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Ann Thorac Surg 1996;61:696-701
© 1996 The Society of Thoracic Surgeons

Original Article: Cardiovascular

Impact of Respiratory Acid-Base Status in Patients With Pulmonary Hypertension

David A. Fullerton, MD, Robert C. McIntyre, Jr, MD, Lyle E. Kirson, DDS, John A. St. Cyr, MD,PhD, Glenn J. R. Whitman, MD, Frederick L. Grover, MD

Department of Surgery, University of Colorado, Denver, Colorado

Accepted for publication October 19, 1995.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background. The perioperative management of patients undergoing mitral valve replacement (MVR) with pulmonary hypertension from mitral stenosis may be complicated by increased pulmonary vascular resistance. The purpose of this study was to examine the influence of respiratory acid-base status on the pulmonary hemodynamic indices of patients with pulmonary hypertension before and after MVR.

Methods. Ten patients with pulmonary hypertension from mitral stenosis (mean preoperative systolic pulmonary artery pressure, 73 ± 8 mm Hg) undergoing MVR were studied in the operating room before and after MVR. Arterial partial pressure of carbon dioxide was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Hemodynamic data were collected as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg and decreased back to 30 mm Hg.

Results. There were no differences in mean pulmonary artery pressure or pulmonary vascular resistance before and after MVR. Before MVR, mean pulmonary artery pressure increased from 32 ± 1 mm Hg to 48 ± 1 mm Hg as the partial pressure of carbon dioxide rose from 30 mm Hg to 50 mm Hg (p < 0.05), and pulmonary vascular resistance rose from 379 ± 30 to 735 ± 40 dynes•second•cm-5 (p < 0.05). These effects on mean pulmonary artery pressure and pulmonary vascular resistance were not different after MVR.

Conclusion. Respiratory acid-base status has a profound impact upon pulmonary vascular resistance in patients with pulmonary hypertension from mitral stenosis undergoing MVR. This impact persists in the immediate postoperative period. We conclude that respiratory acidemia should be avoided in these patients, whereas respiratory alkalemia may be used to help minimize pulmonary vascular resistance.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Pulmonary hypertension may greatly complicate the perioperative management of patients undergoing mitral valve replacement (MVR) for mitral stenosis. Three pathophysiologic mechanisms contribute to this pulmonary hypertension: (1) increased left atrial pressure transmitted retrograde into the arterial circulation, (2) vascular remodeling of the pulmonary vasculature in response to chronic obstruction to pulmonary venous drainage, and (3) pulmonary arterial vasoconstriction [1]. Once the elevated left atrial pressure is relieved by MVR, increased pulmonary vascular resistance (PVR) does not immediately return to normal; several days to weeks may be required [2–4]. In the early postoperative period after MVR, this persistently elevated PVR is derived from pulmonary vasoconstriction superimposed on structural changes in the pulmonary circulation [5].

Although the importance of hypoxemia in the determination of PVR is well known, considerably less attention has been paid to the role of respiratory acid-base status. Data from laboratory animals suggested that hypercarbic acidemia induces pulmonary vasoconstriction, whereas hypocarbic alkalemia results in pulmonary vasodilation [6–8]. These concepts have proven useful in the management of pediatric patients with pulmonary hypertension having cardiac operations; hyperventilation is often effective in lowering PVR [9]. This experience in the management of pediatric patients has prompted a recent appreciation for the influence of respiratory acid-base status on the pulmonary circulation in the adult. When studied in adult patients undergoing cardiac operations without pulmonary hypertension, respiratory acidemia has been shown to increase PVR [10, 11]. However, the influence of respiratory acid-base status in adults with pulmonary hypertension has not been reported previously. Patients with pulmonary hypertension may have an exaggerated response to pulmonary vasoconstricting agents [12]. We therefore hypothesized that hypercarbic acidemia produces a significant increase in PVR in patients with pulmonary hypertension undergoing MVR.

The purpose of this study was to examine the influence of respiratory acid-base status on the pulmonary hemodynamic indices of patients with pulmonary hypertension undergoing MVR for mitral stenosis. Patients were studied before and after MVR. The results of this study demonstrate a profound impact of respiratory acid-base status on the pulmonary hemodynamic indices of patients undergoing MVR with pulmonary hypertension, and suggest that hypocarbic alkalemia may be helpful perioperatively in controlling PVR in patients having cardiac operations.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
To examine both a safe and clinically relevant range of respiratory acid-base status, we reviewed the results of arterial blood gas samples from the surgical intensive care unit at our institution over a 2-month period. During this time, approximately 50 arterial blood gas samples were performed daily. We found that 95% of these samples fell within the pH range of 7.27 to 7.63, and 80% fell within the pH range of 7.30 to 7.50. Thus, the pH range of 7.30 to 7.50 was judged to be a very common clinical occurrence and was therefore chosen as the range of arterial pH for this study.

This protocol was approved by the Human Subjects Review Committee of the University of Colorado Health Sciences Center and the Research and Development Committee, Human Subjects Subcommittee of the Denver Veterans Administration Medical Center. Informed consent was obtained from each participant.

Ten consecutive patients with pulmonary hypertension undergoing MVR for mitral stenosis participated in this study. All patients had isolated mitral stenosis, left ventricular ejection fraction greater than 0.50 (determined by contrast ventriculography), and no coronary artery disease. A St. Jude mechanical prosthetic valve (St Jude Medical, St. Paul, MN) was used in all patients. At preoperative cardiac catheterization (performed on average 1 week before operation, with the patients awake and breathing room air), pulmonary artery systolic pressure was 73 ± 8 mm Hg and mean pulmonary artery pressure was 47 ± 7 mm Hg.

Patients received preoperative medication of morphine sulfate 0.1 mg/kg and scopolamine 0.4 mg intramuscularly 1 hour before arrival in the operating room. Ongoing drug therapy for concomitant medical problems was continued as deemed appropriate by the attending anesthesiologist. Each patient was monitored by a five-lead electrocardiogram, a radial artery line, and a pulmonary artery thermodilution catheter introduced through the right internal jugular vein. To measure pulmonary venous outflow pressure (left atrial pressure) accurately for determination of PVR, we introduced a left atrial pressure line through the right superior pulmonary vein after the pericardium had been opened. This line was subsequently removed under direct vision after completion of data collection and before chest closure. The anesthetic technique consisted of a high-dose narcotic (fentanyl) and relaxant (vecuronium), supplemented with intravenous midazolam. Inhalational anesthetic agents were administered only during cardiopulmonary bypass, not during the periods of data collection.

Mechanical obstruction to pulmonary venous outflow is one of the mechanisms contributing to pulmonary hypertension in patients with mitral stenosis. To examine the impact of this obstruction on the pulmonary vascular response to changes in respiratory acid-base status, we examined patients both before and after MVR. Data were collected in the operating room at two points: (1) after median sternotomy but before cardiopulmonary bypass, and (2) after completion of cardiopulmonary bypass but before chest closure. After weaning from bypass and after protamine administration, all patients were hemodynamically stable and demonstrated normal coagulation. No patients required cardiac pacing, antiarrhythmic therapy, or inotropic or vasoactive drug administration.

The protocol for collection of data proceeded as follows. Tidal volume was set at approximately 10 cm3/kg, and respiratory rate was adjusted to establish an arterial partial pressure of carbon dioxide (pCO2) of 30 mm Hg. To avoid changes in pulmonary hemodynamic indices secondary to changes in ventilatory patterns, ventilator settings were not altered during the study period. Fraction of inspired oxygen was maintained at a mean of 0.97 (range, 0.94 to 0.99), and no patient had application of positive end-expiratory pressure at any point during the study period. Arterial partial pressure of oxygen was maintained at greater than 250 mm Hg throughout the study period to avoid any influence of hypoxia on pulmonary vascular tone. Arterial pCO2 was elevated from 30 to 50 mm Hg by the addition of 5% carbon dioxide to the breathing circuit. Patients were maintained in a steady state for at least 10 minutes at each level of pCO2 before measurement of hemodynamic variables. To return to baseline, carbon dioxide was withdrawn from the breathing circuit to lower the arterial pCO2 to 30 mm Hg. Arterial blood gas samples were obtained at each point of data collection. The hemodynamic variables measured and recorded were heart rate, systemic mean arterial blood pressure, mean pulmonary artery pressure (MPAP), central venous pressure, left atrial pressure, and thermodilution cardiac output (mean of three values). These allowed mathematic determination of pulmonary and systemic resistance, cardiac index, right ventricular stroke work index (RVSWI), and transpulmonary gradient.

To determine what effect the baseline PVR (PVR at pCO2 of 30 mm Hg) had on the response to changing from hypocarbic alkalemia to hypercarbic acidemia, 10 additional patients without pulmonary hypertension undergoing coronary artery bypass grafting were studied using the same experimental protocol. For the combined group of 20 patients, the magnitude of the increase in PVR in response to changing pCO2 from 30 to 50 mm Hg was related to the baseline PVR by regression analysis.

Values are expressed as mean ± standard error of the mean. Statistical analysis used standard one-way classification analysis of variance in conjunction with the Student-Newman-Keuls multiple comparisons procedure. Two-sided statistical evaluation was employed. A p value of less than 0.05 was accepted as statistically significant. Regression analysis was used to determine the effect of baseline PVR on the response to respiratory acidemia.

Hemodynamic formulas included the following:







   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
The study population comprised 10 patients (5 male, 5 female). Patient data included an age of 62 ± 6 years, body surface area 1.8 ± 0.05 m2, aortic cross-clamp time 72 ± 12 minutes, cardiopulmonary bypass time 110 ± 17 minutes, tidal volume 10 cm3/kg, and respiratory rate 12 breaths/min. All patients had a history of cigarette smoking, but none admitted to smoking at the time of operation. All patients had a forced expiratory volume in 1 second of at least 1.5 L/min.

Table 1Go lists the arterial blood gas values and the hemodynamic variables determined at each point of data collection. Within each period of data collection (before and after MVR), there were no significant changes in heart rate, central venous pressure, left atrial pressure, cardiac output, systemic vascular resistance, or mean arterial pressure with changes in respiratory acid-base status. In addition, there were no significant differences in the baseline values of mean pulmonary artery pressure or PVR before and after MVR. As might be expected, baseline cardiac output was higher and left atrial pressure was lower after MVR. Before MVR, cardiac output was 3.8 ± 0.2 L/min; it rose to 4.9 ± 0.3 L/min after MVR (p < 0.05). Left atrial pressure was 14 ± 2 mm Hg before MVR and fell to 10 ± 1 mm Hg after MVR (p < 0.05). Although the baseline values of these variables did change, the values did not change within each period of data collection.


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  		Table 1. . Hemodynamic Dataa
 
When studied preoperatively in the cardiac catheterization suite, MPAP was 47 ± 7 mm Hg. Under the baseline conditions of the present study (pCO2 of 30 mm Hg and general anesthesia) before MVR, MPAP was 32 ± 1.6 mm Hg. As the respiratory acid-base status was changed from hypocarbic alkalemia to hypercarbic acidemia, MPAP rose by 50%, from 32 ± 1.6 to 48 ± 1.2 mm Hg (p < 0.05). With the return to baseline hypocarbic alkalemia, MPAP returned to 32 ± 1.4 mm Hg. As shown in Table 1Go, neither the baseline MPAP nor the magnitude of change in MPAP in response to the change in respiratory acid-base status was different after MVR.

As shown in Figure 1Go, these changes in MPAP were produced without changes in pulmonary artery blood flow (cardiac output) or pulmonary venous outflow pressure (left atrial pressure). Therefore, the changes in MPAP occurred as a result of pulmonary vasoconstriction and vasodilation. In fact, before MVR the transpulmonary gradient nearly doubled from 18 ± 1 mm Hg to 34 ± 1 mm Hg as respiratory acid-base status was changed from hypocarbic alkalemia to hypercarbic acidemia (p < 0.05) (see Table 1Go). The transpulmonary gradient returned to baseline as pCO2 was returned to 30 mm Hg. After MVR, the transpulmonary gradient increased from 21 ± 1 mm Hg to 37 ± 1 mm Hg, a 76% increase (p < 0.05), and returned to baseline with reinstitution of hypocarbic alkalemia (see Table 1Go).



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  		Fig 1. . Changes in mean pulmonary artery pressure (MPAP) with changes in respiratory acid-base status were produced without changes in pulmonary artery flow (cardiac output) or pulmonary venous outflow pressure (left atrial pressure, LAP). (*p < 0.05; MVR = mitral valve replacement; pCO2 = partial pressure of carbon dioxide.)

 
Before MVR, changing the respiratory acid-base status from hypocarbic alkalemia to hypercarbic acidemia produced a 94% increase in PVR, as PVR rose from 379 ± 30 to 735 ± 40 dynes•second•cm-5 (p < 0.05) (Fig 2Go). With reinstitution of hypocarbic alkalemia, PVR returned to baseline. Baseline PVR was unchanged after elimination of mechanical obstruction to pulmonary venous drainage (MVR). After MVR, PVR increased from 342 ± 30 to 688 ± 36 dynes•second•cm-5 as respiratory acid-base status was changed from hypocarbic alkalemia to hypercarbic acidemia (p < 0.05). The magnitude of the increase in PVR was not different before and after MVR. Again, PVR returned to baseline with reinstitution of hypocarbic alkalemia.



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  		Fig 2. . Effect of respiratory acid-base status on pulmonary vascular resistance (PVR) before and after mitral valve replacement (MVR). (*p < 0.05; pCO2 = partial pressure of carbon dioxide.)

 
Right ventricular stroke work index was significantly greater during respiratory acidemia. As shown in Table 1Go, RVSWI increased from 10.5 ± 0.7 g-m/m2 during respiratory alkalemia to 15.7 ± 0.8 g-m/m2 during respiratory acidemia (p < 0.05). Right ventricular stroke work index returned to baseline as respiratory alkalemia was reinstituted. After MVR, RVSWI was higher than before MVR because cardiac output was higher, and it increased from 13.9 ± 0.8 g-m/m2 to 19.9 ± 0.7 g-m/m2 during respiratory acidemia (p < 0.05). Thereafter, RVSWI returned to baseline with respiratory alkalemia.

Figure 3Go presents the combined data from patients with pulmonary hypertension (undergoing MVR) and without pulmonary hypertension (undergoing coronary artery bypass grafting). The baseline PVR influenced the response to changing from hypocarbic alkalemia to hypercarbic acidemia: The higher the baseline resistance, the greater the increase in PVR in response to changing from hypocarbic alkalemia to hypercarbic acidemia.



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  		Fig 3. . Effect of baseline pulmonary vascular resistance (PVR) at a partial pressure of carbon dioxide (pCO2) of 30 mm Hg on the amount of increase in PVR when pCO2 was increased to 50 mm Hg. Patients with pulmonary hypertension and a higher baseline PVR (patients undergoing mitral valve replacement, MVR) had a greater increase in PVR than patients without pulmonary hypertension (patients undergoing coronary artery bypass grafting, CABG).

 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
The results of this study demonstrate that respiratory acid-base status has an important influence on the pulmonary hemodynamic indices of adult patients with pulmonary hypertension from mitral stenosis. Changing the respiratory acid-base status from hypocarbic alkalemia (pCO2 30 mm Hg) to hypercarbic acidemia (pCO2 50 mm Hg) produced a significant increase in MPAP, transpulmonary gradient, and PVR. This influence of respiratory acid-base status was unchanged immediately after MVR. In turn, these effects on the pulmonary circulation resulted in a significant increase in RVSWI. It must be acknowledged that the present study examined only patients with pulmonary hypertension from mitral stenosis, and the results therefore may not necessarily apply to patients with pulmonary hypertension from other causes.

Patients undergoing cardiac operations offered a unique opportunity to examine the influence of respiratory acid-base status on PVR. A homogeneous group of patients could be studied: patients with isolated mitral stenosis. Many variables that affect PVR could be controlled in this select group of patients. Surgical access allowed accurate determination of pulmonary venous outflow pressure (left atrial pressure) for calculation of PVR. The anesthetized, mechanically ventilated patient allowed maintenance of a constant rate of ventilation and tidal volume to avoid mechanical alterations of PVR [13]. Furthermore, partial pressure of oxygen could be well controlled and hypoxia avoided.

Evaluation of the influence of respiratory acid-base status on PVR in mechanically ventilated humans almost certainly requires general anesthesia. In our protocol, a standard cardiac anesthetic technique was used. Intravenous anesthetic agents were administered only before cardiopulmonary bypass, and inhalational anesthetic agents were not administered after the cessation of cardiopulmonary bypass until after the period of data collection. Although the anesthetic technique may or may not influence PVR or the response of the pulmonary vasculature to respiratory acid-base status, the influence was held constant during the period of data collection. In addition, to optimize clinical relevance, we examined early postoperative patients.

As reported by other investigators, PVR in the present study was unchanged immediately after MVR [11, 12]. This persistent elevation in PVR after MVR is in large part derived from avid pulmonary vasoconstriction superimposed on structural changes in the pulmonary circulation [2], and may be refractory to vasodilator therapy. Several pharmacologic agents have been used with variable success to attenuate this pulmonary vasoconstriction, including isoproterenol, prostaglandin E1, dobutamine, nitroglycerin, sodium nitroprusside, amrinone, and inhaled nitric oxide [4, 14–17]. With the exception of inhaled nitric oxide, all of these pharmacologic agents dilate both the systemic and the pulmonary vascular beds. In patients with increased PVR, such nonselective vasodilation may be hazardous; substantial hypotension may result if the reduction of systemic vascular resistance is greater than the reduction in PVR [18]. Such hypotension may in fact be life-threatening if the systemic arterial pressure is lowered enough to decrease coronary arterial perfusion pressure, resulting in right ventricular ischemia and failure [19, 20]. Further, the clinical effectiveness of intravenously administered pulmonary vasodilator agents is often limited because they increase intrapulmonary shunt fraction and thereby lower arterial partial pressure of oxygen.

The results of the present study demonstrate that both before and after MVR, the ``reactive'' (pulmonary vasoconstrictive) component of PVR can be modulated and is very responsive to changes in respiratory acid-base status. These changes in the pulmonary circulation were produced without changes in systemic vascular resistance or in mean systemic arterial pressure. These data suggest that hypocarbic alkalemia may have a clinical role in the perioperative management of patients with pulmonary hypertension undergoing cardiac operations.

Because PVR is the primary clinical determinant of right ventricular afterload, it is important to minimize PVR in the perioperative period to optimize right ventricular function. The present study demonstrated that a significantly greater RVSWI was required to maintain the same cardiac output during hypercarbic acidemia. Although cardiac output was not decreased by this increased PVR in the present study, others have demonstrated that right ventricular ejection fraction is reduced during hypercarbic acidemia–induced pulmonary vasoconstriction [21, 22]. These undesirable influences on right ventricular function may in turn produce hemodynamic compromise if the right ventricle is unable to compensate for this increased afterload.

Patients with higher baseline PVR had a greater increase in PVR in response to respiratory acidemia than did patients with lower baseline PVR (see Fig 3Go). Chronic pulmonary vascular injury may disturb normal pulmonary vasomotor control mechanisms, and such vasomotor dysfunction is related to an exaggerated response to vasoconstricting agents [12]. The chronic vascular injury and pulmonary vascular remodeling produced by chronic pulmonary venous obstruction in mitral stenosis may help explain the greater influence of respiratory acid-base status upon PVR in patients with pulmonary hypertension in this study.

Patients with pulmonary hypertension undergoing cardiac operations are typically mechanically ventilated in the early postoperative period. As revealed by our review of arterial blood gas results in our intensive care unit, mechanically ventilated patients are at particular risk for the development of respiratory acid-base disturbances. The current study suggests that respiratory alkalemia may be used perioperatively to help minimize PVR in adults with pulmonary hypertension having cardiac operations. Changes in respiratory acid-base status simultaneously change pH and pCO2. The influence of respiratory acid-base status on PVR appears to be mediated through [H+] rather than pCO2 [23]. Therefore, in the clinical management of respiratory acid-base status in mechanically ventilated patients with pulmonary hypertension, attention should be focused on pH rather than pCO2.

In summary, respiratory acidemia produced a significant increase in MPAP and PVR in patients with pulmonary hypertension undergoing MVR for mitral stenosis. This impact of respiratory acid-base status on pulmonary hemodynamic indices was unchanged immediately after MVR. We conclude that hypocarbic alkalemia may be used to help minimize PVR in patients with pulmonary hypertension having cardiac operations.


   Footnotes
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 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Fullerton, Cardiothoracic Surgery, University of Colorado Health Sciences Center, Campus Box C-310, 4200 E Ninth Ave, Denver, CO 80262.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Grossman W, Alpert JS, Braunwald E. Pulmonary hypertension. In: Braunwald E, ed. Heart disease, a textbook of cardiovascular medicine. 2nd ed. Philadelphia: Saunders, 1984:830–1.
  2. Dalen JE, Matloff JM, Evans GL, et al. Early reduction of pulmonary vascular resistance after mitral-valve replacement. N Engl J Med 1967;277:387–94.[Medline]
  3. Camara ML, Aris A, Padro JM, Caralps JM. Long-term results of mitral valve surgery in patients with severe pulmonary hypertension. Ann Thorac Surg 1988;45:133–6.[Abstract]
  4. Camara ML, Aris A, Alvarez J, Padro JM, Caralps JM. Hemodynamic effects of prostaglandin E1 and isoproterenol early after cardiac operations for mitral stenosis. J Thorac Cardiovasc Surg 1992;103:1177–85.[Abstract]
  5. Braunwald E, Braunwald NS, Ross J Jr, Morrow AG. Effects of mitral-valve replacement on the pulmonary vascular dynamics of patients with pulmonary hypertension. N Engl J Med 1965;273:509–14.[Medline]
  6. Barer GR, Howard P, Marlow JR. The effect of hypercapnia and blood pH on the pulmonary circulation. J Physiol 1966;182:29–30.
  7. Linde LM, Simmons DH, Lewis N. Pulmonary hemodynamics in respiratory acidosis in dogs. Am J Physiol 1963;205:1008–12.[Abstract/Free Full Text]
  8. Morin FC, Lindgren L, Marshall BE. Metabolic and respiratory hydrogen ion effects on hypoxic pulmonary vasoconstriction. J Appl Physiol 1984;57:545–50.[Abstract/Free Full Text]
  9. Morray JP, Lynn AM, Mansfield PB. Effect of pH and pCO2 on pulmonary and systemic hemodynamics after surgery in children with congenital heart disease and pulmonary hypertension. J Pediatr 1988;113:474–9.[Medline]
  10. Viitanen A, Salmonpera M, Heinoven J, Hynynen M. Pulmonary vascular resistance before and after cardiopulmonary bypass. The effect of PaCO2. Chest 1989;95:773–8.[Abstract/Free Full Text]
  11. Fullerton DA, Kirson LE, St Cyr JA, Albert JD, Whitman GJR. The influence of respiratory acid-base status on adult pulmonary vascular resistance before and after cardiopulmonary bypass. Chest 1993;103:1091–5.[Abstract/Free Full Text]
  12. Dinh-Xuan AT, Higenbottam TW, Clelland CA, et al. Impairment of endothelium-dependent pulmonary artery relaxation in chronic obstructive lung disease. N Engl J Med 1991;324:1539–47.[Abstract]
  13. Fishman AP. Pulmonary circulation. In: Fishman AP, ed. Handbook of physiology. The respiratory system. Vol. 1. Bethesda, MD: American Physiological Society, 1985:93–165.
  14. Tinker JH. Dobutamine for inotropic support during emergence from cardiopulmonary bypass. Anesthesiology 1976;44:281–8.[Medline]
  15. D'Ambra MN, LaRaia PJ, Philbin DM, Watkins WD, Hilgenberg AD, Buckley MJ. Prostaglandin E1: a new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardiovasc Surg 1985;89:567–72.[Abstract]
  16. Girard C, Lehot JJ, Pannetier JC, Filley S, Ffrench P, Estanove S. Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension. Anesthesiology 1992;77:880–3.[Medline]
  17. D'Ambra MN, Beller JP. Pulmonary circulation: pharmacologic management. In: Grillo HC, Austen WG, Wilkens EW, Mathisen DJ, Vlahakes GJ, eds. Current therapy in cardiothoracic surgery. Toronto: BC Decker, 1988:278–82.
  18. Packer M, Greenberg B, Massie B, Dash H. Deleterious effects of hydralazine in patients with pulmonary hypertension. N Engl J Med 1982;306:1326–31.[Abstract]
  19. Vlahakes GJ, Turley K, Hoffman JIE. The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations. Circulation 1981;63: 87–95.[Abstract/Free Full Text]
  20. Prewitt RM, Ghigone M. Treatment of right ventricular dysfunction in acute respiratory failure. Crit Care Med 1983;11:346–52.[Medline]
  21. Rose CE, Van Ben Thuysen K, Jackson JT, et al. Right ventricular performance during increased afterload is impaired by hypercapnic acidosis in conscious dogs. Circ Res 1983;52:76–84.[Abstract/Free Full Text]
  22. Viitanen A, Salmonpera M, Heinoven J. Right ventricular response to hypercarbia after cardiac surgery. Anesthesiology 1990;73:393–400.[Medline]
  23. Fullerton DA, Kirson LE, St Cyr JA, Kinnard T, Whitman GJR. The influence of [H+] versus pCO2 on pulmonary vascular resistance following cardiac surgery. J Thorac Cardiovasc Surg 1993;106:528–36.[Abstract]



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