Relationship between Pulmonary Hemodynamics and Arterial pH and Carbon Dioxide Tension in Critically III Patients* Jaime Figueras, M.D.; Leon Stein, M.D.;oO Victor Diez, J-f.D.; Max Harry Weil, M.D., F.C.C.P.; and Herbert Shubin, M.D.t

To ascertain the cUnicai significance of derangements in arterial pH and arterial carbon dioxide tension (paC02) In modifying pulmonary arterial pressures and pulmonary vascular resistance in critically ill patients, the relationship between these two sets of variables was evaluated In 7S patients. No significant dUferences in pulmonary hemodynamic values were found among patients with acidemia, a normal pH, or alkalemia, even at extreme pH values; and there was no consistent reladonship between PaC02 and each of the pulmonary hemodynamic

T he usefulness of monitoring pulmonary arterial

pressures in critically ill patients has become increasingly recognized, for it provides invaluable information about intravascular filling volume and cardiac competence. The influence of the arterial pH and arterial carbon dioxide tension (PaC02) on the pulmonary vasculature is a subject of considerable controversy. Increased pulmonary vascular resistance has been noted in animals and humans following the production of metabolic acidemia in the presence>" or absencel.,3.4.6.7.9-12 of hypoxia, although several investigators have taken exception to thiS.13-16 When respiratory acidemia with or without hypoxia was induced, some investigators found. an increase in pulmonary arterial pressure and pulwhile others monary vascular resistance,1.2.11 noted either no alteration in the pulmonary vascular tone4.9.10.21 or vasodilation. 4.22,23 The presence of alkalemia, whether meta-

measurements. In patients who initially had a nonnal pH but subsequently developed acidemia or alkalemia, there was also no significant correlation between changes in pH and pulmonary hemodynamic values. We conclude that abnormalities of pulmonary hemodynamic values in seriously ill patients are usually due to factors other than acid-base derangements. Of practical importance is the observation that the predictability of the pulmonary arterial wedge pressure from the pulmonary arterial diastolic pressure is not invalidated by acid-base disturbances.

bolic4.5•7,24 or respiratory,4.5 has been reported clinically and experimentally to reduce pulmonary vascular resistance,2.10.19.25 but this has not been uniformly confirmed. 1.26-28 The present study was undertaken to evaluate the extent to which abnormal pulmonary hemodynamic findings can be accounted for by acid-base derangements in critically ill patients. Special emphasis was placed on the relationship between arterial pH, PaC02, and the pulmonary diastolic gradient (which represents the difference between pulmonary arterial diastolic and wedge pressures), since variations of this gradient affect the reliability of the pulmonary arterial diastolic pressure as an estimate of pulmonary arterial wedge pressure.

jl0

°From the Shock Research Unit and the Department of Medicine, University of Southern California School of Medicine, the Los Angeles County/University of Southern California Medical Center, and the Center for the. Critically Ill, Hollywood Presbyterian Medical Center, Los Angeles. This study was supported by Public Health Service research grants HL-05570 from the National Heart, Lung, and Blood Institute; GM-I6462 from the National Institute of General Medical Sciences; and ROI HS 01462 from the Health Resources Administration, and by the Parker B. Francis Foundation. oOPresently with the Department of Medicine Wishard Memorial Hospital, Indiana University Medical Center, Indianapolis. tDeceased. Manuscript received July 11, 1975; revision accepted April 5. Reprint requests: Dr. Weil, 1300 North Vermont, Los Angeles 90027

466 FIGUERAS ET At

MATERIALS AND METHODS

Clinical Material Seventy-five critically ill patients were the subjects of this study. There were 30 male and 45 female patients, with a mean age of 60 years (range, 15 to 87 years). The primary diagnoses were as follows: acute pulmonary edema or congestive heart failure or both, 11 patients; acute myocardial infarction, 12 patients, among whom five were in cardiogenic shock; sepsis, 15 patients, among whom 13 were or had been in shock; hypovolemic shock, ten patients; coma, 10 patients, among whom two had diabetic ketoacidosis, one had nonketotic hyperosmolality, two had marked hypoosmolality, and five had coma due to other causes; pneumonia, two patients; and chronic obstructive pulmonary disease (COPD), three patients. In addition to these last three patients, there were 14 others who had COPD complicating their primary condition.

CHEST, 70: 4, OCTOBER, 1976

Measurements A double-lumen or triple-lumen radiopaque flow-directed catheter (Swan-Ganz, No. 93/111/7Ft) was inserted either into the femoral vein by the percutaneous approach or into the median basilic vein by surgical cutdown. The catheter was then advanced into the pulmonary artery for measurements of pulmonary arterial and wedge pressures. An eightinch catheter (Longdwell 6723§) was inserted percutaneously into the internal jugular vein or the subclavian vein and was then advanced into the superior vena cava for measurement of the central venous pressure (CVP). The position of the catheter's tip was confirmed in each case both by pressure recordings and chest roentgenograms. A second eightinch catheter (Longdwell 6723§) was inserted percutaneously into the femoral artery by the Seldinger technique. Mean arterial pressure was calculated from the arterial pressure pulse by previously described techniques.2'9 The catheters were connected to a strain-gauge pressure transducer (Statham P23Db), and pressures were recorded on a directwriting Sanborn multichannel recorder ( Hewlett-Packard 964 ). The zero reference was the mid-chest level. The signals were transmitted to a computer (Xerox Data Sigma 5) for processing and display. 30 Cardiac output was measured by the indicator-dilution technique utilizing indocyanine green dye (2.5 or 5 mg ), which was injected into the pulmonary artery. Arterial blood was withdrawn from the femoral artery through a Harvard pump and sampled by a densitometer (Gilson DT1). Four-point calibration was used in each instance. The cardiac output, cardiac index, and stroke volume were calculated utilizing a digital computer.t! The arterial pH, PaC02, and arterial oxygen tension were measured using a standard technique with a blood gas analyzer (Radiometer PHA 927). Arterial oxygen saturation was determined using an oximeter (American Optical 182). The level of blood lactate was measured by a modification of the automated technique previously described by Boyeks and associates .132 Measurements of pulmonary arterial and wedge pressures were obtained during at least two respiratory cycles. Mean :Edwards Laboratory, Santa Ana, Calif. §Becton Dickinson Co.

pressures were derived electronically. The pulmonary arterial diastolic pressure was measured after the "a" wave, when present, or just prior to the systolic upstroke. The pulmonary diastolic gradient was calculated as the pulmonary arterial diastolic pressure minus the pulmonary arterial wedge pressure. The pulmonary vascular resistance (PVR) was calculated by the following formula: PVR

= PAMP-PAWP CO

X 80 (dynes sec cme )

where PAMP is pulmonary arterial mean pressure, PAWP is pulmonary arterial wedge pressure, and CO is cardiac output. Analysis The relationship between arterial pH and pulmonary arterial systolic, diastolic, mean, and wedge pressures and cardiac output were evaluated. For the purpose of evaluation, the patients were classified into the following three groups: (1) arterial pH < 7.35 (acidemia); (2) arterial pH 7.35 to 7.45 ( normal); and (3) arterial pH > 7.45 (alkalemia). To further analyze the relationship between pulmonary arterial pressures, cardiac output, and arterial pH, patients with marked acidemia (arterial pH ~ 7.25) were compared to those with marked alkalemia (arterial pH ~ 7.55). The relationship between sequential changes in arterial pH and changes in pulmonary hemodynamic findings also were evaluated. Among patients with acidemia, those with lactacidemia (blood lactate level 2.0 millimoles/L) were compared to those in whom the lactate level was less than or equal to 2.0 millimoles/L. The relationship between alkalemia and acidemia and pulmonary hemodynamic findings was also evaluated in patients in whom COPD and left ventricular failure, conditions known to affect the pulmonary arterial pressure or pulmonary vascular resistance, or both, were excluded. Patients were categorized as having COPD if there was a history of chronic hypoxia (arterial oxygen saturation < 94 percent) and carbon dioxide retention (PaC02 45 mm Hg). Patients who were considered to have left ventricular failure were those who had a pulmonary arterial wedge pressure greater than 14 nun Hg, bilateral rales, and a history of heart

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Table l-Relatiomhip between Arterial pH and PulmolUlry HemodYJUJmic J'alue. *

No. of patients Arterial pH Arterial oxygen saturation, percent PaC02 , mm Hg Pulmonary arterial pressure, mm Hg Systolic Diastolic Wedge Pulmonary diastolic gradient, mm Hg Pulmonary vascular resistance, dynes sec cm. 6 Cardiac output, L/min Cardiac index, L I minisq m Stroke volume, ml/beat Mean arterial pressure, mm Hg CVP, mm Hg Heart rate, beats per minute

Acidemia (pH < 7.35)

Normal pH (7.35-7.45)

Alkalemia (pH> 7.45)

26 7.28 ± 0.01** 93.5 ± 1.6t 38.0 ± 1.8

26 7.40 ± 0.01** 95.7 ± 0.8 38.7 ± 1.9

23 7.52 ± 0.01 ** 97.6 ± 0.7t 34.5 ± 2.1

28.2 ± 1.5 14.7 ± 1.0 10.1 ± 1.0 4.6 ± 0.7 192 ± 24 4.9 ± 0.4 3.0 ± 0.3 50 ± 3 70 ± 4t 7.8 ± 1.0 99 ± 4

32.6 15.1 10.0 5.1 232 5.2 3.1 53 78 6.6 96

± 2.1 ± 1.1 ± 0.7 ± 0.6 ± 32

± 0.6

± 0.3 ±5 ±4

± 0.8

±4

31.7 16.2 10.4 5.8 256 4.2 2.5 45 81 6.7 97

± 2.9

± 1.3 ± 0.9 ± 0.7 ± 48

± 0.5

± 0.2 ±5

± 4t

± 1.0 ±4

*Values shown are means ± SEe **p < 0.01. tP < 0.05.

CHEST, 70: 4, OCTOBER, 1976 RELATIONSHIP BETWEEN PULMONARY HEMODYNAMICS, ARTERIAL pH & CO 2 TENSION 467

800

RESULTS .... .:.:-:.:-:.:.:-:-:-:.:

•

600

400

200

• o 7.05

125

7.45

pH a , units

"165

FIGURE 1. Relationship between pulmonary vascular resistance and arterial pH. Normal arterial pH is indicated by shaded area (N = 117; r= 0.25).

disease. The relationship between PaC02 and pulmonary hemodynamic findings was evaluated. Patients were initially classified into the following two groups, regardless of their arterial pH: (1) PaC02 > 45 mm Hg; and (2) PaC02 < 35 mm Hg. To further assess the effect of hypercapnia and hypocapnia, these patients were then subclassified into the following three subgroups: (1) arterial pH < 7.35; ( 2) arterial pH, 7.35 to 7.45; and (3) arterial pH 7.45. Statistical analysis was performed using the two-tailed Student's t-test and analysis of correlation.

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Arterial pH and Pulmonary Hemodynamic Values There were no significant differences between the mean values for pulmonary arterial systolic, diastolic, and wedge pressures in patients with acidemia, alkalemia, and those with a normal pH (Table 1). This was also noteworthy in that patients who were acidemic had a significantly lower arterial oxygen saturation than those who were alkalemic. When patients within each of the three groups (acidemia, normal pH, and alkalemia) were further subclassified on the basis of their arterial oxygen saturation, there was no significant difference in the pulmonary arterial pressure, pulmonary arterial wedge pressure, or pulmonary vascular resistance between hypoxemic (arterial oxygen saturation < 94 percent) patients (mean values of 82.4 ± 3.4, 89.6 -+- 0.6, and 90.7 ± 1.2, respectively) and those with a normal (~ 94 percent) arterial oxygen saturation (mean values of 97.6 ± 0.4, 97.8 ± 0.4, and 98.6 ± 0.3, respectively) . The relationship between arterial pH and pulmonary vascular resistance is shown in Figure 1. The low correlation between arterial pH and the variable of pulmonary vascular resistance (r = 0.25) also was found with the following other variables: pulmonary arterial systolic pressure, r = 0.21; pulmonary arterial diastolic pressure, r = 0.07; pulmonary arterial wedge pressure, r = 0.12; and pulmonary diastolic gradient, r = 0.06. All of the correlations were statistically insignificant. The pulmonary hemodynamic values in five patients with marked acidemia (mean arterial pH, 7.15 ± 0.02 [SE]) were compared to those seven patients

Table 2--Pulmonary Hemodynamic Values in Acidemic Patient. M1ith and M1ithout Perfusion Failure *

Blood Lactate Level, millimoles/L --------"---------

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No. of patients Lactate, level, millimoles/L Arterial pH Arterial oxygen saturation, percent PaC02, rom Hg Pulmonary arterial pressure, mm Hg Systolic Diastolic Wedge Pulmonary diastolic gradient, mm Hg Pulmonary vascular resistance, dynes sec cm- 6 Cardiac output, L/min Cardiac index, L/min/sq m Stroke volume, ml/beat Mean arterial pressure, mm Hg CVP, mm Hg

2.0

19 7.7 ± 1.0** 7.27 ± 0.01 94.0 ± 1.6 36.5 ± 1.9 28.8 15.2 10.4 4.8 216 4.4 2.6 45 65 8.0

± ± ± ± ± ±

2.0 1.2 1.2 0.8 24t 0.5t ± 0.3t ± 4** ± 3t ± 1.2