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Left ventricular failure in acute myocardial infarction
MAY
The American
Journal
1970
of CARDIOLOGY VOLUME NUMBER
25 5
Clinical Studies
Left Ventricular Failure in Acute Myocardial Infarction
BENJAMIN MICHAEL
W. LASSERS, MB (Edin.), GEORGE, MB (Edin.),
JOHN L. ANDERTON, MICHAEL R. HIGGINS, MRCP(E) and THOMAS Edinburgh,
PHILP,
MRCP
MRC :P
MB (Edin.) MB (Edin.), MB (Edin.),
MRCP(E)
Scotland
From the Departments of Medicine, Cardiology and Radiology, The Royal Infirmary, Edinburgh, Scotland. This study was supported in part by funds from the British Heart Foundation and a grant from the Scottish Hospitals Endowment Research Trust. Manuscript received March 10, 1969, accepted September 16, 1969. Address for reprints: Dr. Benjamin W. Lassers, King Gustaf V Research Institute, Stockholm 60, Sweden.
VOLUME
25, MAY 1970
In 30 patients with acute myocardial infarction complicated by either advanced atrioventricular or bundle branch block, pulmonary arterial wedge pressures were studied in relation to clinical and radiographic features of left ventricular failure, changes in central venous and pulmonary arterial pressures, and arterial hypoxemia. An increase in mean pulmonary arterial wedge pressure was poorly correlated with the presence of dyspnea, audible third or fourth heart sounds, or persistent basal rales; however, it was significantly related to radiographic evidence of pulmonary venous dilatation or edema, a systolic blood pressure of less than 100 mm Hg, gallop rhythm associated with tachycardia, and heart rate in patients with sinus rhythm and normal atrioventricular conduction. Increased mean .right atrial pressure indicated increased mean pulmonary arterial wedge pressure in patients with isolated anterior infarction, but in several patients with isolated inferior infarction the level of right atrial pressure was disproportionately high. The pulmonary arterial diastolic pressure closely reflected the mean pulmonary arterial wedge pressure in the absence of obstructive airways disease or pulmonary embolism. The level of the arterial oxygen tension fell as the mean pulmonary arterial wedge pressure rose, but it was considerably reduced in some patients with only moderately increased pressures. However, the latter usually had radiographic evidence of pulmonary venous dilatation or edema, suggesting that the pressure had been elevated previously to higher levels.
The detection and assessment of left ventricular failure after acute myocardial infarction has been based principally on clinical signs and radiologic and blood-gas findings.’ These features have seldom been correlated directly with left-sided cardiac pressure measurements*-5 because the hazardous nrocedures reouired to obtain such measurements are seldom justifiable after acute infarction. However, Fluck techniques, related these measurements to pulet a1.,6 using float-in monary arterial pressure levels.
511
15
22
6 5
2
21
20
c :
s
3 E
i
19
18
62
14
E
67
13
62
64
70
64
56
63
70
57
12
16
60
11
17
52
57
10
i
a
(2)
Digoxin, diuretics, lidocaine
0
54
Hypertension+
Myocardial infarction
Congestive cardiac failure
Hypertension+
0
0
0
Myocardial infarction
Hypertension+
0
Myocardial infarction
0
0
Digoxin, diuretics
0
Digoxin, diuretics
0
0
0
0
Digoxin
Digoxin
0
0
0
0
1
1
3
lnferolateral
Anterior
Inferior
lnferolateral
Anterior
1 1
Inferior Inferior
1 4
Inferior +anterior
1
1 ?
1 Inferior
Inferior
2
1
lnferolateral Inferior
2
Anterior
1
Anterior
9
Digoxin, lidocaine 2
Lidocaine
0
48
8
0
Myocardial infarction
Inferior
53
7
Anterior
69
6 3
Anterior
1
45
5 4
Inferior
58
4
0
Inferior
1 2
0
0
50
3
Chronic bronchitis
Anterior
1
0
Hypertension++
60
2
Inferior
66
1
3
(yr)
no. 0
Site of Recent Infarction
Hypertension++
Previous History*
Day? of Infarct
Age
Case
Treatment Before Study
Clinical Features
TABLE I
ii
E
0
0
0
MO/80 105/50 w-
2”HB60 SRlll RBBB
2”HB to SR90
SR120 RBBB
CHB69
SR88 RBBB
SRlOO RBBB
CHB51
2”HB60
SR94 RBBB
SR99 LBBB
2”HB56
2”H 887
2”H B57
CHB75
SRlOO RBBB
SR88 RBBB
SR79 RBBB
85/60
85/-
80/60
90/55
+
+
0
0
S,
Mesodiastolic gallop
0
0
S,
S, 0
0
120/90
0
0 lOO/-
0
S,
0
0
w60 140/100
0
0
160/120
160/80
0
0
W/60
110/60
0
0
85155
+
0
+
0
+
0
0
+
0 0
0 +
0 0
+
+
+
+
+
+
+
0
+
0
0
0
+
0
0
105/80
S,
0
Dead
Dead
Dead
Alive
Dead
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
+
0
+
Alive
0
0
0
Dead
0 +
0
Alive
Dead
0
0
Alive
0
0 0
Outcome
Rales
Dyspnea
120/80
0
Mesodiastolic gallop
S4 0 0
0
110/60
CHB75
2”H B65 +
S,
0
140/100
SR94 RBBB w-
S4
0
160/90
2”HB75
Added Sounds
Shock
Blood Pressure
Clinical Features*
(mm W
Rhythm, Rate (per min) and Conduction
21
21
21
18
17
16
16
16
16
16
15
15
15
14
14
14
12
12
11
8
5
4
(mm W
Pulmonary Arterial Wedge Pressure (mean)
LEFT
+
+
+
+
+
VENTRICULAR
FAILURE
IN
ACUTE
MYOCARDIAL
INFARCTION
The insertion of an electrode-catheter is part of the routine management, of acute heart block, and we have used this opportunity to record the pulmonary arterial wedge pressure, which reflects with reasonable accuracy the mean pressure in the left atrium and pulmonary veins, especially if these pressures are elevated.?-lo This paper examines the relation between the mean pulmonary arterial wedge pressure and the following features of acute myocardial infarction complicated by atrioventricular or bundle branch block: (1) certain clinical and radiologic findings associated with left ventricular failure; (2) changes in central venous pressure ; (3) pulmonary arterial hypertension ; and (4) arterial hypoxemia.
Materials and Methods Patients Thirty patients with acute myocardial infarction admitted to the Coronary Care Unit of the Royal Infirmary, Edinburgh, were studied. There were 26 men and 4 women from 42 to 73 years of age. Pacing electrodes were inserted in all patients as part of the routine managment of either advanced atrioventricular block’l or complete bundle branch b1ock.l” The clinical diagnosis of acute myocardial infarction was confirmed by electrocardiographic and serum enzyme changes in all patients. The diagnosis was considered established if there were (1) pathologic Q waves on the electrocardiogram accompanied by an elevation of the S-T segment and subsequent inversion of the T wave; (2) changes in the S-T segment and T wave suggestive of infarction accompanied by a significant and transient rise in the serum level of aspartate aminotransferase (GOT) ( >50 Reitman and Frankel units) and serum creatine kinase ( >80 International units) ; or (3) left bundle branch block accompanied by similar enzyme changes. An inferior infarct was diagnosed if the Q wave and S-T segment changes appeared in leads III and aVF, and an anterior infarct if these changes occurred in leads Vi to Vs with or without changes in leads I and aVL. An infarct was considered to be inferolateral in site if the changes in leads III and aVF were accompanied by changes in leads I and aVL or in leads V5 and Vs (or both) without changes in the other chest leads. If the changes in leads III and aVF were accompanied by changes in leads Vi to Vq, the infarct was considered to be both anterior and inferior in location. Three patients had elevated serum enzyme levels and the pattern of complete left bundle branch block. In 1, the site of infarction had been determined before bundle branch block developed; in the second, location was based on necropsy findings alone; and in the third, the site was not determined. Seven patients had had previous myocardial infarctions, and 6 others were known to have had hyper-
VOLUME 25, MAY 1970
513
LASSERS ET AL.
TABLE
II
Radiologic,
Hemodynamic
and
Blood
Gas Findings Pressures
Case no.
X-Ray Findings
1 2 3 4 5 6 7 8 9 10
0 0
0
ND ++ 0 0 Alv PVD ++ PVD +++ PVD ++ 0 0 PVD + Alv Alv & int PVD + PVD +
11 12 13 14 15 16 17 18 PVD ++ 19 PVD ++ 0 20 21 22 Int 23 PVD +++ 24 25 Alv & int 26 Alv & int 27 28 Alv 29 Alv 30 Alv & int Mean Standard deviation
Mean PA Wedge 4
5 8 11 12 12 14 14 14 15 15 15 16 16 16 16 16 17 18 21 21 21 23 23 24 26 27 33 34 37 18 8
Blood Gases
(mm Hg) PaO,
PaCOl
CaO*--CYO, (vol 188 ml)
PA
RVED
RA
PA-PAW
(mm Hg)
(mm Hg)
11 11 10 19 30 15 23 17 24 24 19 23 26 30 23 26 20 25 25 28 25 28 29 26 32 38 40 35 60 40 26 10
5 5 9 15 5 5 3 10 10 10 15 10 11 12 15 17 14 12 12 15 6 11 14 -
1 3 7 14 5 4 5 6 9 7 15 11 9 8 11 19 15 8 9 12 4 11 14 4 7 10 20 14 16 9 10 5
7 6 2 8 18 3 9 3 10 9 4 8 10 14 7 10 4 8
-
-
-
86 80 79 82 88 60 62 62 80 88 97 59 59 62 59 57 60 61 69 65 61 -
6.71 5.82 3.82 4.28 6.19 5.67 6.47 4.89 1.91 6.95 5.92 9.02 6.09 6.50 12.69 5.71 7.47 10.00 15.46 10.29 4.52 -
45 69 -
40 35 40 47 35 39 36 35 40 37 33 38 42 34 28 38 43 53 21 29 42 32 38 -
60 39 68 14
44 29 37 7
7.67 9.73 7.03 2.90
10 10 17 15 16 14 11 4
7 4 6 3 8 12 13 2 26 3 8 5
6.69 5.26 -
oxygen content difference; Int = interstitial edema; PA Alv = alveolar edema; CaOl - Cool = arteriovenous pulmonary arterial to pulmonary wedge mean gradient: PaCO* = arterial carbon dioxide tension; PaO, = arterial venous dilation; RVED = right ventricular end-diastolic pressure. tension; PVD = pulmonary 0 = normal lung field; + = mild; ++ = moderate; +++ = severe; - = not recorded.
tension. In 3 patients the hypertension had been mild and had not required treatment; 2 patients had received antihypertensive drugs, and another had severe, untreated hypertension. A further patient, who had cardiac failure due to ischemic heart disease, had been receiving digoxin and diuretic agents for some months before admission. One patient was known to have chronic bronchitis (Table I). Several patients had been given digoxin, or diuretic or antiarrhythmic drugs before study, but none had received analgesic agents within 3 hours or oxygen within 1 hour of study (Table I). Pressure Measurement
and Blood Samples
A no. 6 or 7 Zucker bipolar pacing electrode catheter (U. S. Catheter and Instrument Corp, Glens Falls, New York) was inserted percutaneously into the right subclavian vein and manipulated under fluoroscopic con-
514
PAW = oxygen
trol at the patient’s bedside into the main pulmonary artery to ensure that it had not entered the coronary sinus.13 Pressures were recorded during this procedure. Samples of blood were then drawn simultaneously from the pulmonary artery and from a brachial artery, which was punctured directly with a 21 gauge disposable needle. The electrode catheter was then advanced to the pulmonary arterial wedge position and pressures recorded. Finally, the electrode catheter was withdrawn to the right ventricle and positioned with its tip at the apex of this chamber. The results and complications of insertion of the electrode in cases of advanced atrioventricular block and complete bundle branch block have been presented in detail elsewhere.llJ* The measurements were carried out on the first day after the onset of symptoms of infarction in 19 patients, on the second day in 4 and from the third to the seventh in the remaining 7 patients (Table I).
The American
Journal
of CARDIOLOGY
LEFT-VENTRICULAR
‘7)
40-
0
4o
,
l
/
A
FAILURE IN ACUTE MYOCARDIAL INFARCTION
B
/
l/
/
/ /
30 -
M-
WLMWARY
PULMCWW ARTERIAL
ARTERIAL m-
DIASTOLIC
MEAN mm h
mm.Hp.
y - 1.11x+5-9 50-5.1 ” - 30 r -0469 pcoG4
IO
/
/
/
/
20 y = 1.01x+1.6 SO- 3.1 n= a r = 0935 p
IO
/
/ 0
0 0
chronic krdiia Wipk pllma-ary anbdi 1
40
2Q 30 IO PULMONARY ARTERY WEDGE MEAN
0
IO
20
M
PULMONARY ARTERY WEDGE MEAN
mm Hg
mm. Hp.
Figure 1. Correlation between mean pulmonary arterial wedge pressure and (A) mean pulmonary arterial pressure and (B) pulmonary arterial diastolic pressure (diastolic pressure not obtained in 1 patient). SD = residual standard deviation of y about regression line. Broken line = line of identity.
Pressures were transduced with a Bell and Howell 4-327-L221 strain gauge manometer and recorded on a Devices M4 direct-writing recorder. Zero reference level for the manometer was taken as 5 cm below the level of the manubrium sterni. Mean pressure values were obtained by electrical integration. Right ventricular end-diastolic pressure was taken as the level immediately before the beginning of the upstroke of the systolic portion of the ventricular pressure curve. Arterial
and mixed
venous
blood
samples
were
analyzed immediately for oxygen tension, carbon dioxide tension and pH levels with the use of R.adiometer equipment. The oxygen saturation of the blood was derived from the arterial oxygen tension with a correction for pH and carbon dioxide tension by means of the Severinghaus blood-gas calculator. The hemoglobin capacity was determined by a spectrophotometric technique using a Unicam SP 600, or it was derived from the hemoglobin concentration of the sample. The oxygen content was calculated from the saturation and the hemoglobin capacity. Clinical and Radiological Assessment
Clinical examination was carried out and the findings recorded immediately before the insertion of the pacing electrode. Portable anteroposterior chest roentgenograms were taken within 6 hours of the pressure measurement. The appearance of the lung fields was assessed by a radiologist who had no knowledge of either the clinical features or pressure measurements. The pulmonary veins were recorded as normal or as showing slight-, moderate or marked dilatation. The presence of alveolar or interstitial edema was also recorded.
VOLUME
25, MAY 1970
Necropsies were performed in 12 of the 13 patients who died. All results are presented as mean values +l SD.
Results Pressures
The right atrial, right ventricular, mean pulmonary arterial and mean pulmonary arterial wedge pressures are presented in Table II. The mean pulmonary arterial wedge pressure ranged from 4 to 37 mm Hg and was above the upper limit of normal of 12 mm Hg in 24 patients. The average mean pulmonary arterial wedge pressure in the 13 patients who died was 23 + 9 mm Hg, which was significantly higher than the average level of 14 + 4 in the 17 survivors (P <0.005). Figure 1 shows that there was a significant correlation between the mean pulmonary arterial wedge pressure and both mean pulmonary arterial pressure (Fig. 1A) and pulmonary arterial diastolic pressure (Fig. 1B). However, the diastolic pressures corresponded more closely to the pulmonary arterial wedge values than did the mean pulmonary arterial pressures. The gradient between the mean pulmonary arterial pressure and the mean pulmonary arterial wedge pressure averaged 8 * 5 mm Hg and did not correlate significantly with either the arterial oxygen tension (Pa09) or the arteriovenous oxygen content difference. The correlation between me,an right atria1 and ?nean pulmonary arterial wedge pressures is shown in Figure 2. In patients with anterior infarction there was a sig-
515
LASSERS ET AL.
4or
. .
RIGNT ATRIAI MEAN KIESSUE mmHq
PuLbaxARYARTERY
33
WED&ZMEAN mm.Hp.
25
. T
!
I
-?-
J..
i
4‘: t
I_ .
cl
: Figure 2. Correlation between pulmonary arterial wedge and right atrial pressures. Upper regression line (r = 0.699): patients with acute isolated inferior infarction; lower regression line (r = 0.586): patients with acute anterior infarction. Sites of old infarction have not been considered, and 1 patient (Case 29) with anterior infarction and multiple pulmonary emboli has not been included (significance of difference between slopes of regression lines = 0.10 > P > 0.05).
nificant correlation between the two pressures (r = 0.586; P <0.05), and the right atria1 pressure did not reach abnormal levels until the mean pulmonary arterial wedge pressure was above about 12 mm Hg (slope of regression line = 0.238). In the 5 patients with inferolateral infarction (not shown in Fig. 2), the slope of the regression line was almost identical (0.239). In patients with isolated inferior infarction (r = 0.699; P <0.05)the right atria1 pressure tended to rise more steeply (slope of regression line = 0.812) ; however, the number of cases involved was small and the difference between the slopes of the regression lines did not reach statistical significance (0.10 >P >0.05). Further observations are required to determine whether this trend is a real one. On the other hand, in some patients with an inferior infarction the level of mean right
40
I
301 0
n=25
8
12
16
20
PUlMNARYMEAl
24
28
32
M
40
WEDGEELAN
mm.Hp.
Figure 3. pulmonary
516
Relation
between
pulmonary
arterial
wedge pres(0.10 > P >
atria1 pressure was markedly elevated (14 to 19 mm Hg), whereas the level of mean pulmonary arterial wedge pressure was normal or only mildly elevated (11 to 16 mm Hg). Thus, although the level of elevation of the right atria1 pressure is a fairly reliable guide to the level of elevation of the mean pulmonary arterial wedge pressure in patients with anterior infarction, the right atria1 pressure may be disproportionately high in patients with isolated inferior infarction. Arterial Oxygen Tension (PaO,)
PaOz, measured in 25 patients, ranged from 39 to 97 mm Hg and was below the lower limit of normal of 85 mm Hg in 21 (Table II). There was a significant correlation (Fig. 3) between PaOz levels and the mean pulmonary arterial wedge pressure although PaOz levels ranged widely in patients with mean pulmonary arterial wedge pressures between 14 and 18 mm Hg. The average PaOz level of 69 -t 15 mm Hg in the survivors was not significantly different from the level of 65 t 13 mm Hg in those who died; however, Pa& was not measured in 1 patient who lived or in 4 patients who died. Arterial Carbon Dioxide Tension (PaCOJ
r-0620
p~Ooo1
4
Figure 4.
sure and the presence or absence of dyspnea 0.05).
Correlation between arterial a’rterial wedge pressure.
oxygen tension
and
PaCOz ranged from 21 to 53 mm Hg (Table II). There was evidence of alveolar hyperventilation with PaGO levels of less than 36 mm Hg in 10 patients and mild alveolar hypoventilation with PaCOa levels of 47 and 53 mm Hg in 2 patients, 1 of whom had chronic bronchitis.
The Amarlcan
Journal
of CARDIOLOGY
LEFT
VENTRICULAR
FAILURE
IN
ACUTE
MYOCARDIAL
.
.
..
: FlJlMONhRY WEDGE
INFARCTION
T
APTERY MEAN
f
mm. H9.
I
4 i:
f *
i
s: +-
.
Relation between persistent Figure 5. basal rates and (A) pulmonary arterial wedge pressure (0.10 > P > 0.05). and (B) arterial oxygen tension (PaO?) (P > 0#90).
Arteriovenous Oxygen Content Difference (Ca02 - CVOn)
CaOz - CVO, levels ranged from 1.91 to 12.69 volJlO0 ml and were above the upper limit of normal (4.50 vol/lOO ml ) l4 in all but 3 patients (Table II). There was no significant relation between the mean pulmonary arterial wedge pressure and CaOz - C002 levels. Clinical and Radiologic Features
Dyspnea : Eight patients had dyspnea at the time of study (Table I). The mean pulmonary arterial wedge pressure in these patients ranged from 14 to 33 mm Hg; the average value (23 + 6 mm Hg) was not significantly different from the average mean pulmonary arterial wedge pressure (17 f. 8 mm Hg) in the patients without dyspnea (0.10 >P >0.05) (Fig. 4). Pa09 was not measured in 3 patients with dyspnea; the average value (65 * 4 mm Hg) in the remaining 5 was not significantly different from the average (68 2 16 mm Hg) in the patients without dyspnea. arterial Rales : The average mean pulmonary wedge pressure did not differ significantly between those patients with (20 * 7 mm Hg) and those without (14 f 7 mm Hg) persistent basal rales (0.10 >P >0.05) (Fig. 5A). Rales were present in all 5 patients with mean pulmonary art.erial wedge pressures greater than 25 mm Hg, absent in 3 patients with pressures between 20 to 25 mm Hg and present in 11 patients with normal or slightly increased pressures. There was no significant difference in the average PaOz level between patients with and without rales (P >0.90) (Fig. 5B). There was no significant Added heart sounds: difference between the average mean pulmonary arterial wedge pressure in patients with and without audible added heart sounds (P >0.30) (Fig. 6). Added
VOLUME
25, MAY
1970
-
Z-0
RALES
RALES PRESENT
t---
ABSENT
i
sounds were present in all but 1 patient with a mean pulmonary arterial wedge pressure above 20 mm Hg but were also present in a large proportion of patients with normal or moderately increased pressures. However, there was a group of patients with mesodiastolic gallop rhythms-that is, gallop rhythms observed when tachycardia makes it impossible to determine clinically whether the added sound is a third or fourth heart sound or a summation gallop.ls In these patients the average mean pulmonary arterial wedge pressure was significantly higher than in patients who had no added heart sounds (P
fw4ctw
~nnxw
WEDGE
25-
MEAN
mm.Hg.
.
20 T
.
IS -
IO -
i
. .
0
Figure 6. Relation between pulmonary arterial sure and added heart sounds (P > 0.50).
wedge pres-
517
LASSERS
ET AL.
. ,-
.-’ .
Figure 7. Correlation between heart rate and pulmonary arterial wedge pressure in patients with sinus rhythm and normal atrioventricular conduction. (SD of rate about regression line = lO/min.)
Systemic blood pressure and cardiogenic shock: The systolic blood pressure was unrecordable in 1 patient and ranged from 80 to 160 mm Hg in the remainder. It was less than 100 mm Hg in 13 patients (Table I). There was no significant correlation between the systolic pressure and the mean pulmonary arterial wedge pressure (T = 0.338), but the average mean pulmona,ry arterial wedge pressure was significantly higher in patients with systolic pressures of 100 mm Hg or less than in those with higher systolic pressures (P <0.05). There was no significant relation between PaO,n and systolic blood pressure. Cardiogenic shock, defined as a systolic blood pressure of less than 90 mm Hg accompanied by diminished mental function and evidence of intense cutaneous vasoconstriction, was present in 5 patients. The mean pulmonary arterial wedge pressure was normal in 1 of these patients (11 mm Hg), moderately in-
creased in 2 (21 mm Hg) and markedly increased in the remaining 2 (33 and 37 mm Hg) (Table II). The mean right atria1 pressure level was elevated in 4 of the 5 patients but did not reliably reflect the level of the mean puhnonary arterial wedge pressure. In 1 patient with a mean right atria1 pressure of 4 mm Hg the mean puhnonary arterial wedge pressure was 21 mm Hg, whereas in another patient with a mean right atria1 pressure of 14 mm Hg the mean pulmonary arterial wedge pressure was normal (11 mm Hg) . Chest roentgenograms: These roentgenograms were taken within 6 hours of pressure measurements’ in 27 patients (Table II). There was a significant difference between the average mean pulmonary arterial wedge pressure in patients with normal lung fields and in those with radiographic evidence of pulmonary venous dilatation (2’ <0.05) or pulmonary edema (P <0.005). Although there was no significant difference in the mean pulmonary arterial wedge pressure among patients with slight, moderate or marked pulmonary venous dilatation, the pressure was significantly higher in patients with edema than in patients with dilatation only (PP >0.05). Most patients with radiographic evidence of pulmonary edema had received digoxin or diuretic agents, or both, before pressure measurements were made; in some patients
c-l -
. Qt.
2 fVLp(oNARY UEffiE
ARTERY MEAN
mm. Hq
.
Til
4 .
I +
"9
ea-
mm&q. m-
i i
i .
I
!
j_ .
T M
1. .
I
FiTiFPULMONARY EDEMA
PlJLMONAtW MtiaJS DILATATI’34
DLATAT0N
I
Iwu4DNAFlY EDEMA
Figure 8. Relation between radiographic appearance of lung fields and (A) pulmonary arterial wedge pressure and (8) arterial oxygen tension (Pa&). (See text for levels of significance.)
B 518
The
American
Journal
of
CARDIOLOGY
LEFT
TABLE
VENTRICULAR
FAILURE
IN
ACUTE
MYOCAROIAL
INFARCTION
III
Necropsy
Findings Necropsy
Findings
Pressures
-~ Site of Old Infarction Case no.
Coronary Artery Involved*
Site of Infarct (Electrocardiogram)
Left Ventricle
Left Ventricle
Right Ventricle None None None
Inferior Inferior Lateral,
None None
Right Ventricle
Mean Pulmonary Arterlal Wedge
Mean Right Atrial
Inferior Inferior None
11 21 21
14 12 11
Lateral, inferior Anterior, lateral, inferior
None Inferior
26 27
10 20
None
Septum, lateral
anterior,
None
37
9
None
None
Septum, lateral
anterior,
None
17
8
Inferior
None
Septum, lateral
anterior,
None
21
4
LAD0
Inferior
None
Septum, anterior, lateral, inferior
None
23
14
Anterior Anterior
LAD0 LAD0
Inferior, Inferior,
None None
Septum, Septum, lateral
anterior anterior,
None None
23 33
4 14
Anterior
LAD0
None
None
Septum, lateral
anterior,
None
34
16
4 20 22
Inferior Inferior lnferolateral
26 27
lnferolateral Inferior, anterior
LCO RsapLAD,,, LCss
None None Anterior, lateral, inferior Anterior, lateral Lateral, inferior
30
LBBB
LADss
None
18
Anterior
LAD0
21
Anterior
R ss, LAD,,,
23
Anterior
24 28 29’
* LAD = left anterior descending; stenosis. + Multiple pulmonary emboli.
LBBB
LCss
= left bundle
lateral lateral
branch
this treatment may have resulted in a reduction in mean pulmonary arterial wedge pressure and an increase in Pa02. Individuals having X-ray evidence of pulmonary venous dilatation or edema and those with normal lung fields were clearly demarcated with respect to the relation between Pa& and mean pulmonary arterial wedge pressures (Fig. 8). Necropsies : The necropsy findings are presented in Table III.
Discussion Both atrioventricular and bundle branch block after acute myocardial infarction are often associated with severe underlying myocardial damage.llJ” For this reason, a much larger proportion of our patients had clinical evidence of moderate or severe cardiac failure than would be expected in an unselected group of patients with acute myocardial infarction. In addition, the conduction defects themselves may have affected left ventricular function. Thus, both the loss of atria1 transport function resulting from atrioventricular block and the loss of synchronism of ventricular contraction associated with bundle branch block might affect left ventricular end-diastolic pressure,l’ and, therefore, left atria1 and pulmonary arterial wedge
VOLUME
Site of Recent Infarction --___-
(mm Hg)
25, MAY 1970
block;
inferior
LC = left circumflex;
R = right;
o = occluded;
ss = severe
pressure. However, these considerations should not invalidate t,he relation between left ventricular failure and its clinical manifestations. Left ventricular “failure” after acute myocardial infarction has often been equated with an increase in left ventricular end-diastolic and, therefore, left atria1 pressure. However, although an increase in left ventricular end-diastolic pressure may be one of the first measurable hemodynamic changes in the development of ventricular failure,l* it has limitations as an index of ventricular function. For example, the end-diastolic pressure may be normal in spite of diminished myocardial contractility if there is an increase in ventricular compliance and consequently an increase in ventricular end-diastolic and end-systolic volumes.lOJO Despite these limitations, left ventricular end-diastolic and left atria1 pressures are probably the most reliable indexes of left ventricular failure that have presently been obt.ained in acute myocardial infarction. Therefore, the mean pulmonary arterial wedge pressure, which corresponds closely to the left, atria1 pressure, has been used in our study. Clinical and Radiographic Features of Left Ventricular Failure Dyspnea,
added
heart
sounds
and persistent
basal
519
LASERS
ET AL.
rales are the principal clinical features that usually indicate left ventricular failure after acute myocardial infarction.“l However, our study shows that dyspnea, third and fourth heart sounds and rales are not well correlated with the mean pulmonary arterial wedge pressure. Observer error may account in part for the fact that added heart sounds and rales were not found in some patients with moderately increased mean pulmonary arterial wedge pressures (12 to 20 mm Hg), although they were detected in other patients with similar pressures and in 3 patients with normal pressures. The use of phonocardiography might have eliminated observer error in the detection of added heart sounds. However, phonocardiograms detect fourth heart sounds in more than 90 percent of cases of acute myocardial infarction22 and therefore are of little value in discriminating between the presence and absence of heart failure. The overlap in mean pulmonary arterial wedge pressure levels between the dyspneic and nondyspneic patients may have occurred part’ly because breathlessness is a subjective symptom and often difficult to evaluate. Thus, it is clear fom the PaC02 levels that hyperventilation occurred in several patients who did not complain of breathlessness or appear to be in respiratory distress. Respiratory rate would have provided a more objective assessment, but it was not recorded. It is unlikely that all of the discrepancies between these clinical findings and the mean pulmonary arterial wedge pressures can be attributed to observer error. Part of the explanation may be that elevation o,f the left ventricular end-diastolic or pulmonary venous pressure is not in itself the immediate physical mechanism producing added heart sounds, rales or dyspnea.23-a6 The clinical signs that did have a significant association with elevation of the mean pulmonary arterial wedge pressure were mesodiastolic gallop rhythms, tachycardia and systolic blood pressures of less than 100 mm Hg. In addition, there was a good correlation between the radiographic findings of pulmonary venous dilatation or edema, or both, and the mean pulmonary arterial wedge pressure. Despite this good correlation there was a considerable overlap in mean pulmonary arterial wedge pressures between patients with norma and abnormal lung fields (Fig. 8A). This is probably because fluid produced by an elevation in pulmonary venous pressure will take some time to be absorbed after the pressure falls. The differences in radiographic appearance in patients with similar mean pulmonary arterial wedge pressures emphasize that a pressure measurement reflects the state of pulmonary venous hemodynamics at only one point in time, whereas the roentgenogram also reflects earlier events.
520
Central Venous Pressure Increased central venous pressure after acute myocardial infarction is generally considered to reflect right ventricular failure secondary to failure of the left ventricle.“7 However, Herrick2* in 1912 suggested that right ventricular failure might follow occlusion of the right coronary artery, whereas obstruction of the left artery might produce left ventricular failure; the studies of Fluck et al6 and Lassers et al.“g have shown that this does occur in certain cases, They found some elevation of the right ventricular enddiastolic pressure in some patients with inferior infarction, which could not be accounted for by either pressure or volume overload of the right ventricle. In our study this dissociation of right and left ventricular failure was seen in 4 patients with electrocardiographic evidence of isolated inferior infarction. In addit.ion, patients with isolated inferior infarction tended to have higher mean right atria1 pressures for a given mean pulmonary arterial wedge pressure than did patients with anterior or inferolateral infarction, although this tendency was not statistically significant,. The explanation of dominant right verdricdar failure in some patients with electrocardiographic evidence of isolated inferior involvement is probably that infarction in this site is due to occlusion of the right coronary artery.“” The right’ coronary artery usually supplies the inferior, lateral a’nd most of the anterior wall of the right ventricle and a variable portion of the inferior surface of the left ventricle with collateral circulat,ion provided by the left anterior descending artery. 81~SZOcclusion of this artery can therefore affect the right ventricle more severely than the left,“” but the effect on right ventricular function in an individual patient will depend on the patency of the left anterior descending artery and the distribution and adequacy of anastomotic and collateral circulation. The necropsy findings in our patients support this observation since the 2 patients with elect’rocardiographic evidence of isolated inferior infarction who died had right coronary artery occlusion combined with severe stenosis of the left anterior descending artery (Table III). Pulmonary Arterial Hypertension The pulmonary arterial hypertension that may follow acute myocardial infarction has usually been attributed to left ventricular failure with a consequent increase in left atria1 and pulmonary venous pressure. However, since acute infarction is often accompanied by arterial hypoxemia, which is known to produce an increase in pulmonary vascular resistance,31*85 it is possible that this mechanism could also contribute to the increased pulmonary arterial pressures.
The Americen
Journal
of CARDIOLOGY
LEFT
In our study there was a direct and usually close correlation between the mean pulmonary arterial wedge and mean pulmonary arterial pressures (Fig. 1A). The gradient between these pressures averaged 8 + 4 mm Hg and ranged from 3 to 26 mm Hg (Table 111. However, only 4 patients had gradients of greater than 10 mm Hg, and 1 of these patients (Case 5)) with a gradient of 18 mm Hg, was known to have chronic bronchitis, whereas another (Case 29 1, with a gradient of 26 mm Hg, was found at necropsy to have multiple pulmonary emboli. A closer relation was found between the mean pulmonary arterial wedge pressure and the pulmonary arterial diastolic pressure (Fig. 1B). On the basis of these results it can be concluded that unless some ot.her factor such as obstructive airways disease or pulmonary embolism is present, the mean pulmonary arterial pressure is a fairly reliable reflection of mean pulmonary arterial wedge pressure in acute myocardial infarct,ion but that the pulmonary arterial diastolic pressure is a superior index.
Pulmonary Arterial Wedge Pressure and PaO, The reduction in Pa& which follows acute myocardial infarction has been well documented and is thought to be due to an increased venous admixture resulting from regional inequality of ventilation and perfusion. X-Z+ This abnormality is most marked in patients with evidence of pulmonary congestion,S7-*1 and it has been suggested that left ventricular failure with an elevation in pulmonary venous pressures could produce this abnormality by causing local decreases in pulmonary compliance12 or by alveolar edema and narrowing of airways.““*“D,4z In our patients there was a statistically significant, correlation between the mean pulmonary arterial wedge pressure and Pa@,, (Fig. 31. However, even in
VENTRICULAR
FAILURE
IN
ACUTE
MYOCARDIAL
INFARCTION
those patients with normal pressures at. the tim(a of study there was a mild but’ definite rccluction in P:t( )-. Furthermore, in patient’s with mild elevation of tjho mean pulinonary arterial wedge pressure, t#he Pa(‘),, ranged widely (57 to 97 mm Hgl. It is possible that these patients represent. two ~eparnte groups. In oile group the pulmonary arterial we(Ige pressure may have previously been much higher than tlw level at the time of study, thus accouming for the S-ray findings of pulmonary congestion and the rccluccd Pan, level. In the second group the pulmonary arterial wedge pressure may not have been elevated much above the level found at measurement, and consequently their chest roentgenograms and PaO? levels were normal. Thus, although an elevation of pulmonary venous pressure due to acute left ventricular failure is the most likely initiating cause for the ventilation-perfusion abnormality after acute myorardial infarction the underlying physical mechanism that results from the elevated pressure may persist after the pressure has fallen or returned to normal levels. Further studies with sequential measurements begun very early after the onset of infarction would he necessary to confirm this hypothesis.
Acknowledgments We thank the physicians in charge and the medical and nursing staff of the Coronary Care Unit of the Royal Infirmary for their co-operation; Drs. D. Franklin, M. Godman and C. Vellani, who assisted with some of the studies; Dr. C. Bouch, who provided information from the necropsies; Mr. E. Harding for statistical advice; and Miss Margaret Lawrie and Miss Margaret Duncan for invaluable secretarial help. In particular. we thank Dr. D. CT.*Julian for his advice and generous contribution of ideas.
References 1. Kirby BJ, McNicol MW, Tattersfield 2.
3. 4. 5.
6.
Left ventricular AE: pressures in two patients with myocardial infarction. Lancet 1:944-946, 1968 Lequime J: The circulatory dynamics in coronary thrombosis, in Proceedings of the International Seminar on Arteriosclerosis (Datey KK, ed). New York, Asia Publishing House, 1964, p 151 Left and right ventriCohn JN, Khatri IM, Tristani FE: cular filling pressures in clinical shock (abstr). Ann Intern Med 68:1153, 1968 Nixon PGF: Pulmonary edema with low left ventricular diastolic pressure in acute myocardial infarction. Lancet 2:146-147, 1968 Nixon PGF, Taylor DJE, Morton SD: Left ventricular diastolic pressure in cardiogenic shock treated by dextrose infusion and adrenaline. Lancet 1:1230-1232, 1968 Right heart Fluck DC, Valentine PA, Treister B, et al: pressures in acute myocardial infarction.
VOLUME 25, MAY 1970
&it Heart J 29:748-757,
1967
7. Connolly DC, Kirklin JW, Wood EH: The relationship between pulmonary artery wedge pressure and left atrial pressure in man. Circ Res 2:434-440, 1954 8. Shaffer AB, Sllber EN: Factors influencing the character of the pulmonary arterial wedge pressure. Amer Heart J 51:522-532, 1956 9. Werkd L: The dynamics and consequences of stenosis or insufficiency of the cardiac valves, in Handbook of Physiology, Circulation, Vol 1. (Hamilton WF, Dow P, ed). Washington D. C., American Physiological Society, 1962, p 645-680 10. Sapru RP, Taylor SH, Donald KW: Comparison of the pulmonary wedge pressure with the left ventricular enddiastolic pressure in man. Clin Sci 34:125-140, 1968 11, Lassers BW, Julian Do: Artificial pacing in managment of complete heart block complicating acute myocardial infarction. Brit Med J 2:142-146, 1968 12. Godman MJ, Lassers BW, Julian DG: Pacing in the
521
LASSERS ET AL.
management of complete bundle branch block complicating acute myocardial infarction. New Eng J Med, in press 13. Siddons H, Sowton E: Cardiac Pacemakers. Springfield, Ill., Charles C Thomas, 1967, p 57 14. Wade OL, Bishop JM: Cardiac Output and Regional Blood Flow. Oxford, England, Blackwell Scientific Publications, 1962, p 37 Sound. 8altimore, Wil15. McKusick VA: Cardiovascular liams & Wilkins, 1958, p 174 16. Friedberg CK, Cohen H, Donoso E: Advanced heart block as a complication of acute myocardial infarction. Role of pacemaker therapy. Progr Cardiovasc Dis 10:466-&l, 1968 17. Sarnoff SJ, Mitchell JH: The control of the function of the heart, in Ref 9, Vol 1, p 489-532 18. Davis JO: The physiology of congestive heart failure, in Ref 9, Vol3, p 2071-2122 19. Braunwald E, Ross J Jr: The ventricular end-diastolic pressure. Appraisal of its value in the recognition of ventricular failure in man, Amer J Med 34:147-150. X963 20. Dodge HT, Sandler H, Baxley WA, et al: Usefulness and limitations of radiographic methods for determining left ventricular volume. Amer J Cardiot 18:10-24, 1966 21. Fctwler NO: Physical signs in acute myocardial infares tion and its complications. Progr Cardiovasc Dis 10:287-297, 1968 22. Hill JC, O’Rourke RA, Lewis RP, et al: The diagnostic value of the atrial gallop in acute myocardial infarction. Amer Heart J 78:194-201, 1969 23. Crevasse L, Wheat MW, Wilson JR, et al: The mechanism of the generation of the third and fourth heart sounds. Circulation 25:635-642, 1962 24. Nixon PGF: The genesis of the third heart sound. Amer Heart J 65:712-714, 1963 25. Forgacs P: Crackles and wheazes. Lancet 2:203-205,1967 Disturbances in pulmonary function in 26. Donald Kw: mitral stenosis and left heart failure. Progr Cardiovasc Dis 1:298-308, 1959
27. Sampson JJ, Hutchinson JC: Heart failure in myocardial infarction. Progr Cardiovasc Dis lO:l-29, 1968 28. Herrick JB: Clinical features of sudden obstruction of the coronary arteries. JAMA 59:2015-2020, 1912 29. Lassers BW, Anderton JL, George M, et al: Hemodynamic effects of artificial pacing in complete heart block complicating acute myocardial infarction. Circulation 38:308-323, 1968 30. James TN: The coronary circulation and conduction system in acute myocardial infarction. Progr Cardiovasc Dis 10:410-449. 1968 31. Ferrer-Brown G: Vascular pattern of right ventricle of human heart. 8rit Heart J 30:67Q-686, 1968 32, Hudson REB: Cardiovascular Pathology, Vol I. London, Edward Arnold, Ltd, 1965, p 603 33. Wade WG: The pathogenesis of infarction of the right ventricle. Brit Heart J 21:545-554, 1959 34. Fishman AP: Respiratory gases in the regulation of the pulmonary circulation. Physiol Rev 41:214-280, 1961 35. Rudolph AM, Yuan S: Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes. J Clin Invest 453399-411, 1966 36. MacKenzie GJ, Taylor SH, Flenley DC, et al: Circulatory and respiratory studies in myocardial infarction and cardiogenic shock. Lancet 2:825-832, 1964 37. McNlcol MW, Kirby BJ, Bhoola KE, et al: Pulmonary function in acute myocardial infarction. Brit Med J 2:1270-1273, 1965 38. Valentine PA, Fluck DC, Mounsey JPD, et at: Blood-gas changes after acute myocardial infarction. Lancet 2:837-841, 1966 39. Pain MCF, Stannard M, Sloman 0: Disturbances of pulmonary function after acute myocardial infarction. Brit Med J 2:591-594, 1967 40. Higgs B: Factors influencing pulmonary gas exchange during the acute stages of myocardial infarction. Clin Sci 35:115-122, 1968 41. Shapiro M, Fillmore S, Killip T: Hypoxemia and functional severity in acute myocardiai -infarction (abstr). Circulation 38: Suool 6:178. 1968 42. West JB: Ventilation/Blood Flow and Gas Exchange. Oxford and Edinburgh, Blackwell Scientific Publications, 1965, p 52
The American
Journal
1970
of CARDIOLOGY VOLUME NUMBER
25 5
Clinical Studies
Left Ventricular Failure in Acute Myocardial Infarction
BENJAMIN MICHAEL
W. LASSERS, MB (Edin.), GEORGE, MB (Edin.),
JOHN L. ANDERTON, MICHAEL R. HIGGINS, MRCP(E) and THOMAS Edinburgh,
PHILP,
MRCP
MRC :P
MB (Edin.) MB (Edin.), MB (Edin.),
MRCP(E)
Scotland
From the Departments of Medicine, Cardiology and Radiology, The Royal Infirmary, Edinburgh, Scotland. This study was supported in part by funds from the British Heart Foundation and a grant from the Scottish Hospitals Endowment Research Trust. Manuscript received March 10, 1969, accepted September 16, 1969. Address for reprints: Dr. Benjamin W. Lassers, King Gustaf V Research Institute, Stockholm 60, Sweden.
VOLUME
25, MAY 1970
In 30 patients with acute myocardial infarction complicated by either advanced atrioventricular or bundle branch block, pulmonary arterial wedge pressures were studied in relation to clinical and radiographic features of left ventricular failure, changes in central venous and pulmonary arterial pressures, and arterial hypoxemia. An increase in mean pulmonary arterial wedge pressure was poorly correlated with the presence of dyspnea, audible third or fourth heart sounds, or persistent basal rales; however, it was significantly related to radiographic evidence of pulmonary venous dilatation or edema, a systolic blood pressure of less than 100 mm Hg, gallop rhythm associated with tachycardia, and heart rate in patients with sinus rhythm and normal atrioventricular conduction. Increased mean .right atrial pressure indicated increased mean pulmonary arterial wedge pressure in patients with isolated anterior infarction, but in several patients with isolated inferior infarction the level of right atrial pressure was disproportionately high. The pulmonary arterial diastolic pressure closely reflected the mean pulmonary arterial wedge pressure in the absence of obstructive airways disease or pulmonary embolism. The level of the arterial oxygen tension fell as the mean pulmonary arterial wedge pressure rose, but it was considerably reduced in some patients with only moderately increased pressures. However, the latter usually had radiographic evidence of pulmonary venous dilatation or edema, suggesting that the pressure had been elevated previously to higher levels.
The detection and assessment of left ventricular failure after acute myocardial infarction has been based principally on clinical signs and radiologic and blood-gas findings.’ These features have seldom been correlated directly with left-sided cardiac pressure measurements*-5 because the hazardous nrocedures reouired to obtain such measurements are seldom justifiable after acute infarction. However, Fluck techniques, related these measurements to pulet a1.,6 using float-in monary arterial pressure levels.
511
15
22
6 5
2
21
20
c :
s
3 E
i
19
18
62
14
E
67
13
62
64
70
64
56
63
70
57
12
16
60
11
17
52
57
10
i
a
(2)
Digoxin, diuretics, lidocaine
0
54
Hypertension+
Myocardial infarction
Congestive cardiac failure
Hypertension+
0
0
0
Myocardial infarction
Hypertension+
0
Myocardial infarction
0
0
Digoxin, diuretics
0
Digoxin, diuretics
0
0
0
0
Digoxin
Digoxin
0
0
0
0
1
1
3
lnferolateral
Anterior
Inferior
lnferolateral
Anterior
1 1
Inferior Inferior
1 4
Inferior +anterior
1
1 ?
1 Inferior
Inferior
2
1
lnferolateral Inferior
2
Anterior
1
Anterior
9
Digoxin, lidocaine 2
Lidocaine
0
48
8
0
Myocardial infarction
Inferior
53
7
Anterior
69
6 3
Anterior
1
45
5 4
Inferior
58
4
0
Inferior
1 2
0
0
50
3
Chronic bronchitis
Anterior
1
0
Hypertension++
60
2
Inferior
66
1
3
(yr)
no. 0
Site of Recent Infarction
Hypertension++
Previous History*
Day? of Infarct
Age
Case
Treatment Before Study
Clinical Features
TABLE I
ii
E
0
0
0
MO/80 105/50 w-
2”HB60 SRlll RBBB
2”HB to SR90
SR120 RBBB
CHB69
SR88 RBBB
SRlOO RBBB
CHB51
2”HB60
SR94 RBBB
SR99 LBBB
2”HB56
2”H 887
2”H B57
CHB75
SRlOO RBBB
SR88 RBBB
SR79 RBBB
85/60
85/-
80/60
90/55
+
+
0
0
S,
Mesodiastolic gallop
0
0
S,
S, 0
0
120/90
0
0 lOO/-
0
S,
0
0
w60 140/100
0
0
160/120
160/80
0
0
W/60
110/60
0
0
85155
+
0
+
0
+
0
0
+
0 0
0 +
0 0
+
+
+
+
+
+
+
0
+
0
0
0
+
0
0
105/80
S,
0
Dead
Dead
Dead
Alive
Dead
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
Alive
+
0
+
Alive
0
0
0
Dead
0 +
0
Alive
Dead
0
0
Alive
0
0 0
Outcome
Rales
Dyspnea
120/80
0
Mesodiastolic gallop
S4 0 0
0
110/60
CHB75
2”H B65 +
S,
0
140/100
SR94 RBBB w-
S4
0
160/90
2”HB75
Added Sounds
Shock
Blood Pressure
Clinical Features*
(mm W
Rhythm, Rate (per min) and Conduction
21
21
21
18
17
16
16
16
16
16
15
15
15
14
14
14
12
12
11
8
5
4
(mm W
Pulmonary Arterial Wedge Pressure (mean)
LEFT
+
+
+
+
+
VENTRICULAR
FAILURE
IN
ACUTE
MYOCARDIAL
INFARCTION
The insertion of an electrode-catheter is part of the routine management, of acute heart block, and we have used this opportunity to record the pulmonary arterial wedge pressure, which reflects with reasonable accuracy the mean pressure in the left atrium and pulmonary veins, especially if these pressures are elevated.?-lo This paper examines the relation between the mean pulmonary arterial wedge pressure and the following features of acute myocardial infarction complicated by atrioventricular or bundle branch block: (1) certain clinical and radiologic findings associated with left ventricular failure; (2) changes in central venous pressure ; (3) pulmonary arterial hypertension ; and (4) arterial hypoxemia.
Materials and Methods Patients Thirty patients with acute myocardial infarction admitted to the Coronary Care Unit of the Royal Infirmary, Edinburgh, were studied. There were 26 men and 4 women from 42 to 73 years of age. Pacing electrodes were inserted in all patients as part of the routine managment of either advanced atrioventricular block’l or complete bundle branch b1ock.l” The clinical diagnosis of acute myocardial infarction was confirmed by electrocardiographic and serum enzyme changes in all patients. The diagnosis was considered established if there were (1) pathologic Q waves on the electrocardiogram accompanied by an elevation of the S-T segment and subsequent inversion of the T wave; (2) changes in the S-T segment and T wave suggestive of infarction accompanied by a significant and transient rise in the serum level of aspartate aminotransferase (GOT) ( >50 Reitman and Frankel units) and serum creatine kinase ( >80 International units) ; or (3) left bundle branch block accompanied by similar enzyme changes. An inferior infarct was diagnosed if the Q wave and S-T segment changes appeared in leads III and aVF, and an anterior infarct if these changes occurred in leads Vi to Vs with or without changes in leads I and aVL. An infarct was considered to be inferolateral in site if the changes in leads III and aVF were accompanied by changes in leads I and aVL or in leads V5 and Vs (or both) without changes in the other chest leads. If the changes in leads III and aVF were accompanied by changes in leads Vi to Vq, the infarct was considered to be both anterior and inferior in location. Three patients had elevated serum enzyme levels and the pattern of complete left bundle branch block. In 1, the site of infarction had been determined before bundle branch block developed; in the second, location was based on necropsy findings alone; and in the third, the site was not determined. Seven patients had had previous myocardial infarctions, and 6 others were known to have had hyper-
VOLUME 25, MAY 1970
513
LASSERS ET AL.
TABLE
II
Radiologic,
Hemodynamic
and
Blood
Gas Findings Pressures
Case no.
X-Ray Findings
1 2 3 4 5 6 7 8 9 10
0 0
0
ND ++ 0 0 Alv PVD ++ PVD +++ PVD ++ 0 0 PVD + Alv Alv & int PVD + PVD +
11 12 13 14 15 16 17 18 PVD ++ 19 PVD ++ 0 20 21 22 Int 23 PVD +++ 24 25 Alv & int 26 Alv & int 27 28 Alv 29 Alv 30 Alv & int Mean Standard deviation
Mean PA Wedge 4
5 8 11 12 12 14 14 14 15 15 15 16 16 16 16 16 17 18 21 21 21 23 23 24 26 27 33 34 37 18 8
Blood Gases
(mm Hg) PaO,
PaCOl
CaO*--CYO, (vol 188 ml)
PA
RVED
RA
PA-PAW
(mm Hg)
(mm Hg)
11 11 10 19 30 15 23 17 24 24 19 23 26 30 23 26 20 25 25 28 25 28 29 26 32 38 40 35 60 40 26 10
5 5 9 15 5 5 3 10 10 10 15 10 11 12 15 17 14 12 12 15 6 11 14 -
1 3 7 14 5 4 5 6 9 7 15 11 9 8 11 19 15 8 9 12 4 11 14 4 7 10 20 14 16 9 10 5
7 6 2 8 18 3 9 3 10 9 4 8 10 14 7 10 4 8
-
-
-
86 80 79 82 88 60 62 62 80 88 97 59 59 62 59 57 60 61 69 65 61 -
6.71 5.82 3.82 4.28 6.19 5.67 6.47 4.89 1.91 6.95 5.92 9.02 6.09 6.50 12.69 5.71 7.47 10.00 15.46 10.29 4.52 -
45 69 -
40 35 40 47 35 39 36 35 40 37 33 38 42 34 28 38 43 53 21 29 42 32 38 -
60 39 68 14
44 29 37 7
7.67 9.73 7.03 2.90
10 10 17 15 16 14 11 4
7 4 6 3 8 12 13 2 26 3 8 5
6.69 5.26 -
oxygen content difference; Int = interstitial edema; PA Alv = alveolar edema; CaOl - Cool = arteriovenous pulmonary arterial to pulmonary wedge mean gradient: PaCO* = arterial carbon dioxide tension; PaO, = arterial venous dilation; RVED = right ventricular end-diastolic pressure. tension; PVD = pulmonary 0 = normal lung field; + = mild; ++ = moderate; +++ = severe; - = not recorded.
tension. In 3 patients the hypertension had been mild and had not required treatment; 2 patients had received antihypertensive drugs, and another had severe, untreated hypertension. A further patient, who had cardiac failure due to ischemic heart disease, had been receiving digoxin and diuretic agents for some months before admission. One patient was known to have chronic bronchitis (Table I). Several patients had been given digoxin, or diuretic or antiarrhythmic drugs before study, but none had received analgesic agents within 3 hours or oxygen within 1 hour of study (Table I). Pressure Measurement
and Blood Samples
A no. 6 or 7 Zucker bipolar pacing electrode catheter (U. S. Catheter and Instrument Corp, Glens Falls, New York) was inserted percutaneously into the right subclavian vein and manipulated under fluoroscopic con-
514
PAW = oxygen
trol at the patient’s bedside into the main pulmonary artery to ensure that it had not entered the coronary sinus.13 Pressures were recorded during this procedure. Samples of blood were then drawn simultaneously from the pulmonary artery and from a brachial artery, which was punctured directly with a 21 gauge disposable needle. The electrode catheter was then advanced to the pulmonary arterial wedge position and pressures recorded. Finally, the electrode catheter was withdrawn to the right ventricle and positioned with its tip at the apex of this chamber. The results and complications of insertion of the electrode in cases of advanced atrioventricular block and complete bundle branch block have been presented in detail elsewhere.llJ* The measurements were carried out on the first day after the onset of symptoms of infarction in 19 patients, on the second day in 4 and from the third to the seventh in the remaining 7 patients (Table I).
The American
Journal
of CARDIOLOGY
LEFT-VENTRICULAR
‘7)
40-
0
4o
,
l
/
A
FAILURE IN ACUTE MYOCARDIAL INFARCTION
B
/
l/
/
/ /
30 -
M-
WLMWARY
PULMCWW ARTERIAL
ARTERIAL m-
DIASTOLIC
MEAN mm h
mm.Hp.
y - 1.11x+5-9 50-5.1 ” - 30 r -0469 pcoG4
IO
/
/
/
/
20 y = 1.01x+1.6 SO- 3.1 n= a r = 0935 p
IO
/
/ 0
0 0
chronic krdiia Wipk pllma-ary anbdi 1
40
2Q 30 IO PULMONARY ARTERY WEDGE MEAN
0
IO
20
M
PULMONARY ARTERY WEDGE MEAN
mm Hg
mm. Hp.
Figure 1. Correlation between mean pulmonary arterial wedge pressure and (A) mean pulmonary arterial pressure and (B) pulmonary arterial diastolic pressure (diastolic pressure not obtained in 1 patient). SD = residual standard deviation of y about regression line. Broken line = line of identity.
Pressures were transduced with a Bell and Howell 4-327-L221 strain gauge manometer and recorded on a Devices M4 direct-writing recorder. Zero reference level for the manometer was taken as 5 cm below the level of the manubrium sterni. Mean pressure values were obtained by electrical integration. Right ventricular end-diastolic pressure was taken as the level immediately before the beginning of the upstroke of the systolic portion of the ventricular pressure curve. Arterial
and mixed
venous
blood
samples
were
analyzed immediately for oxygen tension, carbon dioxide tension and pH levels with the use of R.adiometer equipment. The oxygen saturation of the blood was derived from the arterial oxygen tension with a correction for pH and carbon dioxide tension by means of the Severinghaus blood-gas calculator. The hemoglobin capacity was determined by a spectrophotometric technique using a Unicam SP 600, or it was derived from the hemoglobin concentration of the sample. The oxygen content was calculated from the saturation and the hemoglobin capacity. Clinical and Radiological Assessment
Clinical examination was carried out and the findings recorded immediately before the insertion of the pacing electrode. Portable anteroposterior chest roentgenograms were taken within 6 hours of the pressure measurement. The appearance of the lung fields was assessed by a radiologist who had no knowledge of either the clinical features or pressure measurements. The pulmonary veins were recorded as normal or as showing slight-, moderate or marked dilatation. The presence of alveolar or interstitial edema was also recorded.
VOLUME
25, MAY 1970
Necropsies were performed in 12 of the 13 patients who died. All results are presented as mean values +l SD.
Results Pressures
The right atrial, right ventricular, mean pulmonary arterial and mean pulmonary arterial wedge pressures are presented in Table II. The mean pulmonary arterial wedge pressure ranged from 4 to 37 mm Hg and was above the upper limit of normal of 12 mm Hg in 24 patients. The average mean pulmonary arterial wedge pressure in the 13 patients who died was 23 + 9 mm Hg, which was significantly higher than the average level of 14 + 4 in the 17 survivors (P <0.005). Figure 1 shows that there was a significant correlation between the mean pulmonary arterial wedge pressure and both mean pulmonary arterial pressure (Fig. 1A) and pulmonary arterial diastolic pressure (Fig. 1B). However, the diastolic pressures corresponded more closely to the pulmonary arterial wedge values than did the mean pulmonary arterial pressures. The gradient between the mean pulmonary arterial pressure and the mean pulmonary arterial wedge pressure averaged 8 * 5 mm Hg and did not correlate significantly with either the arterial oxygen tension (Pa09) or the arteriovenous oxygen content difference. The correlation between me,an right atria1 and ?nean pulmonary arterial wedge pressures is shown in Figure 2. In patients with anterior infarction there was a sig-
515
LASSERS ET AL.
4or
. .
RIGNT ATRIAI MEAN KIESSUE mmHq
PuLbaxARYARTERY
33
WED&ZMEAN mm.Hp.
25
. T
!
I
-?-
J..
i
4‘: t
I_ .
cl
: Figure 2. Correlation between pulmonary arterial wedge and right atrial pressures. Upper regression line (r = 0.699): patients with acute isolated inferior infarction; lower regression line (r = 0.586): patients with acute anterior infarction. Sites of old infarction have not been considered, and 1 patient (Case 29) with anterior infarction and multiple pulmonary emboli has not been included (significance of difference between slopes of regression lines = 0.10 > P > 0.05).
nificant correlation between the two pressures (r = 0.586; P <0.05), and the right atria1 pressure did not reach abnormal levels until the mean pulmonary arterial wedge pressure was above about 12 mm Hg (slope of regression line = 0.238). In the 5 patients with inferolateral infarction (not shown in Fig. 2), the slope of the regression line was almost identical (0.239). In patients with isolated inferior infarction (r = 0.699; P <0.05)the right atria1 pressure tended to rise more steeply (slope of regression line = 0.812) ; however, the number of cases involved was small and the difference between the slopes of the regression lines did not reach statistical significance (0.10 >P >0.05). Further observations are required to determine whether this trend is a real one. On the other hand, in some patients with an inferior infarction the level of mean right
40
I
301 0
n=25
8
12
16
20
PUlMNARYMEAl
24
28
32
M
40
WEDGEELAN
mm.Hp.
Figure 3. pulmonary
516
Relation
between
pulmonary
arterial
wedge pres(0.10 > P >
atria1 pressure was markedly elevated (14 to 19 mm Hg), whereas the level of mean pulmonary arterial wedge pressure was normal or only mildly elevated (11 to 16 mm Hg). Thus, although the level of elevation of the right atria1 pressure is a fairly reliable guide to the level of elevation of the mean pulmonary arterial wedge pressure in patients with anterior infarction, the right atria1 pressure may be disproportionately high in patients with isolated inferior infarction. Arterial Oxygen Tension (PaO,)
PaOz, measured in 25 patients, ranged from 39 to 97 mm Hg and was below the lower limit of normal of 85 mm Hg in 21 (Table II). There was a significant correlation (Fig. 3) between PaOz levels and the mean pulmonary arterial wedge pressure although PaOz levels ranged widely in patients with mean pulmonary arterial wedge pressures between 14 and 18 mm Hg. The average PaOz level of 69 -t 15 mm Hg in the survivors was not significantly different from the level of 65 t 13 mm Hg in those who died; however, Pa& was not measured in 1 patient who lived or in 4 patients who died. Arterial Carbon Dioxide Tension (PaCOJ
r-0620
p~Ooo1
4
Figure 4.
sure and the presence or absence of dyspnea 0.05).
Correlation between arterial a’rterial wedge pressure.
oxygen tension
and
PaCOz ranged from 21 to 53 mm Hg (Table II). There was evidence of alveolar hyperventilation with PaGO levels of less than 36 mm Hg in 10 patients and mild alveolar hypoventilation with PaCOa levels of 47 and 53 mm Hg in 2 patients, 1 of whom had chronic bronchitis.
The Amarlcan
Journal
of CARDIOLOGY
LEFT
VENTRICULAR
FAILURE
IN
ACUTE
MYOCARDIAL
.
.
..
: FlJlMONhRY WEDGE
INFARCTION
T
APTERY MEAN
f
mm. H9.
I
4 i:
f *
i
s: +-
.
Relation between persistent Figure 5. basal rates and (A) pulmonary arterial wedge pressure (0.10 > P > 0.05). and (B) arterial oxygen tension (PaO?) (P > 0#90).
Arteriovenous Oxygen Content Difference (Ca02 - CVOn)
CaOz - CVO, levels ranged from 1.91 to 12.69 volJlO0 ml and were above the upper limit of normal (4.50 vol/lOO ml ) l4 in all but 3 patients (Table II). There was no significant relation between the mean pulmonary arterial wedge pressure and CaOz - C002 levels. Clinical and Radiologic Features
Dyspnea : Eight patients had dyspnea at the time of study (Table I). The mean pulmonary arterial wedge pressure in these patients ranged from 14 to 33 mm Hg; the average value (23 + 6 mm Hg) was not significantly different from the average mean pulmonary arterial wedge pressure (17 f. 8 mm Hg) in the patients without dyspnea (0.10 >P >0.05) (Fig. 4). Pa09 was not measured in 3 patients with dyspnea; the average value (65 * 4 mm Hg) in the remaining 5 was not significantly different from the average (68 2 16 mm Hg) in the patients without dyspnea. arterial Rales : The average mean pulmonary wedge pressure did not differ significantly between those patients with (20 * 7 mm Hg) and those without (14 f 7 mm Hg) persistent basal rales (0.10 >P >0.05) (Fig. 5A). Rales were present in all 5 patients with mean pulmonary art.erial wedge pressures greater than 25 mm Hg, absent in 3 patients with pressures between 20 to 25 mm Hg and present in 11 patients with normal or slightly increased pressures. There was no significant difference in the average PaOz level between patients with and without rales (P >0.90) (Fig. 5B). There was no significant Added heart sounds: difference between the average mean pulmonary arterial wedge pressure in patients with and without audible added heart sounds (P >0.30) (Fig. 6). Added
VOLUME
25, MAY
1970
-
Z-0
RALES
RALES PRESENT
t---
ABSENT
i
sounds were present in all but 1 patient with a mean pulmonary arterial wedge pressure above 20 mm Hg but were also present in a large proportion of patients with normal or moderately increased pressures. However, there was a group of patients with mesodiastolic gallop rhythms-that is, gallop rhythms observed when tachycardia makes it impossible to determine clinically whether the added sound is a third or fourth heart sound or a summation gallop.ls In these patients the average mean pulmonary arterial wedge pressure was significantly higher than in patients who had no added heart sounds (P
fw4ctw
~nnxw
WEDGE
25-
MEAN
mm.Hg.
.
20 T
.
IS -
IO -
i
. .
0
Figure 6. Relation between pulmonary arterial sure and added heart sounds (P > 0.50).
wedge pres-
517
LASSERS
ET AL.
. ,-
.-’ .
Figure 7. Correlation between heart rate and pulmonary arterial wedge pressure in patients with sinus rhythm and normal atrioventricular conduction. (SD of rate about regression line = lO/min.)
Systemic blood pressure and cardiogenic shock: The systolic blood pressure was unrecordable in 1 patient and ranged from 80 to 160 mm Hg in the remainder. It was less than 100 mm Hg in 13 patients (Table I). There was no significant correlation between the systolic pressure and the mean pulmonary arterial wedge pressure (T = 0.338), but the average mean pulmona,ry arterial wedge pressure was significantly higher in patients with systolic pressures of 100 mm Hg or less than in those with higher systolic pressures (P <0.05). There was no significant relation between PaO,n and systolic blood pressure. Cardiogenic shock, defined as a systolic blood pressure of less than 90 mm Hg accompanied by diminished mental function and evidence of intense cutaneous vasoconstriction, was present in 5 patients. The mean pulmonary arterial wedge pressure was normal in 1 of these patients (11 mm Hg), moderately in-
creased in 2 (21 mm Hg) and markedly increased in the remaining 2 (33 and 37 mm Hg) (Table II). The mean right atria1 pressure level was elevated in 4 of the 5 patients but did not reliably reflect the level of the mean puhnonary arterial wedge pressure. In 1 patient with a mean right atria1 pressure of 4 mm Hg the mean puhnonary arterial wedge pressure was 21 mm Hg, whereas in another patient with a mean right atria1 pressure of 14 mm Hg the mean pulmonary arterial wedge pressure was normal (11 mm Hg) . Chest roentgenograms: These roentgenograms were taken within 6 hours of pressure measurements’ in 27 patients (Table II). There was a significant difference between the average mean pulmonary arterial wedge pressure in patients with normal lung fields and in those with radiographic evidence of pulmonary venous dilatation (2’ <0.05) or pulmonary edema (P <0.005). Although there was no significant difference in the mean pulmonary arterial wedge pressure among patients with slight, moderate or marked pulmonary venous dilatation, the pressure was significantly higher in patients with edema than in patients with dilatation only (P
c-l -
. Qt.
2 fVLp(oNARY UEffiE
ARTERY MEAN
mm. Hq
.
Til
4 .
I +
"9
ea-
mm&q. m-
i i
i .
I
!
j_ .
T M
1. .
I
FiTiFPULMONARY EDEMA
PlJLMONAtW MtiaJS DILATATI’34
DLATAT0N
I
Iwu4DNAFlY EDEMA
Figure 8. Relation between radiographic appearance of lung fields and (A) pulmonary arterial wedge pressure and (8) arterial oxygen tension (Pa&). (See text for levels of significance.)
B 518
The
American
Journal
of
CARDIOLOGY
LEFT
TABLE
VENTRICULAR
FAILURE
IN
ACUTE
MYOCAROIAL
INFARCTION
III
Necropsy
Findings Necropsy
Findings
Pressures
-~ Site of Old Infarction Case no.
Coronary Artery Involved*
Site of Infarct (Electrocardiogram)
Left Ventricle
Left Ventricle
Right Ventricle None None None
Inferior Inferior Lateral,
None None
Right Ventricle
Mean Pulmonary Arterlal Wedge
Mean Right Atrial
Inferior Inferior None
11 21 21
14 12 11
Lateral, inferior Anterior, lateral, inferior
None Inferior
26 27
10 20
None
Septum, lateral
anterior,
None
37
9
None
None
Septum, lateral
anterior,
None
17
8
Inferior
None
Septum, lateral
anterior,
None
21
4
LAD0
Inferior
None
Septum, anterior, lateral, inferior
None
23
14
Anterior Anterior
LAD0 LAD0
Inferior, Inferior,
None None
Septum, Septum, lateral
anterior anterior,
None None
23 33
4 14
Anterior
LAD0
None
None
Septum, lateral
anterior,
None
34
16
4 20 22
Inferior Inferior lnferolateral
26 27
lnferolateral Inferior, anterior
LCO RsapLAD,,, LCss
None None Anterior, lateral, inferior Anterior, lateral Lateral, inferior
30
LBBB
LADss
None
18
Anterior
LAD0
21
Anterior
R ss, LAD,,,
23
Anterior
24 28 29’
* LAD = left anterior descending; stenosis. + Multiple pulmonary emboli.
LBBB
LCss
= left bundle
lateral lateral
branch
this treatment may have resulted in a reduction in mean pulmonary arterial wedge pressure and an increase in Pa02. Individuals having X-ray evidence of pulmonary venous dilatation or edema and those with normal lung fields were clearly demarcated with respect to the relation between Pa& and mean pulmonary arterial wedge pressures (Fig. 8). Necropsies : The necropsy findings are presented in Table III.
Discussion Both atrioventricular and bundle branch block after acute myocardial infarction are often associated with severe underlying myocardial damage.llJ” For this reason, a much larger proportion of our patients had clinical evidence of moderate or severe cardiac failure than would be expected in an unselected group of patients with acute myocardial infarction. In addition, the conduction defects themselves may have affected left ventricular function. Thus, both the loss of atria1 transport function resulting from atrioventricular block and the loss of synchronism of ventricular contraction associated with bundle branch block might affect left ventricular end-diastolic pressure,l’ and, therefore, left atria1 and pulmonary arterial wedge
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Site of Recent Infarction --___-
(mm Hg)
25, MAY 1970
block;
inferior
LC = left circumflex;
R = right;
o = occluded;
ss = severe
pressure. However, these considerations should not invalidate t,he relation between left ventricular failure and its clinical manifestations. Left ventricular “failure” after acute myocardial infarction has often been equated with an increase in left ventricular end-diastolic and, therefore, left atria1 pressure. However, although an increase in left ventricular end-diastolic pressure may be one of the first measurable hemodynamic changes in the development of ventricular failure,l* it has limitations as an index of ventricular function. For example, the end-diastolic pressure may be normal in spite of diminished myocardial contractility if there is an increase in ventricular compliance and consequently an increase in ventricular end-diastolic and end-systolic volumes.lOJO Despite these limitations, left ventricular end-diastolic and left atria1 pressures are probably the most reliable indexes of left ventricular failure that have presently been obt.ained in acute myocardial infarction. Therefore, the mean pulmonary arterial wedge pressure, which corresponds closely to the left, atria1 pressure, has been used in our study. Clinical and Radiographic Features of Left Ventricular Failure Dyspnea,
added
heart
sounds
and persistent
basal
519
LASERS
ET AL.
rales are the principal clinical features that usually indicate left ventricular failure after acute myocardial infarction.“l However, our study shows that dyspnea, third and fourth heart sounds and rales are not well correlated with the mean pulmonary arterial wedge pressure. Observer error may account in part for the fact that added heart sounds and rales were not found in some patients with moderately increased mean pulmonary arterial wedge pressures (12 to 20 mm Hg), although they were detected in other patients with similar pressures and in 3 patients with normal pressures. The use of phonocardiography might have eliminated observer error in the detection of added heart sounds. However, phonocardiograms detect fourth heart sounds in more than 90 percent of cases of acute myocardial infarction22 and therefore are of little value in discriminating between the presence and absence of heart failure. The overlap in mean pulmonary arterial wedge pressure levels between the dyspneic and nondyspneic patients may have occurred part’ly because breathlessness is a subjective symptom and often difficult to evaluate. Thus, it is clear fom the PaC02 levels that hyperventilation occurred in several patients who did not complain of breathlessness or appear to be in respiratory distress. Respiratory rate would have provided a more objective assessment, but it was not recorded. It is unlikely that all of the discrepancies between these clinical findings and the mean pulmonary arterial wedge pressures can be attributed to observer error. Part of the explanation may be that elevation o,f the left ventricular end-diastolic or pulmonary venous pressure is not in itself the immediate physical mechanism producing added heart sounds, rales or dyspnea.23-a6 The clinical signs that did have a significant association with elevation of the mean pulmonary arterial wedge pressure were mesodiastolic gallop rhythms, tachycardia and systolic blood pressures of less than 100 mm Hg. In addition, there was a good correlation between the radiographic findings of pulmonary venous dilatation or edema, or both, and the mean pulmonary arterial wedge pressure. Despite this good correlation there was a considerable overlap in mean pulmonary arterial wedge pressures between patients with norma and abnormal lung fields (Fig. 8A). This is probably because fluid produced by an elevation in pulmonary venous pressure will take some time to be absorbed after the pressure falls. The differences in radiographic appearance in patients with similar mean pulmonary arterial wedge pressures emphasize that a pressure measurement reflects the state of pulmonary venous hemodynamics at only one point in time, whereas the roentgenogram also reflects earlier events.
520
Central Venous Pressure Increased central venous pressure after acute myocardial infarction is generally considered to reflect right ventricular failure secondary to failure of the left ventricle.“7 However, Herrick2* in 1912 suggested that right ventricular failure might follow occlusion of the right coronary artery, whereas obstruction of the left artery might produce left ventricular failure; the studies of Fluck et al6 and Lassers et al.“g have shown that this does occur in certain cases, They found some elevation of the right ventricular enddiastolic pressure in some patients with inferior infarction, which could not be accounted for by either pressure or volume overload of the right ventricle. In our study this dissociation of right and left ventricular failure was seen in 4 patients with electrocardiographic evidence of isolated inferior infarction. In addit.ion, patients with isolated inferior infarction tended to have higher mean right atria1 pressures for a given mean pulmonary arterial wedge pressure than did patients with anterior or inferolateral infarction, although this tendency was not statistically significant,. The explanation of dominant right verdricdar failure in some patients with electrocardiographic evidence of isolated inferior involvement is probably that infarction in this site is due to occlusion of the right coronary artery.“” The right’ coronary artery usually supplies the inferior, lateral a’nd most of the anterior wall of the right ventricle and a variable portion of the inferior surface of the left ventricle with collateral circulat,ion provided by the left anterior descending artery. 81~SZOcclusion of this artery can therefore affect the right ventricle more severely than the left,“” but the effect on right ventricular function in an individual patient will depend on the patency of the left anterior descending artery and the distribution and adequacy of anastomotic and collateral circulation. The necropsy findings in our patients support this observation since the 2 patients with elect’rocardiographic evidence of isolated inferior infarction who died had right coronary artery occlusion combined with severe stenosis of the left anterior descending artery (Table III). Pulmonary Arterial Hypertension The pulmonary arterial hypertension that may follow acute myocardial infarction has usually been attributed to left ventricular failure with a consequent increase in left atria1 and pulmonary venous pressure. However, since acute infarction is often accompanied by arterial hypoxemia, which is known to produce an increase in pulmonary vascular resistance,31*85 it is possible that this mechanism could also contribute to the increased pulmonary arterial pressures.
The Americen
Journal
of CARDIOLOGY
LEFT
In our study there was a direct and usually close correlation between the mean pulmonary arterial wedge and mean pulmonary arterial pressures (Fig. 1A). The gradient between these pressures averaged 8 + 4 mm Hg and ranged from 3 to 26 mm Hg (Table 111. However, only 4 patients had gradients of greater than 10 mm Hg, and 1 of these patients (Case 5)) with a gradient of 18 mm Hg, was known to have chronic bronchitis, whereas another (Case 29 1, with a gradient of 26 mm Hg, was found at necropsy to have multiple pulmonary emboli. A closer relation was found between the mean pulmonary arterial wedge pressure and the pulmonary arterial diastolic pressure (Fig. 1B). On the basis of these results it can be concluded that unless some ot.her factor such as obstructive airways disease or pulmonary embolism is present, the mean pulmonary arterial pressure is a fairly reliable reflection of mean pulmonary arterial wedge pressure in acute myocardial infarct,ion but that the pulmonary arterial diastolic pressure is a superior index.
Pulmonary Arterial Wedge Pressure and PaO, The reduction in Pa& which follows acute myocardial infarction has been well documented and is thought to be due to an increased venous admixture resulting from regional inequality of ventilation and perfusion. X-Z+ This abnormality is most marked in patients with evidence of pulmonary congestion,S7-*1 and it has been suggested that left ventricular failure with an elevation in pulmonary venous pressures could produce this abnormality by causing local decreases in pulmonary compliance12 or by alveolar edema and narrowing of airways.““*“D,4z In our patients there was a statistically significant, correlation between the mean pulmonary arterial wedge pressure and Pa@,, (Fig. 31. However, even in
VENTRICULAR
FAILURE
IN
ACUTE
MYOCARDIAL
INFARCTION
those patients with normal pressures at. the tim(a of study there was a mild but’ definite rccluction in P:t( )-. Furthermore, in patient’s with mild elevation of tjho mean pulinonary arterial wedge pressure, t#he Pa(‘),, ranged widely (57 to 97 mm Hgl. It is possible that these patients represent. two ~eparnte groups. In oile group the pulmonary arterial we(Ige pressure may have previously been much higher than tlw level at the time of study, thus accouming for the S-ray findings of pulmonary congestion and the rccluccd Pan, level. In the second group the pulmonary arterial wedge pressure may not have been elevated much above the level found at measurement, and consequently their chest roentgenograms and PaO? levels were normal. Thus, although an elevation of pulmonary venous pressure due to acute left ventricular failure is the most likely initiating cause for the ventilation-perfusion abnormality after acute myorardial infarction the underlying physical mechanism that results from the elevated pressure may persist after the pressure has fallen or returned to normal levels. Further studies with sequential measurements begun very early after the onset of infarction would he necessary to confirm this hypothesis.
Acknowledgments We thank the physicians in charge and the medical and nursing staff of the Coronary Care Unit of the Royal Infirmary for their co-operation; Drs. D. Franklin, M. Godman and C. Vellani, who assisted with some of the studies; Dr. C. Bouch, who provided information from the necropsies; Mr. E. Harding for statistical advice; and Miss Margaret Lawrie and Miss Margaret Duncan for invaluable secretarial help. In particular. we thank Dr. D. CT.*Julian for his advice and generous contribution of ideas.
References 1. Kirby BJ, McNicol MW, Tattersfield 2.
3. 4. 5.
6.
Left ventricular AE: pressures in two patients with myocardial infarction. Lancet 1:944-946, 1968 Lequime J: The circulatory dynamics in coronary thrombosis, in Proceedings of the International Seminar on Arteriosclerosis (Datey KK, ed). New York, Asia Publishing House, 1964, p 151 Left and right ventriCohn JN, Khatri IM, Tristani FE: cular filling pressures in clinical shock (abstr). Ann Intern Med 68:1153, 1968 Nixon PGF: Pulmonary edema with low left ventricular diastolic pressure in acute myocardial infarction. Lancet 2:146-147, 1968 Nixon PGF, Taylor DJE, Morton SD: Left ventricular diastolic pressure in cardiogenic shock treated by dextrose infusion and adrenaline. Lancet 1:1230-1232, 1968 Right heart Fluck DC, Valentine PA, Treister B, et al: pressures in acute myocardial infarction.
VOLUME 25, MAY 1970
&it Heart J 29:748-757,
1967
7. Connolly DC, Kirklin JW, Wood EH: The relationship between pulmonary artery wedge pressure and left atrial pressure in man. Circ Res 2:434-440, 1954 8. Shaffer AB, Sllber EN: Factors influencing the character of the pulmonary arterial wedge pressure. Amer Heart J 51:522-532, 1956 9. Werkd L: The dynamics and consequences of stenosis or insufficiency of the cardiac valves, in Handbook of Physiology, Circulation, Vol 1. (Hamilton WF, Dow P, ed). Washington D. C., American Physiological Society, 1962, p 645-680 10. Sapru RP, Taylor SH, Donald KW: Comparison of the pulmonary wedge pressure with the left ventricular enddiastolic pressure in man. Clin Sci 34:125-140, 1968 11, Lassers BW, Julian Do: Artificial pacing in managment of complete heart block complicating acute myocardial infarction. Brit Med J 2:142-146, 1968 12. Godman MJ, Lassers BW, Julian DG: Pacing in the
521
LASSERS ET AL.
management of complete bundle branch block complicating acute myocardial infarction. New Eng J Med, in press 13. Siddons H, Sowton E: Cardiac Pacemakers. Springfield, Ill., Charles C Thomas, 1967, p 57 14. Wade OL, Bishop JM: Cardiac Output and Regional Blood Flow. Oxford, England, Blackwell Scientific Publications, 1962, p 37 Sound. 8altimore, Wil15. McKusick VA: Cardiovascular liams & Wilkins, 1958, p 174 16. Friedberg CK, Cohen H, Donoso E: Advanced heart block as a complication of acute myocardial infarction. Role of pacemaker therapy. Progr Cardiovasc Dis 10:466-&l, 1968 17. Sarnoff SJ, Mitchell JH: The control of the function of the heart, in Ref 9, Vol 1, p 489-532 18. Davis JO: The physiology of congestive heart failure, in Ref 9, Vol3, p 2071-2122 19. Braunwald E, Ross J Jr: The ventricular end-diastolic pressure. Appraisal of its value in the recognition of ventricular failure in man, Amer J Med 34:147-150. X963 20. Dodge HT, Sandler H, Baxley WA, et al: Usefulness and limitations of radiographic methods for determining left ventricular volume. Amer J Cardiot 18:10-24, 1966 21. Fctwler NO: Physical signs in acute myocardial infares tion and its complications. Progr Cardiovasc Dis 10:287-297, 1968 22. Hill JC, O’Rourke RA, Lewis RP, et al: The diagnostic value of the atrial gallop in acute myocardial infarction. Amer Heart J 78:194-201, 1969 23. Crevasse L, Wheat MW, Wilson JR, et al: The mechanism of the generation of the third and fourth heart sounds. Circulation 25:635-642, 1962 24. Nixon PGF: The genesis of the third heart sound. Amer Heart J 65:712-714, 1963 25. Forgacs P: Crackles and wheazes. Lancet 2:203-205,1967 Disturbances in pulmonary function in 26. Donald Kw: mitral stenosis and left heart failure. Progr Cardiovasc Dis 1:298-308, 1959
27. Sampson JJ, Hutchinson JC: Heart failure in myocardial infarction. Progr Cardiovasc Dis lO:l-29, 1968 28. Herrick JB: Clinical features of sudden obstruction of the coronary arteries. JAMA 59:2015-2020, 1912 29. Lassers BW, Anderton JL, George M, et al: Hemodynamic effects of artificial pacing in complete heart block complicating acute myocardial infarction. Circulation 38:308-323, 1968 30. James TN: The coronary circulation and conduction system in acute myocardial infarction. Progr Cardiovasc Dis 10:410-449. 1968 31. Ferrer-Brown G: Vascular pattern of right ventricle of human heart. 8rit Heart J 30:67Q-686, 1968 32, Hudson REB: Cardiovascular Pathology, Vol I. London, Edward Arnold, Ltd, 1965, p 603 33. Wade WG: The pathogenesis of infarction of the right ventricle. Brit Heart J 21:545-554, 1959 34. Fishman AP: Respiratory gases in the regulation of the pulmonary circulation. Physiol Rev 41:214-280, 1961 35. Rudolph AM, Yuan S: Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes. J Clin Invest 453399-411, 1966 36. MacKenzie GJ, Taylor SH, Flenley DC, et al: Circulatory and respiratory studies in myocardial infarction and cardiogenic shock. Lancet 2:825-832, 1964 37. McNlcol MW, Kirby BJ, Bhoola KE, et al: Pulmonary function in acute myocardial infarction. Brit Med J 2:1270-1273, 1965 38. Valentine PA, Fluck DC, Mounsey JPD, et at: Blood-gas changes after acute myocardial infarction. Lancet 2:837-841, 1966 39. Pain MCF, Stannard M, Sloman 0: Disturbances of pulmonary function after acute myocardial infarction. Brit Med J 2:591-594, 1967 40. Higgs B: Factors influencing pulmonary gas exchange during the acute stages of myocardial infarction. Clin Sci 35:115-122, 1968 41. Shapiro M, Fillmore S, Killip T: Hypoxemia and functional severity in acute myocardiai -infarction (abstr). Circulation 38: Suool 6:178. 1968 42. West JB: Ventilation/Blood Flow and Gas Exchange. Oxford and Edinburgh, Blackwell Scientific Publications, 1965, p 52