Junpei Nozaki

Phenylephrine increases pulmonary blood flow in children with tetralogy of Fallot

PurposeAlthough it has been reported that the increase in blood pressure improves arterial oxygen saturation (SaO2) in children with tetralogy of Fallot, no prospective study has demonstrated that an increase in blood pressure induces an increase in pulmonary blood flow in these patients. The purpose of this study was to see whether a phenylephrine-induced increase in systemic blood pressure increased pulmonary blood flow, resulting in improved arterial oxygénation in tetralogy of Fallot.MethodsIn 14 consecutive children with tetralogy of Fallot (2–32 months old), transesophageal pulsed Doppler signals of left upper pulmonary venous flow (PVF) velocity were recorded before and four minutes after 10/μg · kg−1 of phenylephrine iv. Simultaneously, arterial blood gas analysis and hemodynamic measurements were performed. The minute distance (MD) was calculated as the product of the heart rate and the sum of time-velocity integrals of PVF.ResultsPhenylephrine iv increased mean arterial blood pressure from 54 ± 8 mmHg to 73 ± 10 mmHg. This phenylephrineinduced hypertension significantly increased SaO2 and MD (92.0 ± 7.5 vs 95.0 ± 5.0% and 1318 ± 344 vs 1533 ± 425 cm · min−1, respectively). There was a significant correlation (r = 0.72) between the change in MD and the change in SaO2.ConclusionOur results suggest that the phenylephrine-induced increase in systemic blood pressure produces an increase in pulmonary blood flow in tetralogy of Fallot. Our results further suggest that this increase in pulmonary blood flow is involved in the mechanism of phenylephrine-induced improvement of arterial oxygenation in tetralogy of Fallot.RésuméObjectifOn a déjà montré qu’une augmentation de la tension artérielle améllore la saturation en oxygène du sang artériel (SaO2), chez les enfants qui présentent une tétralogie de Fallot, mais aucune étude prospective n’a démontré qu’une augmentation de la tension artérielle pouvait induire une élévation du débit sanguin pulmonaire chez ces patients. Nous voullons vérifier si une augmentation de la tension artérielle générale induite par la phényléphrine fait augmenter le débit sanguin pulmonaire et améliore l’oxygénation artérielle dans le contexte d’une tétralogie de Fallot.MéthodeChez 14 enfants porteurs d’une tétralogie de Fallot et traités consécutivement (âgés de 2–32 mois), les signaux Doppler pulsés transœsophagiens de la vitesse du flux de la veine pulmonaire gauche supérieure (DVP) ont été enregistrés avant, puis quatre minutes après l’administration iv de 10 μg · kg−1 de phényléphrine. Une analyse des gaz du sang artériel et des mesures hémodynamiques ont été réalisées simultanément. La distance minute (DM) a été calculée comme le produit de la fréquence cardiaque et de la somme des intégrales de temps-vélocité du DVR.RésultatsLa phényléphrine iv a augmenté la tension artérielle moyenne de 54 ± 8 mmHg à 73 ± 10 mmHg. L’hypertension induite par la phényiéphrine a augmenté la SaO2 et la DM de façon significative (92,0 ± 7,5 vs 95,0 ± 5,0 % et 1318 ± 344 vs 1533 ± 425 cm · min−1, respectivement). Il y avait une corrélation significative (r = 0,72) entre les modifications de la DM et celles de la SaO2.ConclusionNos résultats suggèrent que, chez les patients atteints d’une tétralogie de Fallot, l’augmentation du débit sanguin général induite par la phényiéphrine produit une élévation du débit sanguin pulmonaire. De plus, il apparaît que cette augmentation du débit sanguin pulmonaire contribue à l’amélioration de l’oxygénation artérielle induite par la phényiéphrine.

Transesophageal Echocardiographic Assessment of Pulmonary Arterial and Venous Flow During High-Frequency Jet Ventilation

Abstract Study Objective: To evaluate high-frequency jet ventilation (HFJV) effects on pulmonary arterial and venous flow compared to those of intermittent positive-pressure ventilation (IPPV) by using pulsed Doppler transesophageal echocardiography. Design: Prospective clinical study. Setting: University-affiliated hospital operating room. Patients: 13 ASA physical status I and II patients undergoing lower abdominal or lower extremity surgery. Interventions: Patients had total IV anesthesia with propofol and fentanyl. After anesthesia induction, a transesophageal echocardiography probe was inserted into the esophagus. IPPV (TV, 8–10 mL/kg; respiratory rate, 10–12 cycles/min; I/E ratio, 1:2; FIO 2 , 1.0) and HFJV (driving pressure, 0.5–0.6 kgf/cm 2 ; frequency,3 Hz; I/E ratio, 1:1; FIO 2 , 1.0) were performed under hemodynamically stable conditions. Measurements: Pulmonary-arterial-flow velocity, pulmonary-venous-flow velocity, left ventricular short-axis view, and airway-pressure curve were recorded simultaneously. Parameters measured were: hemodynamic variables, arterial blood gases, inspiratory airway pressure; [from pulmonary-arterial-flow velocity] pre-ejection period (PEP), acceleration time (AT), right ventricular ejection time (RVET), and their ratios (PEP/AT, AT/RVET); [from pulmonary-venous-flow velocity] time-velocity integral of the first systolic wave (S1), second systolic wave (S2), and diastolic wave (D), and systolic fraction (integral S1 + S2/S1+ S2 + D); [from M-mode] left-ventricular-end systolic volume, left-ventricular-end diastolic volume (LVEDV), stroke volume, cardiac output, and ejection fraction, using Teichholzs method. Main Results: Peak inspiratory airway pressure during HFJV was significantly lower than that during IPPV. HFJV significantly decreased PEP/AT, correlating positively with pulmonary arterial pressure, and significantly increased AT and AT/RVET, correlating negatively with pulmonary arterial pressure. Systolic fraction, correlating negatively with left atrial pressure, increased significantly during HFJV, as did LVEDV, stroke volume, cardiac output, and ejection fraction. Conclusions: Our results suggest that, in comparison to IPPV, HFJV significantly decreases pulmonary arterial pressure and left atrial pressure, resulting in significant increases in cardiac output and ejection fraction in healthy anesthetized adults.

Intraoperative Evaluation of Pulmonary Artery Flow During the Fontan Procedure by Transesophageal Doppler Echocardiography

After the Fontan procedure, pulmonary artery (PA) flow is maintained without right ventricular pump function. We evaluated intraoperative PA flow velocity patterns using transesophageal Doppler echocardiography (TEE) immediately after cardiopulmonary bypass (CPB) in patients during Fontan or hemi-Fontan procedures. We studied 10 patients with single-ventricle physiology (age range, 5 mo to 3 yr 1 mo). Anesthesia was induced and maintained with fentanyl. After induction of anesthesia, a pediatric TEE probe was inserted into the esophagus. All patients had surgical repair involving direct anastomosis of the right atrium to the PA. Immediately after completion of CPB, adequacy of the atriopulmonary anastomosis was assessed and PA flow velocity was recorded. In all patients, the atriopulmonary anastomosis was clearly defined using a single-plane TEE probe, and PA flow recording was completed successfully. Intraoperative PA flow velocities showed two distinct patterns. Biphasic forward flows with peak velocities during systole and diastole were observed in six patients. The remaining four patients showed forward flows with flow reversals. The four patients demonstrating flow reversals showed significantly reduced fractional shortening (26.5 ± 2.1% vs 35.5 ± 6.3%) and larger pressure gradient between the right atrium and left atrium (10.8 ± 1.3 mm Hg vs 8.0 ± 0.9 mm Hg) when compared to those without reverse flow. Two patients with reverse flow required reoperation because of hypotension. Because PA flow is influenced by pulmonary vascular resistance and left ventricular function, TEE assessed intraoperative PA flow should be further evaluated as a useful predictor of surgical outcome after a Fontan procedure. Implications We evaluated intraoperative pulmonary artery flow velocity patterns with transesophageal Doppler echocardiography (TEE) in patients during a Fontan procedure. Because pulmonary artery flow is influenced by pulmonary vascular resistance and ventricular function, intraoperative evaluation of pulmonary artery flow using TEE should be further evaluated as a predictor of surgical outcome after a Fontan procedure.

Pulmonary Arterial Pressure Can Be Estimated by Transesophageal Pulsed Doppler Echocardiography

We examined whether pulmonary arterial pressure can be estimated on the basis of pulmonary arterial flow velocity determined via intraoperative pulsed Doppler transesophageal echocardiography (TEE) in 20 patients undergoing cardiac surgery. Standard pulmonary artery measurements were taken as well. Measurements were taken before sternotomy, after pericardiotomy, after cardiopulmonary bypass, and after sternum closure. The variables obtained by TEE included preejection period (PEP), acceleration time (AT), right ventricular ejection time (RVET), and R-R interval (RR). Five ratios were calculated as indices of pulmonary arterial pressure—PEP/AT, PEP/RVET, AT/RVET, PEP/√RR, and AT/√RR—and were compared with pulmonary artery catheterization findings, i.e., systolic pulmonary arterial pressure (sPAP), log sPAP, mean PAP (mPAP), and log mPAP. Before sternotomy, PEP/AT, PEP/√RR, and AT/√RR showed significant correlation with all pulmonary artery catheterization values. AT/RVET showed correlation with all pulmonary artery values except log mPAP. PEP/AT showed the closest correlation with sPAP (r = 0.771) and log sPAP (r = 0.789). PEP/AT also showed close correlation with mPAP (r = 0.764) and log mPAP (r = 0.777). Significant agreement between sPAP and mPAP values calculated from a regression equation and values measured via pulmonary artery catheter was observed by plotting the differences against the mean values of the two measurements. We therefore conclude that noninvasive estimation of pulmonary arterial pressure is feasible via intraoperative TEE when sternotomy is not involved.

Intraoperative transoesophageal echocardiography in a low birth weight neonate with atrioventricular septal defect

An 18‐day‐old male neonate (45 cm, 1.8 kg) with a history of cyanosis and congestive heart failure from an atrioventricular septal defect (AVSD) with a large left‐to‐right shunt was scheduled for surgical repair of the AVSD. After routine induction of anaesthesia with fentanyl and vecuronium, a 4.5‐mm diameter transoesophageal echocardiography (TOE) probe was inserted into the oesophagus, and systematic echocardiographic evaluation was performed during surgery. After cardiopulmonary bypass was stopped, intraoperative TOE revealed mild residual mitral valve regurgitation. Because good left ventricular wall motion was confirmed and haemodynamic parameters were stable, cardiopulmonary bypass was not reinitiated. The patients cardiac output was low in the postoperative intensive care unit. TOE was performed the next day to detect the source of this problem, revealed severe regurgitation compared with that observed intraoperatively. TOE was useful for evaluation of the residual mitral valve regurgitation, and we reconfirmed the importance of continuous monitoring even in a low birthweight neonate undergoing repair of a complete AVSD.

The effects of acute normovolemic hemodilution on left ventricular systolic and diastolic function in the absence or presence of beta-adrenergic blockade in dogs.

Acute normovolemic hemodilution (ANH) increases cardiac output because of a reduction in blood viscosity and enhancement of left ventricular (LV) contractility. The status of LV function, especially LV diastolic function during ANH, remains controversial. We therefore examined LV systolic and diastolic function during ANH. Sixteen dogs were anesthetized with isoflurane in the absence (Group 1) and presence (Group 2) of &bgr;-adrenergic blockade (propranolol 1 mg/kg). LV contractility was quantified by the slope (Mw) of the stroke work and end-diastolic volume relation. Diastolic function was evaluated with the time constant of LV relaxation (T), chamber stiffness constant (Kc), peak LV diastolic filling rate during early filling (peak E) and atrial contraction (peak A), and ratio of peak E to peak A (E/A). Normovolemic exchange of blood (50 mL/kg) for 6% hydroxyethyl starch (ANH50) significantly increased Mw in Group 1 but not in Group 2. In both groups, ANH50 significantly decreased T. ANH50 significantly increased peak E in both groups and peak A in Group 1, and it did not change the E/A ratio or Kc in either group. ANH causes positive inotropic effects and enhances diastolic function without &bgr;-blockade. Even after &bgr;-adrenergic blockade, ANH improves diastolic function through the reduction of LV ejection impedance.

Low-Dose Sevoflurane Inhalation Enhances Late Cardioprotection from the Anti-Ulcer Drug Geranylgeranylacetone

BACKGROUND:We investigated in rabbits whether sevoflurane enhances late cardioprotection induced by geranylgeranylacetone (GGA), a gastric antiulcer drug. METHODS:S(+)-ketamine and xylazine-anesthetized rabbits were assigned to one of seven experimental groups: a control (vehicle only) group, a GGA group, a sevoflurane group, a GGA+sevoflurane group, a sodium 5-hydroxydecanoate (5HD) group, a GGA + 5HD group, and a heat stress group. All rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. Rabbits were pretreated with IV vehicle, GGA (10 mg/kg), or heat stress (42°C for 15 min) 24 h before coronary occlusion. Sevoflurane (0.5 minimum alveolar concentration) or 5HD (5 mg/kg) were administered before myocardial ischemia. Myocardial infarct size and the area at risk for ischemia were measured, and heat shock protein (Hsp) 70 levels in each experimental group were determined. RESULTS:Compared with vehicle only, GGA significantly reduced the size of myocardial infarction in relation to the area at risk (39 ± 10% vs 59 ± 9%, P < 0.02). Sevoflurane enhanced the GGA-induced cardioprotection (23 ± 17%, P < 0.05 vs GGA). The cardioprotective effect of GGA was abolished by administration of 5HD (56 ± 15%, P < 0.01). GGA enhanced Hsp 70 expression compared with that in the control group (0.69 ± 0.15 vs 0.36 ± 0.05, P < 0.02). Administration of GGA with sevoflurane resulted in the same level of Hsp 70 expression as GGA (0.69 ± 0.16, P > 0.98). CONCLUSIONS:GGA appears to reduce myocardial infarct size in association with increased Hsp 70 expression. Sevoflurane enhances the GGA-induced cardioprotective effect.

Effects of sevoflurane on regional myocardial blood flow distribution: quantification with myocardial contrast echocardiography.

BACKGROUND Using myocardial contrast echocardiography, the authors tried to determine whether sevoflurane causes myocardial blood maldistribution in humans and dogs. METHODS In animal experiments, 15 mongrel dogs were organized into dipyridamole (n = 6) and sevoflurane (n = 9) groups. Sonicated albumin was infused into the left main coronary artery. The peak gray level corrected for background was analyzed at the following intervals: (1) at baseline, (2) after stenosis of the left circumflex coronary artery (blood flow reduced by 40%), (3) after administration of dipyridamole (1 mg/kg given intravenously) or sevoflurane (1 minimum alveolar concentration) during stenosis, and (4) after phenylephrine during stenosis and administration of dipyridamole or sevoflurane. In human studies, nine patients undergoing coronary artery bypass grafting were studied. During partial extracorporeal circulation, the peak gray level was analyzed before and 20 min after sevoflurane (1 minimum alveolar concentration). RESULTS In animal experiments, dipyridamole decreased significantly the inner:outer ratio of the peak gray level in the ischemic area and the ischemic:normal ratio of the peak gray level. After arterial pressure was restored with phenylephrine, neither the inner:outer ratio nor the ischemic:normal ratio improved. In contrast, after sevoflurane administration, the inner:outer ratio and the ischemic:normal ratio remained unchanged, but these increased with phenylephrine. In human studies, sevoflurane did not change the inner:outer ratio in the area supplied by the most stenotic coronary artery. CONCLUSION These results suggest that dipyridamole, a potent coronary vasodilator, produces maldistribution of coronary blood flow in our dog models, whereas sevoflurane does not do this in animal or human studies.

Anesthetic management of a patient undergoing cardioverter defibrillator implantation: usefulness of transesophageal echocardiography and near infrared spectroscopy.

A case of a patient with sustained ventricular tachycardia (VT) undergoing implantable cardiovertor defibrillator (ICD) implantation, using transesophageal echocardiography (TEE) and near infrared spectroscopy (NIR) is described. A 67-year-old man with sustained VT associated with old myocardial infarction underwent ICD implantation. Anesthesia was induced with fentanyl and propofol and maintained with nitrous oxide, oxygen, sevoflurane, and fentanyl. Global hypokinesis of the left ventricle was observed in the short-axis view provided by TEE. Intraoperative systolic blood pressure was maintained between 100 and 120 mmHg, and cerebral oxygenated hemoglobin (HbO2) was between 63% and 65%. During periods of induced ventricular fibrillation, systolic blood pressure decreased to 60 mmHg, HbO2 decreased to 59%, and TEE revealed cardiac arrest. These changes were transient; HbO2 returned to baseline values immediately after the restoration of normal rhythm. TEE confirmed no remarkable change in cardiac function after defibrillation testing. TEE and NIR were found to be beneficial for the anesthetic management of a patient with sustained VT who was underdoing ICD implantation.

Effects of acute normovolemic hemodilution on ventriculoarterial coupling in dogs.

Background: Acute normovolemic hemodilution (ANH) causes a decrease in systemic vascular resistance. Similar to vasodilating drugs, ANH might modify ventriculoarterial coupling. Left ventricular elastance (Ees), effective arterial elastance (Ea), stroke work (SW), and pressure volume area (PVA) were used as indicators to examine the effects of ANH on this coupling.