Modeling of the Norwood circulation: effects of shunt size, vascular resistances, and heart rate

2001 ◽  
Vol 280 (5) ◽  
pp. H2076-H2086 ◽  
Author(s):  
Francesco Migliavacca ◽  
Giancarlo Pennati ◽  
Gabriele Dubini ◽  
Roberto Fumero ◽  
Riccardo Pietrabissa ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Compartmental Analysis ◽  
Hypoplastic Left Heart ◽  
Systemic Blood Flow ◽  
Initial Procedure ◽  
Blood Flow Ratio ◽  
Left Heart Syndrome

Hypoplastic left heart syndrome is the most common lethal cardiac malformation of the newborn. Its treatment , apart from heart transplantation , is the Norwood operation. The initial procedure for this staged repair consists of reconstructing a circulation where a single outlet from the heart provides systemic perfusion and an interpositioning shunt contributes blood flow to the lungs. To better understand this unique physiology, a computational model of the Norwood circulation was constructed on the basis of compartmental analysis. Influences of shunt diameter, systemic and pulmonary vascular resistance, and heart rate on the cardiovascular dynamics and oxygenation were studied. Simulations showed that 1) larger shunts diverted an increased proportion of cardiac output to the lungs, away from systemic perfusion, resulting in poorer O2 delivery, 2) systemic vascular resistance exerted more effect on hemodynamics than pulmonary vascular resistance, 3) systemic arterial oxygenation was minimally influenced by heart rate changes, 4) there was a better correlation between venous O2 saturation and O2 delivery than between arterial O2 saturation and O2delivery, and 5) a pulmonary-to-systemic blood flow ratio of 1 resulted in optimal O2 delivery in all physiological states and shunt sizes.

scholarly journals Interstage management of pulmonary blood flow after the Norwood procedure with right ventricle-to-pulmonary artery conduit

2020 ◽  
Vol 58 (3) ◽  
pp. 551-558
Author(s):  
Takashi Yasukawa ◽  
Takaya Hoashi ◽  
Masataka Kitano ◽  
Masatoshi Shimada ◽  
Kenta Imai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Norwood Procedure ◽  
Flow Ratio ◽  
Hypoplastic Left Heart ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Blood Flow Ratio ◽  
Left Heart Syndrome

Abstract OBJECTIVES Our goal was to assess the efficacy of managing pulmonary blood flow from the Norwood procedure with a right ventricle-to-pulmonary artery (RV–PA) conduit until stage 2 palliation (S2P). METHODS Among 48 consecutive patients undergoing the Norwood procedure between 2008 and 2018, 40 (83.3%) patients who survived to discharge were included in this study. The primary diagnosis was hypoplastic left heart syndrome in 28 (70%) patients and hypoplastic left heart syndrome variant in 12 (30%) patients. All patients received bilateral pulmonary artery banding. The median age and weight at the time of the Norwood procedure were 41 (25th–75th percentiles: 27–89) days and 3.2 (2.7–3.9) kg, respectively. In keeping with institutional strategy, S2P was undertaken when body weight exceeded 5.0 kg, and normal gross motor development was confirmed. RESULTS The RV–PA conduit was clipped in 28 (70%) patients during the perioperative period of the Norwood procedure, then partial unclipping was performed in 8 (20%) patients and full unclipping was performed in 20 (50%) patients. Before S2P, the median pulmonary-to-systemic blood flow ratio was 1.0 (0.7–1.3). The median age and weight at the time of S2P were 10.7 (9.0–12.9) months and 6.3 (5.5–7.1) kg, respectively. The survival rate 5 years after Norwood discharge was 85.3%. Pre-S2P pulmonary-to-systemic blood flow ratio was linearly correlated with greater interstage changes in systemic atrioventricular valve regurgitation (R2 = 0.223, P = 0.004). CONCLUSIONS Interstage management of pulmonary blood flow by RV–PA conduit clipping and gradual unclipping provided good interstage outcomes. The median pulmonary-to-systemic blood flow ratio could be controlled to 1.0 at pre-S2P catheter examination.

Leukotriene end organ antagonists increase pulmonary blood flow in fetal lambs

1985 ◽  
Vol 249 (3) ◽  
pp. H570-H576 ◽  
Author(s):  
S. J. Soifer ◽  
R. D. Loitz ◽  
C. Roman ◽  
M. A. Heymann
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Blood Gases ◽  
Physiological Control ◽  
Arterial Blood ◽  
High Pulmonary Vascular Resistance

The factors responsible for maintaining the normally low pulmonary blood flow and high pulmonary vascular resistance in the fetus are not well understood. Since leukotrienes are potent pulmonary vasoconstrictors in many adult animal species, we determined whether leukotrienes were perhaps involved in the control of the fetal pulmonary circulation by studying the effects of putative leukotriene end organ antagonists in two groups of fetal lambs. In six fetal lambs studied at 130-134 days gestation, FPL 55712 increased pulmonary blood flow by 61% (P less than 0.05) and reduced pulmonary vascular resistance by 45% (P less than 0.05). There was a small increase in heart rate but no changes in pulmonary and systemic arterial pressures and systemic arterial blood gases. In six other fetal lambs studied at 130-140 days gestation, FPL 57231 increased pulmonary blood flow by 580% (P less than 0.05) and decreased pulmonary vascular resistance by 87% (P less than 0.05). Pulmonary and systemic arterial pressures decreased (P less than 0.05), and heart rate increased (P less than 0.05). Leukotriene end organ antagonism significantly increases fetal pulmonary blood flow and decreases pulmonary vascular resistance. Leukotrienes may play a role in the physiological control of the fetal pulmonary circulation.

Neonatal hypertrophic cardiomyopathy with duct-independent systemic blood flow

1997 ◽  
Vol 7 (4) ◽  
pp. 446-449
Author(s):  
Kenji Suda ◽  
Darlene P. Horton ◽  
Norman H. Silverman
Keyword(s):  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Ventricular Hypertrophy ◽  
Upper Body ◽  
Left Heart ◽  
Cavity Size ◽  
Hypoplastic Left Heart ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Left Heart Syndrome

AbstractWe describe a newborn who had echocardiogaphic features of severe hypertrophic cardiomyopathy and duct-dependent systemic blood flow. Blood flow to the upper body could be maintained only by prostaglandin El, as in the case of hypoplastic left heart syndrome. Forward flow was gradually established from the left ventricle, and the patient weaned from prostaglandin El. Although the patient's mother had poorly controlled diabetes, the patient at 24 months of age shows residual but lessened ventricular hypertrophy and increased cavity size.

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Blood Content ◽  
Calf Blood Flow ◽  
Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

scholarly journals Cinaciguat, a soluble guanylate cyclase activator, causes potent and sustained pulmonary vasodilation in the ovine fetus

2009 ◽  
Vol 297 (2) ◽  
pp. L318-L325 ◽  
Author(s):  
Marc Chester ◽  
Pierre Tourneux ◽  
Greg Seedorf ◽  
Theresa R. Grover ◽  
Jason Gien ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Left Pulmonary Artery ◽  
Flow Transducer ◽  
Pulmonary Vasodilation

Impaired nitric oxide-cGMP signaling contributes to severe pulmonary hypertension after birth, which may in part be due to decreased soluble guanylate cyclase (sGC) activity. Cinaciguat (BAY 58-2667) is a novel sGC activator that causes vasodilation, even in the presence of oxidized heme or heme-free sGC, but its hemodynamic effects have not been studied in the perinatal lung. We performed surgery on eight fetal (126 ± 2 days gestation) lambs (full term = 147 days) and placed catheters in the main pulmonary artery, aorta, and left atrium to measure pressures. An ultrasonic flow transducer was placed on the left pulmonary artery to measure blood flow, and a catheter was placed in the left pulmonary artery for drug infusion. Cinaciguat (0.1–100 μg over 10 min) caused dose-related increases in pulmonary blood flow greater than fourfold above baseline and reduced pulmonary vascular resistance by 80%. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an sGC-oxidizing inhibitor, enhanced cinaciguat-induced pulmonary vasodilation by >120%. The pulmonary vasodilator effect of cinaciguat was prolonged, decreasing pulmonary vascular resistance for >1.5 h after brief infusion. In vitro stimulation of ovine fetal pulmonary artery smooth muscle cells with cinaciguat after ODQ treatment resulted in a 14-fold increase in cGMP compared with non-ODQ-treated cells. We conclude that cinaciguat causes potent and sustained fetal pulmonary vasodilation that is augmented in the presence of oxidized sGC and speculate that cinaciguat may have therapeutic potential for severe neonatal pulmonary hypertension.

Endothelin-1 vasoactive responses in lambs with pulmonary hypertension and increased pulmonary blood flow

1995 ◽  
Vol 269 (6) ◽  
pp. H1965-H1972 ◽  
Author(s):  
J. Wong ◽  
V. M. Reddy ◽  
K. Hendricks-Munoz ◽  
J. R. Liddicoat ◽  
R. Gerrets ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Heart Diseases ◽  
Main Pulmonary Artery ◽  
Similar Degree ◽  
Fetal Sheep ◽  
Endothelin 1

Increased concentrations of endothelin-1 (ET-1) are found in children with congenital heart diseases that produce increased pulmonary blood flow and pulmonary hypertension, but the role of ET-1 in the pathophysiology of pulmonary hypertension is unclear. Therefore, we investigated ET-1-induced vasoactive responses and ET-1 concentrations in an animal model of pulmonary hypertension and increased pulmonary blood flow. Vascular shunts were placed between the ascending aorta and main pulmonary artery in seven late-gestation fetal sheep. Four weeks after spontaneous delivery, ET-1 increased pulmonary vascular resistance by 29.7 +/- 34.4% (P < 0.05), the ETb-receptor agonist [Ala1,3,11,15]ET-1 (4AlaET-1) had no effect, and the ETa-receptor antagonist cyclo(D-Asp-L-Pro-D-Val-L-Leu-D-Trp) (BQ-123) decreased pulmonary vascular resistance by -16.0 +/- 5.6% (P < 0.05). In contrast, in six control lambs with a similar degree of pulmonary hypertension induced by U-46619, ET-1 and 4AlaET-1 decreased pulmonary vascular resistance by 24.8 +/- 17.6, and 20.0 +/- 13.8%, respectively (P < 0.05). In addition, systemic arterial concentrations of immunoreactive ET-1 were elevated in lambs with pulmonary hypertension (29.2 +/- 9.6 vs. 15.2 +/- 10.7 pg/ml, P < 0.05). Pulmonary hypertension and increased pulmonary blood flow alters the response of ET-1 from pulmonary vasodilation to vasoconstriction. These altered responses suggest a role for ET-1 and its receptors in the pathogenesis of pulmonary hypertension secondary to increased pulmonary blood flow.

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