Left Ventricular Function in Acute Myocardial

Infarction and its Clinical Significance

By CHARLES E. RACKLEY, M.D., AND RICHARD 0. RUSSELL, JR., M.D.

SUMMARY
Investigations on left ventricular function in patients with acute myocardial infarc-
tion and the relatonship to clinical findings have shown: (1) limitations in the use and
interpretation of central venous pressure; (2) pulmonary artery end-diastolic pressure
accurately reflects left ventricular filling pressure in the absence of pulmonary vascular
or mitral valve disease; (3) left ventricular filling pressure is frequently elevated in
mild or clinical uncomplicated infarction; (4) left ventricular function frequently im-
proves during the immediate as well as late convalescent period; (5) the hemodynamic
and clinical evaluations may frequently be at variance; (6) a left ventricular gallop is
usually associated with an abnormally elevated left ventricular filling pressure; (7)
anterior infarctions present greater depression of left ventricular function than inferior
infarctions; and (8) monitoring of hemodynamics can be useful in following the
changes in left ventricular function and the response to therapy in patients with heart
failure and cardiogenic shock.

T HE EVALUATION of patients sustain- findings to the clinical situation in patients

ing an acute myocardial infarction has with acute myocardial infarction.
traditionally involved the description of symp-
Methods
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toms, observations on physical examination,

review of the electrocardiogram, radiographic
assessment of the heart and lungs, and various
laboratory determinations. During the past 20
years hemodynamic measurements from the
right heart, pulmonary circulation, and left
heart have been reported in patients with
acute myocardial infarction. This information
has proved useful in understanding the extent
of altered cardiovascular function, classifying
the severity of the clinical state, measuring the
response to various forms of treatment, and
predicting the prognosis and survival of the
patient. The objective of the present review is
to describe the methods employed for acquir-
ing hemodynamic data, the various findings in
the right heart, pulmonary circulation and left
heart, and the relationship of hemodynamic
From the Cardiovascular Research and Training
Center, Division of Cardiology, Department of
Medicine, University of Alabama, Birmingham, Ala-
bama.
Supported in part by Contract PH 43-67-1441 with
the National Institutes of Health.
Circulation, Volume XLV, January 1972
Techniques utilizing standard cardiac catheter-
ization procedures have been employed to obtain
hemodynamic information from the right and left
heart in patients with acute myocardial infarction.
Catheters have been introduced by the percuta-
neous technique and advanced to the superior
vena cava, right atrium, right ventricle, and
pulmonary artery to record pressure. A significant
development has been the introduction of the
Swan-Ganz balloon-tipped catheter for obtaining
hemodynamic information in patients with acute
myocardial infarction.' This catheter does not
require fluoroscopy and can be advanced with
pressure monitoring to the right atrium, where the
small balloon is inflated, and the balloon flow
directs the catheter into the pulmonary artery
position. Once in the pulmonary artery the
catheter can be deflated and then advanced and
reinflated to obtain pulmonary capillary or wedge
pressure.
Hemodynamic data have also been obtained
from the left heart in patients with acute
myocardial infarction, and several catheterization
techniques have been used. One study involved
transseptal catheterization with recording of left
atrial pressure in patients with acute myocardial
infarction.2 This approach required percutaneous
entry into the right femoral vein and advance-
ment of the catheter and transseptal needle from
231
 232
the right atrium into the left atrium. Other studies
have employed percutaneous puncture of the
femoral artery and retrograde passage of the
catheter into the left ventricle. A preformed
catheter has been developed which permits blind
entry into the left ventricle by this retrograde
technique and requires only electrocardiographic
monitoring.3 Additional approaches include per-
cutaneous entry or open arteriotomy of the
brachial artery with advancement of catheters
into the left ventricle.
The measurement of cardiac output in patients
with acute myocardial infarction has involved
standard catheterization procedures as well as
noninvasive methods. The standard indicator-
dilution technique has been employed with the
dye being injected on the right side of the
circulation and sampled from a peripheral artery.
The Fick method has also been used with
arteriovenous oxygen difference obtained from the
pulmonary artery and a systemic artery with
simultaneous measurement of oxygen consump-
tion. The radioisotope method has been employed
with precordial counting for the estimation of
cardiac output in patients with acute infarction.4
Recently, techniques have been developed for
measuring cardiac output with the use of thermal
indicators, which are injected into the right
atrium with sampling from the pulmonary artery
through a single catheter.5 The noninvasive
technique of ultrasound has been applied in
Downloaded from http://ahajournals.org by on May 11, 2020
patients with acute infarction to estimate stroke
volume and cardiac output.6
Cardiovascular Dynamics
Central Venous Pressure: Venous pressure
measurements have been recorded for several
years in patients with acute myocardial
infarction. In earlier studies measurements
were obtained from an antecubital vein, but in
more recent studies central venous pressure
has been measured directly in the right
atrium. Freis and co-workers7 initially report-
ed venous pressure of 90 mm H20 in patients
with mild myocardial infarction. Patients with
severe infarction were found to have an
average venous pressure of 120 mm H20, and
those in shock had a pressure of 115 mm H20.
These investigators concluded that an increase
in venoconstriction produced an increase in
venous filling pressure in the presence of the
failing heart. Gilbert and associates8 recorded
venous pressure in 20 patients with myocar-
dial infarction, and in mild uncomplicated
infarction the venous pressure was 130 mm
RACKLEY, RUSSELL
H20. In patients with failure the venous
pressure was elevated to 167 mm H20, and
those in shock exhibited an average venous
pressure of 215 mm H20. Gammill and co-
workers9 reported a much narrower range for
venous pressure in patients with acute infarc-
tion. These investigators found patients with
mild infarctions to have an average value of
102 mm H20, while those in heart failure
displayed values of 114, and those in shock
124 mm H20, respectively.
Gunnar and his group10 recorded central
venous pressure in 23 patients in acute
myocardial infarction, 12 of whom presented
in cardiogenic shock. Measurements in two of
the 11 patients without shock revealed a
central venous pressure of 4 and 23 mm Hg,
while the 12 patients in shock revealed central
venous pressures ranging from 0.5 to 22 mm
Hg, with a mean value of 7.9. Smith et al.1"
reported two of 14 patients with cardiogenic
shock in myocardial infarction having a
central venous pressure less than 6 mm Hg. In
15 patients with acute myocardial infarction,
McKenzie and co-workers12 found the right
atrial pressure ranging from 5 to 14 mm Hg in
nine patients without shock, while in six
patients with shock values varied from 13 to
22 mm Hg. Weil and Shubin"3 reported a
central venous pressure of 9.3 mm Hg in 20
patients with acute myocardial infarction and
shock, but in seven patients the value
exceeded 10 mm Hg. Cohn et al.14 studied
nine patients in shock with acute myocardial
infarction and described a range of central
venous pressure from -6 to +6 mm Hg, and
only two patients had values of 5 and 6 mm
Hg. During the infusion of 500 ml of dextran,
elevation in right atrial pressure paralleled left
atrial pressure. Collins and co-workers15 found
the central venous pressure elevated in 21 of
25 patients presenting acute myocardial in-
farction.
The mechanism for the elevation of central
venous pressure in acute infarction has been
explained by venoconstriction, alterations in
effective blood volume, and the development
of heart failure. Nixon and his group'6
proposed dominance of venoconstriction in
Circulation, Volume XLV, January 1972
 LEFT VENTRICULAR FUNCTION IN MI
the elevation of central venous pressure in
acute infarction, but Cohn et al.17 suggested a
relationship between central venous pressure
and left ventricular filling pressure. However,
Hamosh and Cohn'8 have more recently
compared right atrial pressures to the left
ventricular end-diastolic pressure in 40 pa-
tients with acute myocardial infarction and
demonstrated a lack of correlation. Rapaport
and Scheinman19 studied right heart and
pulmonary dynamics in 24 patients with acute
infarction and demonstrated a poor correla-
tion between changes in central venous
pressure and pulmonary artery end-diastolic
pressure. Therefore, the central venous pres-
sure is not regarded as an accurate reflection
of the filling pressure in the left ventricle in
acute myocardial infarction.
Pulmonary Artery Dynamics: Pulmonary
artery pressure has been recorded in patients
with acute myocardial infarction. Fluck and
associates20 found the pulmonary artery pres-
sure abnormally elevated in 21 of 26 patients.
Rutherford and associates21 measured pulmo-
nary artery pressure in 25 patients and found
eight patients with normal mean pulmonary
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artery pressure, while 16 had abnormal
elevations of the mean pressure, and one
patient presented a low mean pressure in the
pulmonary artery. Hunt and associates22
described the risks in measuring pulmonary
artery pressure, as well as methods for
reducing complications. Since the Swan-Ganz
catheter can be advanced to the pulmonary
artery with considerable ease, pulmonary
artery pressure can be measured in patients
with acute infarction, and abnormal elevations
have been found more frequently than eleva-
tions of central venous pressure.
By advancing a catheter in the pulmonary
artery, a wedge or capillary pressure can be
recorded, which has been shown to reflect
mean left atrial pressure. Clinical studies in
various forms of heart disease have demon-
strated that the capillary wedge pressure
accurately reflects the mean pressure in the
left atrium, and in the absence of mitral valve
obstruction the left ventricular end-diastolic
pressure.23 24 Experimentally, heart rates must
Circulation, Volume XLV, January 1972
233
exceed 160-180 beats per minute before a
discrepancy develops between mean left atrial
pressure and left ventricular end-diastolic
pressure.25 Lassers and co-workers26 studied
30 patients with acute myocardial infarction
complicated by advanced forms of heart
block. The mean pulmonary arterial wedge
pressure in this group of complicated infarcts
ranged from 4 to 37 mm Hg, and in 24
patients exceeded the 12 mm Hg, the upper
limit of normal.
In addition to measurements of pulmonary
artery systolic pressure, mean pressure, and
wedge pressure, the diastolic pressure of the
pulmonary artery has also been used as an
indication of left ventricular filling pressure.
Kaltman and co-workers27 studied 47 patients
with congenital and acquired heart disease
and demonstrated a relationship between
pulmonary artery end-diastolic and left ven-
tricular end-diastolic pressures over a range of
5 to 20 mm Hg. In two patients with severe
elevations of left ventricular end-diastolic
pressure the linear relationship was still main-
tained with pulmonary artery end-diastolic
pressure. Hunt and co-workers22 described
simultaneous measurements of pulmonary ar-
tery and left ventricular end-diastolic pressures
in five patients with acute infarction, and re-
ported a linear relationship ranging from 5 to
20 mm Hg. Jenkins and associates28 evaluated
the pulmonary artery end-diastolic pressure as
an indirect estimate of mean left atrial pressure
in 28 patients with acute and chronic disease.
These investigators demonstrated a linear re-
lationship between pulmonary artery end-dias-
tolic pressure and left atrial mean pressure
with normal pulmonary vascular resistance.
However, with abnormal increases in pulmo-
nary vascular resistance, the relationship was
somewhat altered. Even in the presence of
elevated pulmonary vascular resistance, direc-
tional changes still occurred between pulmo-
nary artery end-diastolic and mean left atrial
pressure. Pulmonary artery end-diastolic pres-
sure did not exceed left atrial mean pressure in
any instance. Finally, acute hypoxia and aci-
dosis may exert important effects upon pulmo-
nary artery pressure and must be corrected
 234
before interpretations of left ventricular hemo-
dynamics are made from pulmonary artery
end-diastolic pressure.
Nevertheless, debate persists over the use of
pulmonary artery end-diastolic pressure as an
accurate measure of left ventricular filling
pressure. Falicov and Resnekov29 compared
these two pressures in 71 patients with chronic
heart disease and found a relationship be-
tween pulmonary end-diastolic pressure and
pulmonary artery mean wedge pressure. How-
ever, the pulmonary artery end-diastolic pres-
sure failed to reflect accurately left ventricular
end-diastolic pressure. These investigators did
report a relationship between the A wave in
the pulmonary artery pressure and the left
ventricular end-diastolic pressure. Bouchard
and others30 further demonstrated a discrep-
ancy in pulmonary artery end-diastolic and
left ventricular end-diastolic pressures in
chronic heart disease, and the difference was
further aggravated with the use of various
pharmacologic agents.
The pulmonary artery end-diastolic pressure
has been reported to be abnormally elevated
in approximately 505; of patients with un-
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complicated myocardial infaretion exhibiting
no clinical evidence of left ventricular
failure.31 32, 3 Patients in heart failure consis-
tently demonstrate abnormal elevations in
end-diastolic pressure, but the range is large.
However, patients in cardiogenic shock fre-
quently present severely elevated pulmonary
artery end-diastolic pressures, but on occasion
may exhibit normal or slightly elevated pres-
sures.
Left Heart Dynamics: Physiologists and
investigators have interpreted the level of left
ventricular filling pressure as a reflection of
cardiac performance. In various forms of
chronic heart disease the left ventricular end-
diastolic pressure may be altered by a variety
of mechanisms and cannot be used as a
uniform index of cardiac performance.34 3
Nevertheless, in acute heart failure the eleva-
tion of filling pressure of the left ventricle may
still parallel the end-diastolic pressure-volume
relationship. Left atrial and left ventricular
pressures have been recorded in patients with
RACKLEY, RUSSELL
acute myocardial infarction. Kirby et al.30
reported right and left heart pressures in two
patients with acute myocardial infarction.
Right atrial pressures were 12 and 17 mm Hg,
while left ventricular end-diastolic pressures
were 23 and 33 mm Hg, respectively, in these
two patients. Both these patients presented
clinical evidence of left heart failure. Later,
Nixon and associates2 recorded a left atrial
pressure of 10 mm Hg in myocardial infarc-
tion and shock, and the patient responded
dramatically to volume expansion. Nixon37
subsequently reported a patient with acute
pulmonary edema in myocardial infaretion
with a left ventricular end-diastolic pressure
ranging from 3 to 5 mm Hg. These observa-
tions on left ventricular filling pressure in
cardiogenic shock demonstrated that pressures
could be low, normal, or severely elevated.
Furthermore, the lack of significant linear
correlation between right atrial and left
ventricular end-diastolic pressure in acute
myocardial infarction indicated the necessity
for recording left ventricular filling pressure in
patients with heart failure or cardiogenic
shock. Hamosh and Cohnl8 performed left
ventricular catheterization, and recorded pres-
sure in 40 patients with acute myocardial
infarction. In 14 patients without evidence of
heart failure, left ventricular end-diastolic
pressure ranged from 6 to 22.5 with a mean of
15 mm Hg. In 12 patients with heart failure
the filling pressure ranged from 19 to 40, with
a mean value of 29.9 mm Hg. In 12 patients in
cardiogenic shock the left ventricular end-
diastolic pressure ranged from 8 to 34, with a
mean value of 21.1 mm Hg. This study
indicated that measurements of left ventricu-
lar end-diastolic pressure were similar to
previous observations on pulmonary artery
end-diastolic pressure, in that patients with
uncomplicated infaretion frequently exhibited
abnormal elevations. On the other hand, heart
failure was associated with severe elevations,
and shock revealed a range from mild to
severe elevations.
Cardiac Output: Although it was initially
suspected that cardiac output was significantly
reduced in all patients with myocardial
Circulation, Volume XLV, January 1972
 LEFT VENTRICULAR FUNCTION IN MI
infarction, a range of values has been reported
by various investigators. The indicator-dilu-
tion technique has been the most frequently
employed method for measuring cardiac
output in acute myocardial infarction. Oriol
and McGregor38 have cautioned against the
possible errors in measuring output by the
indicator-dilution method in patients with
shock. Errors can be introduced by a pro-
longed sampling time and are due in part to
recirculation. However, acceptable accuracy
can be obtained by injecting in the pulmo-
nary artery and sampling at a closer systemic
arterial site. Freis and associates7 found a
normal cardiac index averaging 3.4 liters/min/
m2 in patients with mild myocardial infarc-
tion, while those patients with severe infarc-
tions had reduced average index of 2.9
liters/min/m2, and in cardiogenic shock even
lower values of 1.8 liters/min/m2. Similar
values were reported by Gilbert and co-
workers8 in mild infarction, as well as in heart
failure, and shock groups with cardiac indices
of 2.6, 1.9, and 1.0 liters/min/m2, respectively.
Gammill and associates9 reported cardiac-
index values of 4.3 liters/min/m2 in patients
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with uncomplicated infarction, while those
with severe infarction and shock had values of
2.9 liters/min/m2. Patients with intermediate
complications exhibited an average index of
3.2 liters/min/m2. Brock and co-workers39 in
1959 similarly reported cardiac-index values of
3.03 in uncomplicated infarction, and those
with circulatory failure possessed reduced
indices averaging 2.04 liters/min/m2. Fluck
and co-workers20 reported cardiac outputs in
seven patients in acute infarction ranging
from 2.5 to 5.5 liters/min/m2. Gunnar and co-
workers'0 measured cardiac output in 23
patients with acute infarction, 12 of whom
had cardiogenic shock. In the 11 patients
without shock the mean index was 3.8. The 12
patients with shock were divided into two
groups of six patients each. In the six patients
with high peripheral vascular resistance the
average index was 1.66, while in the other six
patients with low resistance values the index
was 2.65 liters/min/m2. In nine patients with
infarction and shock studied by Cohn et al.14
(irculation, Volume XLV, January 1972
235
the average output was 3.2, while Weil and
Shubin13 found a mean cardiac index of 1.3 in
20 patients with shock and infarction. Ramo
and associates40 measured cardiac output in
patients with uncomplicated infarctions as
well as those in mild heart failure, pulmonary
edema, and cardiogenic shock and observed a
wide range of values in each group. Russell
and associateS41 measured cardiac indices in
19 patients with myocardial infarction, and
values ranged from 1.0 to 4.0 liters/min/m2 in
a series that included uncomplicated patients
as well as those with heart failure and
cardiogenic shock. Hamosh and Cohn'8
studied 40 patients with infarction and includ-
ed 14 without complications, 12 in heart
failure, and 14 in shock. Average cardiac index
in the uncomplicated group was 2.98 liters/
min/m2, with values of 2.63 and 1.59 liters/
min/m2 in the heart-failure and shock groups,
respectively. Rutherford and associates2'
studied 25 patients and found eight patients
with a cardiac index greater than 3.0 among
those with a normal mean pulmonary artery
pressure, and a cardiac index less than 3.0
liters/min/m2 in 12 patients with an elevated
mean pulmonary artery pressure.
Peripheral Resistance: Since the measure-
ment of systemic peripheral vascular resis-
tance is determined by the measurements of
pressure and cardiac output, the values
obtained in patients with acute myocardial
infarction exhibit considerable variation espe-
cially in those patients with heart failure and
cardiogenic shock. Freis and co-workers7
reported an average calculated peripheral
vascular resistance of 1175 dynes-sec-cm-5 in
four patients with mild infarction. In five
patients with moderately severe infarction the
vascular resistance was 1325, and in four
patients with cardiogenic shock the value was
2050 dynes-sec-cm-5. Similar values were
reported by Gilbert and co-workers8 in studies
on 20 patients with acute myocardial infarc-
tion. Thirteen patients without shock had a
range of resistance values from 1300 to 3600
dynes-sec-cm-5, while seven patients in shock
exhibited values ranging from 1600 to 3900
 236
dynes-sec-cm-5 . Gammill and his group' re-
ported in patients with mild infarction an
average value of 1272, while in patients with
moderately severe infarction the value was
1555, and in those with shock the measure-
ment was 1781 dynes-sec-cm-5. Sixteen of
these 39 patients were restudied 4 weeks after
admission, and an average decrease in periph-
eral vascular resistance of 373 dynes-sec-cm-8
was recorded, which was attributed to a fall in
blood pressure during the convalescent period.
Gunnar et al.10 studied 23 patients, 12 of
whom were in shock with acute myocardial
infarction. In the 11 patients without shock
the vascular resistance was 26 mm Hg/liter/
min. In 12 patients with cardiogenic shock six
had resistance values from 21 to 97, while the
remainder of the group had values ranging
from 12 to 17. In the study of Cohn et al.14 in
nine patients with shock resulting from
infarction, vascular resistance varied from 703
to 4176 dynes-sec-cm-5. Weil and Shubin13 in
their evaluation of 20 patients with infarction
reported an average value of 2042 826
dynes-sec-cm-5. Therefore, in patients with
acute myocardial infarction the peripheral
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vascular resistance does vary over a wide
range, but there is a definite tendency for
patients with uncomplicated infarctions to
have lower resistance values than in those
patients with heart failure who have elevated
values. Patients who develop shock with acute-
infarction may have normal or severely
elevated values for peripheral vascular resis-
tance.
Left Ventricular Function: Although the
measurement of intracardiac pressures and
flow represent the mechanical performance of
the heart, studies have been performed in
recent years that utilized interventions to alter
cardiac performance and thereby derive a
measure of left ventricular function based on
the response to the intervention. The initial
observation of Nixon et al.2 in a patient with
cardiogenic shock and a normal left ventricu-
lar filling pressure supported earlier physiolog-
ic hypotheses that relative hypovolemia might
be operative in cardiogenic shock, and this
was further substantiated by the dramatic
RACKLEY, RUSSELL
response to volume expansion. Cohn and
associates14 infused low molecular weight
dextran in patients with cardiogenic shock and
related filling pressures to cardiac output
before and after volume expansion. They
concluded that an increase in filling pressure
of 3 cm of H20/ 100 ml of dextran infused was
abnormal and suggested a flat portion of a
ventricular function curve. Russell and co-
workers41 evaluated the effects of raising the
left ventricular filling pressure in 19 patients
with acute myocardial infarction. Ventricular-
function curves were described by relating
cardiac output, stroke index, stroke work, or
stroke power to the left ventricular filling
pressure before and during serial infusions of
low molecular weight dextran (fig. 1). A
spectrum of function curves was described,
and in six patients a descending limb of the
function curve represented a fall in cardiac
output with further increase in filling pressure,
which accompanied the infusion of low
molecular weight dextran (fig. 2). Russell and
his co-workers4' identified the optimum filling
pressure of the left ventricle in patients with
acute myocardial infarction between 20 and
24 mm Hg, which tended to produce the
highest cardiac output in these patients.
Bradley and co-workers42 compared right and
left ventriclar-function curves in six patients
with acute myocardial infarction and shock.
These investigators found.that a small increase
in right atrial pressure could produce consid-
erable increases in left atrial pressure and
resultant improvement in left ventricular
performance. Similarly, small decreases in
right atrial pressure could result in large
decreases in left atrial pressure. In addition to
the possible benefits of reducing sludging and
platelet coagulation, low molecular weight
dextran does provide volume expansion with a
modest stretch on the left ventricle in patients
with acute infarction. The effects of the low
molecular weight dextran infused rapidly in
amounts of 400-600 ml have been observed to
persist for 6-9 hours in patients with acute
infarction (fig. 3). Further observations on
ventricular function were made by Scheidt
and associates43 who calculated cardiac work
Circulation, Volume XLV, January 1972
 LEFT VENTRICULAR FUNCTION IN MI 237
patient: T. A. Acute MI tLMWOJ 250
m
0

5.0 r m
50.0 1-0
ASI m=
* SWI 200 M --Z
m
sha.
a SPI
C
4.0 -40.0
m
._
-J
150
a Lair
A

3.0 L."
= 30.0 W
LA."
m

a2.0 20.0

1.0 Heart Rate 10.0 - Heart Rate

_ 103 c=
C^ 103
110 100 103 110 100 103
. a I 11'
1 a 1 1 1I'
0 10 20 0 10 20
PA DIASTOLIC PRESSURE am
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Figure 1
Left ventricular function curves in a patient with acute myocardial infarction. On the left
cardiac output and on the right stroke index, stroke work index, and stroke power are related
to pulmonary artery end-diastolic pressure. The patient received 600 ml low molecular weight
dextran in 200-ml increments. (Reprinted from J Clin Invest,4' by permission.)

from mean left ventricular systolic pressure,
left ventricular end-diastolic pressure, and
cardiac output in 38 patients with acute
myocardial infarction. Survivors had mean
cardiac-work values of 5.8 kg-m/min, while
the nonsurvivors had values of 2.1 kg-m/min.
Hemodynamic Monitoring: Not only have
the basic measurements of intravascular pres-
sures and cardiac output been recorded in
patients with myocardial infarction, but serial
measurements have been made over periods
of 24 hours to several days. Shillingford and
Thomas44 reported measurements of cardiac
output, brachial arterial pressures, stroke
volume, peripheral resistance, and heart rate
during the initial 3 days of acute infarction in
four patients. Subsequent observations were
Circulation, Volume XLV, January 1972
made in 6-10 days and in 3-4 weeks after the
acute infarction, and improvement was shown
for cardiac output in these four patients.
Later, Fluck and co-workers20 recorded serial
measurements of pulmonary artery systolic
pressure in 22 episodes of acute infarction
during the initial 6 days. In six surviving
patients pulmonary artery systolic pressure
returned to normal at the end of the sixth day,
and similar trends toward normal for the right
ventricular end-diastolic pressure were also
observed by these investigators. Weil and
Shubin13 in their study of 20 patients with
cardiogenic shock and infarction monitored
hemodynamic changes during the initial 24
hours, and survivors were characterized by an
increase in mean arterial pressure with a
 238 RACKLEY, RUSSELL
CRITICL RAISE eF FLLIES PRESSURE
PATIENTS WITH SIHLE STO _ IOSmiSS
PATENTS Wf ly

S..F- Ang
0 to
AI 7.0
af*

"
1I-
--fil "s l

c 20.0

10.0 /

W ,X A
ramakinsummi . LI
a a a1
LEFT RUIAR M MnU ARER E-IAUC PRES m

Figure 2
A composite of left ventricular function curves in patients with acute myocardial infarction.
An increase in stroke index generally continued until left ventricular filling pressure reached
Downloaded from http://ahajournals.org by on May 11, 2020

20-24 mm Hg (solid curves), and beyond this pressure the curves tended to fltten or decrease
(dashed lines). On the right the first and second function curves in a patient are numbered
1 and 2. A star identified each of the five curves whose ratio A stroke index /,A flling pres-
sure was less than 0.30 ml/mm Hg. (Reprinted from J Clin Invest,41 by permission.)

commensurate fall in peripheral vascular dextran. These studies suggested that signffi-
resistance. Hunt and associates" emphasized cant improvement in the hemodynamic func-
the usefulness of monitoring pulmonary artery tion of the left ventricle occurred in the first 3
pressure in acute myocardial infarction to days of myocardial infarction. Rutherford and
measure not only systolic pressure, but also
associates2' have also advocated the value of
end-diastolic pressure. Russell and co-work- monitoring pulmonary artery pressure in acute
ers41 monitored hemodynamic measurements
serially in patients with acute myocardial infarction for the early detection of left
infarction and assessed left ventricular func- ventricular failure. In 25 patients flow-direct-
tion during the first 3 days with the infusion of ed pulmonary artery catheters remained in
low molecular weight dextran (fig. 4). In six place for 4-5 days, and these investigators
patients with ventricular-function curves re- reported that the mean pulmonary artery
corded on days 1, 2, and 3 after the infarction, pressure was consistently elevated prior to the
hemodynamic improvement was demonstrat- usual clinical signs of left ventricular failure.
ed by a shift of the function curve upward Furthermore, the monitoring of mean puhin-
and to the left. On days 2 and 3 after the nary artery pressure provided a guide to
infarction the patients responded with a larger pharmacologic therapy. Porter and asso-
increase in cardiac output than elevation in ciates45 illustrated the usefulness of pulmonary
filling pressure for the same amount of infused artery pressure monitoring in a patient with
Circulation, Volume XLV, January 1972
 LEFT VENTRICULAR FUNCTION IN MI 239
PERSISTENCE OF LMWD INDUCED CHANGES
patient: M . P. day 1 day3
L/mr in/M2 LMWD

-I

C,,
co
C= C-)
09
CL
LAJ
>.
LAJ

aiJ
9=
2.0

20O
0 L.
mm Hg

nU
I _
ILMWD

A I
-
E
A
A

lo
p
AI'

I I 0 l
12 1 4 8 12 4 8
PM PM
TIME OF DAY
Figure 3
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The persistence of changes induced by low molecular weight dextran in a patient is shown
on day 1 and day 3 after acute infarction. The cardiac index increased with LMWD and
returned to control levels over a 6-9-hour period. (Reprinted from J Clin Invest,41 by per-
mission.)
cardiogenic shock due to a ruptured ventricu- pulmonary artery pressure in patients with
lar septum, and pressures were measured for a severe diaphragmatic infarction.20 However,
period of 10 days. In this patient the the more frequent hemodynamic abnormality
monitored pulmonary artery diastolic pressure is that of an elevated left ventricular filling
proved to be an extremely useful guide for pressure in association with a normal central
pharmacologic intervention and later enabled venous pressure. The disparity between cen-
the patient to undergo successful cardiac tral venous pressure and left ventricular filling
surgery. pressure is exaggerated with the infusion of
low molecular weight dextran and the expan-
Clinical Significance sion of blood volume. Therefore, the limita-
Although the central venous pressure has tions of central venous pressure monitoring in
been advocated as a useful guide for the acute myocardial infarction must be appre-
assessment of the blood volume in certain ciated. The central venous pressure can be
forms of shock, studies have now demonstrat- misleading in the recognition, monitoring, and
ed that the central venous pressure does not evaluation of pharmacologic interventions in
accurately reflect the left ventricular filling patients with heart failure or shock complicat-
pressure in patients with acute myocardial ing acute myocardial infarction. Ramo and
infarction. On occasion the central venous associates40 were not able to correlate rales or
pressure may be elevated with a normal left ventricular gallop with elevations in right
Circulation, Volume XLV, January 1972
 240 RACKLEY, RUSSELL
CIRCULATORY FUNCTION CURVES COMPARISON CARDIAC INDEX
* AT a*R 2 A DAY 3
5.0 9attell U P 5.51 alitul C o1*

4.0 40

.c

30 1-
3.0
A *
20 2.0

1.0 1.0

As9 199 111 192 92 A 95 11 98 102

9IA31 RATE I13 1i - *s 9E93T RATE mile9 9137 95 95
0 10 20 30 0 10 20 30 4*A. n
PA END DIASTOLIC PRESS1 RE me Hg PA END DIASTOLIC PRESSURE mm Hg
A,

4.0 pati,el * C 4.0

pat't;e R a

.L'
3.0 *. ._i, 4
/" v-
.7
2.0 = 2.0
1 2
-M

i.0 1.0

132
Downloaded from http://ahajournals.org by on May 11, 2020

A 92 $a 92 It A 99 103
ullt RATE 30 .* 179 As 92 * 3 l11 i1 ' 101 IDIai
' !t
I0 23 30 0 10 2030 49
PA EUI-IIASTILIC PRESSUIE a ig PA EllAIASTSLIC P3ESSI E ME Hg

Figure 4
Serial ventricular function curves are displayed in four patients on days 1, 2, and 3 after
acute infarction. During convalescence the repeat function curve for each patient demon-
strated a higher cardiac index and a lower pulmonary artery end-diastolic pressure. (Reprinted
from J Clin Invest,41 by permission.)

atrial pressure. Similarly, Collins and co-
workers'5 found little correlation between the
central venous pressure and X-ray evidence of
pulmonary edema. An elevated central venous
pressure was associated with serious cardiac
arrhythmias and posterior infarctions, and
when this was greater than 20
fatal outcome was experienced. Therefore,
these studies indicate that the right atrial
pressure is not a sensitive measure of left
ventricular function in patients with acute
myocardial infarction.
The measurement of pulmonary artery
pressures has been useful in assessing the
extent of impairment of left ventricular
function. Lassers and associates26 reported
similar values for pulmonary artery wedge
pressures in those patients presenting with
dyspnea as well as those who were not
dyspneic. In addition, the mean pulmonary
artery wedge pressure was not significantly
cm of H20 a different in those patients with or without
pulmonary basilar rales. Fluck and his group20
observed that the presence of an elevated
pulmonary artery pressure during the acute
stage of infarction proved of prognostic value,
and with prolonged elevations five deaths
were reported in 21 episodes. The persistence
of an elevated pulmonary artery pressure after
the first few days of infarction has also been
Circulation, Volume XLV, January 1972
 LEFT VENTRICULAR FUNCTION IN MI
associated with clinical evidence of chronic
heart failure. In the group of patients with
pulmonary artery pressure monitoring studied
by Rutherford et al.21 those patients that
maintained an elevated mean pulmonary
artery pressure greater than 20 mm Hg over
48 hours demonstrated clinical evidence of
heart failure, experienced major arrhythmias,
and also had a mortality of 25%. Therefore, the
pulmonary artery pressure in acute myocardial
infarction can reflect alterations in left ven-
tricular function but do not consistently
correlate with symptoms or radiographic
findings.
The measurement of left ventricular filling
pressure, either directly or as pulmonary
wedge or end-diastolic pressure, has proved to
be a sensitive reflection of left ventricular
dysfunction in acute myocardial infarction.
Since patients with mild or uncomplicated
infarctions frequently demonstrate abnormal
elevations of the left ventricular filling pres-
sure during the first few days after infarction,
the symptoms and physical findings of left
heart failure do not necessarily manifest the
Downloaded from http://ahajournals.org by on May 11, 2020
altered hemodynamics. The presence of gallop
heart sounds did not correlate with elevations
in pulmonary wedge pressure in the study of
Lassers et al.26 A high incidence of atrial
gallop has been recorded in patients with
acute myocardial infarction,46 but variations in
pulmonary wedge pressure from 4 to 34 mm
Hg have been reported.26 However, left
ventricular gallop is usually associated with an
elevation of left ventricular filling pressure,47
but patients may have elevated pressures
during acute myocardial infarction without
the presence of a ventricular gallop. The left
ventricular filling pressure has been fairly
consistently elevated in those patients mani-
festing heart failure, but the extent of
elevation may be useful in the selection of
pharmacologic agents. Based on the observa-
tions of the ventricular function curves, mild
volume overload may be hemodynamically
beneficial to patients with myocardial infarc-
tion, and diuretics may be most beneficial in
the treatment of pulmonary congestion and ex-
cessive elevation of left ventricular filling pres-
Circulation, Volume XLV, January 1972
241
sures. In cardiogenic shock measurement of the
filling pressure is important in selecting the
various pharmacologic agents such as volume
expansion or sympathomimetic amines.
Although the measurement of cardiac out-
put has been performed by many investigators
in acute myocardial infarction, the range of
values and overlap encountered in uncompli-
cated patients as well as those in heart failure
and cardiogenic shock restricts the interpreta-
tion of a single measurement. The large
collection of data indicates that cardiac output
may be normal or subnormal in mild infarc-
tions, and patients in heart failure and shock
have more severe depression in cardiac
output. Although a range of values for cardiac
outputs in cardiogenic shock has been de-
scribed, those patients with severely reduced
cardiac outputs tend to have an extremely
high mortality, whereas the small percentage
of survivors often have slightly higher values
for output. Even though knowledge of the
cardiac output may not be clinically useful in
uncomplicated patients, this measurement can
be helpful in assessing the prognosis and
pharmacologic management of patients in
cardiogenic shock.48 49
The calculation of peripheral vascular resis-
tance in acute myocardial infarction is a
derived value from cardiac output and pres-
sure and is thus subject to similar clinical
limitations as the basic measurement of
cardiac output. Since normal as well as
elevated values for peripheral vascular resis-
tance may be encountered in cardiogenic
shock, this measurement may possess clinical
value. Studies do suggest that patients with
extremely high peripheral vascular resistance
in cardiogenic shock have a much worse
prognosis than those with normal or slightly
elevated values. Furthermore, the resistance
value may facilitate the selection of drugs in
the management of cardiogenic shock. How-
ever, in patients with heart failure the
measurement of peripheral vascular resistance
does not correlate with clinical findings and
course.
Important clinical information can be de-
rived from the relationship of left ventricular
 242
filling pressure, cardiac output, and aortic
pressure before and after pharmacologic
intervention in patients with acute myocardial
infarction. Left ventricular function has been
reported to be more depressed and hospital
mortality higher in patients with anterior
infarction than those with diaphragmatic
infaretions.5" The ventricular-function curves
aid in quantitating the level of depression of
left ventricular function particularly in heart
failure and cardiogenic shock.41 Furthermore,
the slope of the function curve after volume
expansion indicates the reserve of the myocar-
dium. The observation that improvement of
the ventricular-function curve can occur with-
out treatment in the first 3 days is important in
assessing the effect of any pharmacologic
intervention. Since the optimum cardiac out-
put observed from the function curves occurs
at a filling pressure between 20 and 24 mm
Hg, the use of diuretics can be selected on a
precise physiologic basis. The assessment of
ventricular function by the dextran infusion
not only provides information on the cardiac
performance, but the intervention itself can be
hemodynamically beneficial.
Downloaded from http://ahajournals.org by on May 11, 2020
Serial monitoring of cardiovascular dynam-
ics in acute myocardial infaretion probably
represents the most useful clinical application
of the hemodynamic techniques described.51
Not only can serial changes be related to
baseline measurements, but again the de-
rangements in hemodynamics can be useful in
the selection of pharmacologic agents. In
heart failure and cardiogenic shock indications
for volume expansion or reduction can be
precisely identified with the information pro-
vided by continuous monitoring of pulmonary
artery pressure, cardiac outputs, and systemic
blood pressure. In patients with cardiogenic
shock the control values of various hemody-
namic measurements can be followed more
closely with various drugs, and the lack of
hemodynamic response can be appreciated
more readily. Although patients with mild
infaretion may reveal definite hemodynamic
abnormalities, the generally uncomplicated
course and favorable prognosis do not seem to
justify widespread application of such moni-
RACKLEY, RUSSELL
toring techniques in these situations. How-
ever, the experience of several studies now
indicates that a left ventricular protodiastolic
gallop correlates fairly consistently with ab-
normal elevations in left ventricular filling
pressure and may be the earliest indication for
hemodynamic monitoring in acute myocardial
infarction. As mentioned earlier, the presence
of rales in the chest does not consistently
relate to hemodynamic abnormalities, and the
rise in central venous pressure in most
instances is a very late manifestation of left
ventricular failure. Studies further suggest
that changes of pulmonary vascular conges-
tion on X-ray may be out of phase with left
ventricular and pulmonary artery dynamics.
Therefore, the hemodynamic monitoring can
provide the most accurate indication for the
changes in cardiac function that occur during
the first few days of infaretion.
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Circulation, Volume XLV, January 1972