, and because direct cardiac massage
is more effective than closed-chest cardiac massage, clinicians
should consider refining MID-CM techniques and making the use of
MID-CM devices more widespread. Given that emergency physicians
are already well trained in minor surgical procedures such as chest
tube placement, MID-CM devices should prove easily adaptable to
an emergency department setting. While various drug treatment therapies
are being researched, none has been proven conclusively to be more
effective than the rest. Therefore, drug treatments should continue
to be evaluated in the hopes that the best treatment may be determined
for in-hospital VF-induced CA. While some may find this recommendation
to be premature given the lack of extensive data in this area, it
is clear that the possibility for a more effective drug therapy
than the current epinephrine guidelines exists.
Electrical defibrillation remains the most effective treatment of
VF-induced CA, but more detailed recommendations for its usage must
be made. Because the time to shock may be considerably longer than
the five minutes recommended by the AHA, immediate defibrillation
may be more harmful than beneficial, converting VF to asystole.
Therefore, EMS rescuers should consider the application of 90 seconds
of CPR prior to defibrillation, as this has shown in multiple studies
to produce higher rates of survival. The existence of studies showing
conflicting data must be taken into consideration, but more extensive
research will provide conclusive findings. As for the application
of AEDs, data showing a decrease in survival rates due to the extensive
time required for the AED device to register and diagnose the correct
dysrhythmia are significant, and suggest further research must be
conducted before recommendations are made to provide AED access
to lay people in numerous public settings. The goal of immediate
or quick defibrillation is worthwhile, but even the simplest-to-use
devices require precious time while a lay rescuer with infrequent
practice in defibrillation struggles with a new device. Therefore,
increased emphasis should be placed on maintaining perfusion through
CCC-CPR until trained response personnel arrive on the scene.
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Journal of Young
Investigators. 2003. Volume Seven.
Copyright © 2003 by Holly Cummings and JYI. All rights reserved.
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