***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: OBJECTIVE To compare the effects of propofol and ketamine on systemic and pulmonary circulations in pediatric patients scheduled for elective cardiac catheterization . DESIGN Prospect i ve , r and omized , and blinded . SETTING University hospital . PARTICIPANTS Children ( n = 41 ) undergoing cardiac catheterization . INTERVENTIONS All children were premedicated with oral midazolam 60 minutes before the procedure . Patients were separated into 3 groups according to shunts diagnosed by transthoracic echocardiography before the catheterization procedure : patients without cardiac shunt ( Group I , n = 11 ) , left-to-right shunt ( Group II , n = 12 ) , and right-to-left shunt ( Group III , n = 18 ) . A continuous infusion of propofol ( 100 - 200 microg/kg/min ) or ketamine ( 50 - 75 microg/kg/min ) was r and omly started in all groups to obtain immobility during the procedure . Hemodynamic data , including systemic venous , pulmonary artery and vein , aortic saturations and pressures , were recorded ; Qp/Qs were calculated . The same set of data was recorded before discontinuation of infusions at the end of the procedure . MEASUREMENTS AND MAIN RESULTS After the propofol administration , in all 3 patient groups propofol infusion was associated with significant decreases in systemic mean arterial pressure . In groups with cardiac shunts ( Group II and III ) , propofol infusion significantly decreased systemic vascular resistance and increased systemic blood flow , whereas pulmonary vascular resistance and pulmonary blood flow did not change significantly . These changes result ed in decreased left-to-right shunting and increased right-to-left shunting ; the pulmonary-to-systemic flow ratio decreased significantly . On the other h and , after ketamine infusion , systemic mean arterial pressure increased significantly in all patient groups , but pulmonary mean arterial pressure , systemic vascular resistance , and pulmonary vascular resistance were unchanged . CONCLUSION In children with cardiac shunting , the principal hemodynamic effect of propofol is a decrease in systemic vascular resistance . In children with intracardiac shunting , this results in an increase in right-to-left shunting and a decrease in the ratio of pulmonary to systemic blood flow , which may lead to arterial desaturation . Ketamine did not produce these changes . The authors suggested that during cardiac catheterization in children , both the anesthesiologists and cardiologists need to know that anesthetic agents can significantly alter the hemodynamic status in children with complex congenital heart defects and affect the results of hemodynamic calculations that are important for decision-making and treatment of these patients Background : Sevoflurane and ketamine are commonly used to obtain sedation and facilitate intravenous anesthetic induction in children undergoing cardiac surgery who are uncooperative . We used a new and direct systemic hemodynamic monitoring technique pressure recording analytical method and compared the hemodynamic effects of sevoflurane and ketamine to facilitate intravenous anesthetic induction . Methods : Forty-four children with ventricular septal defect ( 2.2 ± 1.2 years ) were enrolled and r and omized to receive sevoflurane ( Group S ) or intramuscular ketamine ( Group K ) for sedation , followed by intravenous midazolam-sufentanil induction and tracheal intubation . Recorded parameters included heart rate ( HR ) , arterial pressures , stroke volume index ( SVI ) , cardiac index ( CI ) , systemic vascular resistance index ( SVRI ) , the maximal slope of systolic upstroke ( dp/dtmax ) after sedation obtained with sevoflurane or ketamine , 1 , 2 , 5 minutes after midazolam-sufentanil , 1 , 2 , 5 , and 10 minutes after tracheal intubation . Rate-pressure product ( RPP ) and cardiac power output ( CPO ) were calculated . Results : As compared with Group S , Group K had faster decreases during intravenous anesthetic induction in arterial pressures ( P < .01 for all ) , higher HR , arterial pressures , SVRI , dp/dtmax , RPP , lower SVI , CI , CPO ( P < .05 for all ) during the study period . Conclusion : As compared with sevoflurane , ketamine facilitated intravenous anesthetic induction exerts unfavorable effects on systemic hemodynamic and myocardial energetic in children with ventricular septal defect BACKGROUND : The use of ketamine in children with increased pulmonary vascular resistance is controversial . In this prospect i ve , open label study , we evaluated the hemodynamic responses to ketamine in children with pulmonary hypertension ( mean pulmonary artery pressure > 25 mm Hg ) . METHODS : Children aged 3 mo to 18 yr with pulmonary hypertension , who were scheduled for cardiac catheterization with general anesthesia , were studied . Patients were anesthetized with sevoflurane ( 1 minimum alveolar anesthetic concentration [ MAC ] ) in air while breathing spontaneously via a facemask . After baseline catheterization measurements , sevoflurane was reduced ( 0.5 MAC ) and ketamine ( 2 mg/kg IV over 5 min ) was administered , followed by a ketamine infusion ( 10 & mgr;g · kg−1 · min−1 ) . Catheterization measurements were repeated at 5 , 10 , and 15 min after completion of ketamine load . Data at various time points were compared ( ANOVA , P < 0.05 ) . RESULTS : Fifteen patients ( age 147 , 108 mo ; median , interquartile range ) were studied . Diagnoses included idiopathic pulmonary arterial hypertension ( 5 ) , congenital heart disease ( 9 ) , and diaphragmatic hernia ( 1 ) . At baseline , median ( interquartile range ) baseline pulmonary vascular resistance index was 11.3 ( 8.2 ) Wood units ; 33 % of patients had suprasystemic mean pulmonary artery pressures . Heart rate ( 99 , 94 bpm ; P = 0.016 ) and Pao2 ( 95 , 104 mm Hg ; P = 007 ) changed after ketamine administration ( baseline , 15 min after ketamine ; P value ) . There were no significant differences in mean systemic arterial blood pressure , mean pulmonary artery pressure , systemic or pulmonary vascular resistance index , cardiac index , arterial pH , or Paco2 . CONCLUSIONS : In the presence of sevoflurane , ketamine did not increase pulmonary vascular resistance in spontaneously breathing children with severe pulmonary hypertension Ketamine is an induction agent . This experimental study was design ed to investigate the immediate effects of ketamine upon haemodynamics , inotropism and myocardial oxygen consumption during induction . In a circulatory steady state of a piritramide - nitrous oxide - oxygen basic anaesthesia  normoventilated dogs ( n = 8) received intravenous injections of 5.0 and 10.0 mg/kg ketamine within 30 sec at r and om . Immediately after administration of 10.0 mg/kg ketamine the cardiac output ( thermo dilution method ) rose ( 27 % ) on account of tachycardia while the total peripheral resistance ( 40 % ) and the mean arterial pressure ( 23 % ) decreased . The decrease in stroke volume ( 37 % ) and the inotropic parameter dp/dt max ( 42 % ) as well as the increase in the end-diastolic left ventricular pressure ( 31 % ) and in the pressure of the pulmonary artery ( 11 % ) suggest considerable myocardial depressor properties of ketamine . The change in haemodynamics was paralleled with an increase in myocardial oxygen consumption ( 47 % ) , which was initially met by an increase in coronary blood flow ( 25 % ) and an additional oxygen utilization ( 20 % ) . The increase in arterio-coronary venous oxygen difference is believed to be due to a constriction of the coronary arteries after ketamine . Since external cardiac work remained unchanged , while myocardial contractility and myocardial wall tension ( Psyst ) decreased , the increase in heart rate ( 63 % ) explains the rise in myocardial oxygen consumption . The efficiency of cardiac work , which is defined as the ratio of myocardial displacement work to myocardial energy dem and , decreased ( 31 % ) and illustrated the uneconomic work of the heart under the influence of ketamine . The clinical utilization of the data obtained from this study are discussed Little data are available on the hemodynamic effects of premedications and anesthetic agents on infants and children .  Ketamine is the most frequently used anesthetic agent for cardiac catheterization procedures in pediatric patients with congenital heart disease . Previous reports both suggest and deny ketamine 's pulmonary vasoreactive effects . Since the advent of sophisticated noninvasive equipment , one of the few indications for cardiac catheterization is to obtain accurate pressure data . If ketamine alters pulmonary vascular resistance , it would negate the primary reason for the procedure . Because the patient population studied herein resides greater than or equal to 1,200 meters above sea level , concerns about pharmacologic effects on pulmonary vascular resistance are enhanced . Simultaneous pulmonary artery and aortic pressures , thermodilution cardiac outputs , and blood gases were measured in room air ( 16 % oxygen ) and with ketamine infusion in 14 patients at cardiac catheterization . Reaction to hypoxia identified 3 groups : normal , intermediate and hyperresponders . The normal responders had normal resistance ratios ( 0.11 ) in room air and had little resistance ratio response to hypoxia ( + 0.02 ) , hyperoxia ( -0.03 ) or ketamine ( + 0.01 ) . The intermediate responders had a slightly higher but normal resistance ratio ( 0.20 ) in room air , and a moderate reaction to hypoxia ( + 0.13 ) , hyperoxia ( -0.08 ) and ketamine ( + 0.11 ) . The hyperresponders had an elevated resistance ratio ( 0.42 ) in room air and a striking reaction to hypoxia ( + 0.65 ) , hyperoxia ( -0.17 ) and ketamine ( + 0.49 ) . Hypoxia and ketamine have a greater effect on resistance ratio than hypoxia alone in patients with reactive pulmonary vascular beds . Ketamine should not be used in children undergoing procedures to establish operability based on pulmonary vascular resistance or pulmonary vascular reactivity BACKGROUND The safety of ketamine in children with pulmonary hypertension has been debated because of conflicting results of prior studies in which changes in mean pulmonary artery pressure ( mPAP ) and pulmonary vascular resistance ( PVR ) have been widely variable . The goal of this prospect i ve study was to quantitate the effects of ketamine on pulmonary hemodynamics in a cohort of children with pulmonary hypertension under conditions in which variables such as airway/ventilatory management , FiO(2 ) , and use of vasodilating anesthetics were controlled . METHODS The IRB approved this study of 34 children undergoing cardiac catheterization for pulmonary hypertension studies . Following anesthetic induction with sevoflurane and tracheal intubation facilitated by the administration of rocuronium 0.7 - 1 mg·kg(-1 ) iv , sevoflurane was discontinued and anesthesia was maintained with midazolam 0.1 mg·kg(-1 ) iv ( or 0.5 mg·kg(-1 ) po preoperatively ) and remifentanil iv infusion 0.5 - 0.7 mcg·kg(-1 ) · min(-1 ) . Ventilation was mechanically controlled to maintain PaCO(2 ) 35 - 40 mmHg . When endtidal sevoflurane was 0 % and FiO(2 ) was 0.21 , baseline heart rate ( HR ) , mean arterial pressure ( MAP ) , mPAP , right atrial pressure ( RAP ) , pulmonary artery occlusion pressure ( PAOP ) , right ventricular end-diastolic pressure ( RVEDP ) , cardiac output , and arterial blood gases were measured , and indexed systemic vascular resistance ( SVRI ) , indexed pulmonary vascular resistance ( PVRI ) , and cardiac index ( CI ) were calculated . Each child then received a bolus of ketamine 2 mg·kg(-1 ) infused over 2 min . Measurements and calculations were repeated 2 min after the conclusion of the infusion . RESULTS The mean ( 95 % CI ) increase in mPAP  following ketamine was 2 mmHg ( 0.2 , 3.7 ) , which was statistically significant but clinical ly insignificant . PVRI and PVRI/SVRI did not change significantly . Hemodynamic changes did not differ among subjects with differing severity of pulmonary hypertension or between subjects chronically treated with pulmonary vasodilators or not . CONCLUSION Ketamine is associated with minimal , clinical ly insignificant hemodynamic changes in se date d , mechanically ventilated children with pulmonary hypertension 
    Output:
    
Pulmonary vascular resistance , systemic vascular resistance , mean pulmonary artery pressure , mean systemic pressure , heart rate , pH , and arterial oxygen concentration did not significantly change with administration of ketamine .
CONCLUSION Ketamine has minimal impact on hemodynamics in children with congenital heart disease when used at usual clinical doses .
Systemic vascular resistance and pulmonary vascular resistance are not significantly altered .
Blood gas values are also only minimally affected by ketamine