(Circulation. 1997;96:2102-2112.)
© 1997 American Heart Association, Inc.
Articles |
Key Words: AHA Medical/Scientific Statements death, sudden cardiopulmonary resuscitation ventilation
| Introduction |
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Because early CPR plays a central role in saving lives, the Ventilation Working Group of the Basic Life Support (BLS) and Pediatric Life Support Subcommittees of the AHA Emergency Cardiovascular Care (ECC) Committee reviewed the scientific evidence on mouth-to-mouth ventilation. The ECC Committee and its subcommittees prepare guidelines and recommendations for providing emergency cardiovascular care and cardiopulmonary resuscitation in the United States and will formally review and publish updated guidelines in the year 2000. Although this report represents a focused analysis and serves as a consensus statement regarding the role of mouth-to-mouth ventilation during CPR, it is not intended to change any current AHA recommendations or guidelines for performance of CPR. The specific purpose of this report is to review the historical rationale for providing mouth-to-mouth ventilation during CPR and to critically analyze, using the available scientific literature, the following questions: (1) Does assisted ventilation during CPR result in improved physiological status or survival? (2) Are there adverse effects that result from inclusion of mouth-to-mouth ventilation in basic CPR techniques? (3) Could mouth-to-mouth ventilation be deferred or delayed in certain cases of bystander CPR? Finally, new recommendations are presented, particularly regarding the ethics of human clinical trials on the performance of CPR techniques without mouth-to-mouth ventilation.
| Historical Rationale for Mouth-to-Mouth Ventilation |
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In a landmark study in the 1950s, Safar and
colleagues26 demonstrated that the tongue and soft palate
commonly obstructed the upper airway in unconscious persons. They
further demonstrated that the manual ventilation techniques developed
in the 1900s were relatively ineffective in the presence of such
obstruction. The chin-lift and jaw-thrust techniques for opening the
airway of the supine patient were developed to remove obstructions and
maintain airway patency.27 28 Safar and
colleagues29 30 then demonstrated a practical advantage of
expired breath ventilation over previous manual methods with the
patient lying supine. Specifically they compared tidal volumes
generated during mouth-to-mouth (or mouth-to-airway) ventilation with
those generated using the older manual techniques in paralyzed and
anesthetized adults with normal circulation. Although the
Holger-Nielsen method (one of the most effective manual techniques)
generated >340 mL/min tidal volume in five of six patients, it was
still less effective than mouth-to-mouth ventilation (Fig 1
). On the
basis of these and similar confirmatory studies, mouth-to-mouth
ventilation became the therapy of choice for out-of-hospital
respiratory arrest by the 1960s.31 32
While these studies on ventilatory techniques were being
conducted, other laboratories sought a practical method of providing
circulatory support during cardiac arrest. Because external chest
compression could provide partial circulatory support, the
mouth-to-mouth ventilation technique was added to chest compression to
create modern CPR. The "ABC" sequence of
resuscitationAirway patency, Breathing (with
mouth-to-mouth ventilation), and Circulation (chest
compression)emerged as a practical and empirical means of
CPR (Fig 2
).33 34 Because
most adult cardiac arrest victims become apneic or generate abnormally
diminished respiratory efforts, it has long been assumed that
mouth-to-mouth ventilation should be an integral component of CPR. On
the basis of the physiological principle of rapidly
restoring "normal" breathing and circulation and the subsequent
success of CPR in the clinical setting, a sequence of mouth-to-mouth
ventilation at a rate of 10 to 12 breaths per minute for adults, with
each breath followed by five chest compressions (two rescuers), was
recommended by consensus and adopted by the AHA.1 35
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Effectiveness of Traditional Techniques of Cardiopulmonary
Resuscitation
Over the past 25 years many studies have reinforced the
empirical practice of the ABC sequence for CPR by confirming the
effectiveness of bystander-initiated CPR.2 4 5 36 37 38 39 The
outcome of most cases of adult cardiac arrest depends primarily on the
time interval from cardiac arrest until
defibrillation.5 40 41 42 43 44 Therefore, rapid provision of
defibrillation is considered the most important determinant of
successful outcome.1 40 41 43 44 However, traditional CPR
extends the time available for successful defibrillation and
resuscitation.43 44 Specifically investigations of
"adult" type cardiac arrest in laboratory animals indicate that
(1) maintenance of adequate coronary perfusion pressure
and resultant myocardial blood flow during chest compression are
critical for optimal survival and (2) the window for successful
bridging until defibrillation is 10 to 18 minutes.45 46 47 48 49 50 51 52 53
Clinical studies similarly indicate that success of CPR improves when
(1) the cardiac arrest is witnessed, (2) immediate bystander CPR is
provided, (3) adequate coronary perfusion pressures are
obtained during CPR, (4) the initial rhythm is ventricular
fibrillation, and (5) early defibrillation is
provided.5 36 40 41 42 43 44 54 55 56 57 58 59 60 61 Data from both animals and
humans concur: time is of the essence. Traditional bystander-initiated
CPR can improve survival when it is started within 4 to 6 minutes from
the time of collapse and followed with advanced cardiac life support
within 10 to 12 minutes of collapse.43 44 Nevertheless,
although these studies have reinforced the value of the ABC technique,
few studies have focused on the relative efficacy of mouth-to-mouth
ventilation or chest compression alone.
| Does Assisted Ventilation Improve Outcome of Cardiopulmonary Resuscitation? |
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Traditionally the ventilatory goals of CPR training techniques have stressed empirically that minute ventilation be more or less normal.34 However, current techniques for mouth-to-mouth ventilation were developed in paralyzed anesthetized subjects with normal circulation, conditions not typically present during CPR scenarios. Both oxygenation and ventilation requirements may be altered during circulatory arrest because cardiac output and pulmonary blood flow generated even during CPR that is well performed are far lower than blood flow during spontaneous circulation. With low blood flow, end-organ tissues become ischemic, extract a higher percentage of O2, and accumulate higher levels of CO2 ("tissue acidosis"),66 67 but arterial blood gases may not reflect these tissue conditions.68 As a result, the goals of oxygenation and ventilation during CPR have not been established, and interpretation of arterial blood gases is not clear.68 69 Therefore, it is difficult to evaluate current oxygenation/ventilation techniques. Collectively there is little evidence that oxygenation and ventilation need to be "normalized" during fibrillatory cardiac arrest because the primary disorder is due to low blood flow, not respiratory insufficiency.
Sources of Ventilation During Cardiopulmonary
Resuscitation
Although active mouth-to-mouth ventilation has been stressed in
traditional CPR training, it is also important to consider that many
other sources of gas movement can contribute to
oxygenation and ventilation in patients receiving CPR.
Indeed, there are several potentially important sources of ventilation
during cardiac arrest with attempted resuscitation including
compression-induced ventilation and gasping respiration.
Compression-induced ventilation commonly results when gas is expelled
from the lungs and is "passively inhaled" following elastic
recoil of the chest wall during the relaxation phase.70 71 72 73 74 75 76
In multiple animal studies, compression-induced ventilation alone has
proved quite substantial when measured.71 74 75 76 77
However, measured minute ventilation and arterial
oxy-genation decrease after 4 to 10 minutes of CPR with
or without assisted ventilation, possibly because of progressive chest
compressioninduced atelectasis and thoracic
deformity.71 78 Thus, with longer periods of cardiac
arrest, ventilation may become more important. This is supported by
animal studies in which chest compression periods were more prolonged,
demonstrating that chest compression with assisted ventilation and
adequate lung inflation result in better oxygenation
compared with chest compression without assisted
ventilation.71 74 In addition to compression-induced
ventilation, spontaneous respiration, usually in the form of agonal or
gasping breathing, commonly occurs during cardiac arrest in both
animals and humans, further contributing to total
ventilation.75 76 78 79 Several recent investigations in
animals have specifically established that spontaneous gasping occurs
early during CPR and is associated with a better
outcome.74 75 76 78 79 Spontaneous gasping may simply
reflect improved oxygen delivery to the medulla during CPR, or it may
reflect a shorter cardiac arrest interval. However, the mechanics of
gasping may also improve the effectiveness of CPR because of (1)
improved venous return during the negative-pressure inspiratory
efforts, (2) augmentation of cardiac output due to increased
intrathoracic pressure during the expiratory phase of gasping, and (3)
improved pulmonary gas exchange due to both increased airflow
and the more physiological "pulling open" of
those dependent lung zones subject to deflation. In one study of swine,
spontaneous gasping contributed approximately half of the measured
minute ventilation during chest-compression-only CPR, compared with
<10% during chest compression plus mechanical
ventilation.74
Therefore, in human and animal studies some component of compression-induced ventilation and gasping respirationwhich by themselves may be important sources of gas exchangeis present unless specifically prevented. In turn, studies reporting CPR performed "without ventilation" may not be strictly accurate; the authors more likely mean "without mouth-to-mouth ventilation" or "without assisted ventilation." Although not necessarily measured or reported, the contributions of compression-induced ventilation and gasping respiration may still be substantial in the absence of mouth-to-mouth ventilation. In contrast to the original studies of mouth-to-mouth ventilation in which anesthetic and paralytic agents were administered to subjects with normal circulation, these components of ventilation during CPR may be sufficient for a short time to produce survival when coupled with effective chest compression.
Experimental Studies of Assisted Ventilation
With the recognition that ventilatory requirements during cardiac
arrest are unclear and acknowledging that compression-induced
ventilation and gasping respiration may be important sources of gas
movement, the requirement for and timing of mouth-to-mouth ventilation
can be questioned. A canine study on the effects of mechanically
assisted breathing (as an approximation of human mouth-to-mouth
ventilation) was performed in 1983 by Meursing et al.80 In
this study CPR was delayed for 5 minutes following sudden circulatory
arrest, and no significant fall in arterial
PO2 or rise in PCO2 was
observed. Chest compression was then initiated, but assisted
ventilation was withheld for 2 minutes. No significant fall in
arterial PO2 or rise in
PCO2 was demonstrated over the next 30 seconds.
This study, reported only in an abstract, was a key consideration in
CPR guidelines developed in the Netherlands and reflects a lack of
conviction regarding the importance of immediate ventilation. Instead
of using the ABC sequence, the Netherlands approach to sudden witnessed
arrests is "CAB" (Circulation, Airway,
Breathing). Rescue breathing is delayed (several seconds
and, infrequently, several minutes) to enable prompt provision of chest
compression. Survival outcomes with CAB appear to be similar to, if not
better than, those reported with ABC CPR.81
Many laboratory studies support this concept. Berg and colleagues82 demonstrated that fibrillatory cardiac arrest in swine provided with chest compression alone for 9.5 minutes maintained an arterial pH of 7.33 and arterial PCO2 of 48 mm Hg. In a nonintubated canine cardiac arrest model, Chandra et al70 demonstrated that arterial oxygen saturation could be maintained above 90% with a measured minute ventilation of 5 L/min being generated during the fourth minute of chest compression alone without any assisted ventilation.
The need for assisted ventilation during CPR for fibrillatory arrest
has been evaluated in four swine studies with long-term survival. Each
reported nearly identical 24-hour survival and neurological outcome
with chest compression alone versus chest compression plus assisted
ventilation.74 75 76 82 Fibrillatory cardiac arrest
intervals varied from 30 seconds to 5 minutes, and CPR was provided for
8 to 12 minutes. In a more recent study swine underwent a 5-minute
fibrillatory cardiac arrest interval, followed by 8 minutes of (1)
chest compression alone, (2) chest compression plus assisted
ventilation, or (3) no CPR at all. Assisted ventilation (at 15 mL/kg
tidal volume) was provided with 17% oxygen and 4% carbon dioxide to
better simulate the exhaled gas delivered during human mouth-to-mouth
ventilation. The results showed that without CPR there were no
survivors. Both the chest-compression-alone group and the
chest-compression-plus-assisted-ventilation group had significantly
better survival than the no-CPR group. However, whether or not assisted
ventilation was performed made no detectable difference on either
return of spontaneous circulation or 24-hour survival
rates (Fig 3
).76
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Idris and colleagues83 have demonstrated that with prolonged arrest intervals beyond 6 minutes, supplemental oxygenation and assisted ventilation should still be considered critical determinants of CPR success. In one study, swine underwent 6 minutes of untreated ventricular fibrillation, followed by 10 minutes of chest compression plus assisted ventilation (12 mL/kg) with 85% oxygen versus chest compression without assisted ventilation. The nonventilated animals were paralyzed to prevent gasping and its effect on total ventilation. Return of spontaneous circulation was achieved in 9 of 12 (75%) ventilated animals versus only 1 of 12 (8%, P<.002) nonventilated animals. However, with arrest intervals of less than 6 minutes, these differences were not apparent. The investigators further demonstrated that assisted ventilation with either hypoxic or hypercarbic gas admixtures during CPR resulted in lower resuscitation rates compared with assisted ventilation with 85% oxygen.84
In summary the published experimental data on animals collectively suggest that assisted ventilation may not be critical in the early minutes after onset of sudden fibrillatory cardiac arrest if adequate chest compression is provided. However, after relatively longer intervals of untreated fibrillatory cardiac arrest, some form of ventilatory support is likely to become critical for successful resuscitation outcomes. Whether mouth-to-mouth ventilation as the form of ventilatory support is helpful during even prolonged fibrillatory cardiac arrest remains unclear.
Clinical Studies of Mouth-to-Mouth Ventilation
Are the results obtained from animal studies applicable to CPR in
human beings? Upper airway anatomy of animals differs from that
of human beings; thus, upper airway obstruction during cardiac arrest
may differ among species. Many animal species demonstrate frequent and
prolonged gasping. Laboratory animals also do not have coronary
artery disease. Unlike animal studies, the adequacy of
oxygenation and ventilation during
chest-compression-only CPR (ie, without mouth-to-mouth ventilation) has
not yet been demonstrated in human beings receiving CPR.
Nevertheless, the available human data to date are consistent with findings in animals.38 75 85 86 For example, Weil et al86 demonstrated that during the first few minutes of CPR in humans, arterial pH, PaCO2, and bicarbonate change little from prearrest values. In addition, agonal respiration or gasping has also been documented in 40% of 445 out-of-hospital cardiac arrest victims and 55% of those victims with witnessed arrests.85 Furthermore, as in animal studies, agonal respiration or gasping was associated with improved survival. Survival was 27% when gasping was present, compared with 9% when it was not. It is uncertain if the gasping was a marker for better central nervous system perfusion or shorter arrest intervals or if the agonal breaths themselves contributed to improved outcome.
Notably, recent investigations in humans with the active compression-decompression CPR device (plunger type) demonstrated that excellent minute ventilation (>6 L/min) was maintained in four cardiac arrest victims without assisted ventilation or intubation of the airway.87 New investigations are still necessary to determine whether standard chest compression consistently results in adequate gas exchange for successful resuscitation of human victims of cardiac arrest.
Although physiological studies are informative,
long-term survival in the clinical setting is the major therapeutic end
point of CPR. The Belgian Cerebral Resuscitation
Group38 39 prospectively evaluated 3053 out-of-hospital
arrests. Physicians on the ambulances evaluated the quality of
bystander CPR for compression and ventilation. Long-term survival of
those treated with good-quality chest compression alone and those
treated with good-quality chest compression plus mouth-to-mouth
ventilation was comparable (15% and 16%, respectively)
(Fig 4
). Survival when either of these
techniques was used was significantly superior to survival without any
CPR (6%, P<.001). The data confirm that bystander CPR can
be lifesaving but also suggest that mouth-to-mouth ventilation may not
be necessary for survival of cardiac arrest, at least during the
immediate moments after arrest. The authors of the study cautioned that
conclusions drawn from these observations should be limited to adult
patients with witnessed fibrillatory cardiac arrest.
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Lengthier periods of arrest may require earlier ventilatory support. The observation that some ventilatory interventions are helpful after prolonged fibrillatory cardiac arrest may indicate an oxygenation or lung inflation requirement as much as a need for ventilation (CO2 elimination). It seems probable that progressive lung deflation and airway closure occurs during chest compression without gasping or mouth-to-mouth ventilation. Such lung deflation will lead to increased pulmonary shunting and progressive hypoxemia. Reversal of lung deflation with an occasional lung inflation may be the critical pulmonary intervention to prevent hypoxia. If so, it may still be unnecessary to "normalize" respiratory rates in fibrillatory cardiac arrest until spontaneous circulation returns. Future studies should therefore attempt to delineate the critical timing, tidal volumes, and rates for optimal resuscitation.
| Are There Adverse Effects of Mouth-to-Mouth Ventilation? |
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Lower esophageal sphincter tone usually prevents regurgitation of gastric contents and provides resistance to gastric air flow during positive pressure ventilation. The normal esophageal sphincter opening pressure is about 20 to 25 cm H2O.90 91 However, this energy-dependent muscular tone decreases rather quickly after circulatory arrest. In a swine model of CPR, mean esophageal sphincter opening pressure decreased from 20.6 cm H2O before cardiac arrest to 5.6 cm H2O after 5 minutes of cardiac arrest.92 In anesthetized patients with adequate circulation, gastric insufflation commonly occurs with bag-valve mask ventilation unless cricoid pressure is provided.93 During cardiac arrest and CPR, pulmonary compliance decreases, increased inspiratory pressures may be needed to inflate the lung, and lower esophageal sphincter tone may decrease, all factors that increase gastric insufflation. Regurgitation was noted to occur primarily after the stomach was insufflated with air.16 Not surprisingly, in one series gastric insufflation and pulmonary aspiration were documented in nearly half of cardiac arrest victims after CPR with mouth-to-mouth ventilation.17
Another consideration is whether there are important differences between exhaled gas and ambient air. While room air has 21% O2 and 0.03% CO2, exhaled gas was observed to contain a mean O2 concentration of 16.6% to 17.8% and a mean CO2 concentration of 3.5% to 4.1% during one- and two-rescuer CPR.19 Thus, as provided during mouth-to-mouth ventilation, expired gas is slightly hypoxic and contains considerably more CO2 than ambient air ventilation achieved with gasping and compression-induced ventilation alone.94
Although expired gas rescue breathing is safe and may be life-saving for patients with respiratory arrests, the hypercarbia may have adverse cardiovascular effects when compared with ambient air ventilation during circulatory arrest. In one study of isolated hypercarbia, animals ventilated (12 mL/kg) with 95% O2 and 5% CO2 did as poorly as animals receiving no assisted ventilation at all during CPR.84 Another investigation showed that swine ventilated with room air during 6 minutes of CPR had a rate of successful resuscitation (83%) twice that of animals ventilated with simulated exhaled gas ventilation when both groups received similar tidal volumes (38%, P<.01).95 Consistent with animal studies are cellular studies that demonstrate modest increases in concentration of CO2 can inhibit the rate and force of cardiac contraction, suggesting that elevated CO2 has a direct cardiodepressive effect.96 97
Circulatory Effects
Obviously a single rescuer performing CPR on an adult or
child cannot provide chest compression and mouth-to-mouth ventilation
simultaneously. Thus, it follows that with more time spent
attempting ventilation, less time will likely be allocated to chest
compression and vice versa. As noted, successful resuscitation has been
highly correlated with the timing and degree of restored myocardial
blood flow and coronary perfusion pressure, which are in turn
dependent on the effective provision of chest compression of a
sufficient rate and depth.98 99 100 101 Therefore, time spent
attempting ventilation may take away valuable coronary
perfusion. In support of this concept are recent studies that suggest
that when rescuers attempt ventilation using current AHA
recommendations, the compression rate and depth become
inadequate.102 Current AHA guidelines for adult CPR
recommend a chest compression rate of 80 to 100 per minute and a
respiratory rate of approximately 12 breaths per minute, with
compression/ventilation ratios of 15:2 with one rescuer and 5:1 with
two rescuers. However, achieving these recommended guidelines in the
real world has been demonstrated as problematic for both
one- and two-rescuer adult CPR with mouth-to-mouth
ventilation.18 19 20 101 102 103 One study of in-hospital
two-rescuer CPR found that only 2 of 12 rescuers gave 80 compressions
or more per minute,103 whereas another investigation of
simulated two-rescuer CPR on a manikin found that compression rates
averaged 75 per minute and that the depth of compression was inadequate
in 14% to 22%.101 These inadequacies of chest
compression observed in two-rescuer CPR appear to be even worse in
studies of one-rescuer CPR.18 19 20 In a study of healthcare
professionals performing one-rescuer CPR on a manikin, only 15%
achieved a rate of 80 compressions per minute despite continuous
coaching.19 Further investigation confirmed that even
immediately after successful completion of a basic CPR course,
compression rates were particularly inadequate; on average, only 56
compressions per minute were provided by the 129 medical students
studied.20
These data suggest that the competition between time for ventilation and time for compression during one-rescuer CPR is a "zero-sum" game; time spent on ventilation takes precious time away from chest compression and support of myocardial blood flow. It is surprising that this aspect of CPR as practiced in the real world (ie, cycle time spent on ventilation versus cycle time spent on compression) has not been studied. It is worrisome that multiple studies have demonstrated survival rates to be consistently correlated with coronary perfusion pressure whereas no studies of fibrillatory arrest have shown improved rates of survival with early ventilation. Future studies need to take these real-world factors into account and not assume that performance of CPR is in complete adherence with AHA guidelines (which appears to be infrequently achieved).
Does Mouth-to-Mouth Ventilation Inhibit Performance of
Bystander Cardiopulmonary Resuscitation?
Despite widespread acknowledgment of its value and efficacy, CPR
is not performed by bystanders in the majority of cases for which it is
indicated. Furthermore, several recent studies have documented a lower
overall frequency of bystander CPR performance compared with
earlier investigations.3 Although this latter finding may
have several possible explanations (including the failure of the
medical community and public health officials to effectively teach the
public the skills of CPR), the perceived risk of disease transmission
during CPR, even by healthcare workers, has become increasingly suspect
as a major factor.
The actual risks of disease transmission during mouth-to-mouth ventilation are quite small. There are isolated reports of possible transmission of Helibacter pylori,104 Mycobacterium tuberculosis,105 meningococcus,106 herpes simplex,107 108 109 shigella,110 streptococcus,111 and salmonella.112 No reports on transmission of HIV can be found. Nevertheless, despite the remote chances of its occurring, fears regarding disease transmission are common in the current era of universal precautions. Indeed, not only laypersons but physicians, nurses, and even BLS instructors are extremely reluctant to perform mouth-to-mouth ventilation.7 8 9 12 113 The most commonly stated reason for not performing mouth-to-mouth ventilation is fear of contracting AIDS.13 In one survey, only 15% of 975 respondents reported a willingness to perform chest compression with mouth-to-mouth ventilation on a stranger, whereas 68% would "definitely" perform chest compression alone if it was offered as an effective alternative CPR technique.12
Fear of disease transmission may not be the only reason that mouth-to-mouth ventilation inhibits bystanders from initiating CPR. When mouth-to-mouth ventilation is combined with chest compression, the CPR technique becomes a complex psychomotor task that can be difficult to teach, learn, remember, and perform.82 114 Educational principles suggest that a simpler technique, such as chest compression without mouth-to-mouth ventilation, would be far easier to teach the public. If it were known that the use of chest compression alone was nearly as efficacious as when combined with mouth-to-mouth ventilation, potential rescuers might start chest-compression CPR faster and more frequently because it is easier to perform in an actual emergency. In addition, the greater ease of learning, retaining, and performing such a simple procedure could lead to more widespread performance of bystander CPR, thereby improving survival rates for victims of cardiac arrest.
| Special Considerations: Implications for Future Guidelines |
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It is also important to note that the current discussion and available research focus only on the contribution of mouth-to-mouth ventilation in the setting of sudden adult fibrillatory cardiac arrest. The potential application of mouth-to-mouth ventilation may be much broader than merely responding to fibrillatory arrest. Intuitively, mouth-to-mouth ventilation seems clearly indicated in cases of cardiopulmonary arrest associated with airway obstruction, water submersion, or preceding respiratory symptoms. Likewise, in children and young adults, respiratory compromise, not cardiac arrest, is the more common threat to life; thus, respiratory management should not be deferred. Submersion and respiratory problems are the typical precipitating causes of nontraumatic cardiac arrest in pediatric patients and young adults.6 115 116 In addition, a child's pulse may be difficult to locate and measure.117 118 119 120 These children may only be hypotensive (or even normotensive), and ventilatory support from mouth-to-mouth ventilation seems the highest priority under these circumstances.
Although the above recommendation on usefulness of mouth-to-mouth ventilation during asphyxial arrest for children with respiratory failure is logical, not even this is supported by data comparing the effectiveness of mouth-to-mouth ventilation with chest compression alone. A large amount of research is needed before the role and timing of mouth-to-mouth ventilation can be better clarified. As in adults, the relative importance of mouth-to-mouth ventilation and prompt defibrillation may be quite different among the many subgroups of cardiac arrest victims.121 Unfortunately, as with adults, in the majority of pediatric out-of-hospital arrest patients, basic bystander CPR is not attempted. The working group continues to recommend prompt ventilatory support in the form of mouth-to-mouth ventilation for apneic, pulseless, unresponsive children.
| Conclusions and Recommendations |
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Although it seems possible that mouth-to-mouth ventilation is not needed during the first minutes of sudden witnessed circulatory arrest with suspected ventricular fibrillation, it is likely that mouth-to-mouth ventilation should be the initial intervention for arrest of suspected respiratory etiology. If a delay in mouth-to-mouth ventilation is being considered, the overall net impact on the public for saving lives from all causes of arrest, not merely sudden fibrillatory circulatory arrest, must also be taken into account. Updated guidelines on CPR are published at regular intervals. It is the hope of the working group that additional data will be available for consideration at the international conferences on CPR planned for the year 2000.
The working group recommends that
| Footnotes |
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This article also appears in Annals of Emergency Medicine (November 1997), Journal of Respiratory Care (September 1997), and Resuscitation.
A single reprint is available after September 30, 1997 by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0118. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or
© 1997 American Heart Association, Inc.
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