Myocardial and Body Metabolism in Fatal Cardiogenic Shock after

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Myocardial and Body Metabolism
in Fatal Cardiogenic Shock
after Valvular Replacement
By EMERSON A. MOFFITT, M.D., GEORGE D. MOLNAR, M.D.,
AND
DWIGHT C. MCGOON, M.D.
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SUMMARY
Cellular energy substrates and metabolites, electrolytes, oxygenation, and acid-base
balance, in arterial and coronary sinus blood of seven adult patients who died after
valvular replacements, were studied and compared with these measurements from five
patients having aortic replacement who survived. Six of the patients were in New
York Heart Association class IV. All but one died within 24 hr of acute circulatory
failure, with excessive bleeding being a contributing factor. Plasma potassium and
osmolality remained higher in the first postoperative hours in nonsurvivors. Ketone
bodies, growth hormone, and lactate levels rose precipitously as shock became severe.
Increased arterial blood osmolality and potassium, plus a still-rising lactate concentration, were evident 2 hr after operation in patients who died in the next 24 hr. Low
cardiac output, hyperosmolality, and the degree of lactic acidosis were the only early
changes predicting the fatal outcome.
Additional Indexing Words:
Energy metabolism
Postoperative mortality
Lactic acidosis
follow these metabolic changes until death in
seven critically ill patients who died after
valvular surgery. They were the nonsurvivors
from a group of 85 patients2-7 in whom we
have studied the myocardial and whole-body
metabolic response during and after wholebody perfusion for repair of acquired and
congenital lesions. The data from analysis of
arterial and coronary sinus blood, and from
cardiac output, from these nonsurvivors are
compared with those from five patients who
survived aortic valve replacement. Our purpose was to ascertain whether changes in
metabolism could be detected early in postoperative shock, and possibly lead to better and
successful treatment.
I NABILITY of the myocardium to maintain
sufficient contractility for a satisfactory
circulation is the most frequent cause of death
after open-heart operations. Acute failure, or
low output syndrome, causes deficient perfusion of body tissues. Profound effects on
cellular oxygenation, energy metabolism, acidbase balance, and electrolyte patterns occur in
the end stages of shock, including that of the
cardiogenic type.1 We had the opportunity to
From the Department of Anesthesiology, Division
of Endocrinology and Internal Medicine, and Section
of Thoracic, Cardiovascular and General Surgery of
the Mayo Clinic and Mayo Foundation, Rochester,
Minnesota 55901.
Supported in part by Research Grant GM-14919
from the National Institutes of Health, U. S. Public
Health Service.
Read at the meeting of the American Heart
Association, Atlantic City, New Jersey, November 1215, 1970.
Received January 8, 1971; revision accepted for
publication April 12, 1971.
Circulation, Volume XLIV, August 1971
Open-heart surgery
Methods
Information on Patients
Clinical details on the seven patients and their
operative courses are shown in table 1. All were
in New York Heart Association functional class
IV, except patient 6 who was in class III. All had
237
238
MOFFITT ET AL.
been taking digitalis, and all but one, diuretics.
All therapeutic manipulations possible and available to us were used postoperatively, including
mechanical ventilation via endotracheal tube,
digitalis (when indicated), isoproterenol by drip,
and adjustment of blood volume as allowed by
monitoring of right atrial, left atrial, and arterial
pressures. Despite these combinations of treatment, the downhill course continued with
ventricular fibrillation being the usual terminal
event, after a prolonged period of severely
depressed cardiac output. A fresh left ventricular
infarct was found at autopsy in two instances.
The group used for comparison consisted of five
patients surviving aortic valve replacement.2 No
significant differences were found in previous
similar studies between patients having aortic
replacement and those more seriously ill patients
having double valve replacements,5 or those in
other studies having similar hormonal determinations.7
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Anesthesia and supportive care were as
previously reported.2 Perfusing flow averaged 2.4
liters/min/m2 at 30°C except for patient 7
(36°C). In all cases involving aortic valve
replacement direct perfusion of both coronary
arteries was done, except in patient 2 in whom
the right coronary artery was not able to be
cannulated. The priming solution for the vertical
sheet oxygenator was two-thirds acid-citratedextrose (ACD) blood diluted with 5% dextrose in
0.45% NaCl and tris(hydroxymethyl)aminomethane (THAM). All valve prostheses were of the
Starr-Edwards type.
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Arterial blood was drawn before induction of
anesthesia, with the patient breathing air. After
thoracotomy, a small catheter was inserted deep
into the coronary sinus, initially via the right
atrium and after the onset of perfusion through
the wall of the coronary sinus. Serial samples
were taken simultaneously of arterial and coronary venous blood throughout perfusion and
operation, and postoperatively for 3 days. The
fractional concentration of 02 in inspired gas
(F102) was 0.4-0.5 during anesthesia, 0.98 during
perfusion, and 0.4-1.0 from the ventilator after
operation.
Biochemical analyses of blood were performed
as previously outlined,2 for electrolytes (Na, K,
and Ca), osmolality, and energy-producing
substrates: glucose, nonesterified fatty acids
(NEFA), total ketone bodies, lactate, and
pyruvate. Blood gases were determined by
electrodes at 37°C, and temperature corrections
were made when body temperature was below
Circulation, Volume XLIV, August 1971
239
METABOLISM IN FATAL CARDIOGENIC SHOCK
Electrolytes- Nonsurvivors
150
150
1< 1 Anesthesia
|
-1^
Postoperative
1r45
__
__
__
_
~-140////
135
125
305
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*Prime
tPP (005
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-
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120
120
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-
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353Qj
295 353-=~*~°A
:
oArterial
xCoronary sinus
lN
Nonsurvivors
group
-.-:,OAortic
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j
~~ 295
~ ~ ~ ~Normal range
285
275
Downloaded from http://circ.ahajournals.org/ by guest on September 30, 2016
~265
255
I
iii
Pre- k-Perfusion---4
induction
Day 1
I
I
I
2hr
L
L
L....
a.m. p.m. a.m. P.M. a.m. p.m.
-4-3-2-
Figure 1
Plasma sodium was lower during operation, and hyperosmolality was present preterminally
in nonsurvivors.
Abbreviations for all figures: NEFA = nonesterified fatty acids; IRI
immunoreactive
insulin; GIK - glucose-insulin-potassium.
Metobolism-Nonsurvivors
120
' 40
0
Anesthesia
Postoperotive
o Arteriol
xCoronary sinus
1444
1440 l
|
i!
°Nonsurvivors
-I T
'
500
Aortic group
I C-------0Non GIK group
*
,400
-
300
-
X
O
l
l
l l l
2Z00
100
before deth.
O
l
lNormal roange
*Prime
.
3eO- c-Perf usion--of 2hhor
i
induction P
Day 1
am. p.m. acm. p.m. a.m. p.m.
-3-2-4
F'igure 2
Cardiac index
was
mar.kedly low early after operation; growth hormone increased steeply
before death.
36C. Oxygen content of hemoglobin
was
calculated from oxygen saturation. Plasma immuCirculation, Volume XLIV, August 1971
noreactive insulin (IRI)8 and growth hormone'.
concentrations were measured by double antibodv
MOFFITT ET AL.
-240
vate similarly was above control at all
subsequent sample times.
radioimmunoassay. Cardiac output was obtained
by dye dilution, with injection of indocyanine
green via a left atrial catheter and blood sampling
from a catheter in the thoracic aorta.10
Analyses of paired data were performed by the
Student t-test in the nonsurvivor group, comparing arterial to coronary sinus levels at each sample
time and subsequent arterial levels to the control
taken before anesthesia. Comparisons between
arterial levels in the nonsurvivor and survivor
groups were also made (unpaired data) using the
t-test. Only differences significant at the 5% level,
or greater, are reported.
Comparisca
Table 2 focuses on pertinent findings from
the end of operation through the next
morning, when the last preterminal sample
was taken. No differences in arterial oxygenation or acid-base balance were found. Coronary sinus oxygen tension was lower in
nonsurvivors during perfusion and from the
end of operation through the next morning.
Similarly oxygen content was lower in coronary sinus blood of nonsurvivors from the end
of perfusion through 2 hr postoperatively.
Cardiac index in nonsurvivors was lower, and
growth hormone, lactate, and osmolality
higher, on the morning of day 2. Plasma
potassium was higher in nonsurvivors from the
end of operation through the next morning.
Results
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Mean concentrations of variables in arterial
and coronary sinus blood, plus cardiac index,
for both groups are shown in figures 1-5, with
identification of significant arterial-coronary
sinus differences.
Nonsurvivor Group
Mean arterial Po2 (Pao2) remained above the
preanesthetic level all of day 1, while oxygen
content was below control early in perfusion
from hemodilution. Arterial PCo2 (Paco2) was
below and pH above control during perfusion; buffer base was below control 2 hr
postoperatively. Plasma sodium fell during
perfusion, because of dilution. Plasma osmolality, potassium, and calcium became elevated above control on beginning perfusian and
remained so through the morning of day 2,
instead of decreasing shortly after the end of
operation as in the other group. Blood glucose
increased before perfusion without any being
infused; the high level in the priming solution
caused elevated blood levels through the
remainder of day 1. IRI increased from the
end of perfusion through the end of operation.
NEFA were higher than control before and
during perfusion but fell shortly after perfusion. Ketone bodies were elevated before and
during perfusion and became extremely high
preterminally. Growth hormone had two
periods of increase: at the end of operation,
and then an even higher one preterminally on
the next morning. Cardiac index was lower 2
hr postoperatively than before perfusion.
Lactate increased steadily from preperfusion,
with a marked elevation before death. Pyru-
Between Survivor
and Nonsurvivor Groups
Mtetabphism - Nonsurvyof s
Z-0
F*
'l0
Kt~
2400 2000 4- 1600 1200
z
800 E
--
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;t
induction
D
Doy l
-
-2-
-3-
-4-
Figure 3
Ketone bodies were elevated at aU times, and highest
preterminally; NEFA were not different between
groups postoperatively.
Circulation, Volume XLIV, August 1971
241
METABOLISM IN FATAL CARDIOGENIC SHOCK
Survivors vs. Nonsurvivors
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Figure 4
Blood glucose level was higher in nonsurvivors early postoperatively, and both blood glucose
and IRI fell by the next morning.
Metabolism-N onsurvivors
am..
P.M.
-2-
am.
p.m.
-3-
a.m.
p.m.
-4-
Figure 5
Lactate
rose
steadily postoperatively in nonsurvivors, while it fell in survivors.
Circulation, Volume XLIV, August 1971
MOFFITT ET AL.
242
Table 2
Differences Between Groups: Mean Levels and Significance
Variable
Cardiac index
(liters/min/m2)
Osmolality
(mGsm/kg H20)
K (mEq/liter)
Na (mEq/liter)
Glucose
(mg/100 ml)
Insulin (pU/ml)
NEFA (mEq/liter)
Total ketones
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(mg/m1)
Lactate
(mmole/liter)
Pcso2 (mm Hg)
Growth hormone
(ng/ml)
Group
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
Survivors
Nonsurvivors
End of operation
2 hr postop
P < 0.03
3.73
4.47
NS
P < 0.05
280
301
3.80
4.60
NS
153
243
NS
NS
13.2
25.1
3.33
5.84
25.2
17.5
NS
P < 0.05
NS
NS
3.64
4.44
138
133
NS
NS
NS
14.7
24.9
P < 0.05
P < 0.02
P < 0.05
NS
25.2
18.4
NS
Abbreviations: NEFA = nonesterified fatty acids;
nificant; P < 0.05.
P < 0.0o
Pcso, = tension
Sodium remained lower in nonsurvivors,
compared to the level before anesthesia,
through the end of operation. Blood glucose
was higher in nonsurvivors 2 hr postoperatively, with no differences in IRI between groups.
Before perfusion NEFA were more elevated
in the survivor group than in nonsurvivors.
Total ketone bodies remained higher in
nonsurvivors from the end of operation
through the final sampling on the next
morning.
Blood Loss
Mean volume of drainage from chest tubes
from the end of operation until midnight for
the nonsurviving patients was 2,280 ml, while
blood replacement averaged 3,230 ml for that
period. In comparison, mean volume of chest
drainage in the aortic valve replacement
group for the same period was 850 ml.
Discussion
Several factors contributed to the fatal
outcome. These patients were critically ill, in
advanced stages of their disease. In every case
but one, more than replacement of one valve
was required, with five of the perfusions
Morning of day 2
2.18
1.22
NS
NS
P < 0.05
P < 0.05
P < 0.01
NS
NS
40.8
129.1
1.47
9.04
25.4
17.7
7.7
48.8
P < 0.05
P < 0.0o
P < 0.05
P < 0.05
P < 0.02
P < 0.05
of oxygen in coronary sinus; NS = not sig-
lasting over 2 hr. The hearts were grossly
enlarged with reduced contractility. Cardiac
index before perfusion averaged below 2
liters/min, and the sizeable increase in index
seen with stronger hearts after valve replacement did not occur. The mean index 2 hr after
operation, of 1.2 liters/min, revealed the
severity of cardiogenic depression present
early in the interval between operation and
death. All resuscitative measures were ineffective, and ventricular arrhythmias were prominent in the final hours.
Though death was attributed to myocardial
and circulatory failure, an additional critical
factor was excessive bleeding. During and
after these longer perfusions more blood than
usual had to be transfused in the operating
room. Impaired coagulation of blood continued postoperatively. Reopening of the thoracotomy was necessary in one patient and
acute tamponade occurred in another, so that
tamponade may have been primarily responsible for the demise of these two patients. The
mean volume of chest drainage for the first 10
hr was four times that during 24 hr after
multivalvular replacement in another series.'1
Circulation, Volume XLIV, August 1971
METABOLISM IN FATAL CARDIOGENIC SHOCK
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With the circulation precarious from poor
myocardial contractility, the adverse effects on
the heart of large amounts of ACD blood, and
retention of blood in the pericardium, proba-bly served to tip the scale against survival.
Both oxygenation and acid-base balance of
the arterial blood remained satisfactory in
relatively prolonged cardiogenic shock in
patients on ventilators. The extreme degree of
extraction of oxygen by one tissue, the
myocardium, is evident from the low oxygen
content of coronary sinus blood. Little evidence of electrolyte exchanges across the heart
was detected. The only consistent finding was
a higher coronary sinus content of sodium,
possibly due to a loss of water from blood to
myocardium. Evidence of water loss from
blood to the interstitial space, or of solute
entering the plasma, appears in the increased
osmolality postoperatively. Patients progressing well in the first 24 hr after operation
diurese both water and potassium,'2 and often
need extra potassium to avoid or treat
ventricular hyperirritability. However, the
patient in shock develops hemoconcentration,
elevated plasma potassium, high catecholamine levels, and, as in these patients, arrhythmias. Another explanation for the elevated
plasma potassium may be the excessive
amount in the large volume of whole blood
transfused.
The effects of cardiogenic shock on energy
metabolism are multiple, with a host of
interrelated actions and feedback effects.13
Diminution of oxygen supply to cells impairs
oxidative phosphorylation, and the severe
preterminal rise in lactate attests to the high
rate of anaerobic metabolism of glucose and
glycogen. Patients with an adequate circulation began to reduce their arterial levels of
lactate and pyruvate by the end of operation.
Those who died within 24 hr continued to
increase their arterial lactate levels and to lose
pyruvate from the myocardium up to the time
of their death.
Blood levels of the catecholamines increase
with various stresses, including open-heart
surgery.'4 Growth hormone also is released in
greater amounts during stress15 as well as in
Circulation, Volume XLIV, August 1971
243
hypoglycemia, exercise, and fasting.16 Growth
hormone values in these patients in cardiogenic shock became five times normal before
death. According to Randle and associates,'7
the body uses for energy predominantly
glucose or lipid, depending on glucose intake
or hormonal stimulation. The stress hormones
stimulate lipid mobilization tending to elevate
circulating levels of NEFA. With unavailability or underuse of carbohydrate, ketone bodies
are produced in the liver'8 from acetyl
coenzyme A that cannot enter the Krebs cycle.
The severe ketosis before death shows the
high rate of NEFA metabolism in the liver,
with ketone bodies produced faster than other
tissues could use them. Accumulation of
NEFA, unbound to protein, in hypoxic
myocardial cells is hypothesized as causing
arrhythmias after acute infarction.19 Certainly
our nonsurvivors suffered severe NEFA mobilization and had ventricular arrhythmias in
their final hours.
The stress hormones enhance glycogenolysis
in the liver and muscles, possibly accounting
for the higher blood glucose levels toward the
end of operation in nonsurvivors than in
survivors. The pancreas was still able to
respond with a high rate of IRI release, or the
rate of its inactivation may have been slowed.
However, on the next morning, after hours of
inadequate circulation, both blood glucose
and IRI had fallen. The catecholamines
inhibit both IRI release20 and its effects in the
cell. By this time glucose and glycogen
supplies were likely depleted from the massive
production of lactate. Central to the concept
of the glucose-fatty acid cycle is that NEFA
and ketone bodies inhibit glucose uptake by
muscle.17 During operation the myocardium
used NEFA, ketone bodies, and lactate, but a
significant arteriovenous difference of glucose
was not found. With both blood glucose and
IRI reaching low levels in shock, with IRI
activity depressed in cardiogenic shock,21 and
with the known ability of IRI to decrease
mobilization of fat,'6 the administration of
additional glucose to these patients, possibly
also with insulin, may be an effective method
of treatment.
MOFFITT ET AL.
244
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The relative lack of changes in the constituents of blood early in cardiogenic shock that
might help in predicting prognosis and in
treatment is disappointing. Many findings
were similar in patients doing well and those
with low output, until just before death.
Arterial oxygenation and acid-base balance
remained satisfatory as long as sampled.
Sodium and calcium levels were not different.
Neither were fatty acid, blood glucose, or IRI
concentrations of help in this regard. Both
growth hormone and total ketone bodies rose
severely but only shortly before death. However, a few positive signs did appear early
after operation. Plasma potassium remained
in normal range. Osmolality remained elevated instead of falling, at the end of operatior,
in patients who died within 24 hr, indicating a
deteriorating circulation. A rising, instead of a
falling, lactate concentration without pyruvate
change, in the early postoperative hours,
reflected the low cardiac output at that time.
Both the high lactate and low cardiac output
were grave prognostic signs. Serial monitoring
of cardiac output is probably the most
valuable measurement in anticipating a grave
prognosis and in evaluating the effect of
therapeutic efforts.
Acknowledgments
The valuable help of Mrs. Rita M. Nelson, Mrs.
Peggy S. Quimby, and Mr. A. Paul Servick is
acknowledged.
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Myocardial metabolism in children having
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4. MOFFITT EA, ROSEvEAx JW, McGOoN DC:
Myocardial metabolism during and after mitral
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5. Mormirr EA, ROSEzEAR JW, TARHAN S, MCGOON DC: Myocardial metabolism during and
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Cwrc*ati,a, Vo4,e XLIV, Aagost 1971
Myocardial and Body Metabolism in Fatal Cardiogenic Shock after Valvular
Replacement
EMERSON A. MOFFITT, GEORGE D. MOLNAR and DWIGHT C. MCGOON
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Circulation. 1971;44:237-244
doi: 10.1161/01.CIR.44.2.237
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX
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Copyright © 1971 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
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KINOSHITA, KOBAYASHI
538
It is known that, when the vectorcardiogram is observed in a single plane, the
greatest accuracy in interpretation is attained
by using the horizontal plane.4 In order to
obtain the "color vectorcardiogram," therefore, a vector loop in the horizontal plane was
usually employed. In cases in which the
amplitude of the deflection in the Y axis was
unusually large or unusually small, the sensibility to the voltage in the Y axis was
respectively decreased or increased to such an
extent that differences in color of the spots
could be readily appreciated.
We think that the use of these procedures,
as compared with the use of three-plane
vectorcardiograms, can remove the abovementioned complication in the graphic inter-
pretation, without greatly diminishing the
accuracy.
References
1. CRONVICH JA, ABILDSKOV JA, JACKSON CE,
BURCH GE: An approximate derivation for
stereoscopic vectorcardiograms with the equilateral tetrahedron. Circulation 2: 126, 1950
2. GUYTON AC, CRowELL JW: A stereovectorcardiograph. J Lab Clin Med 40: 726, 1952
3. KWnosm'rA S, KOBAYASHI T: The "color
vectorcardiogram": Its study with an apparatus
for spatial representation by coloring. Shinzo
(Heart) In press (in Japanese)
4. HAYASHI H, YoKoI M, AmIARA N, OKAMOTO N,
MizUNo Y, YASUI S, OKAJIMA H, IwAzuxA T,
YAMADA K: Comparison in diagnostic accuracy
between each of three plane vectorcardiograms. Shinzo (Heart) 2: 889, 1970 (in
Japanese)
Correction
Moffitt EA, Molnar GD, McGoon DC: Circulation
44: 237, 1971. Legends for figures 2 and 4 are reversed.
Circulation, Volume XLIV, October 1971
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