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2. CAPITULO II

3.2 TEORÍA DEL LEVANTAMIENTO DEL VELO SOCIETARIO

3.2.2. Análisis de la teoría del levantamiento del velo societario y su

Background. Respiration manipulations and management are vital for infants with a

univentricular heart. Positive pressure ventilation (PPV) has been shown to have a

deleterious effect on blood flow in patients with a univentricular physiology. Postoperative length of stay in the intensive care unit is predominantly determined by need for mechanical ventilation and respiratory insufficiency. With a passive pulmonary physiology and with the pulmonary and systemic circulations now connected in series, keeping the pulmonary

vascular resistance (PVR) and systemic vascular resistance (SVR) as low as possible is vital. However, endotracheal intubation and PPV promote increased PVR. Management is

dependent on adequate ventilation. To date, management strategies are decided by individual institutions. This study examines the effect of positive pressure ventilation (PPV) on

hemodynamic parameters in normal and Fontan circulations. The overall hypothesis for this research is that a fundamental understanding of the AP and various TCPC geometries will lead to improved surgical planning and designs and thus the potential for improved long term outcomes in patients. In order to address this hypothesis, investigation will occur for the following specific aims: (1) Qualitative and quantitative assessment of Fontan flow dynamics

vivo animal studies performed in lambs. (2) Examine the effect of PPV on hemodynamic variables both in normal and Fontan circulations.

Methods. In-vivo experiments were performed in lambs. Normal and four Fontan

modification procedures have been examined. These are the atriopulmonary connection (AP), total cavopulmonary connection without a synthetic graft (TCPC), extracardiac total cavopulmonary connection (TCPX), and the total cavopulmonary connection using a Y- shaped graft (TCPY). Multiple pressure and flow transducers were introduced. Ventilation manipulation varying ventilation rate, stroke volume, and minute ventilation was performed under both normal and Fontan circulations. Data were recorded at 200 Hertz. Data analysis was performed using MATLABTM. Hemodynamic changes and systemic and vascular resistances were calculated.

Results. AP. A reduction in cardiac output (CO) amounting to 63% was observed between normal and AP conditions. SVR increased by 54% and PVR increased 137% between circulations. SVR increased significantly as respiration rate increased. No significant changes occurred in pressure and flows with varying ventilation rate. Also, no significant changes occurred with varying stroke volume. SVR showed a decreasing trend as stroke volume increased. No significant changes occurred in IVCQ, SVCQ, and PAQ with varying minute ventilation. Vascular resistances remained statistically unchanged with varying minute ventilation. TCPC. CO decreased by 61% between normal and TCPC circulations. PVR increased by 136% to 736.2±54.1 dyne•sec•cm-5. Respiration rate had little effect on hemodynamic variables. Statistically significant decreases in pressure occurred for all parameters as stroke volume increased. Extremely low and high stroke volumes decreased the flow by 47% from middle range stroke volumes. Stroke volume had no significant

difference on LPAQ or SVCQ. No significant changes occurred in vascular resistance with changing stroke volumes. Pressure waveforms showed minimal change throughout the constant minute ventilation range. TCPX. Normal flow contributions, IVC (74%), SVC (26%), and LPA (41%), are present in the TCPX circulation [IVC (72.4%), SVC (27.6%), and LPA (48.4%)]. Extremely high vascular resistances were created. The SVR was

4579.8±1603.5 dyne•sec•cm-5 and the PVR was 45.8±16.8 dyne•sec•cm-5. A 68% decrease in CO from 32.0±2.5 cc/sec under normal circulation to 10.2±5.4 cc/sec under TCPX

circulations were a result of the high resistances. Mean pressures for the IVC, SVC, and PA were 25.2±5.3 mm Hg, 24.0±4.6 mm Hg, and 28.9±4.3 mm Hg respectively. No significant effects were observed with varying respiration rate. CO showed a decreasing trend as rate increased. SVR decreased when high rates were imposed. Significant increases in pressure occurred at low stroke volumes (300-400 mL). No changes were seen in SVR across varying stroke volumes. TCPY. PVR increased 26% from 543.8±303.6 dyne•sec•cm-5 to

688.5±267.8 dyne•sec•cm-5. SVR increased 4% from 27.3±3.7 dyne•sec•cm-5 to 26.1±17.6 dyne•sec•cm-5. Flow contributions remained similar, with LPA flow comprising of 39% of the flow under normal conditions to 32% in TCPY conditions. IVC flow was 79% of systemic flow under normal circulation to 78% in the TCPY circulation. Cardiac output decreased 51% between circulations. All pressures increased significantly with increasing respiratory rates keeping stroke volume constant. However, IVC flow increased as

respiration increased. Furthermore, SVC and LPA flows significantly increased at a lower rate as respiration increased. PVR increased with respiration rate. At low stroke volumes, SVR decreased sharply as rate increased. PVR significantly increased as stroke volume

increased at various rates. SVR decreased as volume increased for low rates and increased as stroke volume increased for high rates.

Conclusions. Significant hemodynamic changes occurred between anatomic Fontan

connections. Systemic and vascular resistances differed according to procedure. Overall, stroke volume and ventilation rate had a predominantly instantaneous effect on

hemodynamics, but minimal effects on averages. Promising hemodynamics were observed in the novel TCPY procedure. Flow ratios, flow distribution, and resistances approached normal circulation values for the TCPY circulation. However, systemic pressures remained high that may lead to postoperative complications. To improve recovery time and perfusion efficiency, ventilation management may be beneficial if prescribed dependent on Fontan procedure. Limitations to this study are the acute, open chest study performed on an animal with previously normal circulation. Hemodynamic adaptations are not available.