Respiratory Muscle Strength and

Respiratory Muscle Strength and
Hemodynamics in Chronic Heart Failure*
Yoshihiro Nishimura, M.D.; Hitoshi Maeda, M.D.; Katsuji Tanaka, M.D.;
Hirofumi Nakamura, M.D.; Yukako Hashimoto, M.D.; and
Mitsuhiro Yokoyama, M.D.
To examine whether respiratory muscle weakness is
associated with cardiac function andlor exercise capacity
in chronic heart failure (CHF), 23 patients with CHF
were evaluated with respiratory muscle strength,
pulmonary function tests, cardiac catheterization, and
exercise test The subjects were divided lntothree groups
on their New York Heart Association (NYHA) functional
class. Group A consisted of 13 patients with NYHA
functional classification class 3 or 4, group B consisted
of 10 patients with NYllAclassification class 2, and group
C consisted of 15 age-matched normal controls.
Respiratory muscle strength was assessed with maximal
static inspfratory mouth pressure at residual volume level
andexplratory mouthpressure at total lung capacity level
(Pimax, PEmax, respectively). Pulmonary functions In
entswith CHF showed almostnormaL Pimaxm group
A was significantly less than that In group B or C,
although Punaxin group B was not Significantly different
from that in group C. In the patients with CHF, Pimax
correlated positively with cardiac Index and maximal
oxygen consumption (r = 0.460 and r = 0.503, p < 0.05,
respectively). These findings suggest that lnspiratory
muscle strength, which was Impaired In patients with
severe CHF, may be dependent on cardiac function and
may be one ofthe limiting factors on Impaired exercise
capacity In the patients with CUE
(Chest 1994; 105: 355-59)
PAP = pulmonary artery pressure; PAWP pulmona
arterywedge pressure; Pasnax maximal expiratory mou
pressure; Pimax meximal inspiratory mouth pressure;
So5maz = mpima1 oxygen consumption
R espiratory muscle dysfunction has been reported in
various respiratory neuromuscular, and cardiac diseases.’4
Respiratory muscle strength is dependent on sex,
age, pulmonary function, respiratory muscle blood flow,
and nutritional status.” Until now, the relationship between
respiratory muscle strength and cardiac function
has not been well determined. Hammond et al6 documented
the respiratory muscle weakness in patients with
congestive heart failure and suggested that reduction in
respiratory muscle blood flow might be responsible for
the mechanism in respiratory muscle weakness. They,
however, did not show the relationship between respiratory
muscle strength and blood flow.
Ifrespiratory muscle strength is dependent on the systemic
blood flow level, we postulated that patients with
chronic heart failure (CHF) should exhibit respiratory
muscle weakness, which was responsible for reduction
ofblood flow in cardiac dysfunction. In the present study,
we evaluated the relationship among respiratory muscle
strength, cardiac function, and exercise capacity in patients
with CHF, and compared the results with those
from age-matched normal subjects. We demonstrated
that reduction in respiratory muscle strength in patients
with CHF was responsible for impaired cardiac function
and exercise capacity.
#{176}Fromthe First Department of Internal Medicine, Kobe University
School ofMedicine, Kobe, Japan.
Manuscript received October 27, 1993; revision acceptedJuly 1, 1993.
Reprint requests: Dr Nishimura. Takatsuki GenerefHospital, 1-3-13
Kosobe-cho, Takatsuki, Osaka 569, Japan
Patient
Population
METHODS
We studied 23patients with CHF (18 male and 5 female, mean age
± SD, 59.3 ± 9.2 years) and 15 age-matched healthy volunteers (12
male and 3 female, 60.2 ± 6.2 years). Patients with CHF consisted of
seven with old myocardial infarction, eight with old myocardial
infarction and anginapectoris, fourwith mitral valve disease, and four
with dilated cardiomyopathy (Table 1). Each patient was examined
while in a stable hemodynamic condition and free ofacute exacerbation,
although all the patients with CHF complained of exertional
dyspnea. We divided the subjects into three groups on their severity
ofdyspneaon effort. Group A consisted ofl3 patients with New York
Heart Association (NYHA) functional classffication class 3or4. Group
B consisted oflOpatients with NYHA functional classification class 2.
GroupC consistedofl5 age-matthedcontrob. Subjects whohad some
evidence ofneuromyopathic disease, recent surgery, hypoproteinemia,
and/or electrolyte abnormalities were excluded. Informed consent was
obtained from each person for this protocol.
Measurement ofRespiratory Muscle Strength
Maximal static inspiratosy and expiratory mouth pressures were
measuredin all patients accordingtothe technique ofBlack and Hyatt7
(using Vitalopower KH1O1, Chest MI, Co Ltd. Tokyo). This device
consists oftwo parts: a plastic cylinder and a calculator. The cylinder
has a closed end with a strain gauge pressure sensor and a small side
hole that minimizes oral pressure artifacts. The opposite end is fitted
with a mouthpiece. The time-pressure curve is displayed on a chart.
Maximal inspiratosymouth pressurewas measured at level of residual
volume (RV) (Pimax) and maximal expiratory mouth pressure was
obtained at level oftotal lung capacity (TLC) (Psmax). Patients performed
the maneuver for the measurement of respiratory muscle
powerin theirmaximal inspiratosyand expiratoryefforts atleast three
times at two lung volume levels and we adopted the maximal values in
their maneuver for analysis. The predicted values for age and sex were
corrected by our institution formulas, and percentages of Pimax and
for predicted values were calculated (percent Pimax and per-
CHEST I 105 I 2 I FEBRUAR 1994 355
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No.
Age, yr/
Sex
Table 1-Characteristics in fldients With
Chronic Heart Thilure#{176}
Height,
cm
V.ight,
kg
Clinical
Diagnosis
Myocardial
Ischemia
During
Exercise
GroupA .
NYHA
1167/F 144 46 MVD - 4
2/69/M 155 45 MVD - 4
3/66/M 162 68 OMI - 3
4/48/F 158 55 DCM - 3
5rwM 157 51 DCM - 3
6/63/M 170 76 DCM - 3
7/4WF 146 42 MVD - 3
8/68/M 165 60 OMI,AP + 3
93/M 162 63 OMI,AP + 3
12/M 160 56 OMI, AP + 3
1V6’F 158 67 OMI,AP + 3
12/TIJM 165 63 OMI, #{192}Y + 3
13/6WM 165 60 OMI,AP + 3
Group B
14162/M 158 58 OMI - 2
15164/M 162 54 OMI - 2
1&7/M 169 70 OMI - 2
17/45/M 160 54 OMI - 2
18/63’M 161 55 OMI - 2
19/4S/M 165 63 OMI - 2
20158/M 173 62 DCM - 2
21151fF 153 42 MVD - 2
2214WM 167 71 OMI,AP + 2
23/6WM 152 62 OMI,AP + 2
NYHA= New York Heart Association functional classification;
M = male; F = female; OMI old myocardial infarction;
AP= angina pectons; MVD = mitral valve disease; DCM = dilated
cardiomyopathy.
cent PEmax, respectively). The formulas established for Japanese
healthy persons are as follows.5
Male: PEmax 149 - 0.59 X AGE cm H2O(r = - 0.325,
p , 0.05)-.(1)
Pimax = 131 - 0.76 x AGE cm H2O(r = - 0.476,
p < 0.01)-(2)
Female: PEmax 93 - 0.33 X AGE cm H2O(r = - 0.277,
p < 0.05)-(3)
Pimax 102 - 0.69 X AGE cm H2O(r -0.438,
p < 0.01)-(4)
Pulmonanj Function Test
Vital capacity (VC), forced vital capacity (FVC), forced expiratory
volume in 1 S (FEy1), and TIC were measured using the spirometer
ofcomputer processing (Autospirometer System-55, Minato Medical
Science Co Ltd. Osaka, Japan) and the ratio of FEy1 for forced vital
capacity (FEV1/FVC) was calculated.
Cardiac Catheterization and Exercise Studies
Mean pulmonary artery pressure (PAP) and mean pulmonary artery
wedge pressure (PAWP) were measured with a Swan-Ganz catheter
that was advanced into the right pulmonary artery. The direct
Fick method was employed for measurement of the cardiac output
from which the cardiac index (CI) was calculated.
Exercise capacity was studied on an electrically braked bicycle ergometer
in a supine position. An incremental exercise was performed
to a symptom-limited maximum. The work load was increased by 25
W every 3 mm. The expired gas was analyzed for fractions of oxygen
and carbon dioxide by RM-300 (Minato Medical Science, Co. Ltd.,
Osaka, Japan), and maximal oxygen consumption (Vo2max) was calculated.
Statistical
Analysis
All values are given as mean ± SD. Statistical differences for vanables
of respiratory muscle strength and pulmonary function were
anal by analysis ofvaniance (ANOVA). Differences for hemodynamic
data between two CHF groups were evaluated by Students t
test. Relationships between respiratory muscle functions and hemodyn
amic parameters were assessed by linear regression analysis. Values
ofp < 0.05 were considered to be statistically significant.
RESULTS
The anthropometric data are shown in Table 2. Ages
were not significantly different among group A, group
B, and controls. Height and body weight did not differ
significantly among three groups. Plasma albumin level
in group A was not significantlylower than that in group
B (3.7 ± 0.2 and 3.9 ± 0.3 g/dl, respectively). Six of 13
patients with group A and 2 of 10 patients with group B
showed myocardial ischemic response during exercise
test.
Mean values ofpulmonary function variables showed
within normal limits in both group A and B. There were
no significant differences in pulmonary function variables
among three groups. In cardiac catheterization, PAP and
PAWP of group A were significantly higher than those
ofgroup B. The CI and Vo2max ofgroup A were significantly
lower than those ofgroup B.
Figure 1 shows respiratory muscle strength in the patients
with CHF and normal subjects. The mean value
of Pimax in group A was 60 ± 15 cm H20, which was
significantly smaller than the values in group B and group
C (92 ± 32, 84 ± 24 cm H20, p < 0.05, respectively).
Percent Pimax in group A was also significantly smaller
than those in the other two groups. PEmaX and percent
PEmax were not significantly different among three
groups.
There was a significant positive correlation between
percent Pimax and CI in patients with CHF (r 0.460,
p < 0.05) (Fig 2). Percent Plmax had a significant correlation
with Vo2max (r 0.503, p < 0.05) in 15 patients
with CHF without myocardial ischemic response during
exercise test (Fig 3).
DISCUSSION
We have demonstrated that respiratory muscle
strength exhibited reduction in patients with severe CHF
and that the impairment in inspiratory muscle strength
was intimately related to the deterioration in cardiac
function and to the impaired exercise capacity. This may
support our hypothesis that, if respiratory muscle
strength is dependent on the cardiac dysfunction, the
patients with CHF should exhibit respiratory muscle
weakness related to cardiac output.
Our present study showed that patients with severe
CHF (group A) exhibited inspiratory muscle weakness
compared with patients with mild heart failure (group
356 Respiratory Muscle Strength In Chronic Heart Failure (Niahimura et aQ
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Table 2-Anthropometric Data, IWmonary Function Thst Hemodynamics and Respiratory Muscle Strength in }btients
With CUP and Age-Matched Normal Subjects
CHF
Age-Matched
-
Control
Data Group A Group B Group C
Anthropometnic data
n 13 10 15
Sex, maleffemale 9/4 9/1 12/3
Age,yr 62.2±8.1 55.4±10.1 60.2±6.2
Height,cm 159.0±7.1 162.0±6.4 160.2±8.7
ight, kg 57.8±9.6 59.1 ±8.1 62.1 ± 10.4
Pulmonary function test
VC, L 3.03±0.68 3.38±0.57 3.39±0.73
%pred 99.6±12.7 99.5±12.8 108.2±16.2
FEY1, L 2.28±0.49 2.74±0.58 2.57±0.61
FEVI/FVC, % 77.8±9.0 80.1±7.5 78.6±5.0
TLC, % pred 92.3± 11.5 82.3± 14.2 96.1±26.5
Hemodynamics
PAI mm Hg 19.9±5.lt 12.8±2.6
PAWP, mm Hg 12.2±4.9t 6.6± 2.2
CI,LImin/m’ 2.49±O.73t 3.10±0.72
Vo2max, mi/mm/kg 11.9±2.8t 18.6±3.2
Respiratory muscle strength
Punax, cm HO 60± 15fl 92±32 84±24
%_ 80±2ltt 107±34 106±24
Pnmax, cm HO 84± 18 104±34 106±34
%_ 85±25 90±24 102±29
0VC = vital capacity; FEV1 = forced expiratory volume in 1 5; PVC = forced vital capacity; PAP = mean pulmonary artery pressure;
PAWP = mean pulmonary artery wedge pressure; CI = cardiac index; Vo2max = maximal oxygen consumption; Pimax = maximal inspiratory
mouth pressure; % Pimax = percent of maximal inspiratory mouth pressure for predicted value5; Psmax = maximal expiratory mouth
pressure; % PEmax = percent of maximal expiratory mouth pressure for predicted value.5 Values are mean ± SD.
tp

%Plmax (%)
200.
150
100.
50.
A-
VO2max/BW
(mI/mm/kg)
8
6
4
2
0
. #{149}11 #{149}. #{149}
.
1 3 5
.
Cl U2)
FIGURE 2. Relationship between percent Pimaxand CI in patients with
CHF. The real line is the regression line. Percent Plmax is significantly
correlated with CI (r = 0.460, p < 0.05).
The second is generalized skeletal muscle weakness.
Lecarpentier et al reported that reduction in respiratory
muscle function in a rabbit model with CHF was
associated with cardiac cachexia, suggesting that respiratory
muscle weakness was related to the generalized
muscle weakness. Although our anthropometric data
showed no cachexic condition among three groups, generalized
muscle weakness resulting from cardiac dysfunction
plays an important role in part for inspiratory muscle
weakness in patients with CHF.
Pulmonary function abnormalities and nutritional status
influence respiratory muscle function.5 Decreased
TLC should cause reduction in expiratory muscle
strength, and augmentation in RV should induce deterioration
in inspiratory muscle strength. Furthermore,
.
#{149}#{149}
0 50 100 150
.
%PI max (%)
.
malnutrition might be responsible for respiratory muscle
weakness. There was, however, no significant difference
of variables of pulmonary function tests among three
groups, and no subject was included in this study who
exhibited abnormalities of pulmonary function and nutritional
status.
In the present study, Vo2 max significantly correlated
with Pimax. Sera’#{176} showed that patients with severe CHF
exhibited much more increase in airway resistance and
decrease in dynamic pulmonary compliance during exercise
than do patients with mild heart failure, suggesting
that the respiratory muscle in patients with severe
CHF might be loaded much more than in patients with
mild CHF. In skeletal muscles, on the other hand, the
perception of heaviness of a lifted object or of achieved
force in an isometric contraction depends on sensing the
grade of effort, or voluntarily generated input to monotones,
rather than an afferent sensation signaling the
muscular force achieved.” The sense ofeffort increased
in relation to the augmentation of inspiratory loading
pressure and the intensity of sense of effort in fatigued
muscle was stronger than that in fresh muscle.’ It is suggested
that respiratory muscle in patients with severe
CHF plays a more important role in exercise capacity
than it does in patients with mild CHF, and that inspiratory
muscle function may be one of the limiting factors
ofexercise capacity in patients with CHF, while myocardial
ischemia should play an important role in exercise
capacity in the ischemic patients.
We used maximal inspiratoiy and expiratory mouth
pressures to estimate inspiratory and expiratoiy muscle
strength, because measurements ofmaximal mouth pressure
could be performedwith an easy maneuver and with
good reproducibility.5 As two components, the pressure
generated by respiratory muscles and the recoil pressure
ofthe respiratory system, were intimately associated with
maximal mouth pressure, the pure mouth pressure generated
with the respiratory muscles should be obtained
aftercorrection forthe factor induced by recoil pressure.’3
In this study, actual lung volume was not simultaneously
measured while the maximal mouth pressure was measured.
Therefore, both Pimax and PEmaX might be overestimated.
We concluded that inspiratory muscle strength, which
may be responsible for cardiac output, is significantly
correlated with Vo2max in the patients with CHF without
myocardial ischemia. This may suggest that inspiratory
muscle may be dependent on cardiac function and
200 may be one of the limiting factors in impaired exercise
capacity in the patients with CHF.
FIGURE 3. Relationship between percent Pimax and Vo5max in the
patients with CHF without myocardial ischemia during exercise. The
real line is the regression line. Vo2max is significantly correlated with
percent Plmax (r 0.503, p < 0.05).
ACKNOWLEDGMENT: The authors thank H. Yamabe, M.D., and
A. Hashimoto, M.D., for invaluable help in exercise data collection.
358 Respiratory Muscle Strength in Chroi* Heart Failure (Nishimura at al) 2
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