684
Myocardial Acidosis Associated With CO2
Production During Cardiac Arrest
and Resuscitation
Martin von Planta, MD, Max Harry Weil, MD, PhD, Raul J. Gazmuri, MD,
Joe Bisera, MSEE, and Eric C. Rackow, MD
Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed
(pulmonary artery) blood in animals and human patients during cardiac arrest and
cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the
myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in
11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes.
During CPR, there was rapid onset of profound myocardial acidosis with an increase in
intramyocardial [H'] from 54±5 to 146±20 nmol/l (7.27±0.04 to 6.88±0.20 pH units). Great
cardiac vein Pco2 increased from 57±2 to 158±+12 mm Hg. Profound hypercarbic acidosis in
great cardiac vein blood was associated with myocardial lactate production to levels of 8.1±0.7
mmol/1. Only moderate decreases in cardiac vein bicarbonate concentrations from 31±1 to
23±1 mmol/l were observed. These acid-base changes were almost completely reversed over an
interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The
Pco2 in cardiac vein blood was significantly greater than that of mixed venous blood,
demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is
CO2 production during ischemia that is implicated as the predominant mechanism accounting
for myocardial [H'] increases during cardiac arrest. Important clinical implications for buffer
therapy during CPR and, in particular, treatment with bicarbonate emerge from these
observations. (Circulation 1989;80:684-692)
venous
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In prospective investigations of the pH, Pco2,
and HCO3- in both arterial and mixed venous
blood in pigs, rats, and human patients during
CPR, we observed that acidemia is predominantly
due to increases in Pco2 in mixed venous (pulmonary artery) blood. This contrasted with decreases
in Pco2 in arterial blood. The venoarterial Pco2
gradient exceeded 30 mm Hg, but there was no
bicarbonate gradient.1-3 Both excesses of CO2 generated by HCO3- buffering of lactate and flowlimited pulmonary excretion of CO2 were implicated
as mechanisms accounting for increases in mixed
From the Department of Medicine, University of Health
Sciences-The Chicago Medical School, North Chicago, Illinois.
Supported by a grant (85BS16) from the Swiss Scientific
Foundation to M.v.P.; by The Laerdal Foundation for Acute
Medicine, Stavanger, Norway; by a grant-in-aid (861262) from
the American Heart Association; by National Institutes of Health,
NHLBI Grant IR01-HL-39148-01; and by The Institute of Critical Care Medicine, Rancho Mirage, California.
Address for correspondence: Max Harry Weil, MD, PhD,
Professor and Chairman, Department of Medicine, UHS/The
Chicago Medical School, 3333 Green Bay Road, North Chicago,
IL 60064.
venous PCo2.'14 Striking increases in cardiac venous
PCO2 to levels exceeding 150 mm Hg during experimental CPR were observed. The PCO2 of cardiac
vein blood consistently exceeded the Pco2 of mixed
venous blood.5 Similar observations were subsequently reported by Capparelli and his associates.6
Such profound acidemia has important clinical
implications because the efficacy of adrenergic agents
may be decreased,7 the administration of CO2 generating buffer agents may be counterproductive,8'9
and intracellular respiratory acidosis may further
reduce myocardial contractility.'0"11
It was, therefore, of interest to quantitate myocardial acidosis in relation to both myocardial CO2
production and coronary perfusion during CPR.
Accordingly, we measured myocardial [H'] and
myocardial production and extraction of [H'], PCO2,
HCO3 , S02, and lactate before, during, and after
resuscitation from cardiac arrest. Because mean
aortic and coronary perfusion pressures have been
identified as major determinants of resuscitability,
we also monitored these parameters in conjunction
with continuous measurements of end-tidal PCo2
von Planta et al Myocardial Acidosis During Cardiac Arrest
tension (PETCO2) and intermittent measurement of
cardiac output.4,12
Methods
Animal Preparation
Eleven domestic pigs weighing between 22 and 30
kg were investigated. The animal care and procedures were in accord with the guidelines stated in
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the Guide for the Care and Use of Laboratoty
Animals. The domestic pig was selected because
the porcine coronary circulation,13 conduction
system,14 and epicardial blood supply15 are more
like those of the human than other nonprimate
animal species.
Anesthesia was induced with 20 mg/kg ketamine
and 25 mg/kg pentobarbital, which was subsequently supplemented with 5 mg/kg bolus injections
of pentobarbital at intervals of 30 minutes. After
endotracheal intubation, constant minute ventilation with a volume-controlled ventilator (Model
MA-1, Puritan Bennett, Los Angeles, California)
was initiated. FiO2 was maintained at 0.5, the
frequency between 12 and 15/min, the tidal volume
at 15 ml/kg, and a maximal flow rate at 40 1/min. The
tidal volume was subsequently adjusted such as to
maintain baseline arterial Pco2 in the physiologic
range of 40-45 mm Hg.
For hemodynamic monitoring, catheters were
advanced from the right femoral artery into the
thoracic aorta (USCI Model 6523-8F, CR Bart Inc,
Billerica, Massachusetts), from the right femoral
vein into the pulmonary artery (thermodilution catheter, Model SP5527, Gould Inc. Oxnard, California)
and from the left cephalic vein through the coronary
sinus into the great cardiac vein (USCI Model
5470-7F, CR Bart Inc, Billerica, Massachusetts).
All catheter positions were confirmed by fluoroscopy and characteristic pressure pulse morphology,
and appropriate oxygen saturation and lactate content of blood sampled from the catheters. Patency
of the catheters was maintained with minimal pressure flushes with physiologic saline containing 10
IU heparin/ml saline using the Intraflow system
(Gould Inc, Oxnard, California). Fluid losses were
replaced with physiologic saline infused in amounts
of 10 ml/kg/hr.
Measurements
Cardiac index was measured by bolus injection of
thermal tracer using the thermodilution technique.
The reproducibility and validity of this method in
this experimental setting was previously reported.16
Coronary perfusion pressure was computed as the
difference between diastolic aortic and time coincident diastolic right atrial pressure.
End-tidal CO2 concentration was continuously
measured with a side-stream infrared absorption
CO2 analyzer (Model 200, Instrumentation Laboratory Inc, Lexington, Massachusetts). The CO2 analyzer was calibrated with room air and CO, gas
685
standards (Air Products, Allentown, Pennsylvania).
Linearity of the measurement was confirmed by
stepwise 1% increases in the CO2 concentration
from 1% to 5 %. The maximal error of the CO2
measurement was less than 2% over the range of
0-40 mm Hg on 35 trials (r=0.99; y=0.99x+0.01).
PETCO2 was derived from the end-tidal CO2 concentration corrected for barometric pressure and temperature. The sidewall sample manifold of the CO2
analyzer was adapted to the endotracheal tube, and
the gas was sampled at a flow rate of 200 ml/min.
Dynamic data including electrocardiogram (lead
II), intravascular pressures, tidal volume, and
PETCO2 were continuously recorded with the aid of
an eight-channel physiologic amplifier-thermoprinter
system (Model 7758A, Hewlett-Packard Inc,
Waltham, Massachusetts). Blood temperature was
maintained in the range of 36-37° C with the aid of
external infrared heat lamps. Arterial, pulmonary
artery (mixed venous) and cardiac vein [H+], Pco2,
Po2, SO2, and lactic acid were measured before and
during cardiac arrest, during chest compression,
and after resuscitation by techniques previously
described.1718 Bicarbonate was computed from [H'],
Pco2, and hemoglobin with corrections for blood
temperature, which was measured by the thermistor in the pulmonary artery. The acid-base nomograms for immature domestic pigs developed by
Hannon19 were used.
For measurement of intramyocardial [H'], a midline laparotomy was performed. The tendinous portion of the diaphragm was excised, and a 1.5 cm
vertical incision was made in the pericardium overlying the diaphragmatic left ventricular myocardium. Earlier studies had demonstrated that neither
the precardiac arrest hemodynamic status nor the
effectiveness of precordial compression and resuscitation was compromised by these interventions in
this porcine model.20 A 1-mm, steel-jacketed, glasstipped pH electrode was advanced into a position
midway between the epicardial and the endocardial
surfaces of the diaphragmatic left ventricle. The
electrode was then anchored in the myocardium. A
temperature sensor was placed in the myocardium
within 1 cm of the pH electrode and secured with a
suture; the pericardial incision was then closed with
sutures. A potassium chloride reference electrode
was placed in a subcutaneous pocket in the neck.
[H4] was measured with a Khuri pH monitor at
intervals of 20 seconds. The 95% in vitro response
time to step changes in [H'] was less than 3 seconds
with a linear response over the range of interest.21,22
It was calibrated in vitro before and after completion of the experiment with buffer solutions representing 4.0 and 7.0 pH units.
Experimental Protocol
After baseline hemodynamic, blood gas, and
intramyocardial [H4] measurements were obtained,
ventricular fibrillation was induced by 10 mA AC
current delivered to the right ventricular epicar-
686
Circulation Vol 80, No 3, September 1989
PORCINE CPR 1: ACID - BASE ( N - 1 1 )
VENTRICULAR FIBRILLATION
a CHEST COMPRESSION
CONTROL
RESUSCITATION
*
15011
110 L
70
30 L
H+
PH
units
nmol/L
A
vi
689
7.0
72
7.5
13U [
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90 L
mmynol/L
30
30r
10
or---
-
-------
-
.
.-.
-.
-.---
HC05
*
*
=E9*
mrrnoJ/L
I
I
-2
0
* p<QD1
I
I
2
I
-I
4
I
1
a
6
8
MINUTES
,
10
12
12
,
14
h
+60
UHS/CMS MvP. MHW 4/88
VF =11', Prec Comp 8'
FIGURE 1. Plots of mean+±SEM of intramyocardial [He] andpH, great cardiac vein (GCV), mixed venous (pulm. art.)
and aortic [H'], Pco2, and HCO3- before, during, and after resuscitation from ventricularfibrillation in ]pigs. External
chest compression was begun after 3 minutes, and spontaneous circulation was restored by defibrillation at 11 minutes.
dium. After 3 minutes of ventricular fibrillation,
external chest compression with a mechanical compressor (Thumper@, Model 1000, Michigan Instruments, Grand Rapids, Michigan) was begun at a
rate of 60/min, an equal compression-relaxation
interval (i.e., 50% duty cycle), and a compression
depth of 25-30% of the animal's anteroposterior
chest width and continued for another 8 minutes.
After 11 minutes of ventricular fibrillation, DC
defibrillation with 300 J (Model 911, PhysioControl, Redmond, Washington) was attempted.
All animals were successfully resuscitated and
observed for an additional interval of 60 minutes.
The animals were then killed by injection of saturated potassium chloride. Autopsy was performed
for confirmation of appropriate placement of catheters and to ensure that there were no adverse
effects from the invasive procedures or major injuries stemming from external chest compression.
Statistical Analysis
The significance of changes over time were analyzed by single-factor repeated-measures ANOVA.
Measurements are reported as mean±SEM. A p
value of less than 0.01 was regarded as significant.
Results
The baseline intramyocardial [H'] after 30 minutes of equilibration was 54±5 nmol/l (7.27±0.04
pH units) with a myocardial temperature of
36.5+± 0.50 C. After 11 minutes of ventricular fibrillation, there was a significant increase in intramyocardial [H'] to 146±20 nmol/1 (6.88±0.20 pH units)
with an intramyocardial temperature of 36.8±0.20 C.
Restoration of spontaneous circulation was followed by a prompt decline in intramyocardial [H'].
It declined to 58±6 nmol/l (7.24±0.04 pH units)
during the 60-minute interval that followed successful defibrillation (Figure 1).
Highly significant increases in cardiac vein [H'],
Pco2, and lactate were observed, which peaked
during the fourth minute of ventricular fibrillation
(i.e., 1 minute after start of external chest compression). This was associated with lesser increases in
mixed venous Pco2 and small decreases in arterial
Pco2 (Figures 1 and 2). Most impressive were the
augmented [H'] and C02 gradients between the
aorta and the pulmonary artery (Figure 3) and
between the aorta and the great cardiac vein (Figure
4). These were rapidly reversed after restoration of
von Planta et al Myocardial Acidosis During Cardiac Arrest
687
PORCINE CPR lI: METABOLIC AND HEMODYNAMIC ( NI 1 )
CONTROL
CHEST COMPRESSION
;
S02O
100
RESUSCITATION
VENTRICULAR FIBRILLATION
U--
%
-----------
*.
--
LACTATE mmol/L
-
*
PULM. ART.
*---*
/
----r--*-- ----------------
1-
MAP
c" mmHg
a
50
-
*
*;
mmHg
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v
v
-1
T
*
*
v
__
v
7
*
T
**
Cl
40 -120
ETCO2
20 -60
*
m*
ml/kglrn
Aa
-2
*
F
Cl km
0L0
p<W1
1
.
a
.
0
1
.
AA
2
5.
5.
4
1.
Ia
A
a
1
8
6
MINUTES
1.
9
10
1
,
,
i1r
12-
a
14
1Hl
-,
+60
UHS/CMS MvP. MHW 4/88
VF= 11', Prec Comp 8'
FIGURE 2. Plots of oxygen saturation (SO2), lactate, mean aortic pressure (MAP), coronary perfusion pressure (CPP),
end-tidal CO2 tension (PETCO2), and cardiac index (CI) before, during, and after resuscitation. Values given are
mean +SEM. GCV, great cardiac vein; mixed venous, pulm. art.
normal sinus rhythm. Accordingly, there was marked
myocardial production of CO2 during CPR. However, cardiac venous HCO3- was only modestly
reduced from 31±1 to 23±1 mmol/l during precordial compression. Myocardial oxygen extraction
increased from 69+4% to 82+1% at 2 minutes and
to 84±1% after 6 minutes of precordial compression. Immediately after resuscitation, it decreased
to 24±4% (p<0.01) (Figure 2).
Mean aortic pressure declined from 100±6 to
16±1 mm Hg after onset of ventricular fibrillation
(p<0.01). During precordial compression, it
increased to a plateau level of between 43±3 and
45+3 mm Hg (p<0.01). It increased to 93+5 mm Hg
60 minutes after resuscitation, which was not significantly different from the prearrest values. Cardiac index declined from 125 + 11 to 33+3 ml/kg/min
after 2 minutes of precordial compression (p<0.01)
and insignificantly increased to 38±3 ml/kg/min
after 6 minutes of precordial compression (Figure 2
and Table 1). After successful defibrillation, it
increased to 93+±14 mm Hg within 2 minutes after
restoration of spontaneous circulation. There was
close correspondence between changes in coronary
perfusion pressure and PETCO2.
Discussion
Earlier studies from our laboratories in a similar
porcine model of CPR demonstrated significant
increases in the arteriovenous CO2 and pH gradients during cardiac arrest.' These findings were
later confirmed in patients during CPR by our
group.3 However, the HCO3- before and during
CPR in a subset of 13 patients was not altered.
Accordingly, the gradients between arterial and
mixed venous blood CO2 were solely due to CO2.
We demonstrated that these were associated with
decreases in pulmonary blood flow such that pulmonary CO2 elimination was critically reduced.
This accounted for corresponding decreases in the
end-tidal CO2 concentration.4'16,23
Pilot studies subsequently demonstrated striking
increases in cardiac venous CO2 that exceeded the
mixed venous CO2.5 We, therefore, anticipated and
found profound intramyocardial acidosis during the
course of the present studies and related such to the
myocardial production of both carbon dioxide and
688
Circulation Vol 80, No 3, September 1989
GRADIENTS BETWEEN PULMONARY ARTERY AND AORTA
VENTRICULAR FIBRILLATION
+ CHEST COMPRESSION
CONTROL
H+nmol/L
|
p<OOl
*
*
20 -
RESUSCITATION
'f
DEF
PC02
10
5
HCO3 nmwol/L
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LACTATE
I
mmol/L
ElM
-1
*
60
OXYGEN
EXTRACTION, AS02%
lr
30 L
-2
0
2
i
.
6
4
8
MINUTES
,
,
10
,
.
,
12
11.
i
+60
UHS/CMS MvP. MHW 4/88
VF = 1 1. Pr.c CoMp 8'
FIGURE 3. Plots ofgradients between mixed venous (pulm. art.) and aortic blood for [H+], Pco2, HCO3- lactate, and
saturation during CPR independent of changes in coronary blood flow. Values given as mean ±SEM.
oxygen
lactic acid.24 These acid-base alterations occurred
under conditions of constant mechanical ventilation. The high ventilation-to-perfusion ratio
accounted for arterial alkalemia in association with
acidemia in blood sampled from the pulmonary
artery and the great cardiac vein. Comparable or
even higher Pco2 levels in mixed venous and cardiac
vein blood have been reported in experimental and
clinical CPR settings in which arterial Pco2 is reduced
to average levels ranging from 16 to 35 mm Hg.6,25,26
Accordingly, increases in systemic and coronary
venoarterial Pco2 gradients are more closely related
to decreases in blood flow rather than changes in
alveolar ventilation. Whether more vigorous ventilation would alter CO2 clearance by increasing
intrathoracic pressure and, therefore, blood flow is
as yet unresolved.
Parallel reductions in coronary perfusion pressure, cardiac index, and PETCO2 were observed. A
close relation between coronary perfusion pressure
and microsphere determined myocardial blood flow
has been demonstrated by other workers.27-29
Accordingly, decreases in coronary perfusion pressure and, therefore, in myocardial blood flow
accounted for failure to match the metabolic demand
of the heart for oxygen with the blood supply to the
myocardium. The buffering capacity of cardiac myocytes is greater than that of skeletal muscle, nervous tissue, or extracellular fluids, including blood.
The present data, therefore, support the concept
that it is bicarbonate buffering of the anaerobically
generated lactate that accounts for the increases in
intramyocardial CO2.29 32
[H'], Pco2, and lactate peaked in cardiac vein
blood after 4 minutes; the intramyocardial [H']
peaked after 11 minutes. The early changes in blood
sampled from the great cardiac vein are attributed
to partial restoration of coronary blood flow during
precordial compression with washout of metabolites accumulated during the no-flow interval of
cardiac arrest. Nevertheless, coronary perfusion
during precordial compression was not sufficient to
reverse anaerobic metabolism. Consequently, the
severity of intramyocardial acidosis was progressive during the 9-minute interval of ventricular
fibrillation even though coronary venous Pco2
remained stable or decreased. The generation of
additional protons by lipolysis and ATP hydrolysis
in association with continuing lactate production
would account for continued increase of intramyocardial [HW].32 Indeed, intramyocardial lactate may
be substantially increased during acute myocardial
von Planta et al Myocardial Acidosis During Cardiac Arrest
689
MYOCARDIAL PRODUCTION / EXTRACTION
CONTROLf
VENTRICllAR FIBRLLATION
F ESUSCITATION
M ,M
CHEST COMPRESSION
*
DEF
70
*
p<0.01
50 F
30 L
10 _
90 _
WL
t
M~~~ROUCTION
1-
*~~~~~
PC02 mmHg
PRODUCTION
4
LLZ
HCO3- mmol/L
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*
I[
LACTATE mmol/L
PRODUCTIO
.
-1 t X
r0; AS02%
I
-2
0
2
I
I
I
4
I
I
6
MINUTES
I
I
8
10
12
+60
UHSICMS MvP. M*W 4188
VF = 11. Prec Comp 8'
FIGURE 4. Plots of myocardial production of [H'], Pco2, and lactate are accompanied by extraction of HCO3- and
during CPR and reversal after successful resuscitation. Values given as mean +SEM.
oxygen
ischemia without parallel increases of cardiac vein
lactate.33 After successful resuscitation with restoration of near-normal cardiac index and coronary
perfusion pressures, lactate production and intramyocardial acidosis were reversed. The observations of
Lai et al34,35 would support this explanation.
Myocardial acidosis associated with CO2 production is likely to be of clinical import. Experimentally, intracellular acidosis due to rapid CO2 accumulation is associated with rapid loss of myocardial
contractility.10"11 The myocardial depressant effect
of CO2 was recognized as early as 1910 by Ernest
Starling and his coworker, E. Jerusalem.36 PooleWilson and Langer37 confirmed these findings on rat
and rabbit myocardium. Both Steenbergen et a138 in
studies on the perfused rat heart and MacGregor
and his associates39 in dogs demonstrated marked
depression of myocardial contractility when myocardial pH was decreased in association with
increases in myocardial CO2 tension. We confirmed
in our laboratories in the isolated rat heart the
earlier observations of Williamson et a140 that
increases in Pco2 rather than changes in pH of the
perfusate adversely affect contractility over the pH
range of 6.80-7.40.
The pH of myocardium and, therefore, its contractility are likely to be rapidly reduced in the
setting of myocardial ischemia because of the ease
with which CO2 diffuses into myocardial cells and
thereby increases in intracellular C02.41 In studies
by Case et a142 in dogs, the intramyocardial CO2
increased within 7-10 seconds after experimental
coronary occlusion and progressively increased to
430 mm Hg when ventricular fibrillation was induced
by coronary occlusion.
Changes in cardiac vein CO2 at varying coronary
flows and respiratory rates closely parallel those of
intramyocardial CO2.43 Unfortunately, we have not
as yet been successful in our efforts to produce a
reliable and rapid response electrode for measurement of myocardial Pco2 during cardiac resuscitation. However, in studies that used slower response
mass spectrometry methods, increases in myocardial CO2 during ischemia correlated highly with
increases in myocardial [H'], intramural ST segment changes, anaerobic generation of high energy
phosphates, and histologic injury.44,45
The interpretation of our findings may be challenged because our technique for measurement of
intramyocardial [H'] includes extracellular or interstitial [H'] and is not selective for intracellular
690
Circulation Vol 80, No 3, September 1989
TABLE 1. Acid-Base and HemOdynamic Parameters Before, During, and After CPR in 11 Domestic Pigs
Ventricular fibrillation
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Minutes
H+ (nmol/L)
AO
MV
CV
MYO
PCO2 (mm Hg)
AO
MV
CV
HCO3- (mmOl/l)
AO
MV
CV
Lactate (mmol/1)
AO
MV
CV
Control
-2
Chest compression
2
42±2
43±2
54±5
40+2 (10)
43±2 (10)
60±6 (10)
60±7
44±1
52±2
57±2
46±2
53±2
66±4
(10)
(10)
27±1
30±1
31±1
28±1
30±1
27-1
(10)
(10)
(10)
1.2±0.1
1.1±0.1
0.8±0.2
1.1±0.1 (10)
1.2+0.2 (10)
2.6±0.5 (10)
38+2
5
4
(10)
Resuscitation
9
13
+60
38+1
42±2
57±3*
49±2
48±2
54±2*
66±3*
57±3*
162±14 (5)*
77±9
102±8
86±10
93±7
132±16*
69±6
91±9
56±3
58±6
39±1
158±12 (5)*
59+3
113±9*
38±2
58±2
96±6
55±4
71±3*
66±5
47±2
61±2
61±2
25±1
29+1
26±1
21±1*
26±1*
25±1
23±1*
26±1*
23±1*
23±3*
27±1*
27±1
2.0±0.1
2.1±0.2
6.8±0.7*
2.6±0.2
2.6±0.2*
6.6±0.6*
3.8±0.3*
3.8±0.3*
4.7±0.4*
2.4±0.2
2.4±0.2
2.0±0.2
23±1
(5)
8.1+0.7 (5)*
S02 (%)
97+1
95±1 (10)
92±2
92±2
96±2
93±2
62+4 (10)
47±4
49±5
62±3
35±4*
35±3*
28±4
34±5 (10)
8±2 (5)
10±2
10±2
69±5*
33±4
16±1*
74±9*
100±6
44±3*
43±3*
93±5
45+3*
75±5
4±1*
85±7
23±2*
21±3*
15±2*
53+9*
4±1*
17±2*
39±4
34±1
15±3*
17±2*
35+1
PETC02 (mm Hg)
93±14
90±6
33±3*
38±3*
125±11
CI (ml/kg/min)
end-tidal
cardiac
mean
aortic
MAP,
PCO2; CI,
index; AO, aorta; MV, mixed
pressure; CPP, coronary perfusion pressure; PETCO2,
venous (pulmonary artery); CV, great cardiac vein; MYO, intramyocardial.
Values are given as mean±SEM.
Single-factor repeated-measures ANOVA: *p<0.01 compared with baseline. Note: In instances in which less than 11 measurements
were obtained, the numbers are shown in parenthesis. During chest compression (minute 4), the low-flow conditions allowed withdrawal
of only five blood samples.
AO
MV
CV
MAP (mm Hg)
CPP (mm Hg)
[H']. However, Walters et at46 had previously
observed a high correlation between tissue electrode pH and intracellular pH by enzyme assay.
Intracellular and tissue pH are closely related such
that changes in intracellular pH are rapidly followed
by changes in myocardial tissue pH.47-49
We conclude that myocardial acidosis during
cardiac arrest is associated with intramyocardial
CO2 and lactate production with only minor effects
on extracellular bicarbonate. Such increases in
intramyocardial CO2 during reduced perfusion of
the myocardium adversely affect myocardial contractility and, therefore, resuscitability.
This has potential implications for buffer therapy.
If the administration of bicarbonate increases CO2
production, this buffer therapy might be counterproductive.50 This indeed may explain the recent
documentation of adverse cardiac effects of sodium
bicarbonate in the setting of lactic acidosis by Arieff
and his coworkers (Arieff et al,51 Graf et al,52 and
Bersin et a153). However, this is not securely established. We have investigated the effects of both
C02-generating and C02-consuming buffer agents
on myocardial H' in our porcine model. Preliminary data demonstrated that intramyocardial [H']
was not altered by the buffers; and cardiac resuscitability was not changed.54 This would suggest
that the sodium buffer fails to diffuse into the
myocardium in the setting of cardiac arrest. Additional studies are in progress to define more precisely these pharmacodynamics of buffer therapy.
References
1. Grundler WG, Weil MH, Rackow EC: Arteriovenous carbon
dioxide and pH gradients during cardiac arrest. Circulation
1986;74:1071-1074
2. von Planta I, Weil MH, von Planta M, Bruno S, Bisera J,
Rackow EC: Cardiopulmonary resuscitation in the rat. J
Appl Physiol 1988;65:2641-2647
3. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL,
Griffel M: Difference in acid-base state between venous and
arterial blood during CPR. N'Engl JMed 1986;315:153-157
4. Gudipati CV, Weil MH, Bisera J, Deshmukh HG, Rackow
EC: Expired carbon dioxide: A noninvasive monitor of
cardiopulmonary resuscitation. Circulation 1988;77:234-239
von Planta et al Myocardial Acidosis During Cardiac Arrest
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Circulation Vol 80, No 3, September 1989
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KEY WORDS * acid-base imbalance * cardiac arrest
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Myocardial acidosis associated with CO2 production during cardiac arrest and
resuscitation.
M von Planta, M H Weil, R J Gazmuri, J Bisera and E C Rackow
Downloaded from http://circ.ahajournals.org/ by guest on July 31, 2017
Circulation. 1989;80:684-692
doi: 10.1161/01.CIR.80.3.684
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