Hans Tydén

Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study.

Background: Respiratory failure after cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors tested the hypothesis that atelectasis is an important factor responsible for the increase in intrapulmonary shunt after CPB. Methods: Six pigs received standard CPB (bypass group). Six other pigs had the same surgery but without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ventilation‐perfusion distribution was measured with the inert gases technique, extravascular lung water was quantified by the double‐indicator distribution technique, and atelectasis was analyzed by computed tomography. Results: Intrapulmonary shunt increased markedly after bypass but was unchanged over time in the control group (17.9 +/‐ 6.2% vs. 3.5 +/‐ 1.2%; P < 0.0001). Shunt also increased in the sternotomy group (10 +/‐ 2.6%; P < 0.01 compared with baseline) but was significantly lower than in the bypass group (P < 0.01). Extravascular lung water was not significantly altered in any group. The pigs in the bypass group showed extensive atelectasis (32.3 +/‐ 28.7%), which was significantly larger than in the two other groups. The pigs in the sternotomy group showed less atelectasis (4.1 +/‐ 1.9%) but still more (P < 0.05) than the controls (1.1 +/‐ 1.6%). There was good correlation between shunt and atelectasis when all data were pooled (R2 = 0.67; P < 0.0001). Conclusions: Atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy and it explains most of the marked post‐CPB increase in shunt and hypoxemia. Surgery per se contributes to a lesser extent to postoperative atelectasis and gas exchange impairment.

Atelectasis and gas exchange after cardiac surgery.

Background Sometimes a high intrapulmonary shunt occurs after cardiac surgery, and impairment of lung function and oxygenation can persist for 1 week after operation. Animal studies have shown that postoperative shunt can be explained by atelectasis. In this study the authors tried to determine if atelectasis can explain shunt in patients who have had cardiac surgery. Methods Nine patients having coronary artery bypass graft surgery and nine patients having mitral valve surgery were examined using the multiple inert gas elimination technique before and after operation. On the first postoperative day, computed tomography scans were made at three levels of the thorax. Results Before anesthesia, the average shunt was low (2 +/‐ 3%; range, 0–13%), but on the first postoperative day shunt had increased to 12 +/‐ 6% (range, 3–28%). The computed tomography scans showed bilateral dependent densities in all patients but one. The mean area of the densities was 8 +/‐ 8% (range, 0–37%) of total lung area, corresponding to a calculated fraction of collapsed lung tissue of 20 +/‐ 14% (range, 0–59%). In the basal region, the calculated amount of collapsed tissue was 28 +/‐ 19% (range, 0–73%). One mitral valve patient was an outlier and had a large shunt both before and after the operation. Conclusions Large atelectasis in the dorsal part of the lungs was found on the first postoperative day after cardiac surgery. However, there was no clear correlation between atelectasis and measured shunt fraction.

Ventilation-perfusion inequality in patients undergoing cardiac surgery.

BackgroundImpaired gas exchange is a major complication after cardiac surgery with the use of extracorporeal circulation. Blood gas analysis gives little information on underlying mechanisms, in particular if the impairment is multifactorial. In the current study we used the multiple inert gas technique with recordings of hemodynamics to analyze the separate effects of intrapulmonary shunt (&OV0422;s/&OV0422;r), ventilation-perfusion (&OV0312;A/&OV0422;) mismatch, and low mixed venous oxygen tension on arterial oxygenation during cardiac surgery. Methods&OV0312;A/&OV0422; distribution was studied in nine patients undergoing coronary artery revascularization surgery. The obtained data related to &OV0312;A/&OV0422; distribution were perfusion of lung regions with &OV0312;A/&OV0422; < 0.005 (&OV0422;s/&OV0422;r), perfusion of lung regions with 0.005 < &OV0312;A/&OV0422; < 0.1 (“low”-&OV0312;A/&OV0422; regions), ventilation of lung regions with 10 < &OV0312;A/&OV0422; < 100 (“high”-&OV0312;A/&OV0422; regions), and ventilation of lung regions with &OV0312;A/&OV0422; > 100 (dead space [&OV0312;D/&OV0312;T]). In addition, arterial and mixed venous oxygen and carbon dioxide tensions and systemic and pulmonary hemodynamics were analyzed. Recordings were made before and after induction of anesthesia, after sternotomy, 45 min after separation from extracorporeal circulation, 4 h postoperatively during mechanical ventilation, and on the 1st postoperative day during spontaneous breathing. ResultsIn the awake state, &OV0422;s/&OV0422;r was 4 ± 4%, and perfusion of low-&OV0312;A/&OV0422; regions was 3 ± 5%. The sum of &OV0422;s/&OV0422;r and low-&OV0312;A/&OV0422; units correlated with the alveolar-arterial oxygen tension gradient (PA-ao2) (r = 0.63, P < 0.05). After induction of anesthesia, &OV0422;s/&OV0422;r increased to 10 ± 9% (P = 0.069). Sternotomy had little effect on shunt, but &OV0422;s/&OV0422;r increased to 22 ± 8% (P < 0.01) after separation from extracorporeal circulation, which was correlated with a significantly higher PA-ao2 (r = 0.77, P < 0.05). Postoperatively, gas exchange improved rapidly, as assessed by a decrease of PA-ao2 from 341 ± 77 to 97 ± 36 mmHg (P < 0.01) and a reduced &OV0422;s/&OV0422;r (5 ± 4%, P < 0.05). On the 1st postoperative day, arterial oxygen tension was significantly lower than preanesthesia values (58 ± 6 vs. 68 ± 8 mmHg, P < 0.05). &OV0422;s/&OV0422;r had increased to 11 ± 6% (P < 0.05), but little perfusion of low-&OV0312;A/&OV0422; units was observed. A correlation was found between PA-ao2 and &OV0422;s/&OV0422;r (r = 0.82, P < 0.03). Conclusions&OV0422;s/&OV0422;r is a major component of impaired gas exchange before, during, and after cardiac surgery. &OV0422;s/&OV0422;r increases after induction of general anesthesia, probably because of development of atelectasis. After separation from extracorporeal circulation, accumulation of extravascular lung water or further collapse of lung tissue may aggravate &OV0422;s/&OV0422;r-Postoperatively, oxygenation improves, possibly because of recruitment of previously nonventilated alveoli or resolution of extravascular lung water. During spontaneous breathing, additional mechanisms such as altered mechanics of the chest, perfusion of low-&OV0312;A/&OV0422; regions, and decreased mixed venous oxygen tension may contribute to impaired gas exchange.

Early extubation after coronary artery surgery in efficiently rewarmed patients: A postoperative comparison of opioid anesthesia versus inhalational anesthesia and thoracic epidural analgesia

Twenty-eight patients were studied after uncomplicated aortocoronary bypass surgery with hypothermic cardiopulmonary bypass (CPB). In all patients residual hypothermia was effectively treated by the use of extended rewarming during CPB and postoperatively by an external heat source. This treatment almost eliminated postoperative shivering, and it resulted in the lowering of oxygen uptake, carbon dioxide production, and required ventilatory volumes to stable levels where spontaneous breathing could be used safely. The patients were divided into two groups. In group I (n = 12), intraoperative anesthesia was based on an intravenous (IV) opioid (phenoperidine), which caused persistent respiratory depression and made mechanical ventilation necessary for a mean postoperative time period of 10.7 +/- 3.8 hours even with the rewarming. In group II (n = 16), thoracic epidural analgesia and intraoperative general anesthesia with enflurane were used. In this group, postoperative metabolic and ventilatory requirements were stable and low, finger skin temperature was normalized earlier, systemic vascular resistance was lower, and stroke index was higher. Emergence from anesthesia was uneventful and was achieved early postoperatively in Group II. The patients had good pain relief and were mentally alert. Adequate spontaneous breathing was resumed quickly and endotracheal extubation was performed within the first two postoperative hours (1.6 +/- 0.5 hours). No complications or increased morbidity occurred, and no patient needed to be reintubated in Group II.

Thoracic Intravascular and Extravascular Fluid Volumes in Cardiac Surgical Patients

BackgroundOne possible mechanism of impaired oxygenation in cardiac surgery with extracorporeal circulation (ECC) is the accumulation of extravascular lung water (EVLW). Intrathoracic blood volume (ITBV) and pulmonary blood volume (PBV) also may increase after separation from ECC, which can influence both cardiac performance and pulmonary capillary fluid filtration. This study tested whether there were any relationships between lung fluid accumulation and pulmonary gas exchange during the perioperative period of cardiac surgery and ECC. MethodsTen patients undergoing myocardial revascularization were studied. ITBV, PBV, and EVLW were determined from the mean transit times and decay times of the dye and thermal indicator curves obtained simultaneously in the descending aorta. Gas exchange was assessed by arterial and mixed venous partial pressure of oxygen (Po2) and carbon dioxide (Pco2), and calculation of alveolo-arterial Po2 gradient (Pa-ao2) and venous admixture (Qva/Qt). Recordings were made after Induction of anesthesia, after sternotomy, 15 min after separation from ECC, and 4 and 20 h postoperatively. ResultsAfter induction of anesthesia, EVLW (6.0 ± 1.0 ml/kg, ± ± SD), PBV (3.6 ± 1.3 ml/kg), and ITBV (18.4 ± 2.7 ml/kg) were within normal ranges. Oxygenation was moderately impaired, as indicated by an increased Pa-ao2 (144 ± 46 mmHg) and Qva/Qt (11 ± 4%). After separation from ECC, EVLW had increased to 9.1 ± 2.6 ml/kg, which was accompanied by an increase of ITBV (26.0 ± 4.4 ml/kg) and PBV (5.6 ± 1.9 ml/kg). Paa-02 (396 ± 116 mmHg) and Qva/Qt (29 ± 7%) also were increased. ITBV and PBV remained increased 4 and 20 h post-operatively, but EVLW decreased to presurgery values. No correlations were found between thoracic intravascular and extravascular fluid volumes and gas exchange. ConclusionsCardiac surgery with the use of ECC induces alterations of thoracic intravascular and extravascular fluid volumes. Postoperatively, increased ITBV and PBV need not be associated with higher EVLW. Thus, sufficient mechanisms protecting against lung edema formation or providing resolution of EVLW probably are maintained after ECC. Since oxygenation is impaired during and after cardiac surgery, it is concluded that mechanisms other than or in addition to changes of ITBV, PBV, and EVLW predominantly influence gas exchange.

Use of a Vital Capacity Maneuver to Prevent Atelectasis after Cardiopulmonary Bypass An Experimental Study

Background Respiratory failure secondary to cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors previously found that the increase in intrapulmonary shunt was well correlated with the amount of atelectasis. They tested the hypothesis that post‐CPB atelectasis can be prevented by a vital capacity maneuver (VCM) performed before termination of the bypass. Methods Eighteen pigs received standard hypothermic CPB (no ventilation during bypass). The VCM was performed in two groups and consisted of inflating the lungs during 15 s to 40 cmH2 O at the end of the bypass. In one group, the inspired oxygen fraction (FIO2) was then increased to 1.0. In the second group, the FIO2 was left at 0.4. In the third group, no VCM was performed (control group). Ventilation‐perfusion distribution was measured with the inert gas technique and atelectasis by computed tomographic scanning. Results Intrapulmonary shunt increased after bypass in the control group (from 4.9 +/‐ 4% to 20.8 +/‐ 11.7%; P < 0.05) and was also increased in the vital capacity group ventilated with 100% oxygen (from 2.2 +/‐ 1.3% to 6.9 +/‐ 2.9%; P < 0.01) but was unaffected in the vital capacity group ventilated with 40% oxygen. The control pigs showed extensive atelectasis (21.3 +/‐ 15.8% of total lung area), which was significantly larger (P < 0.01) than the proportion of atelectasis found in the two vital capacity groups (5.7 +/‐ 5.7% for the vital capacity group ventilated with 100% oxygen and 2.3 +/‐ 2.1% for the vital capacity group ventilated with 40% oxygen. Conclusion In this pig model, postcardiopulmonary bypass atelectasis was effectively prevented by a VCM.

Thoracic epidural anesthesia does not influence the occurrence of postoperative sustained atrial fibrillation.

BACKGROUND To evaluate whether thoracic epidural anesthesia (TEA) can reduce the incidence of atrial fibrillation (AF) after coronary artery bypass grafting (CABG). METHODS Forty-one patients undergoing CABG were treated with TEA intraoperatively and postoperatively. Another 80 patients served as the control group. The sympathetic and parasympathetic activities were evaluated by analysis of neuropeptides, catecholamines and heart rate variability (HRV), preoperatively and postoperatively. RESULTS Postoperative AF occurred in 31.7% of the TEA-treated patients and in 36.3% of the untreated patients (p = 0.77). TEA significantly suppressed sympathetic activity, as indicated by a less pronounced increase of norepinephrine and epinephrine (p = 0.03, p = 0.02) and a significant decrease of neuropeptide Y (p = 0.01) postoperatively in TEA-treated patients compared to untreated patients. The HRV variable expressing sympathetic activity was significantly lower and the postoperative increase in heart rate was significantly less in the TEA group than in the control group after surgery (p = 0.01, p < 0.001). Among patients developing AF, the maximal number of supraventricular premature beats per minute increased significantly in untreated patients postoperatively but remained unchanged in TEA-treated patients (p = 0.004 versus p = 0.86). CONCLUSIONS TEA has no effect on the incidence of postoperative sustained AF, despite a significant reduction in sympathetic activity.

Thoracic epidural anesthesia as an adjunct to general anesthesia for cardiac surgery: Effects on ventilation-perfusion relationships

OBJECTIVE To determine the effects of thoracic epidural anesthesia (TEA) on ventilation-perfusion (VA/Q) relationships, atelectasis, and oxygenation before and after coronary artery bypass graft surgery (CABG). DESIGN Prospective, controlled, unblinded, randomized trial. SETTING Cardiothoracic clinic at a major university referral center. PARTICIPANTS Twenty-eight patients undergoing elective CABG. INTERVENTIONS Perioperative and postoperative TEA was added to general anesthesia (GA) in 14 patients, and 14 patients receiving GA alone served as controls. MEASUREMENTS AND MAIN RESULTS VA/Q relationships were measured by the multiple inert gas elimination technique, and, 20 hours postoperatively, atelectasis was assessed by computerized tomographic scans. Arterial and mixed venous blood gases and hemodynamic variables were measured by standard techniques. TEA per se caused no change in shunt, VA/Q matching, or oxygenation. Induction of GA in the control group and induction of TEA caused similar reductions in mean arterial pressure. The TEA patients needed less morphine analgesia postoperatively and were extubated earlier. Extubation caused significant improvement in VA/Q matching. On the first postoperative day, a slight reduction in PaCO2 was seen in the TEA group, but no differences in shunt, VA/Q matching, or oxygenation compared with the GA group. Both groups showed extensive bilateral atelectasis. CONCLUSION TEA can reduce respirator time and the need for morphine analgesics after CABG without negative effects on VA/Q matching, oxygenation, or atelectasis formation.

Is cerebral blood flow/metabolic mismatch during rewarming a risk factor after profound hypothermic procedures in small children?

The relation between cerebral blood flow and oxygen consumption was studied in six children during cardiac operations with profound hypothermia. A combination of topical cooling and core cooling was used to reduce the nasopharyngeal temperature to 15 degrees C. The alpha-stat principle for pH management was used. Blood flow and oxygen consumption decreased significantly with temperature. At a nasopharyngeal temperature of 15 degrees C, blood flow was reduced to 25% of the awake level, corresponding to 34% of the asleep value obtained 15-30 min after intubation. Oxygen consumption decreased to 25% of the asleep value. During stable profound hypothermia, venous saturation in the jugular bulb was at the same level as 15 min after intubation (70%). Markedly lower values were observed during topical cooling, and particularly during rewarming (down to 21%), indicating a mismatch between cerebral blood flow and oxygen consumption. The speed of rewarming correlated with the fall in venous oxygen saturation (rs = 0.82, P less than 0.05). It is suggested that periods of cerebral blood flow/metabolic mismatch during topical cooling and rewarming may explain postoperative cerebral dysfunction after deep hypothermic procedures. A moderate speed of rewarming is advocated.

Coagulation, fibrinolysis and bleeding after open-heart surgery

To investigate the disputed pathogenesis of excessive bleeding after open-heart surgery, variables representing different hemostatic systems were correlated to postoperative blood loss in 29 patients. The general bleeding tendency in the early postoperative phase was probably attributable to depletion of hemostatic agents due to hemodilution, decreased antiplasmin activity, instantaneous but reversible platelet dysfunction following protaminization, and the natural interval to development of complete hemostasis. Heavy bleeding (greater than 800 ml/16 h) occurred in ten patients, who had significantly reduced levels of von Willebrand factor and lower active platelet count than in eight patients with minor bleeding. Defective primary hemostasis thus seemed to be the main cause of increased postoperative bleeding in these patients. Determination of platelet function by glass retention test showed good clinical relevance and gave considerably more reliable diagnosis than conventional platelet count alone. The patient with the greatest blood loss also showed drastic decrease in the plasminogen-binding form of alpha 2-antiplasmin, suggesting that additionally impaired fibrinolysis inhibition may contribute to development of severe hemorrhagic complications.