Intraabdominal carbon dioxide insufflation in the pregnant ewe. Uterine blood flow, intraamniotic pressure, and cardiopulmonary effects

BACKGROUND: Laparoscopic surgical procedures are being performed in pregnant women with increasing frequency. Maternal-fetal physiologic changes occurring during intraabdominal carbon dioxide insufflation are poorly understood, and maternal-fetal safety is of concern during carbon dioxide pneumoperitoneum. A previous pilot study using end-tidal carbon dioxide-guided ventilation resulted in maternal and fetal acidosis and tachycardia during carbon dioxide pneumoperitoneum. Using serial arterial PCO2 to guide ventilation, this study was designed to evaluate maternal-fetal cardiopulmonary status, uterine blood flow, and the intraamniotic pressure effects of intraabdominal carbon dioxide insufflation in singleton pregnant ewes between 120 and 135 days of gestation. METHODS: In a prospective randomized cross-over study, nine ewes were to receive either abdominal insufflation with carbon dioxide to an intraabdominal pressure of 15 mmHg (n = 9; insufflation group) or receive no insufflation (n = 9; control group). Anesthesia was induced with thiopental and maintained with end-tidal halothane (1 to 1.5 minimum alveolar concentration/100% oxygen). Mechanical ventilation was guided by serial maternal arterial blood gas analysis to maintain PaCO2 between 35 and 40 mmHg. Data from insufflated animals were collected during insufflation (60 min) and after desufflation (30 min). Control group data were collected and matched to similar time intervals for 90 min. Ewes were allowed to recover, and after a rest period (48 h) they were entered in the cross-over study. RESULTS: During insufflation there was a significant increase (P < 0.05) in maternal PaCO2 to end-tidal carbon dioxide gradient and minute ventilation, with concomitant decreases in maternal end-tidal carbon dioxide and PaO2. Intraamniotic pressure increased significantly during insufflation. No significant changes were observed in maternal hemodynamic variables, fetal variables, or in uterine blood flow during the study. There were no fetal deaths or preterm labor in any of the animals during the experiment. CONCLUSIONS: During the 1-h insufflation, a marked increase in PaCO2-to-end-tidal carbon dioxide gradient was observed, suggesting that capnography may be an inadequate guide to ventilation during carbon dioxide pneumoperitoneum in the pregnant patient. No other significant circulatory changes were observed.     

Sputum and serum pharmacokinetics of loracarbef (LY163892) in patients with chronic bronchial sepsis

BACKGROUND: Carbon dioxide absorption into the blood during laparoscopic surgery using intraperitoneal carbon dioxide insufflation may lead to respiratory acidosis, increased ventilation requirements, and possible serious cardiovascular compromise. The relationship between increased carbon dioxide excretion (VCO2) and intraperitoneal carbon dioxide insufflation pressure has not been well defined. METHODS: In 12 anesthesized pigs instrumented for laparoscopic surgery, intraperitoneal carbon dioxide (n = 6) or helium (n = 6) insufflation pressure was increased in steps, and VCO2 (metabolic cart), dead space, and hemodynamics were measured during constant minute ventilation. RESULTS: VCO2 increases rapidly as intraperitoneal insufflation pressure increases from 0 to 10 mmHg; but from 10 to 25 mmHg, VCO2 does not increase much further. PaCO2 increases continuously as intraperitoneal insufflation pressure increases from 0 to 25 mmHg. Hemodynamic parameters remained stable. CONCLUSIONS: By considering Fick's law of diffusion, the initial increase in VCO2 is likely accounted for by increasing peritoneal surface area exposed during insufflation. The continued increase in PaCO2 without a corresponding increase in VCO2 is accounted for by increasing respiratory dead space.     

Femoral vein stasis during laparoscopic cholecystectomy: effects of graded elastic compression leg bandages in preventing thrombus formation

Venous stasis of the legs during laparoscopic cholecystectomy was compared between patients without graded compression leg bandages (Group 1; n = 12) and patients with such bandages (Group 2; n = 12) by measuring mean blood flow velocity and cross-sectional area of the femoral vein using a color Doppler ultrasonography. In Group 1, when velocity and area were measured in the supine position, a significant decrease in velocity (p < .05) and a significant increase in area (p < .05) occurred after abdominal insufflation to 10 mm Hg. These changes were greater during abdominal insufflation in the reverse Trendelenburg position than during abdominal insufflation in the supine position. In Group 2, flow velocity was significantly higher (p < .05) before abdominal insufflation as compared with Group 1. After abdominal insufflation to 10 mm Hg and a postural change, velocity significantly decreased (p < .05) and area significantly increased (p < .05) in Group 2, similar to the results in Group 1. During abdominal insufflation at 5 mm Hg or lower, the use of the graded compression bandage was found to be useful for preventing femoral vein stasis. During abdominal insufflation at 10 mm Hg or in the reverse Trendelenburg position, the bandage did not prevent femoral vein stasis.     

Cardiorespiratory effects of induction and maintenance of anesthesia with ketamine-midazolam combination, with and without prior administration of butorphanol or oxymorphone

Cardiorespiratory effects of an IV administered bolus of ketamine (7.5 mg/kg of body weight) and midazolam (0.375 mg/kg) followed by IV infusion of ketamine (200 micrograms/kg/min) and midazolam (10 micrograms/kg/min) for 60 minutes was determined in 6 dogs. Ketamine-midazolam combination was administered to dogs on 3 occasions to determine effects of prior administration of IV administered saline solution (1 ml), butorphanol (0.2 mg/kg), or oxymorphone (0.1 mg/kg). The infusion rate of ketamine and midazolam was decreased by 25% for anesthetic maintenance after opioid administration. There were no significant differences in cardiorespiratory variables after saline solution or butorphanol administration; however, oxymorphone caused significant (P < 0.05) increases in mean arterial blood pressure, systemic vascular resistance, and breathing rate. Bolus administration of ketamine-midazolam combination after saline solution caused significant (P < 0.05) increases in heart rate, mean arterial blood pressure, cardiac index, mean pulmonary blood pressure, venous admixture, and significant decreases in stroke index, pulmonary capillary wedge pressure, arterial and mixed venous oxygen tension, arterial oxygen content, and alveolar-arterial oxygen gradient. Opioid administration was associated with significantly (P < 0.05) lower values than was saline administration for heart rate, mean arterial blood pressure, and arterial and mixed venous pH and with higher values for stroke index, pulmonary capillary wedge pressure, and arterial and mixed venous carbon dioxide tension. Prior oxymorphone administration resulted in the highest (P < 0.05) values for mean pulmonary blood pressure, venous admixture, and arterial and mixed venous carbon dioxide tension, and the lowest values for arterial oxygen tension, and arterial and mixed venous pH. Each treatment provided otherwise uncomplicated anesthetic induction, maintenance, and recovery.(ABSTRACT TRUNCATED AT 250 WORDS)     

The left ventricular contractility of the rat heart is modulated by changes in flow and alpha 1-adrenoceptor stimulation

Myocardial contractility depends on several mechanisms such as coronary perfusion pressure (CPP) and flow as well as on alpha 1-adrenoceptor stimulation. Both effects occur during the sympathetic stimulation mediated by norepinephrine. Norepinephrine increases force development in the heart and produces vasoconstriction increasing arterial pressure and, in turn, CPP. The contribution of each of these factors to the increase in myocardial performance needs to be clarified. Thus, in the present study we used two protocols: in the first we measured mean arterial pressure, left ventricular pressure and rate of rise of left ventricular pressure development in anesthetized rats (N = 10) submitted to phenylephrine (PE) stimulation before and after propranolol plus atropine treatment. These observations showed that in vivo alpha 1-adrenergic stimulation increases left ventricular developed pressure (P < 0.05) together with arterial blood pressure (P < 0.05). In the second protocol, we measured left ventricular isovolumic systolic pressure (ISP) and CPP in Langendorff constant flow-perfused hearts. The hearts (N = 7) were perfused with increasing flow rates under control conditions and PE or PE + nitroprusside (NP). Both CPP and ISP increased (P < 0.01) as a function of flow. CPP changes were not affected by drug treatment but ISP increased (P < 0.01). The largest ISP increase was obtained with PE + NP treatment (P < 0.01). The results suggest that both mechanisms, i.e., direct stimulation of myocardial alpha 1-adrenoceptors and increased flow, increased cardiac performance acting simultaneously and synergistically.     

Bitter taste of monosaccharide pentaacetate esters

We investigated the possibility of using argon, an inert gas, as a replacement for carbon dioxide (CO2). The tolerance of argon pneumoperitoneum was compared with that of CO2 pneumoperitoneum. Twenty pigs were anesthetized with enflurane 1.5%. Argon (n = 11) or CO2 (n = 9) pneumoperitoneum was created at 15 mm Hg over 20 min, and serial intravenous injections of each gas (ranging from 0.1 to 20 mL/kg) were made. Cardiorespiratory variables were measured. Transesophageal Doppler and capnographic monitoring were assessed in the detection of embolism. During argon pneumoperitoneum, there was no significant change from baseline in arterial pressure and pulmonary excretion of CO2, mean systemic arterial pressure (MAP), mean pulmonary artery pressure (PAP), or systemic and pulmonary vascular resistances, whereas CO2 pneumoperitoneum significantly increased these values (P < 0.05). During the embolic trial and from gas volumes of 2 and 0.2 mL/kg, the decrease in MAP and the increase in PAP were significantly higher with argon than with CO2 (P < 0.05). In contrast to CO2, argon pneumoperitoneum was not associated with significant changes in cardiorespiratory functions. However, argon embolism seems to be more deleterious than CO2 embolism. The possibility of using argon pneumoperitoneum during laparoscopy remains uncertain. Implications: Laparoscopic surgery requires insufflation of gas into the peritoneal cavity. We compared the hemodynamic effects of argon, an inert gas, and carbon dioxide in a pig model of laparoscopic surgery. We conclude that argon carries a high risk factor in the case of an accidental gas embolism.     

New technique for knife and radial keratotomy

Low-flow (1 litre min-1) sevoflurane anaesthesia was used in 16 patients undergoing laparoscopic cholecystectomy (group LSC, n = 8) or tympanoplasty (group TP, n = 8), and concentrations of sevoflurane degradation products were measured. Degradation products in the circuit were measured hourly, and end-tidal carbon dioxide concentration, inspired and end-tidal sevoflurane concentrations, and carbon dioxide elimination were monitored. The only degradation product detected was CF2=C(CF3)-O-CH2F (compound A). The mean maximum concentrations of compound A were 21.6 (SEM 1.6) ppm and 19.6 (0.8) ppm in the LSC and TP groups, respectively (ns). The maximum temperatures of soda lime were 46.4 (0.5) degrees C and 44.8 (0.5) degrees C, respectively (P < 0.05). Hourly end-tidal sevoflurane concentrations and concentrations of sevoflurane degradation products were the same for both groups. Carbon dioxide elimination was the same for both groups 1 h after the start of anaesthesia, but was higher in group LSC after 2 h (P < 0.05). Intraperitoneal carbon dioxide insufflation associated with laparoscopic cholecystectomy had no effect on the concentration of sevoflurane degradation products.     

8-year experience with force vector rhinoplasty by J.B. Tebbetts: comparative results

BACKGROUND: Previous studies have suggested that diagnostic laparoscopy may be contraindicated in multiple trauma patients with closed head injuries because of the detrimental effects of carbon dioxide (CO2) pneumoperitoneum on intracranial pressure (ICP). In this study we compared the effects of two alternative inflation gases, helium (He) and nitrous oxide (N2O), against the standard agent used in most hospitals, CO2. ICP was monitored in experimental animals both with and without a space occupying intracranial lesion designed to simulate a closed head injury. METHODS: Twenty-four domestic pigs (mean, 30 kg) were divided into four groups (6 CO2, 6 He, 6 N2O, and 6 control animals without insufflation). All animals were monitored for ICP, intraabdominal pressure, mean arterial pressure, end-tidal CO2 (ETCO2), and arterial blood gases. These parameters were measured for 30 minutes prior to introducing a pneumoperitoneum and then for 80 minutes thereafter. The measurements were repeated after artificially elevating the ICP with a balloon placed in the epidural space. RESULTS: The mean ICP increased significantly in all groups during peritoneal insufflation compared with the control group (P < 0.005). The CO2-insufflated animals also showed a significant increase in PaCO2 (P < 0.05) and ETCO2 (P < 0.05), as well as a decrease in pH (P < 0.05). After inflating the epidural balloon the ICP remained significantly higher in animals inflated with CO2 as compared with the He and N2O groups (P < 0.05). CONCLUSIONS: Peritoneal insufflation with He and N2O resulted in a significantly less increase in ICP as compared with CO2. That difference was most likely due to a metabolically mediated increase in cerebral perfusion (PaCO2) in the CO2 group. Further studies need to be conducted to determine the safety and efficacy of using He and N2O as inflation agents prior to attempting diagnostic or therapeutic laparoscopy in patients with potential closed head injuries.     

Blood gas changes during laparoscopic cholecystectomy--comparative study of N2O pneumoperitoneum and CO2 pneumoperitoneum

During laparoscopic cholecystectomy by alternative insufflation of nitrous oxide and carbon dioxide, the changes of blood gas tensions were measured and analyzed in 12 patients. During N2O insufflation, PaO2 decreased by about 25 mmHg and PaCO2 was unaltered compared with the values before pneumoperitoneum. While during CO2 insufflation, PaO2 decreased by about 13 mmHg and PaCO2 increased by about 6 mmHg. We considered that decrease in PaO2 during N2O insufflation was associated with not only uneven ventilation/blood flow ratios but also with the reduction in the alveolar O2 tension caused by the diffusion of N2O absorbed from the peritoneum. PaCO2 increases during CO2 insufflation because CO2 is absorbed from the peritoneum, and is not excreted entirely through the lungs.     

Mechanical output and electromyographic parameters in males and females during fatiguing knee-extensions

Although extensive research has been carried out on the respiratory and renal effects of intra-abdominal pressure increase, there is limited research with regard to its effects on bacterial translocation. The objective of this study was to discuss whether the high intra-abdominal pressure due to carbon dioxide (CO2) insufflation during laparoscopy leads to bacterial translocation. Eighteen male dogs, 7 of which constituted the control group, were used in the study. Two study groups, in which the intra-abdominal pressure was raised to 15 mm Hg and kept at that level for 30 and 120 minutes, respectively, were set. Blood gases and blood pressure values were observed throughout the experiments. Samples of peritoneal smear, portal vein blood, mesenteric lymph node, liver, spleen, and cecum were examined to detect bacterial translocation. Histopathological examinations of all samples were also carried out. No translocation was detected in the samples of peritoneal smear, portal blood, mesenteric lymph node, liver, or spleen, but in the samples of cecum, bacterial colonization for the second group (p<0.05) and for the third group (p<0.05) was significantly higher compared with the control group. There was a considerable difference between the second and third groups (p<0.05). The changes in the mesenteric lymph nodes were interpreted to be a result of bacterial drainage. Histopathological examination disclosed active changes in the mesenteric lymph nodes in all groups, but there was considerable sinus histiocytosis only in the third group. We conclude that the intraabdominal pressure of 15 mm Hg created by carbon dioxide insufflation does not lead to bacterial translocation but causes intraluminal bacterial colonization in the cecum after 30 minutes and after 2 hours.     

An ovine model of acute myocardial infarction and chronic left ventricular dysfunction

In order to develop and validate an ovine model of myocardial infarction with subsequent impairement of left ventricular function, 15 instrumented sheep underwent selective microembolization of the left coronary arteries with 0.5 mL 90 microns polystyrene beads. Hemodynamics and plasma hormones were measured preembolization (baseline) and then at hours 2, 4, 6, and 12 and days 1, 2, 3, 5 and 7 postembolization. Of the 15 sheep studied, 2 (13%) died on the day of embolization from arrhythmias. In the remaining sheep, left ventricular systolic pressure and stroke work (both P < 0.001) were reduced promptly and remained below basal levels. Mean arterial pressure (P < 0.001) increased initially, then decreased to below basal levels by hour 6. Heart rate (P < 0.001) and left atrial pressure (P < 0.05) were increased while cardiac output was decreased (P < 0.05). Left ventricular ejection fraction at day 7 was reduced (38.8 +/- 3.5 vs 46.0 +/- 3.9% preembolization; P < 0.05). The cardiac enzymes creatine kinase (P < 0.001) and troponin-T (P < 0.001) were increased following microembolization and returned to basal levels by days 2 and 5 respectively. Plasma atrial and brain natriuretic peptides (both P < 0.001) and plasma renin activity (P < 0.005) were all increased following embolization. This ovine model mimics the hemodynamic and neurohumoral features of acute myocardial infarction, resulting in left ventricular dysfunction, and should prove suitable for the study of interventions in a number of these conditions.     

Coronary pressure as a determinant of B-type natriuretic peptide gene expression in isolated perfused adult rat heart

The role of coronary flow in the regulation of ventricular B-type natriuretic peptide (BNP) gene expression was studied in isolated perfused rat heart preparation. The increase of coronary flow from 5 ml/min to 20 ml/min for 2 h resulted in a 132+/-6 mm Hg increase in aortic perfusion pressure. The changes in BNP mRNA and immunoreactive BNP (IR-BNP) levels in response to hemodynamic stress were compared to those of c-fos and adrenomedullin (ADM) gene expression. The increase of coronary flow resulted in 1.5-fold increases in the left ventricular BNP mRNA (P < 0.001) and IR-BNP (P < 0.05) levels in 2-month old rats. There was also a 1.5-fold (P < 0.05) increase in ventricular c-fos mRNA levels, whereas ADM mRNA levels decreased by 74% (P < 0.001) in the left ventricle. In 18-month old rats, the increase in coronary flow decreased left and right ventricular BNP mRNA levels by 18% (P < 0.05) and 39% (P < 0.001), respectively. There were no changes in IR-BNP peptide and c-fos mRNA levels, whereas ADM mRNA levels decreased by 46% (P < 0.001) in the left ventricles. The results show that increased aortic perfusion pressure results in differential expression of cardiac genes including up-regulation of ventricular BNP and c-fos gene expression and down-regulation of ADM gene expression. Furthermore, aging seems to elevate the threshold at which hemodynamic stress of the heart results in a response at BNP gene level.     

Hemodynamic effects of a calcium channel promoter, BAY y 5959, are preserved after chronic administration in ischemic heart failure in conscious dogs

BAY y 5959 is a dihydropyridine derivative that binds to L-type calcium channels in a voltage-dependent manner and promotes calcium entry into the cell during the plateau of the action potential by influencing mean open time. Because myofilament responsiveness to calcium is preserved in congestive heart failure (CHF), the inotropic responsiveness to this compound should be preserved in CHF, and tolerance should not develop despite long-term treatment. To test these hypotheses, CHF was induced in 14 chronically instrumented dogs by daily (30 +/- 5 days) intracoronary microsphere injections. The effects of BAY y 5959 (2-h i.v. infusions of 3 microg/kg/min and 10 microg/kg/min) were determined before heart failure, after heart failure was established and then 2 h after the end of a 5-day continuous BAY y 5959 intra-atrial infusion. Before CHF, the positive inotropic effect of BAY y 5959 at a dose of 10 microg/kg/min [left ventricular dP/dt (LVdP/dt) increased from 2955 +/- 132 mmHg to 4897 +/- 426 mmHg, P < .05] was associated with bradycardia (HR decreased from 92 +/- 4 to 78 +/- 6 b/min, P <.05), slight increases in mean arterial pressure (it increased from 100 +/- 2 mmHg to 113 +/- 5 mmHg, P <.05) and did not alter left ventricular end-diastolic pressure. In CHF, BAY y 5959 continued to induce dose-dependent increases in left ventricular systolic pressure, LVdP/dt and mean arterial pressure, as well as causing bradycardia and a significant decrease in left ventricular end-diastolic pressure. After a 5-day infusion of BAY y 5959, base-line LVdP/dt and left ventricular end-diastolic pressure improved. The responses of LVdP/dt and mean arterial pressure to BAY y 5959 were similar to those of the control state. The sustained responses in CHF and after long-term infusion suggest that BAY y 5959 may be an effective and potent inotropic agent for treatment of CHF that does not lead to tolerance to its positive inotropic effects.     

Changes in left ventricular structure and function in patients with white coat hypertension: cross sectional survey

OBJECTIVES: To assess the relation between white coat hypertension and alterations of left ventricular structure and function. DESIGN: Cross sectional survey. SETTING: Augsburg, Germany. SUBJECTS: 1677 subjects, aged 25 to 74 years, who participated in an echocardiographic substudy of the monitoring of trends and determinants in cardiovascular disease Augsburg study during 1994-5. OUTCOME MEASURES: Blood pressure measurements and M mode, two dimensional, and Doppler echocardiography. After at least 30 minutes' rest blood pressure was measured three times by a technician, and once by a physician after echocardiography. Subjects were classified as normotensive (technician <140/90 mm Hg, physician <160/95 mm Hg; n=849), white coat hypertensive (technician <140/90 mm Hg, physician >=160/95 mm Hg; n=160), mildly hypertensive (technician >=140/90 mm Hg, physician <160/95 mm Hg; n=129), and sustained hypertensive (taking antihypertensive drugs or blood pressure measured by a technician >=140/90 mm Hg, and physician >=160/95 mm Hg; n=538). RESULTS: White coat hypertension was more common in men than women (10.9% versus 8.2% respectively) and positively related to age and body mass index. After adjustment for these variables, white coat hypertension was associated with an increase in left ventricular mass and an increased prevalence of left ventricular hypertrophy (odds ratio 1.9, 95% confidence interval 1.2 to 3.2; P=0.009) compared with normotensive patients. The increase in left ventricular mass was secondary to significantly increased septal and posterior wall thicknesses whereas end diastolic diameters were similar in both groups with white coat hypertension or normotension. Additionally, the systolic white coat effect (difference between blood pressures recorded by a technician and physician) was associated with increased left ventricular mass and increased prevalence of left ventricular hypertrophy (P<0.05 each). Values for systolic left ventricular function (M mode fractional shortening) were above normal in subjects with white coat hypertension whereas diastolic filling and left atrial size were similar to those in normotension. CONCLUSION: About 10% of the general population show exaggerated inotropic and blood pressure responses when mildly stressed. This is associated with an increased risk of left ventricular hypertrophy.     

Permissive hypercapnia with and without expiratory washout in patients with severe acute respiratory distress syndrome

BACKGROUND: Permissive hypercapnia is a ventilatory strategy aimed at avoiding lung volutrauma in patients with severe acute respiratory distress syndrome (ARDS). Expiratory washout (EWO) is a modality of tracheal gas insufflation that enhances carbon dioxide removal during mechanical ventilation by reducing dead space. The goal of this prospective study was to determine the efficacy of EWO in reducing the partial pressure of carbon dioxide (PaCO2) in patients with severe ARDS treated using permissive hypercapnia. METHODS: Seven critically ill patients with severe ARDS (lung injury severity score, 3.1 +/- 0.3) and no contraindications for permissive hypercapnia were studied. On the first day, hemodynamic and respiratory parameters were measured and the extent of lung hyperdensities was assessed using computed tomography. A positive end-expiratory pressure equal to the opening pressure identified on the pressure-volume curve was applied. Tidal volume was reduced until a plateau airway pressure of 25 cm H2O was reached. On the second day, after implementation of permissive hypercapnia, EWO was instituted at a flow of 15 l/min administered during the entire expiratory phase into the trachea through the proximal channel of an endotracheal tube using a ventilator equipped with a special flow generator. Cardiorespiratory parameters were studied under three conditions: permissive hypercapnia, permissive hypercapnia with EWO, and permissive hypercapnia. RESULTS: During permissive hypercapnia, EWO decreased PaCO2 from 76 +/- 4 mmHg to 53 +/- 3 mmHg (-30%; P < 0.0001), increased pH from 7.20 +/- 0.03 to 7.34 +/- 0.04 (P < 0.0001), and increased PaO2 from 205 +/- 28 to 296 +/- 38 mmHg (P < 0.05). The reduction in PaCO2 was accompanied by an increase in end-inspiratory plateau pressure from 26 +/- 1 to 32 +/- 2 cm H2O (P = 0.001). Expiratory washout also decreased cardiac index from 4.6 +/- 0.4 to 3.7 +/- 0.3 l.min-1.m-2 (P < 0.01), mean pulmonary arterial pressure from 28 +/- 2 to 25 +/- 2 mmHg (P < 0.01), and true pulmonary shunt from 47 +/- 2 to 36 +/- 3% (P < 0.01). CONCLUSIONS: Expiratory washout is an effective and easy-to-use ventilatory modality to reduce PaCO2 and increase pH during permissive hypercapnia. However, it significantly increases airway pressures and lung volume through expiratory flow limitation, reexposing some patients to a risk of lung volutrauma if the extrinsic positive end-expiratory pressure is not substantially reduced.     

Effects of antihypertensive therapy on left atrial function

OBJECTIVES: To investigate left atrial (LA) function as a reservoir, as a conduit and as a booster pump in essential hypertension (EH). LA volumes were echocardiographically measured in 28 untreated hypertensive patients and in 20 control subjects. BACKGROUND: LA makes a large contribution in left ventricular filling, especially in patients with impaired diastolic function. LA function is fundamental in left ventricular filling in hypertensive patients as hypertension results in left ventricular diastolic dysfunction. METHODS: Diagnosis of EH (blood pressure > 140/90 mm Hg) was based on three repeated readings of blood pressure (BP). Patients with myocardial infarction, cardiomyopathy, valvular or congenital heart disease were excluded. Doppler diastolic early (E) and late (A) velocity of mitral inflow were measured. The following indexes were calculated: left ventricular mass index (LVMI) using the Penn convention; left ventricular stroke volume (LVSV); LA reservoir volume (LARV = LA maximal volume at mitral valve opening minus minimal volume); LA conduit volume (LACV = LVSV-LARV). Atrial systolic function was assessed by calculating the active emptying fraction (volume at onset of atrial systole minus minimal volume/volume at onset of atrial systole, the E/A ratio and the LA ejection force (0.5 rho A2 MOA, where rho = the density of blood, MOA = mitral orifice area from the parasternal short axis view). Measurements were obtained in all hypertensive patients before and after 16 weeks administration of either enalapril (10 or 20 mg) or enalapril +/- chlorthalidone (20/25 mg) once a day. RESULTS: After 16 weeks of treatment, BP was reduced significantly (from 172/110 to 137/86 mm Hg, P < 0.001). LVMI decreased significantly as well (from 141 to 123 g/m2) although it was higher compared to controls (94 g/m2, P < 0.001). LARV decreased significantly (from 35.4 to 29.3 cm3, P < 0.05) while LACV increased significantly (from 43.8 to 51.3 cm3, P < 0.05), LA active emptying fraction and E/A ratio did not change. LA ejection force decreased significantly (from 20.9 to 18.1 kdynes, P < 0.05) but it was greater than controls (16.7 kdynes, P < 0.01). There was a positive relationship of LVMI to LARV (P < 0.01) in controls (r = 0.77) which held true in hypertensive patients, before (r = 0.72) and after treatment (r = 0.69). There was a negative relationship of LVMI to LACV (P < 0.01) in controls (r = -0.65), and in hypertensive patients untreated (r = -0.74) and after treatment (r = -0.72). CONCLUSIONS: Our results showed that in hypertensive patients, LA reservoir function increases and LA conduit function decreases, while LA ejection force increases. Antihypertensive treatment with enalapril and/or thiazide, induces normalisation of the LA function in parallel to left ventricular hypertrophy regression.     

Central nervous system metabolic and physiologic effects of laparoscopy

We set out to determine whether the increases in intracranial pressure (ICP) associated with CO2 insufflation had any metabolic effect on the central nervous system in a head injury when compared with gasless laparoscopy (GL). To test this hypothesis, we looked at both the ICP and jugular bulb venous saturation (JVS), with and without a coexisting cerebral mass lesion. Twenty-five kilogram male pigs had tracheostomy, epidural balloon, pulmonary arterial catheter, arterial line, and jugular bulb catheter placed. Intravenous Pentobarbital was used for anesthesia. Either CO2 laparoscopy (CL; n=7) or GL (n=7) were performed both with and without an epidural balloon inflated to a baseline ICP of 25. Data were analyzed using the Student's t test with a P value <0.05 being significant. Cerebral perfusion pressure and most hemodynamic values did not differ. Both central venous pressure and peak inspiratory pressure were significantly elevated whenever CO2 insufflation took place, reflecting an increased intrathoracic pressure. When comparing both study groups, the partial pressure of CO2 did not differ. CL increases ICP significantly above the gasless group in our head injury model. This is most likely secondary to increased intrathoracic pressure. The question still remains whether these changes are clinically significant. We could not demonstrate significant metabolic effects secondary to laparoscopy. In patients suffering head injury, GL rather than CL might be safer to avoid ICP elevation. Additional studies looking at central nervous system metabolic and objective histopathologic effects should be undertaken with larger numbers of study animals.     

Effect of chronotropic and inotropic stimulation on the coronary pressure-flow relation in left ventricular hypertrophy

Left ventricular hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during increased cardiac work. The present study was performed to study the effects of chronotropic and inotropic stimulation on the coronary pressure-flow relation of the hypertrophied left ventricle of dogs and to determine the individual contributions of increases in heart rate and contractility to the exaggerated exercise-induced increases in effective back pressure (pressure at zero flow; Pzf). Ascending aortic banding in seven dogs increased the LV to body weight ratio to 7.7 +/- 0.3 g/kg compared to 4.8 +/- 0.2 g/kg in 10 normal dogs (p < or = 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. During resting conditions maximum coronary blood flow in the pressure overloaded hypertrophied left ventricle was impaired by both an increase in Pzf (25.1 +/- 2.6 vs 13.8 +/- 1.2 mmHg in hypertrophied vs normal ventricles, respectively, p < or = 0.01) and a decrease in maximum coronary conductance (slope of the linear part of the pressure-flow relation, slopep > or = linear) (8.6 +/- 1.1 vs 12.7 +/- 0.9 ml/min/mmHg, p < or = 0.01). Right atrial pacing at 200 and 250 beats/min resulted in similar rightward shifts of the pressure-flow relation in hypertrophied and normal hearts with 3.1 +/- 0.8 and 4.7 +/- 0.8 mmHg increases in Pzf in LVH and normal dogs, respectively; stepwise multivariate regression analysis indicated that the exaggerated decrease in filling pressure (10 +/- 2 vs 6 +/-2 mmHg) and decrease in left ventricular systolic pressure (45 +/- 5 vs 3 +/- 3 mmHg, p < or = 0.01) may have blunted a greater rightward shift of the pressure-flow relation produced by atrial pacing in the hypertrophied hearts. Inotropic stimulation with dobutamine (10-20 micrograms/kg/min, i.v.) resulted in minimal flow changes in normal hearts but produced a 4.4 +/- 1.5 mmHg (p < or = 0.05) rightward shift of the pressure-flow relation in hypertrophied hearts. which correlated with a greater increase in left ventricular systolic pressure (83 +/- 16 vs 18 +/- 4 mmHg. p < or = 0.05). Exercise resulted in a rightward shift in both normal and hypertrophied left ventricles, but the increase in Pzf was significantly greater in the hypertrophied hearts (15.2 +/- 0.9 vs 10.3 +/- 0.9 mmHg. p < or = 0.05). Stepwise multivariate regression analysis indicated that not only increases in left ventricular filling pressure, but also increases in heart rate and LV systolic pressure contributed to the abnormally great increase in effective coronary back pressure which results in limitation of myocardial perfusion during exercise in the pressure overloaded hypertrophied left ventricle.     

Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.