3070
Observations of Ventilation During
Resuscitation in a Canine Model
Nisha Chibber Chandra, MD; Kreg G. Gruben, PhD; Joshua E. Tsitlik, PhD; Roy Brower, MD;
Alan D. Guerci, MD; Henry H. Halperin, MD; Myron L. Weisfeldt, MD; Solbert Permutt, MD
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Background Fear of infection limits the willingness of
laymen to do cardiopulmonary resuscitation (CPR). This study
assessed the time course of change in arterial blood gases
during resuscitation with only chest compression (no ventilation) in an effort to identify the time for which ventilation
could be deferred.
Methods and Results Aortic pressures and arterial blood
gases were monitored in seven 20- to 30-kg dogs in ventricular
fibrillation (VF) at 2-minute intervals during chest compression alone (no ventilation) at 80 to 100 compressions per
minute. Before the induction of ventricular fibrillation, all
animals were intubated and ventilated with room air, 10
mL/kg. The endotracheal tube was removed when VF was
induced. Pre-VF arterial pH, Pco2, and 02 saturation were
(mean±SEM) 7.39±0.02, 27.0+1.5 mm Hg, and 97.5 ±0.5%,
respectively, with aortic pressures being 143.2±5.7/116.2±4.6
mm Hg. At 4 minutes of chest compression alone, the corresponding values were 7.39±0.03, 24.3±3.1 mm Hg, and
93.9±3.0%, with an arterial pressure of 48.1±7.7/22.6±3.9
mm Hg. Mean minute ventilation during the fourth minute of
CPR, measured with a face mask-pneumotachometer, was
5.2± 1.1 L/min.
Conclusions These data suggest that in the dog model of
witnessed arrest, chest compression alone during CPR can
maintain adequate gas exchange to sustain 02 saturation
>90% for >4 minutes. The need for immediate ventilation
during witnessed arrest should be reexamined. (Circulation.
1994;90:3070 -3075.)
Key Words * ventilation * cardiopulmonary resuscitation
T Nhe traditional teaching of cardiopulmonary resuscitation (CPR) in the United States and
many other countries is based on the "A-B-C"
is probably in the range of several seconds and possibly
>1 minute. No study has addressed the issue of when
ventilation must be initiated during CPR to ensure
favorable results. This becomes particularly applicable
in the 1990s because fear of infection has prompted
many laymen and medical personnel to avoid performing mouth-to-mouth ventilation in unknown victims of
cardiac arrest.78 Laymen would probably be willing to
perform chest compression alone and activate emergency medical system personnel, who on arrival could
then initiate ventilation with the necessary protective
equipment. These issues become particularly important
to explore because clinical studies have previously
shown that prompt bystander CPR after arrest improves
outcome.9
During CPR, of the various indexes of respiratory
function, arterial oxygen saturation and content are of
significant importance because they, along with blood
flow, determine the delivery of oxygen to tissue such as
the brain and heart. In most clinical situations, tissue
oxygenation is adequate if arterial oxygen saturation is
maintained >90%.10 The present recommendations for
ventilation during CPR are based on studies that were
conducted in the 1960s and are founded on the premise
that the ventilatory requirements during CPR are comparable to those during normal circulation.2,311 However, substantially less ventilation may be sufficient to
maintain arterial oxygenation and CO2 clearance during
CPR, because venous return and cardiac output are
only 10% to 15% of normal during manual chest
compression.12 The goal of ventilation during CPR is to
provide adequate oxygenation and CO2 removal. What
is "adequate" has never been established. Data from
Bishop et al suggest that an arterial Pco2 <35 mm Hg
during CPR is effective in correcting the metabolic
sequence, ie, the prompt initiation of Airway patency,
Breathing, and Circulation (chest compression), a sequence that reflects the historical development of these
techniques.1-4 However, an alternative approach is that
of C-A-B: Chest compression, Airway, Breathing, in
which airway manipulation is deferred for several seconds. In dogs with cardiac arrest, Meursing et a15
delayed CPR 5 minutes after arrest and then initiated
chest compression but withheld ventilation for 2 minutes and demonstrated no significant fall in arterial Po2
or rise in Pco2 for 30 seconds. At 45 seconds after the
initiation of chest compression alone, arterial Po2 was
lower, but still 52.3 mm Hg, which probably reflected an
arterial hemoglobin saturation of 70% to 80%. Based on
these and other data in the Netherlands, clinical CPR
does not employ the "A-B-C" rule; rather, the approach
is "C-A-B" (Circulation-chest compression, Airway,
Breathing), with ventilation being delayed and chest
compression being initiated as soon as possible. Using
the "C-A-B" approach, survival data from the Netherlands suggest resuscitation rates comparable to those
seen in the best paramedic response centers in the
United States.6 The actual delay between chest compression and ventilation has never been reported, but it
Received September 2, 1993; revision accepted May 20, 1994.
From The Peter Belfer Laboratory for Myocardial Research,
Cardiology Division, Department of Medicine, The Johns Hopkins
Medical Institutions, Baltimore, Md.
Correspondence to Nisha C. Chandra, MD, Division of Cardiology, Francis Scott Key Medical Center, 4940 Eastern Ave,
Baltimore, MD 21224.
©0 1994 American Heart Association, Inc.
Chandra et al Ventilation During CPR
Sample Data
3071
(Dog #2,4 wini.)
a
E 40
0U
bt
0
,n
60
E.E0
30-
.
0
FIG 1. Photograph of face mask used, which was conical in
shape. The narrow end was fitted with a removable patent
stopper and could be connected to a pneumotachometer.
-1
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acidosis of hypoperfusion during CPR.13 Also, a lower
Pco2 (in the range of 25 to 35 mm Hg) may limit
cerebral edema. From these observations, it would
that ventilation sufficient to produce a Paco2
<35 mm Hg and an arterial O2 saturation >90% would
probably be sufficient and meet bodily needs during the
initial phases of resuscitation.
The specific goal of this study was to measure in dogs,
during resuscitation with chest compression alone, the
time course of rise in arterial Pco2 and fall in arterial pH
and
saturation. We reasoned that the time course of
fall in oxygen saturation and pH would help identify the
time when ventilation must be initiated during CPR.
appear
02
Methods
This study was approved by the Animal Care and Use
Committee of The Johns Hopkins University. This committee
conforms strictly to the guiding principles of the American
Physiological Society. Seven mongrel dogs weighing 20 to 30 kg
were anesthetized with intravenous pentobarbital, intubated,
and positioned supine in a special cradle as previously described.'4 Additional anesthetic was given as needed. All
animals were ventilated with a Harvard ventilator (model 607),
10 mL/kg tidal volume, at a frequency of 10 to 12 breaths per
minute. Millar micromanometer-tipped catheters (model PC470) were inserted retrograde into the right atrium and
ascending aorta via femoral cutdowns, and a pacing catheter
was positioned in the right ventricle. The neck of the dog was
carefully maintained in a neutral position, avoiding extension
or flexion. The head of the animal was not specifically positioned in any holding device. A special face mask was constructed for purposes of this study and is depicted in Fig 1.
This conical mask was fitted over the snout, glued into
position, and then taped to provide an airtight seal. This mask
had at its apex a removable stopper with an opening that could
be connected to a pneumotachometer (Fleisch model 3).
Before intervention, the endotracheal tube exited through this
opening. When the cone was positioned, care was taken not to
compress subpharyngeal structures. Baseline hemodynamics
were recorded on a Gould 4 channel recorder (model 2406),
and baseline arterial blood gases were drawn. All blood gases
measured on a Radiometer ABL 3 electrode and analyzer system that was calibrated and set to the animal's body
temperature. The animal's temperature was recorded with a
rectal mercury thermometer before arrest and twice during
the period of chest compression. After the induction of
ventricular fibrillation (via the right ventricular pacing electrode), the endotracheal tube was removed, and the face mask
stopper was replaced and connected to a pneumotachometer.
were
0
1
2
3
4
Time (sec)
FIG 2. Tracings showing hemodynamics and air flow during
chest compression in the fourth minute of resuscitation. Aortic
pressure (P), right atrial pressure, air flow (in liters per second,
I/s), and chest compression force (in newtons, N) are depicted.
Air flow above the zero line represents air flow out of the lungs,
or expiration. With the release of chest compression, vascular
pressures fall, and air enters the chest. Tidal volume recorded in
this animal was 102.7 mL per breath.
To minimize dead space during CPR, the pneumotachometer
connected to the exit port for measurements of air flow for
only 5 to 10 seconds every 60 seconds. Hemodynamic and air
flow data were digitized at a rate of 200 Hz and recorded on
magnetic disk and also on a Gould 4 channel recorder. Tidal
volumes were obtained by integration of the expiratory air
flow. Chest compression was initiated, and chest compression
force was maintained constant at 400 N for 14 minutes by use
of a hand-held device (previously described)." Chest compression force was chosen to be 375 to 400 N on the basis of prior
studies that have shown that vital organ perfusion is optimal
and trauma less likely at this compression force.'4 Arterial
blood gases were measured at 2-minute intervals.
Data are reported as mean±SEM. Arterial Pco2, Po2, and
pH were analyzed as a function of time with custom-written
software. For vascular pressures (aortic and right atrial), 10
beats were analyzed before arrest and at 2, 4, and 6 minutes
after the initiation of ventricular fibrillation. Means and SEM
were calculated for each animal for each period in time and
then the mean was developed for the overall group for each of
the time intervals indicated. Tidal volume was similarly calculated by analysis of five representative beats. Minute ventilation was calculated by multiplying the tidal volume by the chest
compression rate.
was
Results
Fig 2 is a representative tracing of a dog in the fourth
minute of chest compression alone. With chest compression, aortic and right atrial pressures increase by a
similar amount and air leaves the chest. On chest
compression release, marked by a fall in chest compression force, air enters the upper airway. The tidal volume
for Fig 2 was 103 mL per breath, with the minute
3072
Circulation Vol 90, No 6 December 1994
AVG 02 Sat
AVG pH
X
AVG pCO2
02
Sat
8
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nm
Tkm
(
()
FIG 3. Graphs of composite data from seven dogs, showing change average arterial 02 saturation (upper left, AVG 02 Sat), average
arterial pH (upper right, AVG pH), and average PCO2 (lower left, AVG PC02) over the period of study. The lower right frame (02 Sat)
depicts each individual dog studied and shows change in percent 02 saturation over the time period of study. Means±SEM are plotted.
in
ventilation during the fourth minute of resuscitation
being 8.7 L/min.
Fig 3, upper left, shows pooled data from seven dogs
and depicts the change in 02 saturation during chest
compression without ventilation over a 14-minute time
period. At 4 minutes after the onset of ventricular
fibrillation with chest compression alone, oxygen saturation was still approximately 94% (Table). The range
Of 02 saturation at 4 minutes was from 77% to 97.8%,
with six of seven dogs being >90% (Fig 3, lower right).
At 6 minutes, it had fallen to 87%.
Fig 3, upper right, also shows the changes in arterial
pH over 14 minutes in seven dogs. At 4 minutes, the
mean pH was still 7.39±0.03 (range, 7.24 to 7.47) (Table). At 6 minutes it had fallen to 7.36±0.12. Fig 3, lower
left, depicts the change in arterial Pco2. Arterial Pco2 did
not rise above 35 mm Hg until after 8 minutes, well after
oxygen saturation had already fallen below 75%.
The Table also shows aortic systolic and diastolic
pressures, right atrial pressure, minute ventilation, and
tidal volume before arrest and at 2, 4, and 6 minutes
during resuscitation with chest compression alone.
Ventilation During Only Chest Compression
Time (2-M;n Intervals During Resuscitation)
AO sys,
mm Hg
AO dia,
mm Hg
RA mean,
mm Hg
Min vent,
L/min
4 Mmn
6 Mmn
8 Mmn
10 Min
12 Mln
14 Min
49.6±5
48.1±7.7
52.2±10.2
36.1 ±7.8
33.6±4.7
34.4±4.8
33.7±4.1
116.2±4.6
25.4±3
22.6±3.9
24.6±6.0
21.8±4.8
19.5+3.3
19.3±3.2
18.1±2.4
5.3±1.4
17.1±1
14.8±0.8
12.9±0.7
13.4±0.5
12.2±0.7
11.3±1.0
11.2±0.9
5.2±1.1
6.1±1.2
6.7±1.3
5.6±1.1
5.7±1.1
5.1±0.8
79.5±12.2
7.19±0.05
69.7±12.8
7.15±0.04
46.9+7.3
48.5+6.8
Prearrest
2 Min
143.2±5.7
...
Tidal vol,
4.9±0.9
78.1
89.5±16.1
81.7±16.1
73.3±17.7
70.2±17.9
7.19±0.04
7.29±0.05
7.36±0.05
7.39±0.02
7.39±0.03
38.8+6.4
34.3±4.9
26.3±5.3
24.3±3.1
27+1.5
25.7±1.3
PCo2
42.0±9.4
57.3±9.7
84.3±14.6
95.8±11.7
101.6±7.9
108.9±7.5
P02
70.4±10.6
75.2±1.0
87.5±6.8
93.9±2.8
% 02 Sat
97.5±0.5
96.44±1.2
AO sys indicates aortic systolic pressure; Ao dias, aortic diastolic pressure; RA mean, right atrial mean
ventilation; and tidal vol, tidal volume. Arterial pH, PCO2, P02, and % 02 saturation values are also noted.
mL/breath
pH
...
7.39±0.02
36.1±5.7
50.7±9.9
pressure; Min vent, minute
40.9±7.5
58.8±10.5
Chandra et al Ventilation During CPR
These time intervals are chosen for display because they
are clinically meaningful and span the time periods
when arterial 02 saturation falls below 90%. Vascular
pressures are low, since epinephrine was not administered, but are similar to those that have been reported
previously during conventional CPR without epinephrine.16 Despite a fall in pH and Po2, there is no
substantial hemodynamic effect and specifically no decrease in arterial pressure observed for >6 minutes.
Tidal volume during chest compression alone also remains fairly constant over time. The range of tidal
volume in the dogs studied was 21 to 127 mL per breath.
Discussion
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Resuscitation research over the past 20 years has
been broad based and has encompassed the study of the
epidemiology of arrest, the hemodynamics of CPR, and
the role of early defibrillation and vasopressors in
resuscitation.9121417-21 Based on the results of these
studies, recommendations have been developed that
have formed the basis for the changes in the American
Heart Association Standards and Guidelines for CPR.'
Despite this growth in knowledge, little is known of the
role of ventilation during CPR. The 1990s have ushered
in an era in which a perceived risk of disease transmission may undermine the significant public education
effort of bystander CPR that marked the 1970s and
1980s.7,8 Although often considered, transmission of
HIV during CPR has never been documented.22 Nevertheless, the risk of transmission of other diseases during
CPR, such as herpes simplex, has been documented,
and transmission of drug-resistant tuberculosis is also a
matter of concern.23 Although most cardiac arrest victims collapse at home and hence are attended to by
relatives and friends, several surveys and studies have
identified the lack of willingness of most laymen and
medical personnel to initiate CPR in unknown victims
of cardiac arrest.7,8
When should ventilation be initiated during CPR in
adults? What is the tidal volume necessary during CPR
to maintain adequate gas exchange? There is little in the
literature that gives concrete answers to these basic
questions about ventilation during resuscitation. This
preliminary study was designed to initiate the process of
reevaluating ventilation during CPR. The pioneering
work of Safar and Elam in the 1950s established the
superiority of the mouth-to-mouth technique of ventilation compared with the manual techniques of ventilation that did not require any oral contact between
rescuers and victim. Safar et a12 compared tidal volumes
during mouth-to-mouth or mouth-to-airway respiration
with manual ventilation in anesthetized and curarized
apneic adults studied with natural airways and an
artificial oral pharyngeal airway. These studies suggested that of all the manual techniques of ventilation,
the Holger-Nielsen method, although inferior to the
mouth-to-mouth technique, was probably the most effective in maintaining tidal volume. On the basis of
these and other studies in 1961, these investigators
recommended the preferential use of mouth-to-mouth
ventilation during CPR. It was further recommended
that mouth-to-mouth ventilation be initiated immediately and interposed after every five chest compressions,
since chest compression alone moved relatively small
volumes of air." Whether ventilation could be delayed
3073
in relation to chest compression was never assessed, and
the studies of ventilation frequency during CPR were
also limited in scope.11 These earlier studies of manual
and mouth-to-mouth ventilation cannot be readily extrapolated to the human cardiac arrest situation. In
most of these studies, the patients were alive, with
nearly normal cardiac output.2 In addition, these studies
presumed that the goal of ventilation during CPR was to
achieve nearly normal tidal volumes and minute ventilation; hence, the emphasis in all of these studies was
the prompt institution of ventilation with normal or
higher than normal tidal volumes.
Our data show that in a canine model of witnessed
cardiac arrest when chest compressions were started
within 1 minute of arrest, arterial oxygen saturation
remained >90% for 4 minutes after initiation of chest
compressions without ventilation. Changes in arterial
pH and Po2 that occurred were not of sufficient magnitude to affect vascular tone, as judged by the lack of
change in aortic diastolic pressure. Our observations
are supported by data from Berg et al,24 who demonstrated no change in survival in dogs with witnessed
cardiac arrest in whom only chest compressions were
performed before defibrillation (compared with conventional CPR).
Weil et a125 demonstrated that during CPR in humans
(in-hospital arrest victims), arterial pH, Pco2, and bicarbonate change little from prearrest values. This
observation can probably be explained by the reduced
cardiac output of CPR and adequate alveolar ventilation. On the basis of these observations and studies, we
hypothesize that the recommended parameters for tidal
volume and minute ventilation may be unnecessarily
high for CPR in most clinical situations. In addition,
because of the reduced cardiac output of CPR, if
cardiac arrest occurs with the blood relatively well
oxygenated, ventilation could well be briefly deferred if
chest compression is initiated promptly. CPR Registry
data from Belgium further support the concept of
deferred ventilation.26 Using an observational database
of 2971 victims of cardiac arrest, Bossaert et a126 examined 21-day survival in patients undergoing out-ofhospital resuscitation. Of those who had no bystander
CPR, 6% survived (123 of 2055 patients). Of those who
had external chest compression and mouth-to-mouth
ventilation (probably initiated in an A-B-C sequence,
since this is the preferred technique in Belgium), 12%
survived (67 of 561 patients) (P<.001). However, 9%
(24 of 258) of those who had external chest compression
alone and no ventilation survived (P<.05 compared
with no bystander CPR). This compares with only 5 of
97 patients who survived from those who had only
mouth-to-mouth ventilation (P=NS versus no bystander
CPR).26 Since these data represent an observational
database, ie, a registry, it is unknown whether the
groups were balanced in terms of downtime, accuracy of
diagnosis, etc. Nevertheless, by virtue of the large
numbers and the fact that cardiac arrest was confirmed
in all patients by physicians (who were part of the
Emergency Medical Response System in Belgium),
these observations are intriguing and support the hypothesis that ventilation may be delayed if chest compressions are initiated immediately.
The applicability of animal data to the human cardiac
arrest situation can obviously be questioned, and the use
3074
Circulation Vol 90, No 6 December 1994
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of the dog to model ventilation during CPR in humans
may be regarded by some as a limitation. Although the
dog has been used extensively as the standard model to
study circulation and the hemodynamics of CPR, there
is relatively little published information regarding the
similarity of canine and human respiratory function
during resuscitation.17 However, dog models have
proved extremely useful in the study of various pathological and physiological states such as the adult respiratory distress syndrome,27'28 pulmonary embolism,29
pneumonia,30 pulmonary fibrosis, and emphysema.3'
Moreover, despite anatomic differences in chest configuration, intrathoracic vascular pressures during chest
compression in humans and large dogs have been shown
to be similar.17 Thus, it is probable that the transmission
of chest compression forces to the lungs is also similar.
We recently demonstrated that cineradiographic images
of medium-sized bronchi during chest compression in
dogs are similar to those obtained during forced expiratory efforts in humans.32
Another limitation of this study is that the mean
Paco2 before cardiac arrest was approximately 27
mm Hg. This low Paco2 probably reflects respiratory
compensation for tissue acidosis that occurred from
femoral artery ligation for catheter placement. The low
initial Paco2 values could potentially cause a longer
period of time for Paco2 to rise to values considered
unacceptable. However, Paco2 initially decreased during the 4 to 6 minutes after cardiac arrest, indicating
that the level of ventilation that occurred with chest
compression only was more than sufficient to clear the
relatively small amount of CO2 delivered to the lungs
during this phase. From 6 to 14 minutes after cardiac
arrest, Paco2 increased from approximately 26 to approximately 48 mm Hg (Fig 3, lower left). The rate of
rise in Paco2, even when starting from a level of 30
mm Hg, indicates that it took at least 3 to 4 minutes for
the Pco2 to rise by 5 mm Hg (Fig 3, lower left).
Unfortunately, there are no data on actual ventilation
during chest compression alone in patients with true
cardiac arrest. The data that exist were obtained in
patients with beating hearts. Their relevance to human
CPR, in which cardiac output is reduced and upper
airway obstruction is common, is unclear. Upper airway
obstruction can be overcome by positioning the head
and neck as shown by Elam et a133 in 1958, but an
in-depth knowledge of ventilation during resuscitation
is lacking. Our study was designed to initiate the process
of reevaluating ventilation during CPR because of the
increasing concern of even health care professionals to
initiate mouth-to-mouth ventilation.7
Our data suggest that in the animal model, ventilation
can be deferred for several minutes in a witnessed arrest
and arterial saturation maintained >90%. These data
are clearly not sufficient to warrant any change in the
performance of human CPR, nor do they represent a
call to cease ventilation during resuscitation. They
should be regarded only as a stimulant to study ventilation during resuscitation more intensely. The prompt
institution of ventilation during CPR is undoubtedly
ideal but is causing great concern in our present health
care environment. The preliminary Belgian Registry
data are intriguing and suggest that brief periods of
chest compression alone are clearly superior to no CPR
at all and nearly as effective as conventional CPR (chest
compression plus ventilation) in terms of survival. In
light of our present health care environment, these data
should prompt a reexamination of the recommendations for ventilation and specifically the need for immediate ventilation during witnessed arrest. Ventilatory
requirements in victims of unwitnessed arrest may be
quite different, to judge by preliminary animal data.34
Reluctant rescuers should be encouraged to activate the
Emergency Medical Service system and at least open
the airway and initiate chest compressions, pending the
arrival of trained and equipped rescuers/paramedics.
Further detailed studies to better identify the timing of
ventilation and tidal volumes during resuscitation in
humans are clearly needed.
Acknowledgment
This study was supported by Ischemic Heart Disease SCOR
grant 5P50-HL-17655 from the National Heart, Lung, and
Blood Institute.
References
1. American Heart Association. Standards and Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care
(ECC). JAMA. 1992;268:2171-2302.
2. Safar P, Escarraga LA, Elam JO. Comparison of mouth-to-mouth
and mouth-to-airway methods of artificial respiration with chest
pressure arm lift methods. N Engl J Med. 1958;258:671-677.
3. Safar P, Brown TC, Holtey WJ, Wilder RJ. Ventilation and circulation with closed-chest cardiac massage in man. JAMA. 1961;176:
574-581.
4. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest
cardiac massage. JAMA. 1960;173:1064-1067.
5. Meursing BTJ, Zimmerman ANE, Van Heyst ANP. Experimental
evidence in favor of a reversed sequence in cardiopulmonary resuscitation. JAm Coll Cardiol. 1983;1:610. Abstract.
6. Simoons ML, Kimman GP, Ivens EMA, Hartman JAM, Hart HN.
Follow up after out of hospital resuscitation. Read before the
XIIth Annual Congress of the European Society of Cardiology;
September 16-20, 1990; Stockholm, Sweden.
7. Brenner BE, Kauffman J. Reluctance of internists and medical
nurses to perform mouth-to-mouth resuscitation. Arch Intern Med.
1993;153:1763-1769.
8. Ornato JP, Hallagan L, McMahan SB, Peeples EH, Rostafinski
AG. Attitudes of BCLS instructors about mouth-to-mouth resus-
citation during the AIDS epidemic. Ann Emerg Med. 1990;19:
151-156.
9. Thompson RG, Hallstrom AP, Cobb LA. Bystander-initiated cardiopulmonary resuscitation in the management of ventricular
fibrillation. Ann Intern Med. 1979;90:737-740.
10. Guenter CA. Arterial blood gas analysis: the final yardstick of
overall adequacy of lung function. In: Guenther CA, Welch MH,
eds. Pulmonary Medicine. Philadelphia/Toronto: JB Lippincott Co;
1977:124-130.
11. Harris LC, Kirimli B, Safar P. Ventilation-cardiac compression
rates and ratios in cardiopulmonary resuscitation. Anaesthesia.
1967;28:806-812.
12. Koehler RC, Chandra NC, Guerci AD, Tsitlik J, Traystman RJ,
Rogers MC, Weisfeldt ML. Augmentation of cerebral perfusion by
simultaneous chest compression and lung inflation with abdominal
binding following cardiac arrest in dogs. Circulation. 1983;67:
266-275.
13. Bishop RL, Weisfeldt ML. Sodium bicarbonate administration
during cardiac arrest: effect on arterial pH, pCO2, and osmolality.
JAMA. 1976;235:506-509.
14. Halperin HR, Tsitlik JE, Guerci AD, Levin HR, Shi AY, Chandra
NC, Weisfeldt ML. The determinants of vital organ flow during
cardiac arrest in dogs. Circulation. 1986;73:539-551.
15. Gruben KG, Romlein J, Halperin HR, Tsitlik JE. System for
mechanical measurements during cardiopulmonary resuscitation
in humans. IEEE Trans Biomed Eng. 1990;37:204-210.
16. Michael JR, Guerci AD, Koehler RC, Shi AY, Tsitlik J, Chandra
NC, Niedermeyer E, Rogers MC, Traystman RJ, Weisfeldt ML.
Mechanisms whereby epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in
Circulation. 1984;69:822-835.
dogs.
Chandra et al Ventilation During CPR
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
17. Chandra NC, Tsitlik J, Halperin HR, Guerci AD. Observations of
hemodynamics during human cardiopulmonary resuscitation. Crit
Care Med. 1990;18:929-934.
18. Paradis NA, Martin GB, Goetting MG, Rosenberg JM, Rivers EP,
Appleton TJ, Nowak RM. Simultaneous aortic, jugular bulb, and
right atrial pressures during cardiopulmonary resuscitation in
humans: insights into mechanisms. Circulation. 1989;80:361-368.
19. Eisenberg MS, Copass MK, Hallstrom AP, Blake B, Bergner L,
Short F, Cobb LA. Treatment of out-of-hospital cardiac arrests
with rapid defibrillation by emergency medical technicians. N Engl
J Med. 1980;302:1379-1383.
20. Brown CG, Martin D, Pepe P, Steuven H, Cummins RO, Gonzalez
E, Jazktremski M, and the Multicenter High Dose Epinephrine
Study Group. Standard versus high dose epinephrine in out-ofhospital cardiac arrest: a controlled clinical trial. N Engl J Med.
1992;327:1051-1055.
21. Weaver WD, Hill D, Fahrenbruch CE, Copass MK, Martin JS,
Cobb LA, Hallstrom AP. Use of the automatic external defibrillator
in the management of out-of-hospital cardiac arrest. N Engl J Med.
1988;319:661-666.
22. Centers for Disease Control Update. Human immunodeficiency
virus infections in health-care workers exposed to blood of infected
patients. MMWR. 1987;36:285-289.
23. Hendricks AA, Shapiro E. Primary herpes simplex infection following mouth-to-mouth resuscitation. JAMA. 1980;242:257-258.
24. Berg RA, Kern KB, Sanders AB, Otto CW, Hilwig RW, Ewy GA.
Bystander cardiopulmonary resuscitation: is ventilation necessary?
Ann Emerg Med. 1993;22:174-885.
25. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel
MI. Difference in acid base state between venous and arterial
blood during CPR. N Engl J Med. 1986;315:153-156.
3075
26. Bossaert L, Van Hoeyweghen R, and the Cerebral Resuscitation
Study Group. Bystander cardiopulmonary resuscitation (CPR) in
out-of-hospital cardiac arrest. Resuscitation. 1989;17(suppl):
555-569.
27. Koyama I, Toung TJK, Rogers MC, Gurtner GH, Traystman RJ. 02
radicals mediate reperfusion lung injury in ischemic O2-ventilated
canine pulmonary lobe. JAppl Physiol. 1987;63:111-115.
28. Parker JC, Hernandez LA, Longnecker GL, Peevy K, Johnson W.
Lung edema caused by high peak inspiratory pressures in dogs:
role of increased microvascular filtration pressure and permeability. Am Rev Respir Dis. 1990;142:321-328.
29. Wagner PD. Mechanisms of hypoxemia in pulmonary embolism.
Appl Cardiopulm Pathophysiol. 1987;1:63-71.
30. Light RB, Mink SN, Wood LDH. Pathophysiology of gas exchange
and pulmonary perfusion in pneumococcal lobar pneumonia in
dogs. JAppl Physiol. 1981;50:524-530.
31. Mink SN. Expiratory flow limitation and the response to breathing
a helium-oxygen gas mixture in a canine model of pulmonary
emphysema. J Clin Invest. 1984;73:1321-1334.
32. Halperin HR, Guerci AD, Brower R. Air trapping in the lungs
during cardiopulmonary resuscitation in dogs: a mechanism for
generating changes in intrathoracic pressure. Circ Res. 1989;65:
946-954.
33. Elam JO, Greene DG, Schneider MA. Head tilt method of oral
resuscitation. JAMA. 1960;172:812-815.
34. Idris AH, Melker RJ, DelDeca KD, Staple ED, O'Brien DJ, Rush
W, Falk JL. The effect of ventilation on pH, PCO2, and end tidal
carbon dioxide during low blood flow states. Circulation. 1986;
4(suppl I):I-547. Abstract.
Observations of ventilation during resuscitation in a canine model.
N C Chandra, K G Gruben, J E Tsitlik, R Brower, A D Guerci, H H Halperin, M L Weisfeldt
and S Permutt
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Circulation. 1994;90:3070-3075
doi: 10.1161/01.CIR.90.6.3070
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