2016 Volume 80 Issue 6 Pages 1378-1385
Background: Home oxygen therapy (HOT) is used to adapt patients to the bidirectional Glenn (BDG) physiology. However, the precise cardiovascular effect of oxygen inhalation is still unknown. We used phase-contrast MRI to evaluate the cardiovascular effects of oxygen inhalation in young patients with BDG physiology.
Methods and Results: The 56 sessions of cardiac MRI were performed in 36 patients with BDG circulation. Oxygen saturation (SpO2) and heart rate (HR) were monitored under both room air and nasal 100% oxygen inhalation, and the blood flow volumes of the ascending aorta (AA), superior vena cava (SVC), and inferior vena cava (IVC) were measured by phase-contrast MRI. Systemic-to-pulmonary collateral flow (SPCF) volumes were calculated by subtracting the sum of flow volumes through the SVC and IVC from the flow volume through the AA, and used for further comparative examination. Under nasal oxygen inhalation, SpO2 significantly increased from 82% to 89%, while HR decreased from 115 to 110 beats/min. AA (5.0 vs. 4.9 L·min–1·m–2), SVC (1.85 vs. 1.77 L·min–1·m–2), and systemic blood flow volume (=SVC+IVC) significantly decreased (3.60 vs. 3.46 L·min–1·m–2). In contrast, SPCF and the pulmonary-to-systemic blood flow ratio (Qp/Qs) remained unchanged.
Conclusions: Oxygen inhalation improved arterial blood oxygenation and lowered HR in patients with BDG circulation without an increase in Qp/Qs. HOT would be protective of the cardiovascular system in patients with BDG circulation. (Circ J 2016; 80: 1378–1385)
We have introduced home oxygen therapy (HOT) to smoothly adapt congenital heart disease (CHD) patients to the bidirectional Glenn (BDG) circulation and transition them to Fontan circulation. In general, the administration of oxygen in patients with a left-to-right shunt such as a ventricular septal defect is known to cause an increase in the pulmonary-to-systemic blood flow ratio, leading to negative effects on the patient’s circulation. However, the effects of oxygen administration on the BDG circulation are still unknown. Recently, phase-contrast MRI has been introduced to accurately measure blood flow volume in any plane in the region of interest (ROI). It has confirmed the existence of a significant left-to-right shunt in BDG circulation, which was proved by the systemic-to-pulmonary collateral flow (SPCF), calculated from the differences in blood flow volume between the aorta and venae cavae, or between the pulmonary vein and pulmonary artery. SPCF has been reported as 46–54% of total pulmonary blood flow volume and 36% of cardiac output volume.1–3 In addition, previous studies reported that the SPCF after Fontan operation had a positive correlation with the volume of pleural effusion, duration of drain placement, and length of hospital stay, showing that high SPCF had a negative effect on prognosis.3–5 The aim of the present study was to use phase-contrast MRI flow measurements to elucidate the cardiovascular effects of nasal oxygen inhalation on BDG circulation in young patients with a single-ventricle heart.
We studied 56 cardiac MRI examinations performed in 36 patients with BDG circulation between February 2010 and September 2012. Among them, patients with conserved antegrade pulmonary flow as additional pulmonary blood flow were excluded. All patients enrolled in the study had started continuous HOT immediately after the BDG procedure. The primary cardiac diagnoses of the patients enrolled were hypoplastic left heart syndrome in 18 patients, unbalanced atrioventricular septal defect in 8, pulmonary atresia with intact ventricular septum in 2, tricuspid atresia in 2 and other conditions in 6. Of the 36 patients enrolled in the study 10 had asplenia and 3 had undergone DKS anastomosis. Left superior vena cava (SVC) was observed in 6 patients (7 studies). There were no major veno-venous collaterals or pulmonary arteriovenous malformations. The ratio of male to female was 21:15, and the mean age of patients at the time of the imaging examination was 2.3 years. The details of the patients are shown in Table 1.
| No. of studies (n=56) | |
|---|---|
| M/F (studies) | 35/21 |
| Age at MRI (years) | 2.3±1.3 |
| Weight (kg) | 9.8±2.0 |
| Body surface area (m2) | 0.456±0.074 |
| Age at BDG (years) | 0.46 (0.29–0.90) |
| Time between BDG and MRI (years) | 1.7±1.0 |
| Diagnosis | |
| HLHS | 27 (18*) |
| Unbalanced AVSD | 12 (8*) |
| PAIVS | 3 (2*) |
| TA | 3 (2*) |
| Other morphology | 11 (6*) |
| Drugs (mg·kg−1·day−1) | Median dose (n=no. of studies/patients) |
| Imidapril | 0.15 (n=51/32*) |
| Carvedilol | 0.24 (n=34/20*) |
| Candesartan | 0.18 (n=3/2*) |
| Diuretics# | 1.0 (n=22/14*) |
| Bostentan | 2.3 (n=5/5*) |
Data are mean±SD. *Number of patients. #Combination of both furosemide and spironolactone at the same dose. AVSD, atrioventricular septal defect; BDG, bidirectional Glenn; HLHS, hypoplastic left heart syndrome; PAIVS, pulmonary atresia with intact ventricular septum; TA, tricuspid atresia.
As a part of our routine assessment after BDG operation, cardiac MRI was performed in all the enrolled patients under intravenous thiamylal sodium sedation (3–5 mg/kg).
Each patient’s blood flow volume, peripheral arterial blood oxygen saturation (SpO2), and HR under room air conditions and with nasal oxygen inhalation (1–3 L/min) were compared. First, they were examined under room air conditions, then they continued on oxygen inhalation for 25 min until the examination ended. The flow measurements under oxygen inhalation were carried out during the last 15 min (Figure 1).
Transition of peripheral oxygen saturation and heart rate under routine cardiac magnetic resonance (CMR) imaging.
In this study, we placed an emphasis on noninvasive procedures to obtain stable SpO2 and HR, and tried to exclude clinical procedures that might affect the vital signs of the child patients.
Although measurement of systemic blood pressure with sphygmomanometer, as well as examination by blood vessel puncture, would be required under ordinary circumstances, we preferred not to perform these procedures to avoid arousing the sedated patients.
During sedation, the children’s conditions were monitored by continuous recording of SpO2 and ECG, and by television camera.
We palpated the dorsalis pedis artery immediate after sedation, paid attention to the risk of excessive hypotension, and confirmed the condition of the patient was stable before the examination.
Accordingly, safety was secured and no unexpected adverse events occurred. Because each patient awoke from sedation without harmful phenomena, we considered that the sedation level was constant.
The study protocol was approved by the Fukuoka Children’s Hospital Ethics Committees.
MRI Protocol All MRI examinations were performed with 1.5-T Avanto magneton (Siemens Medical Solutions, Erlangen, Germany). The phase-contrast MRI data were obtained using the following imaging parameters: minimum echo time and repetition time; flip angle 30 degrees; bandwidth, 241 Hz/Px; slice thickness, 3 mm; matrix, 256×256; upper velocity limit, 250 cm/s for artery and 150 cm/s for vein; 30 reconstructed phases per a cardiac cycle. A schematic of the imaging plane slice measurement setting is shown in Figure 2.
Schematic showing the location of the phase-contrast velocity used to calculate collateral flow. Red and blue squares represent the location of the velocity maps. AA, ascending aorta; DA, descending aorta; IVC, inferior vena cava; LA, left atrium; RA, right atrium; PA, pulmonary artery; QAA, flow volume through the AA; QIVC, flow volume through the inferior vena cava; Qs, systemic blood flow volume; QSVC+LSVC, sum of flow volumes through the right and left superior venae cavae; SVC, superior vena cava; SPCF, systemic-to-pulmonary collateral flow.
The imaging plane for the AA was set at a level distal to the Valsalva sinus. In the 3 patients with DKS anastomosis it was set at the level distal to the anastomotic site. The imaging plane for the SVC was set just upstream of the confluence of the pulmonary artery and downstream of the azygos and innominate veins. For the bilateral SVC, the location of each imaging plane was set just upstream of the confluence of the pulmonary artery and the azygos or hemiazygos vein. The imaging plane for the inferior vena cava (IVC) was set just downstream of the confluence of the hepatic vein and the atrium. However, when the flow volume of the IVC was unable to be measured at a single ROI, the volumes of blood flow through the hepatic vein and IVC were measured separately, and the sum of these volumes were used for further assessment.
The imaging plane for each vessel was based on 2 localizer images that were parallel to the vessel’s long axis and orthogonal to each other. Special-purpose analytical software (Argus Flow; Siemens Medical Solutions) was used for quantification of flow volumes. Flow volumes through the AA (QAA), the descending aorta (DA) at the diaphragm level (QDA), SVC (QSVC+LSVC), and IVC (QIVC) were measured, and then the QAA values were validated by comparing them with the calculated ventricular output using cine MR images.
When the measured QAA and calculated ventricular output values differed substantially, modifications of the ROI were repeated until the values agreed.
Moreover, when QDA was compared with QIVC and the values differed drastically, the ROI was modified after confirming no large azygos veins were nearby.
The following variables were calculated from the measured flow volume.
· Systemic blood flow volume (Qs)=QSVC+LSVC+QIVC.
· SPCF volume (SPCF)=QAA–(QSVC+LSVC+QIVC).
· Pulmonary blood flow volume (Qp)=QSVC+LSVC+SPCF.
The values of QAA, QSVC+LSVC, QIVC, and SPCF at baseline and after oxygen inhalation were converted into volume per heartbeat, and used for comparison.
Similarly, each value of SAA, SSVC+LSVC, SIVC, and SSPCF was compared.
Statistical AnalysisContinuous variables that followed a normal distribution are presented as mean±SD. Non-normally distributed variables are presented as medians and interquartile ranges. Proportions are presented as percentage (%). Each index was examined by paired t-test at baseline and after oxygenation. Statistical significance was defined by P<0.05.
Statistical analysis was performed with commercial statistical software (SPSS ver. 16.0.1; SPSS Inc, Chicago, IL, USA).
The changes in SpO2 and HR during the examination are shown in Figure 1. Because every SpO2 and HR value fluctuated, the plateau values were used in our assessment. The results are shown in Table 2 and Figure 3.
| Hemodynamic parameter | Baseline | After oxygen | P value |
|---|---|---|---|
| Vital signs | |||
| SpO2(%) | 82.2±6.1 | 89.0±4.4 | <0.001 |
| Heart rate (beats/min) | 115±15.9 | 110±17.0 | <0.001 |
| Measured flows (L·min−1·m−2) | |||
| QAA | 5.00±1.05 | 4.90±1.09 | 0.003 |
| QDA | 1.63±0.46 | 1.59±0.41 | 0.084 |
| QSVC+LSVC | 1.85±0.36 | 1.77±0.41 | 0.009 |
| QIVC | 1.74±0.61 | 1.68±0.56 | 0.011 |
| Calculated flows (L·min−1·m−2) | |||
| Qs (QSVC+LSVC+QIVC) | 3.60±0.82 | 3.45±0.79 | <0.001 |
| SPCF | 1.41±0.55 | 1.45±0.64 | 0.261 |
| Qp (QSVC+LSVC+SPCF) | 3.26±0.61 | 3.22±0.69 | 0.270 |
| Flow distribution | |||
| QSVC+LSVC/QAA(%) | 37.8±7.3 | 37.0±8.0 | 0.208 |
| SPCF/QAA(%) | 27.8±8.9 | 29.0±9.7 | 0.126 |
| Qp/Qs | 0.93±0.20 | 0.95±0.20 | 0.147 |
| Stroke index (ml/m2) | |||
| SAA | 43.9±9.7 | 45.0±10.5 | 0.042 |
| SSVC+LSVC | 16.3±3.7 | 16.3±4.1 | 0.971 |
| SIVC | 15.4±5.5 | 15.5±4.5 | 0.646 |
| SSPCF | 12.2±4.5 | 13.2±5.4 | 0.019 |
Data are mean±SD. BDG, bidirectional glenn; QAA, flow in ascending aorta; QDA, flow in descending aorta; QSVC+LSVC, flow in combined right and left superior venae cavae (SVC); QIVC, flow in inferior vena cava (IVC); Qs, systemic flow=sum of flow in SVC, LSVC and IVC; SPCF, systemic-to-pulmonary collateral flow=difference between QAA and Qs; Qp, pulmonary flow=sum of QSVC+LSVC and SPCF; Qp/Qs, pulmonary to systemic blood flow ratio; SAA, SSVC+LSVC, SIVC, SSPCF: stroke flow of QAA, QSVC+LSVC, QIVC, SPCF, respectively; SpO2, saturation of peripheral oxygen.
Change in peripheral oxygen saturation (A) and heart rate (B). *P<0.001.
SpO2 increased and HR declined significantly under all oxygen inhalation conditions (82±6 to 89±4%, P<0.001, and 115±16 to 110±17 beats/min, P<0.001, respectively).
Among the measured minute volumes of blood flow, QAA (5.00±1.05 to 4.90±1.09 L·min–1·m–2, P=0.003), QSCV+LSVC (1.85±0.36 to 1.77±0.41 L·min–1·m–2, P=0.009), and QIVC (1.74±0.61 to 1.68±0.56 L·min–1·m–2, P=0.011) decreased significantly, and QDA (1.63±0.46 to 1.59±0.41 L·min–1·m–2, P=0.084) showed a decreasing trend.
Of the calculated parameters, Qs (QSVC+LSVC+QIVC) was significantly decreased (3.60±0.82 to 3.45±0.79 L·min–1·m–2, P<0.001), and no changes were found in SPCF (1.41±0.55 to 1.45±0.64 L·min–1·m–2, P=0.261) or Qp (=QSVC+LSVC+SPCF) (3.26±0.61 to 3.22±0.69 L·min–1·m–2, P=0.270). The difference in Qp/Qs was not significant (0.93±0.20 to 0.95±0.20, P=0.147).
With regard to stroke indexes, SAA (43.9±9.7 to 45.0±10.5 ml, P=0.042) and SSPCF (12.2±4.5 to 13.2±5.4 ml, P=0.019) increased, but SSVC+LSVC (16.3±3.7 to 16.3±4.1 ml, P=0.971) and SIVC (15.4±5.5 to 15.5±4.5 ml, P=0.646) remained unchanged. A schematic of the changes in flow volumes is shown in Figure 4.
Schematic showing the change in flow volume by oxygen inhalation. (A) Minute volumes of blood flow. (B) Stroke indices of blood flow. ↓, decreased, →, unchanged, ↑, increased. AA, ascending aorta; DA, descending aorta; IVC, inferior vena cava; SPCF, systemic to pulmonary collateral flow; SVC, superior vena cava.
Most of the subjects (34 cases/53 studies) were on renin-angiotensin system (RAS) inhibitors, which can lower systemic vascular resistance (SVR), but may not cause a decrease in HR.
As decreased HR may be influenced by administration of β-blockers, the effect on HR according to administration of carvedilol is shown in Table 3. There was a tendency for a greater degree of HR reduction to be observed in the non-carvedilol group, even though a smaller degree of SpO2 elevation was found. The changes in flow volume by HOT were not significantly different between the 2 groups.
| Carvedilol (+) | Carvediol (−) | P value | |
|---|---|---|---|
| No. of patients and studies | 20/34 | 16/22 | |
| Age (years) | 2.1±1.0 | 2.8±1.6 | 0.065 |
| SpO2 (%) | |||
| 1. Baseline (room air) | 81.8±6.9 | 82.9±4.3 | 0.510 |
| 2. After oxygenation | 89.3±4.3 | 88.5±4.7 | 0.550 |
| Δ (2–1) | +7.5±3.9 | +5.6±1.3 | 0.035 |
| Heart rate (beats/min) | |||
| 1. Baseline (room air) | 117±15 | 112±17 | 0.274 |
| 2. After oxygenation | 113±16 | 106±19 | 0.114 |
| Δ (2–1) | −3.8±4.1 | −6.5±8.0 | 0.094 |
Data are mean±SD. Abbreviations as in Table 2.
The results from the present study suggested that oxygen inhalation is beneficial for patients with BDG circulation because it simply improves systemic oxygenation and may inhibit stimulation of sympathetic nerve activity (SNA) without a significant increase in Qp/Qs. Reduced oxygen saturation has been found to strongly correlate with impaired brain growth in infants with CHD,6 and it is also believed that their physical growth in childhood is influenced by the degree of cyanosis and cardiac performance. Consequently, oxygen inhalation may lessen the developmental and growth impairments in CHD patients.
Bradycardia by Oxygen InhalationIn healthy individuals, inhalation of 100% oxygen reduces the HR and cardiac index, and increases SVR and blood pressure.7 No change in stroke volume is observed with inhalation of 100% oxygen.7 In short, the reduction in cardiac index is caused by the slowing of HR, which can be blocked by atropine; therefore, it is considered a phenomenon via the vagal reflex. In the present study, there were reductions in HR and cardiac index, and no change in the stroke volume of the SVC and IVC with oxygen inhalation by patients with BDG circulation, suggesting that the mechanism of oxygen inhalation is the same as in healthy individuals. On the other hand, SAA and SSPCF were increased with oxygen inhalation, which is different from healthy persons. The details will be described later.
Furthermore, it is considered that higher inspiratory oxygen concentrations cause more slowing of the HR in healthy individuals.7 The concentration of inhaled oxygen was estimated to be 34% (29–44%) of the body constitution and ventilation volume of the patients with BDG circulation (eg, given tidal volume as 15 ml/kg, respiratory rate as 30 breaths/min, and inspiratory time as 0.67 s in an infant weighing 10 kg with ventilation volume of 2 L/min: inhaled air volume is 150 ml×30=4,500 ml/min, 100% oxygen inhalation duration is 0.67×30=20 s, inhaled volume of 100% oxygen is 2,000×20/60=667 ml, giving a total ventilation volume of (4,500–667)×0.21+667=1,472 ml, resulting in an estimated fraction of inspiratory oxygen of 1,472/4,500=32.7%). HR slightly decreased from 67.1 to 66.8 beats/min with 30% oxygen inhalation in healthy adults,7 whereas it apparently decreased from 115 to 110 beats/min in patients with BDG circulation. There is no significant correlation between the degree of HR decrease and the volume of inhaled oxygen. This result may be based on small differences in the oxygen concentration inhaled. This increased action in patients with BDG circulation under constant low-oxygen conditions might be caused by amplified reactivity of the chemoreceptor to high oxygen exposure. On the other hand, there is a report that RAS inhibitors may increase the sensitivity of the chemoreceptor,8 and thus the sensitivity of the patients in this study may also have been affected. It has been reported that the sensitivity of the chemoreceptor to a low-oxygen concentration decreased in patients with cyanotic CHD.9 Therefore, it is no wonder that patients under chronic exposure to low-oxygen conditions are highly sensitive to high-oxygen conditions.
SNA Under Low-Oxygen ConditionsArterial oxygen saturation in patients is chronically lower than in healthy subjects. In previous publications regarding the human response to a low-oxygen environment, studies were conducted under low-oxygen conditions by adding nitrogen or conducted under low atmospheric pressure at high altitude. In the present study, the research conditions were not identical to those in previously published studies; that is, chronic low-oxygen conditions in patients with BDG circulation were under ordinary atmospheric pressure and ordinary partial pressure of oxygen in air.
In general, the effects of chronic low-oxygen conditions on individuals can be classified as: (1) direct action on pulmonary blood vessels at the level of exposed pulmonary alveoli, (2) responses of the chemoreceptor that detects low oxygen levels in arterial blood, and (3) direct action on peripheral arterioles and venules. In BDG circulation with decreased arterial oxygen saturation and ordinary inspiratory oxygen concentration, the effects of low oxygen fall into categories (2) and (3); in other words, the responses are mediated by the chemoreceptor and peripheral vessels and the effects of this pathway are considered as the same as in the previous publications. Hypoxia stimulates excitatory impulses from the chemoreceptor to the brainstem vasomotor center, and enhances systemic SNA. Thus it is possible that SNA is activated constitutively in BDG circulation. In fact, in healthy individuals who live at high altitudes and are exposed to hypoxic stimulation equivalent to BDG circulation, both blood pressure and the plasma level of noradrenaline are increased.10 In the Fontan circulation, which is a right heart bypass circulation as well as a BDG circulation, muscle SNA (MSNA) is considered to be enhanced.11 As in (3), it is considered that low-oxygen conditions dilate peripheral vessels to increase blood flow, whereas high-oxygen conditions constrict them. Even when peripheral blood vessels are constricted by oxygen administration, the oxygen effects on stroke volume play only a small or negligible role, as shown in Table 2 and in the previous study.7 It is thought that SNA could promote myxomatous degeneration in mitral valve prolapse, propagating disease severity.12 Inhibiting SNA by oxygen administration may also prevent worsening of atrioventricular valvular regurgitation in CHD.
Effects of Oxygen Inhalation in Individuals Under Low-Oxygen ConditionsAs reported by Querido et al,13 acute hypoxic stress with 81% SpO2 increases blood pressure, HR, and MSNA. MSNA has a positive correlation with cardiac SNA.14 An increase in SpO2 by oxygen inhalation can inhibit stimulated SNA under chronic low-oxygen conditions through an enhanced inhibitory impulse to the chemoreceptors. The tendency toward a large degree of HR reduction in the non-carvedilol group (Table 3) in the present study also supports this idea. Though the effect of long-term oxygen inhalation is unknown, it is possible that the acute effect lasts longer. The present study showed sustainable HR slowing during oxygen inhalation in BDG circulation. If the patients’ SNA is enhanced, oxygen inhalation could inhibit it.
SPCF in BDG CirculationWhitehead et al1 reported that SPCF was 1.8±0.6 L·min–1·m–2 and 37% of aortic blood flow volume, using the same method as ours [SPCF=QAA −(QSVC+LSVC+QIVC)]. Grosse-Wortmann et al2 reported a median SPCF of 1.4 L·min–1·m–2 and a proportion of aortic blood flow of 36% using an alternative formula [SPCF=QPV–QPA]. The SPCF was 1.4 L·min–1·m–2 in the present study, consistent with the values in the 2 published studies. The SPCF proportion of 28% of aortic blood flow in our study was slightly less than in the previous reports and the precise reason is unknown. One reason may be routine use in our institute of oral systemic vasodilators (angiotensin-converting enzyme inhibitor (ACEI), angiotensin-receptor blocker or α,β-adrenoreceptor antagonist) to protect the cardiovascular system (Table 1). It was reported that intravenous ACEI significantly decreased Qp/Qs in patients with BDG circulation, according to measurement of pulmonary and systemic blood flows.15 It is suggested, in short, that a decrease in SVR by vasodilator administration may have resulted in a slight decrease in the proportion of SPCF of aortic blood flow in the present study compared with the published data.
It is thought that SPCF is a vital reaction to hypoxia. The extent of SPCF may reflect the degree of adaptation to right heart bypass circulation. A large SPCF may mean that the patient cannot secure enough pulmonary blood flow by right heart bypass circulation only. SPCF may be essential in cases of maladaptation to the Fontan circulation, but may be troublesome in cases of adaptation. Oxygen inhalation improves arterial blood oxygenation without a significant large increase in pulmonary blood flow.
Oxygen Administration and Blood FlowBoth SSVC+LSVC and SIVC were unchanged by oxygen inhalation and the level of increase in SAA mostly agreed with that in SSPCF. Pulmonary blood flow showed a trend of slight increase with oxygen inhalation through SPCF. It is well known that oxygen inhalation decreases pulmonary vascular resistance and increases SVR. An increase in the pressure gradient between the systemic and pulmonary circulations by oxygen inhalation might result in an increase in SPCF. However, in the present study Qp/Qs only showed a slight increasing trend, from 0.93 to 0.95, which may reflect underpowering of this study and we can estimate that Qp/Qs actually increased, while the alteration of Qp/Qs was only slight in comparison with the significant increase in SpO2. It is suggested that the improvement in arterial oxygenation by oxygen inhalation would not mainly result from an increase in pulmonary blood flow volume but from other factors (eg, improvement of local ventilation-perfusion mismatch because of uneven distribution of blood flow). It is utterly groundless that inhalation of a high concentration of oxygen by patients with BDG circulation might cause an inappropriate increase in pulmonary blood flow. Unlike alterations in the flow indexes (SAA, SSVC+LSVC and SIVC), the QAA, QSVC+LSVC and QIVC decreased with oxygen inhalation. It is feasible that a decrease in cardiac minute output would mainly cause a decrease in HR. We speculate, therefore, that peripheral vasoconstriction by oxygen inhalation has a minor effect on BDG circulation. Consequently, there is little risk of worsening heart failure by pulmonary high-flow or peripheral vasoconstriction with oxygen inhalation.
Oxygen Inhalation and Ventricular PreloadThe HR decrease with oxygen inhalation leads to a prolongation of the time available for ventricular filling. Prolonged ventricular filling time may most contribute to the increase in SAA because oxygen inhalation does not decrease SVR,7 and may not improve ventricular contractility alone. Oxygen inhalation-induced increase of SAA without a change in SSVC+LSVC+SIVC in BDG circulation suggests that the amount of increase in SAA can be ascribed to that in SPCF. Because cardiac minute output (=QAA) decreased with decreasing HR, cardiac workload might be decreased. On the other hand, the cardiac preload of a single beat (=ventricular filling volume=SAA) was increased. This effect of oxygen inhalation would be quite favorable for adaptation of the cardiac ventricle to right heart bypass circulation by avoiding drastic preload reduction causing acute ventricular decompression with diastolic dysfunction.
Introduction of HOT in Patients Who Have Undergone BDG ProcedureWe administer HOT (1–2 L/min) to patients who have undergone BDG procedure without additional pulmonary blood flow as a combination therapy. As discussed, HOT has physiologic advantages for BDG circulation, but also disadvantages, such as discomfort from the nasal cannula, mechanical irritation of skin, and a requirement to carry an oxygen cylinder.
Fortunately, in our experience adverse effects of HOT in young patients are very rare. It is conceivable that HOT has more advantages than disadvantages because of the improvement in both oxygenation and hemodynamics in patients with BDG circulation.
Study LimitationsThis study investigated an acute effect of oxygen and the chronic effect is unknown. However, HR continues to be lowered during oxygen inhalation, so the favorable effect may last as long as the patient inhales oxygen.
We did not measure blood pressure during our examination, to avoid arousing the sedated patients. However, if measured, more detailed analysis would be possible.
Furthermore, even in the parameters without a statistically significant difference because of the small number of patients in this study, it is possible to show a statistically significant difference by conducting a further study with an increased number of cases.
Oxygen administration for patients with BDG circulation increased SpO2, and decreased HR and cardiac output. However, it induced little change in the SPCF.
It is possible that HOT in patients with chronic hypoxemia who have BDG circulation will allow the BDG circulation to function properly and this will in turn, contribute to improving prognosis.
None.
