Annals of Clinical Cardiology

: 2020  |  Volume : 2  |  Issue : 2  |  Page : 60--69

Pulmonary dysfunction: A predictor of postoperative outcome in severe mitral stenosis

Usha T Parvathy1, Rajesh Rajan2, AG Faybushevich1, Kobalava D Zhanna2,  
1 MPS Hospital, Podbelskovo Street, Department of Cardiac Surgery, RUDN University, Moscow, Russia
2 Department of Internal Medicine with the Subspecialty of Cardiology and Functional Diagnostics Named after V.S. Moiseev, RUDN University, Moscow, Russia

Correspondence Address:
Dr. Usha T Parvathy
Department of Cardiac Surgery, MPS Hospital, Podbelskovo Street, RUDN University, Moscow


Background: Pulmonary function (PF) derangements in mitral stenosis (MS) can have an impact on the postmitral valve-replacement (MVR) period, which is not well studied. Objectives: The objectives were (1) to study the impact of the preoperative PF derangements intrinsic to MS on the early postoperative outcome and (2) to assess the prognostic relevance of spirometric tests as to the postoperative complications and morbidity. Methods: Prospective observational study: The spirometric pulmonary function tests (PFTs) performed in 25 patients with isolated MS (nonrandomized sampling) and arterial blood gas (ABG) were correlated to postoperative (post-MVR) variables: duration of ventilation, intensive care unit (ICU) stay, hospital stay, ABG, pulmonary complications, and outcome. Data were analyzed and compared under types, grades, and risk-based groups using nonparametric (Spearman's correlation, Kruskal–Wallis, and Mann–Whitney) tests. Results: The significant correlations were forced vital capacity (FVC)%, forced expiratory volume in 1 s (FEV1), FEV1%, peak expiratory flow rate (PEFR), and oxygen status to ventilation duration (P < 0.05); FEV1, PEFR, forced expiratory flow (FEF)-50, and oxygenation with ICU duration (P < 0.05); FVC, PEFR, and FEF-50 with hospital stay (P < 0.05); FVC, FEV1, and oxygenation to postoperative oxygen status (P = 0.02); FVC and FEV1 to pulmonary complications (P < 0.05); and FVC, PEFR, and FEF-50 with ventilation modification (P < 0.05). The morbidity and respiratory events showed a higher incidence with the mixed and severe categories (though not significant) and also with high-risk group in terms of postoperative pulmonary complications (P = 0.044) and prolonged ventilation. Mild trend toward hypercarbia needed ventilation optimization. Conclusions: PFT derangements in MS play an impact on the postoperative course to varying degrees. The advanced (severe and mixed) derangements and the high-risk group associate with greater morbidity and complications, calling for precautionary care, but on the whole do not contraindicate surgery. Spirometric evaluation can to a certain extent predict the postoperative morbidity risk.

How to cite this article:
Parvathy UT, Rajan R, Faybushevich A G, Zhanna KD. Pulmonary dysfunction: A predictor of postoperative outcome in severe mitral stenosis.Ann Clin Cardiol 2020;2:60-69

How to cite this URL:
Parvathy UT, Rajan R, Faybushevich A G, Zhanna KD. Pulmonary dysfunction: A predictor of postoperative outcome in severe mitral stenosis. Ann Clin Cardiol [serial online] 2020 [cited 2021 May 8 ];2:60-69
Available from:

Full Text


Various controversies have been raised regarding the correlation of the pulmonary function test (PFT) derangements with the clinical and hemodynamic grading of the disease in mitral stenosis (MS).[1],[2] Reports on the degree of postoperative improvement in pulmonary function test (PF) and its correlation with the hemodynamic improvement have also shown conflicting findings. The changes in PFTs varied from no improvement,[2] to partial improvement [3] and considerable improvement.[4],[5],[6] However, the degree of its impact on the immediate postoperative outcome variables is not well studied.


This study was undertaken to determine the correlation of the early postoperative pulmonary complications (PPC), morbidity, and mortality after mitral valve-replacement (MVR) in patients with MS, with PFT derangements of varying degrees and types and with individual parameters.


Study design: Prospective observational study

The study population consisted of 25 patients with isolated/predominant MS (by nonrandomized sampling based on their fitting the selection criteria), who underwent spirometric PFTs with computerized system within a week prior to the mitral valve surgery. Parameters such as forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, peak expiratory flow rate (PEFR), and forced expiratory flow at 50% VC (FEF-50) were recorded. The measured or observed values were expressed as percentage predictive of age, sex, weight, and height, and the results were interpreted with Miller (type)[7] and Conrad's criteria (grades).[8] The preoperative arterial blood gas (ABG) was also recorded. The selected group were nonsmokers with no previous respiratory disease (as on symptoms and chest X-ray) and had good ventricular function. Their mean age was 37.2 years, and the mean duration of symptoms was 6.5 years. The patients were classified as high risk for surgery and anesthesia if one of the FVC, FEV1, and FEF-50 was <50% of predicted or FEV1/FVC ratio was <70.[4] MVR was performed with standard median sternotomy, under cardiopulmonary bypass (CPB), with blood cardioplegia and topical and systemic hypothermia to 30°C in all cases.

The patients were ventilated overnight except those with normal pulmonary pressures or mild pulmonary artery hypertension (PAH) and stable hemodynamics who were extubated within few hours after the procedure. Postoperatively, apart from routine hemodynamic monitoring, the ABG was particularly analyzed. Ventilatory adjustments were made to avoid hypercarbia and to maintain normocarbia or mild hypocarbia (PaCO2 – 35 mmHg). A regimen of chest physiotherapy and pain control was followed after extubation, and early mobilization was encouraged. The complications within 30 days post surgery were recorded as present or absent. The PPCs (respiratory) were classified as follows: mild grade I (mild atelectasis, collapse, consolidation, pneumothorax, pleural effusion, or opacities, mild bronchospasm, secretions, needing no intervention); moderate-II (larger areas of collapse or effusion causing symptoms, and or alteration in ABG [hypoxia or hypercarbia], needing some intervention); and severe-III (symptomatic, significant alteration in ABG: respiratory failure, requiring prolonged ventilation, reintubation, and tracheostomy).

Those with hypercarbia needing ventilatory adjustments were also recorded separately. A PaCO2 of 36–40 mmHg was considered as mild hypercarbia, 41–50 mmHg as moderate, and >50 mmHg as significant. Nonpulmonary complications were arrhythmias, low cardiac output (CO), cardiac tamponade, other system complications (renal, etc.), and nonrespiratory infections. The complications and need for respiratory intervention were graded as follows: 0 = absent, 1 = mild, 2 = moderate, and 3 = significant. These and the need for intervention (various types and degrees), reintubation, duration of ventilation, and intensive care unit (ICU) and hospital stay were taken as arbitrary indices of morbidity and postoperative outcome. Informed consent was obtained from all patients after a full explanation of all the evaluation procedures and the operative procedure. As this was only an observation made from the routine operative and postoperative protocol, and did not include any invasive tests on the patient, ethical committee approval was not obtained.

Statistical analysis

Data analysis was done using SPSS-18 PASW (SPSS Inc., Chicago, USA). The associations and correlations of individual parameters were performed using Spearman's rank correlation (coefficient rho and two-tailed significant P obtained). Comparison between groups was done using Kruskal–Wallis (KW) [groups of types – [Table 1]a, grades – [Table 1]b, and Mann–Whitney test (groups based on: [a] duration of ventilation, [b] ICU stay, and [c] classified-risk groups), and the morbidity and outcome differences were charted. P < 0.05 was considered statistically significant.{Table 1}


In our study, 12 patients had restrictive, 1 had obstructive, and 8 had mixed-type derangements. Three patients with normal values of conventional spirometry had only early sign of airway obstruction (ESAO) (decreased FEF-50), and in one, both were normal. The disturbances were mild in 10 patients, moderate in 10, and severe in 4. Of those with severe dysfunction, the FEV1 was <1 L in 3 and 1.1 in 1. The median and range for preoperative ABG were SPO2: 97.95% (94.9–99); PaO2: 100.00 (77.6–128) mmHg; and PaCO2:35.00 (31–38.1 mmHg), and postoperatively: SPO2: 99.00% (93–100); PaO2: 195.00 (72–370) mmHg; and PaCO2: 38.45 (30–54) mmHg. The duration of ventilation ranged from 4 to 154 h (mean ± standard deviation = 17.31 ± 31.49 and median: 8); ICU stay 1–15 days (3.84 ± 2.64, and 3); and hospital stay 6–30 days (11.72 ± 5.52, and 10).

Relation to postoperative course

The correlations to the various spirometric and ABG indices [Table 2] show that the postoperative variables such as duration of ventilation and ICU stay, respiratory complications, postoperative oxygen status, and need for ventilation modification have significant/striking correlations with FEV1, FVC, PEFR, FEF-50, and preoperative oxygen status; lower functional values were definitely associated with higher morbidity and complications. Few other minor associations were noted: FVC with ventilation modification, PEFR with postoperative oxygen status, FEF-50 with respiratory complications, and PaO2 with hospital stay.{Table 2}

Relation to complications

The distribution of respiratory-related events (complications and ventilation modification), and their degree in relation to the preoperative PF abnormality type and grade, was assessed. All groups had some events, while the incidence was higher in the restrictive (50%), mixed (75%), and the severe grades (100%), major complications were confined to the mixed and severe groups. Small sample size, however, makes its validity questionable.

The KW method of comparison of postoperative parameters between the groups based on types and grades [Table 1]a and [Table 1]b showed no significant differences, though the morbidity shows a higher incidence in the mixed type and severe grades [Figure 1]a and [Figure 1]b (with higher values and a direct correlation Spearman's rho for related variables such as ventilatory hours [rho = 0.489, P = 0.013; rho = 0.425, P = 0.034] and lower oxygenation [rho = −0.528, P = 0.007; rho = −-0.396, P = 0.050]).{Figure 1}

Respiratory complications as seen in six patients (24%) included Grade I (4) mild atelectasis in 2; bronchospasm occurred in one of these, and increased secretions troubled two patients. However, none of them required any intervention like bronchoscopic drainage. Chest physiotherapy and nasal and endotracheal suctioning were adequate. In Grade III (2) patients needed prolonged ventilation; one due to pulmonary cause (severe mixed type, with postoperative atelectasis, secretions, needing reintubation and ventilation for 154 h after which was gradually weaned off), and another with ventricular dysfunction and low CO who succumbed after 3 days. The postoperative PaCO2 ranged from <35 mmHg in 8, 36 to 40 in 9, 41 to 50 in 6, and >50 in 2 patients. Fourteen of these needed ventilatory adjustments to maintain desired levels of PaCO2 (normocarbia or mild hypocarbia).

The nonrespiratory complications (12/25 [48%]) included Grade I (6) – minor arrhythmias (atrial fibrillation with rapid ventricular rate – 4 and sinus bradycardia – 2); Grade II (5) low CO due to ventricular dysfunction (which improved with inotropes) 3 and moderate ventricular dysfunction and arrhythmias – 2; and Grade III (1) severe low CO in one who died after 72 h. This was the only early mortality in this series (4%). Separate comparison of data based on ventilation duration and ICU duration is shown in [Table 3]a and [Table 3]b, respectively. The salient ones (of correlation) here were impaired FVC% and FEV1 on the preoperative side, and the altered blood gas and complications on the postoperative side, which were associated with longer duration of each. An additional analysis and comparison under risk-based groups (Kadam's criteria) showed a significant difference, with considerably impaired tests in the high-risk group preoperatively [Table 4]a and slightly higher morbidity (ventilation and ICU duration) and comparatively lower PaO2, with statistical significance only for the respiratory complications postoperatively [Table 4]b.{Table 3}{Table 4}


PF derangements in MS have shown varying degrees of correlation to the severity and chronicity of the disease and the degree of PAH.[1],[9] The changes of early obstruction or restriction and generally those related to increased congestion and edema may regress and show improvement with hemodynamic improvement, while the advanced ones due to fibrotic changes in the lung are unlikely to reverse.[3],[9] Thus results of reports vary with regard to the degree of improvement.[2],[3],[4],[5],[6] In addition, the changes are likely to have effect on oxygenation (SPO2 and PaO2) and blood carbon dioxide status (PaCO2), the airway changes contributing to edema, retention of secretions, and its consequences in the postoperative period. The present article has attempted to show the correlations on this aspect.

Pulmonary complications after cardiac surgery are known,[10],[11],[12] with the incidence quoted being 3%–16% for coronary artery bypass grafting (CABG) and 5%–7% following valvular surgery.[11],[12],[13] However, with no explicitly standardized definition for PPC, and a variety of terms being used to classify them, their frequency and severity in clinical practice are not well documented; there is a dramatic wide variation from 2% to 40%,[14] or 8%–79%[12] in the surgical setting. Although the recent improvements in operative and postoperative management have reduced the complications, patients with preexisting respiratory dysfunction are at an increased risk.[14],[15]

Unlike thoracic and lung surgeries, PFTs are not routinely done before cardiac surgery, and studies on the impact of deranged PFT on the postoperative outcome are limited. Controversies have been raised regarding its predictive value to the postoperative outcome.[15],[16],[17],[18] Few authors noted that with advanced disease with severe derangements, the morbidity and mortality are likely to be high,[18],[19] and some have advised early surgery.[3]

However, the risk of PPC has been usually estimated in heterogeneous population and in varied surgical procedures, making it difficult to exactly ascertain their relation with the previous spirometric derangements. Many of the earlier studies have been on noncardiothoracic surgery followed later by cardiac surgery as a whole, with little or no attention to valvular surgeries.[11],[15],[16],[20]

In MS, though the PFT may correlate with the Functional Class I, the preoperative respiratory symptoms may not exactly correlate with the degree of PFT derangements and the postoperative complications, unlike the respiratory disorders. Bulow et al. were the earliest to study the PPCs in MS which they classified according to their severity.[21] However, there were no PFT guidelines for correlating these. Stepanov on grounds of his clinicomorphologic and autopsy-based study opined that PPCs ought to be common postoperatively in advanced-stage MS with destructive lung changes and deranged function.[22]

Bevelaqua et al.'s and Yamashiro et al.'s retrospective analysis of patients undergoing different types of cardiac surgeries showed the group with impaired PFT to have more PPCs, which Bevelaqua et al. noted more with obstructive impairment and after valve surgery.[15],[23] The recent additions have also only assessed the impact on CABG patients.[17],[19],[24] A good number of studies have included PFT disorders in patients with respiratory disease-chronic obstructive pulmonary disease (COPD) and smokers,[15],[18],[20],[24] and many are retrospective, where evaluations are based on records.[15],[16],[23],[24] Studies correlating PFT directly with postoperative outcome variables in MS are very limited;[22],[25] even the recent literature on mitral disease concentrates on the effect of surgery on the postoperative PFT changes.[6],[26],[27],[28]

We concentrated on patients with isolated/predominant MS with no previous respiratory disease, with varying PFT results from normal spirometry, or only ESAO, to varying degrees of derangements. Each of the preoperative PF indices correlated to various arbitrary indices of postoperative outcome. Hence, we have very few reports to compare our results.

The statistical correlations obtained in this study point to the higher association of deranged functional parameters, especially FVC, FEV1, flow rates, and oxygen saturation, with postoperative respiratory problems and oxygenation derangements, with slightly higher morbidity in terms of longer ventilation and ICU duration, and thereby the hospital stay. This result stands somewhat similar to that of Bevelaqua et al. and Durand et al.,[15],[29] who have related PFT to ventilation and ICU duration, raising the predictive value of PFT. However, they had investigated coronary and multivalvar disease (with only few mitral patients), whereby the hemodynamic picture and hence the true functional status may be different, precluding a direct comparison.

In the large retrospective review on cardiac and thoracic surgery, Silva et al. could find mild association between only FVC and PPCs.[20] The preoperative oxygen levels had significant association with postoperative oxygen status, and with ventilation and ICU duration. Although arterial desaturation reflects pulmonary membrane structural damage, hypercarbia indicates pulmonary vascular resistance and pulmonary vascular disease, and thereby is expected to have adverse effects postoperatively, the mild desaturation and mild-to-moderate hypercarbia seen in our setting did not have major/adverse effect on the postoperative outcome. This somewhat complies with the general observations of Arozullah, which has not found PaCO2 to be an important predictor of PPC.[30] A low preoperative PaO2 was considered as risk factor for PPC,[13],[29] where the inclusion of smokers and COPD has presented significantly low PaO2, unlike our mitral patients where the oxygenation is related to the pulmonary congestion, pressures, and or structural changes, which, in turn, is related to the severity of MS. A relative improvement in oxygenation was noted postoperatively.

The incidence of PPC in this series was 24%, though may look higher than few of the recent reports on such complications in cardiac surgery,[11],[13],[23] which correlated with the significantly deranged PFT in the high-risk groups. This can alert one with the thought that these mitral patients, though do not have much respiratory symptoms correlating with the deranged PF (unlike the COPD patients), can be troubled in the postoperative phase.

Further analysis relating complications to the PF types and severity noted that though there was no statistically significant intergroup difference, the respiratory-related events showed a higher prevalence in the restrictive and mixed types and in the severe grades.

This is somewhat similar to the recent reports by Fuster et al. and Sato et al.,[19],[24] but their study was solely on coronary disease wherein the derangements could be due to added respiratory factor, with most patients being smokers, unlike the present study which has particularly focused on derangements in MS. The findings in our mitral patients where restrictive disease predominated are slightly dissimilar to the earlier observation of higher complication rate with obstructive type by Bevelaqua et al.[15] which included COPD. All our patients in the severe grade had complications, with one being major, pointing to the greater pulmonary structural damage as mentioned by Bulow et al. and Stepanov.[21],[22] Studies on CABG patients have shown that moderate-to-severe disease, both of obstructive and restrictive types, increases the peri- and post-operative mortality and complications,[18],[19] while Cain et al. and Jacob et al. could not find any difference.[16],[17]

The major complications and morbidity in our series were restricted to two patients who needed prolonged ventilation. One with severely impaired preoperative PFT showed persistently low PaO2 and high PaCO2 postoperatively, with atelectasis and secretions, and development of pneumothorax needing drainage, however recovered gradually over a week. The other had unsatisfactory cardiopulmonary conditions related to ventricular dysfunction. The single early mortality was rather related to cardiac, and not to pulmonary factor.

Of course, quite a good number of patients had high PaCO2 or borderline high PaCO2 (>35 mmHg) postoperatively and needed ventilatory adjustments with increase in minute volume to maintain normocarbia/mild hypocarbia. This is an interesting finding noted only in few studies.[31],[32] In MS, with pulmonary venous congestion and hypertension, the increased blood volume and interstitial fluid reduce pulmonary compliance and cause ventilation/perfusion mismatching. Postoperatively, the decreasing PAP and blood volume lead to increased alveolar dead space, with inequalities in dead space/tidal volume ratio and ventilation/perfusion ratio, which results in deranged acid–base status.[31],[32]

The need and importance of maintaining normocarbia postsurgically comes from the point that hypercarbia tends to raise the pulmonary vascular tone and resistance, which may affect the right ventricular (RV) stroke volume index and depress the RV function.[31] Tempe et al. advised elective ventilation in patients with PAH to avoid even mild hypercarbia.[31] We electively ventilated patients with moderate and severe PAH for 10–12 h and extubated them when they satisfied the hemodynamic and respiratory criteria. The incidence of hypercarbia (based on our definition range) may appear to be high (17 [68%]), as we intentionally aimed at a low level of normocarbia or even mild hypocarbia.

We attempted correlating this factor of postoperative hypercarbia with certain other relevant factors. The simple correlative analysis did not show any of the preoperative PF or blood gas indices to have a direct association or impact on this. However, the trend was to have a higher incidence in mixed and severe categories (though not statistically significant).

Few nonpulmonary complications encountered did not have a direct correlation with the presurgical PFT. Probably, a comparison with patients with normal PFT may give an improved idea on this. However, mitral patients without PFT derangements are rare as most of them have some alterations due to the congestive and later fixed pulmonary structural components of the disease.

The lower PFT values and higher incidence of complications in patients with ICU stay >5 days as noted in our comparative analysis are somewhat similar to that of few earlier studies.[15] Nearly 75% of these patients in our study were of the mixed and higher grade category. Though the associations of preoperative impaired PFT with prolonged ICU stay have been noted earlier by Bevelaqua et al., Cain et al., and Durand et al.,[15],[16],[29] and recently Adabag et al. and Ozyilmaz et al.,[18],[28] few authors could not obtain direct/exact association between PFT and PPC or ICU duration, contradicting its predictive value,[17] Cain et al. noted no difference in the mean ICU duration, and/or risk rate of PPC between grades of PFT impairment.[16] As regards the duration of ventilation, literature shows some variation in the definition of prolonged ventilation.[9],[15],[33] Vaidya et al. marked that mitral patients with impaired PFT, and smoking, needed prolonged ventilation, which they defined as >10 h, and their postoperative PFT deterioration was more than others,[9] while Chandra et al. found no such correlations.[26] In view of this diversity in the definition, and as we electively ventilated patients for 10–12 h, we compared those who needed >12 h' ventilation with the rest.

Our finding that those with impaired PFT (FVC%, FEV1) fell under the former longer-ventilation group, and the definite association of higher morbidity (oxygenation, hypercarbia, and complications) with this group, (though other PF parameters did not show significant intergroup difference), suggesting greater pulmonary damage, fairly supports what Vaidya et al. have stated earlier.[9]

One study by Ota concentrated on mitral disease with severely impaired PFT (FEV1 < 1 L/s), who have survived surgery and shown reasonably good results, though their morbidity was slightly high.[25] Kadam et al. have brought out this point, but they have not discussed the exact correlations.[4] Bevelaqua et al. and Yamashiro et al. also gave a positive opinion on the favorable general outcome of these patients, though the PPCs were higher.[15],[23]

Looking at our data on Kadam's (4) terms and angle, 11 (44%) of our patients were in the high-risk group for surgery and anesthesia. Their significantly impaired PFT did not seem to have major or adverse impact on the outcome, but was portent to the comparatively higher incidence of respiratory complications and a higher morbidity.

Limitations and recommendations

The limitations may be that in the early postoperative period, pulmonary status and function may be influenced by the CPB-related alterations in the cardiac and pulmonary hemodynamics. Hence, the effect of this confounding factor in the interpretation of results cannot be ruled out. Some authors have reported on the prolonged duration of CPB (>80 m)[9],[13] and ventilation >10 h to cause more pulmonary damage postoperatively, though the correlations were not statistically significant.[9] As there was no significant difference in the CPB time among our patients, we did not correlate these with the postoperative variables.

A review by Wynne and Botti showed that currently the frequency of PPCs remains similar for patients who have CPB and those who do not.[12] We did not repeat PFTs postoperatively because though expected to improve with the improved hemodynamics, the pain and restriction due to surgery may prevent proper estimation of these, and also may show derangements, as noted by many authors.[2],[9],[26] Instead, the study was mainly focused to document the impact of PFT derangements on the immediate postoperative parameters and complications. Whether a correlative analysis of PPCs to postoperative PFT may give clearer ideas is questionable as the latter tends to be affected by a multitude of factors.[26],[27] In contrast to many other studies, this article (though based on small sample) has been restricted to isolated/predominant MS, which suggests that, overall, patients with deranged PF of severe degree, and the restrictive and the mixed type, had a tendency for complications in the early postoperative period, with mild impact on the postoperative course and morbidity.

These simple preoperative tests can alert the surgeon of these possibilities and point to the need for better postoperative care though definite cutoff limits could not be made. However, the derangements including the severely impaired ones by themselves do not affect the mortality and cannot be preclusion for valve surgery as noted in our study. This supports the view of few earlier observers.[4],[23],[25] The uniqueness of the study is that it tried to analyze pulmonary factors intrinsic to the mitral disease with the postoperative outcome. A larger cohort study of this subset is awaited which may prove and provide the percentage predictivity of PFT. A pathological analysis would further reveal the degree of damage.


PF derangements in MS showed varying degrees, which, with proper postoperative care, did not have major/adverse impact on the surgical outcome. What directly correlated was the slightly but definitely increased incidence of pulmonary complications and a higher morbidity in terms of increased ventilation and ICU period in the advanced disease. Ventilation optimization for mild hypercarbic trend is effective. PFTs should guide/direct the surgeon for an early surgery and alert to the possible postoperative complications. Stratification into risk groups also adds informative results and emphasizes these points.


This is an investigator-initiated, single-center study conducted at MPS Hospital, Podbelskovo Street, Department of Cardiac Surgery, Institute of Medicine, Peoples' Friendship University of Russia (RUDN University), Moscow, Russian Federation.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Rhodes KM, Evemy K, Nariman S, Gibson GJ. Relation between severity of mitral valve disease and results of routine lung function tests in non-smokers. Thora×1982;37:751-5.
2Seboldt H, Stunkat R, Keppeler F, Hoffmeister HE, Hilpert T. [Reversibility or irreversibility of pulmonary function changes after cardiac surgery on insufficient or stenotic cardiac valves (author's transl)]. Thoraxchir Vask Chir 1975;23:431-6.
3Gómez-Hospital JA, Cequier A, Romero PV, Cañete C, Ugartemendia C, Iràculis E, et al. Persistence of lung function abnormalities despite sustained success of percutaneous mitral valvotomy: The need for an early indication. Chest 2005;127:40-6.
4Kadam PP, Pantvaidya SH, Jagtap SR, Rajgor KD. Effect of closed mitral valvotomy on spirometric pulmonary function tests in mitral stenosis. J Postgrad Med 1997;43:38-40.
5Rhodes KM, Evemy K, Nariman S, Gibson GJ. Effects of mitral valve surgery on static lung function and exercise performance. Thorax 1985;40:107-12.
6Mansuri ZH, Vala EB, Kaji BC, Talwar R. Comparison of pre and post interventional pulmonary function tests in patients with mitral valve heart disease-(A study of 50 cases). Med Sci 2014;3:335-6.
7Miller WF, Wu N, Johnson PL. Miller's Prediction Quadrant. Anesthesiology 1956;17:480-93.
8Conrad SA. Pulmonary Function: Principles and Practices. 11th ed. Oxford: Oxford 1BH Publishing Co.; 1983.
9Vaidya R, Husain T, Ghosh PK. Spirometric changes after open mitral surgery. J Cardiovasc Surg (Torino) 1996;37:295-300.
10Gass GD, Olsen GN. Preoperative pulmonary function testing to predict postoperative morbidity and mortality. Chest 1986;89:127-35.
11Weissman C. Pulmonary function after cardiac and thoracic surgery. Anesth Analg 1999;88:1272-9.
12Wynne R, Botti M. Postoperative pulmonary dysfunction in adults after cardiac surgery with cardiopulmonary bypass: Clinical significance and implications for practice. Am J Crit Care 2004;13:384-93.
13Ji Q, Mei Y, Wang X, Feng J, Cai J, Ding W. Risk factors for pulmonary complications following cardiac surgery with cardiopulmonary bypass. Int J Med Sci 2013;10:1578-83.
14Canet J, Mazo V. Postoperative pulmonary complications. Minerva Anestesiol 2010;76:138-43.
15Bevelaqua F, Garritan S, Haas F, Salazar-Schicchi J, Axen K, Reggiani JL. Complications after cardiac operations in patients with severe pulmonary impairment. Ann Thorac Surg 1990;50:602-6.
16Cain HD, Stevens PM, Adaniya R. Preoperative pulmonary function and complications after cardiovascular surgery. Chest 1979;76:130-5.
17Jacob B, Amoateng-Adjepong Y, Rasakulasuriar S, Manthous CA, Haddad R. Preoperative pulmonary function tests do not predict outcome after coronary artery bypass. Conn Med 1997;61:327-32.
18Adabag AS, Wassif HS, Rice K, Mithani S, Johnson D, Bonawitz-Conlin J, et al. Preoperative pulmonary function and mortality after cardiac surgery. Am Heart J 2010;159:691-7.
19Fuster RG, Argudo JA, Albarova OG, Sos FH, López SC, Codoñer MB, et al. Prognostic value of chronic obstructive pulmonary disease in coronary artery bypass grafting. Eur J Cardiothorac Surg 2006;29:202-9.
20Silva DR, Gazzana MB, Knorst MM. Merit of preoperative clinical findings and functional pulmonary evaluation as predictors of postoperative pulmonary complications. Rev Assoc Med Bras (1992) 2010;56:551-7.
21Bulow K, Biorck G, Axen O, Krook H, Wulff HB, Winblad S. Studies in mitral stenosis. VI. Pulmonary vessels in mitral stenosis. Am Heart J 1955;50:242-59.
22Stepanov VV. Pulmonary complications in the surgery of advanced stages of mitral stenosis. Vestn Khir Im I I Grek 1980;124:22-7.
23Yamashiro S, Sakata R, Nakayama Y, Ura M, Arai Y, Morishima Y. Cardiac operations in patients with severe pulmonary impairment. Ann Thorac Cardiovasc Surg 2000;6:100-5.
24Sato M, Nishida H, Endo M, Tomizawa Y, Shiikawa A, Akazawa T, et al. Postoperative complications after coronary bypass operations in patients with pulmonary impairment. Jpn J Thorac Cardiovasc Surg 1998;46:145-9.
25Ota T, Tsukube T, Matsuda H, Iwahashi K, Okada M. Effect of mitral valve surgery on severely impaired pulmonary function. Thorac Cardiovasc Surg 1994;42:94-9.
26Chandra A, Srivastava S, Dilip D. Spirometric changes following open-heart surgery on rheumatic mitral valves. Asian Cardiovasc Thorac Ann 1998;6:28-33.
27El-Sobkey SB, Gomaa M. Assessment of pulmonary function tests in cardiac patients. J Saudi Heart Assoc 2011;23:81-6.
28Ozyilmaz S, Demir R, Hatemi AC, Ziyaettin M, Muammer K, Muammer R, et al. Retrospective analysis of clinical and pulmonary data in valve patients. Pak J Med Sci 2011;27:971-75.
29Durand M, Combes P, Eisele JH, Contet A, Blin D, Girardet P. Pulmonary function tests predict outcome after cardiac surgery. Acta Anaesthesiol Belg 1993;44:17-23.
30Arozullah AM, Conde MV, Lawrence VA. Preoperative evaluation for postoperative pulmonary complications. Med Clin North Am 2003;87:153-73.
31Tempe D, Cooper A, Mohan JC, Nigam M, Tomar AS, Ramesh K, et al. Closed mitral valvotomy and elective ventilation in the postoperative period: Effect of mild hypercarbia on right ventricular function. J Cardiothorac Vasc Anesth 1995;9:552-7.
32Muralidhar K, Rupert E, Singh R, Gowda N, Kumar V, Kumar S. Influence of changes in the pulmonary artery pressure on ventilation requirements in patients undergoing mitral valve replacement. Ann Card Anaesth 2004;7:144-8.
33Serrano N, García C, Villegas J, Huidobro S, Henry CC, Santacreu R, et al. Prolonged intubation rates after coronary artery bypass surgery and ICU risk stratification score. Chest 2005;128:595-601.