Transesophageal echocardiography: an objective tool in defining maximum ventricular response to intravenous fluid therapy

Ventricular preload is an important determinant of cardiac function, which is indirectly measured in the clinical setting by the pulmonary capillary wedge pressure (PCWP). Transesophageal echocardiography (TEE) is rapidly gaining acceptance as a monitor of cardiac function. Although it provides high-resolution images of cardiac structures, clinical assessment of ventricular preload using TEE has been subjective, since quantitative measurements have been difficult to perform in a timely fashion. Automated border detection (ABD) is a new technology used in conjunction with TEE that allows quantitative real-time, two-dimensional measurement of cavity areas. To determine whether enddiastolic area (EDA) measured by ABD can be used to determine an appropriate end point for intravenous fluid administration, nine mongrel dogs were studied. Anesthetized animals were hemorrhaged to achieve a central venous pressure of 0-5 mm Hg. Each animal was then given intravenous fluid (autologous blood followed by hetastarch) until a peak in thermodilution cardiac output (CO) was achieved. Measures of PCWP, EDA, CO, and left ventricular stroke work (LVSW) were obtained after each fluid bolus. Bivariate plots displaying administered volume versus CO, LVSW, and EDA revealed parallel curves for each of these variables with peaks evident at cumulative volumes of 50-55 mL/kg. Multiple regression with mixed model analysis of covariance was performed to determine the significance of EDA in relation to changes in CO and LVSW. Analysis was likewise performed comparing the relationship between PCWP and changes in CO or LVSW. A significant relationship was demonstrated when comparing EDA to changes in CO and LVSW (P = 0.03 and P < 0.0001, respectively). Similar analysis comparing PCWP to changes in CO and LVSW failed to demonstrate a significant relationship (P = 0.54 and P = 0.36, respectively). These data suggest that changes in EDA measured using TEE with ABD are related to trends in cardiac function and can suggest an appropriate end point for intravenous fluid administration as defined by maximum CO and LVSW. PCWP did not demonstrate a significant relationship to changes in CO and LVSW.     

Laparoscopically assisted abdominal aortic aneurysm repair: first 20 cases

PURPOSE: Laparoscopic surgery decreases postoperative pain, shortens hospital stay, and returns patients to full functional status more quickly than open surgery for a variety of surgical procedures. This study was undertaken to evaluate laparoscopic techniques for application to abdominal aortic aneurysm (AAA) repair. METHODS: Twenty patients who had AAAs that required a tube graft underwent laparoscopically assisted AAA repair. The procedure consisted of transperitoneal laparoscopic dissection of the aneurysm neck and iliac vessels. A standard endoaneurysmorrhaphy was then performed through a minilaparotomy using the port sites for the aortic and iliac clamps. Data included operative times, duration of nasogastric suction, intensive care unit days, and postoperative hospital days. Pulmonary artery catheters and transesophageal echocardiography were used in seven patients. For these patients data included heart rate, pulmonary artery systolic and diastolic pressures, mean arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, and end diastolic area. Data were obtained before induction, during and after insufflation, during aortic cross-clamp, and at the end of the procedure. RESULTS: Laparoscopically assisted AAA repair was completed in 18 of 20 patients. Laparoscopic and total operative times were 1.44 +/- 0.44 and 4.1 +/- 0.92 hours, respectively. Duration of nasogastric suction was 1.3 +/- 0.7 days. Intensive care unit stay was 2.2 +/- 0.9 days. The mean length of hospital stay was 5.8 days excluding three patients who underwent other procedures. There were two minor complications, one major complication (colectomy after colon ischemia), and no deaths. For the eight patients who had intraoperative transesophageal echocardiographic monitoring, no changes were noted in heart rate, pulmonary artery systolic pressure, pulmonary capillary wedge pressure, and cardiac index. Pulmonary artery diastolic pressure and central venous pressure were greatest during insufflation without changes in end-diastolic area. Volume status, as reflected by end-diastolic area and pulmonary capillary wedge pressure, did not change. CONCLUSIONS: Laparoscopically assisted AAA repair is technically challenging but feasible. Potential advantages may be early removal of nasogastric suction, shorter intensive care unit and hospital stays, and prompt return to full functional status. The hemodynamic data obtained from the pulmonary artery catheter and transesophageal echocardiogram during pneumoperitoneum suggest that transesophageal echocardiography may be sufficient for evaluation of volume status along with the added benefit of detection of regional wall motion abnormalities and aortic insufficiency. Further refinement in technique and instrumentation will make total laparoscopic AAA repair a reality.     

Laparoscopy in high-risk cardiac patients

Fifteen patients with severe cardiac disease (American Society of Anesthesiologists III or IV) underwent laparoscopy using radial artery and pulmonary artery catheters to determine intraoperative hemodynamic changes. Cardiac output (CO), mean arterial blood pressure (MAP), central venous pressure, heart rate, systemic vascular resistance (SVR) and mixed venous oxygen saturation (SVO2) were recorded before anesthetic induction, after induction, but before peritoneal insufflation, after insufflation and after release of pneumoperitoneum. Peritoneal insufflation led to significant elevations in MAP and SVR and reduction in CO. For seven patients, a decrease in SVO2 after peritoneal insufflation was predictive of significant worsening of hemodynamic parameters, suggesting inadequate cardiac reserve. In all patients, hemodynamic parameters returned toward baseline once pneumoperitoneum was released. There were no perioperative cardiac complications. While it is evident that laparoscopy presents serious hemodynamic stress, it can be performed safely in high-risk patients, using aggressive intraoperative monitoring.     

Thoracic electric impedance and fluid balance during aortic surgery

Indices of fluid balance were evaluated during and after aortic surgery in 16 consecutive patients. Thoracic electrical impedance (TI), heart rate (HR), central venous (CVP), pulmonary artery mean (PAMP), pulmonary wedge (PWP) and mean arterial (MAP) pressures as well as fourteen arterial and venous blood gas variables were followed. Consistent with a reduction of TI during the operation, fluid balance was in excess, and it remained elevated on the first postoperative morning. The HR, MAP and PWP remained stable, while CVP and PAMP decreased. Of the determined variables only TI revealed a meaningful correlation to fluid balance (rho = -0.41; p < 0.01). The results indicate that while central venous and pulmonary artery mean pressures gave the impression of a volume deficit, the positive fluid balance was mirrored by thoracic electrical impedance.     

Acute effects of transjugular intrahepatic portosystemic stent-shunt (TIPSS) procedure on renal blood flow and cardiopulmonary hemodynamics in cirrhosis

OBJECTIVE: An acute increase in portal pressure is associated with an immediate reduction in renal blood flow. It has been suggested that this supports the presence of an hepatorenal reflex. In this study, we used TIPSS placement as a model to investigate the effect of an acute reduction in portal pressure on renal blood flow and cardiopulmonary hemodynamic parameters. METHODS: Eleven cirrhotic patients were studied during elective TIPSS placement for variceal hemorrhage (n = 9) or refractory ascites (n = 2). Unilateral renal blood flow (RBF) was measured before and at 5, 15, 30, 45, and 60 min after shunt insertion. Heart rate (HR), mean arterial pressure (MAP), right atrial pressure (RAP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and systemic vascular resistance (SVR) were also measured before and 30 min after TIPSS placement. RESULTS: Despite significant increases in CO (p = 0.001), RAP (p < 0.001), PAP (p < 0.001), and PCWP (p = 0.001), and a fall in SVR (p = 0.003), no change was observed in RBF, HR, or MAP after TIPSS placement. The fall in the portoatrial pressure gradient correlated only with the rise in CO (p < 0.05) and the drop in SVR (p < 0.05). CONCLUSION: Despite the fall in portal pressure and the systemic hemodynamic changes caused by TIPSS placement, there is no immediate effect on RBF. Any improvement in renal function after TIPSS procedure does not appear to be due to an acute increase in RBF.     

Effect of artificial ventilation on pulmonary capillary pressure in acute respiratory insufficiency

To determine the influence of intermittent positive pressure breathing (IPPB), the level of pulmonary capillary wedge pressure (PCWP) was compared during IPPB and after a short period off the respirator in 68 occasions on 42 patients with an acute respiratory failure (ARF) of various etiologies. During IPPB, the average PCWP was in the normal range in patients with toxic or neurologic comas and in cases of increased pulmonary capillary permeability edema (IPCPE), PCWP slightly increased within chronic obstructive pulmonary disease (COPD) complicated with ARF and in hemodynamic acute pulmonary edema (HAPE). During the weaning stage, PCWP decreased in the groups of coma, COPD, and IPCPE, but increased in HAPE. The weaning test demonstrates that IPPB influenced PCWP in all patients. Therefore, PCWP cannot be assumed to represent the left ventricle filling pressure. The weaning test allows differentiation of IPCPE from HAPE. In the event of over-infusion or hypovolemia, PCWP measured under IPPB can lead to misinterpretation if not followed up by a second measurement off the respirator.     

Planimetric quantification of aortic valve stenoses using multiplanar transesophageal echocardiography

Standard techniques used in order to quantify the severity of aortic valve stenoses in clinical practice comprise: transthoracic echocardiography, namely, by determining maximum and mean transvalvular gradients and evaluating aortic valve areas, as well as invasive techniques which quantify aortic valve areas through hemodynamic pressure measurements and application of the Gorlin formula. Since the introduction of the multiplane TEE technique, it has become feasible to scan the aortic valve in a strictly horizontal plane and quantify the aortic valve orifice by planimetry. In this study, we investigated 23 patients with various degrees of aortic valve stenoses. We compared aortic valve areas, which had been planimetrically determined by multiplane TEE scans, and mean aortic valve gradients (standard TEE technique) with pressure gradients and valve areas derived from hemodynamic measurements obtained during cardiac catheterization, and have found that the valve areas as well as the mean pressure gradients correlate well.     

Hemodynamic changes in acute respiratory insufficiency: the role of the right ventricle

Acute respiratory failure, particularly if associated with sepsis, results in diffuse changes in pulmonary vascular geometry and the afterload characteristics against which the right ventricle must perform. Therapy in these patients frequently requires replacement of intravascular volume which, if pulmonary vascular resistance is abnormally elevated, may cause a substantial enlargement in right ventricular (RV) end-diastolic volume. The low compliance characteristics of the RV invalidate the use of filling pressure (CVP) as a guide to RV size. We have examined RV volume in critically ill patients by means of the gated 99TAc scan and noted a substantial increase in RV volume despite filling pressure in the upper normal range. This enlargement appears to encroach upon LV function because the ejection fraction of the LV remained high despite elevation of pulmonary capillary wedge pressure (PCWP). Older patients with "silent" right coronary artery disease may become hemodynamically limited during therapy for acute respiratory failure and sepsis due to RV enlargement, increased wall tension and RV ischemia, a condition not readily diagnosed at the bedside with the usual monitoring techniques.     

Cardiac tamponade during transesophageal echocardiography in the patient of circumferential aortic dissection

A 43-year-old woman, whose physical findings were consistent with Marfan's syndrome, presented with acute chest pain. Transthoracic two-dimensional echocardiography demonstrated dilated ascending aorta with a circular shape intimal flap at the root level. Subsequently, the patient required transesophageal echocardiography (TEE), but during esophageal intubation, the patient developed acute pericardial tamponade which resulted in death in spite of cardiopulmonary resuscitation. Although, some investigators recommend TEE as the first choice of diagnostic method of aortic dissection, hemodynamic stability is very important during TEE study. Therefore, aggressive sedation may be required in the case of circumferential dissection of the ascending aorta to prevent the increases of the blood pressure and the heart rate which suggested an extensive tear of the aortic intima during TEE procedure.     

Prediction of pulmonary capillary wedge pressure and assessment of stroke volume by noninvasive impedance cardiography

Early recognition of heart failure is important because early treatment reduces mortality and hospitalization rates. In screening for this disease, there is a need for a simple, safe, and cost-effective method to obtain cardiovascular variables. Therefore we developed a noninvasive impedance cardiographic method to predict the pulmonary capillary wedge pressure (PCWP) from the impedance cardiogram. The impedance cardiographic technique, though, was originally designed for stroke volume (SV) determination. The objectives of this study were to validate both variables by comparison with the paired, invasively obtained equivalents. PCWP, measured with a pulmonary artery catheter, was related to the O/C ratio from the impedance cardiogram. The O/C ratio was calculated as the amplitude of the impedance cardiogram during diastole (O) divided by the maximum height during systole (C). Stroke volume was also calculated from the impedance cardiogram according to the equation of Kubicek (SVIC) and compared with thermodilution (SVTD). Data analysis was performed in 24 stable patients who underwent diagnostic heart catheterization. Linear regression analysis showed that the O/C ratio was strongly related to the invasively measured PCWP over a range of 3 to 30 mm Hg (r = 0.92, standard error of the estimate, 3.2 mm Hg). Between SVIC and SVTD a moderate correlation was established (r = 0.69), but after exclusion of the data from patients with an aortic valve disorder (n = 5), the correlation increased considerably (r = 0.87). No significant differences between SVIC and SVTD were found (mean difference +/- 2 SD = 1.8 +/- 28.8 ml). These preliminary observations suggest that impedance cardiography can predict PCWP and measure SV over a wide range of clinically relevant values. The combined measurement of SV and PCWP by impedance cardiography might be a clinical useful tool in screening for heart failure.     

Complement resistance of capsulated strains of Aeromonas salmonicida

1. We investigated the effect of exercise on plasma adrenomedullin, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations and studied the relationship between these peptides and haemodynamic parameters in nine patients with old myocardial infarction (MI) and in eight normal subjects. 2. The exercise protocol consisted of two fixed work loads (40 and 80 W) for 4 min each and venous blood samples were taken at rest, during each exercise stage and after exercise while monitoring the mean arterial pressure (MAP) and heart rate (HR). In MI, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), left ventricular end-diastolic pressure (LVEDP) and cardiac output (CO) were measured throughout exercise. 3. Adrenomedullin levels did not significantly increase with exercise. Adrenomedullin levels correlated with PAP and PCWP at rest (P < 0.05). Atrial natriuretic peptide levels correlated with PAP, PCWP and LVEDP throughout exercise (P < 0.05) but, on multiple regression analysis, PCWP correlated only with ANP (P < 0.01). Brain natriuretic peptide levels correlated with LVEDP throughout exercise (P < 0.01) and its increment correlated closely with basal BNP levels at rest (P < 0.01). 4. These results suggest that adrenomedullin does not respond to the acute haemodynamic changes of exercise, whereas ANP responds to it and PCWP is the major stimulus factor. Brain natriuretic peptide responds to exercise in proportion to the basal synthesis of BNP in patients with left ventricular dysfunction and LVEDP may play a role in increasing BNP during exercise.     

Serum erythropoietin and granulocyte-macrophage-colony stimulating factor levels with megadose methylprednisolone treatment

We described an anesthetic management of a patient with abdominal aortic aneurysm associated with dilated cardiomyopathy (DCM) focusing on preanesthetic evaluation of cardiovascular reserve and on intraoperative continuous circulatory monitoring with transesophageal echocardiography (TEE) and continuous cardiac output measurement (CCO). Based on echocardiographic and hemodynamic measurements after a 50 m-walk load, we predicted the allowable range of alteration of preload (LV diastolic dimension; Dd), myocardial performance (arterial blood pressure and ejection fraction) and of heart rate. During anesthesia and operation, we continuously monitored Dd, arterial blood pressure, heart rate and cardiac output, and maintained these variables within the allowable range. The changes in preload after clamping or unclamping of the aorta was promptly reflected by Dd as compared to pulmonary capillary wadge pressure. The CCO was also usuful in detecting abrupt changes in myocardial performance. In conclusion, we suggest preanesthetic stress test to be performed to evaluate cardiovascular reserve and to predict the allowable range of alteration of hemodynamic variables. Continuous monitoring of preload (Dd) by TEE and of myocardial performance by CCO is useful to detect early changes in these variables.     

Protective effects of halothane but not isoflurane against global ischaemic injury in the isolated working rat heart

The effects of equi-anaesthetic concentrations of halothane (HAL) and isoflurane (ISO) on myocardial performance, perfusion, oxygenation and lactate release were studied before, during and after a low-flow, global ischaemic insult in isolated, paced rat left heart preparations. An antegrade perfusion technique was used, where left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other. Aortic flow, coronary flow (CF) and PO2 in venous coronary effluent were continuously recorded and stroke volume, myocardial oxygen consumption (MVO2) and myocardial oxygen extraction as well as lactate release were calculated. The hearts were exposed for at least ten minutes to the perfusate without (control, n = 10) or with HAL (n = 10) or ISO (n = 10) at a MAP of 80 mmHg (10.4 kPa) and a LAP of 7.5 mmHg (1.0 kPa). After baseline measurements, MAP was reduced to 25 mmHg (3,2 kPa) for a total of nine minutes. Thereafter MAP was increased to 80 mmHg (10.4 kPa) for another nine minute period. During the whole experimental procedure, LAP was maintained at 7.5 mmHg (1.0 kPa) and heart rate at 325 beats per minute. In the pre-ischaemic control period, MVO2 was lower with HAL compared to ISO (P < 0.05) and control (P < 0.05). Stroke volume was also lower with HAL compared to control (P < 0.05). During hypoperfusion, lactate release was twice as high in the control group (P < 0.01) and with ISO (P < 0.01) compared to HAL.(ABSTRACT TRUNCATED AT 250 WORDS)     

Kaposi''s sarcoma-associated herpesvirus and human herpesvirus 8 (KSHV/HHV8)-associated lymphoma of the bowel. Report of two cases in HIV-positive men with secondary effusion lymphomas

BACKGROUND: We evaluated the ability of the standards issued by the Danish Society of Anaesthesiologists to reflect a blood loss. METHODS: In 9 pigs bled (0-24 ml kg-1 and retransfused (to 28 ml kg-1) during halothane anaesthesia central cardiovascular, thoracic electrical impedance (TI), oxygen, acid-base and temperature variables were recorded. RESULTS: With the recommendation for minor surgery (mean arterial pressure (MAP) and heart rate (HR)), the correlation to the blood loss was 0.74 (P < 0.001) and with that for major surgery (MAP, HR, central venous pressure (CVP) and rectal temperature (Tempr)) it was 0.79 (P < 0.001). With the recommendation for extensive surgery (MAP, HR, CVP, pulmonary artery catheter variables and the central-peripheral temperature difference (delta Tempr-t)), the correlation was 0.84 (P < 0.001). Non-invasive monitoring (MAP, HR, delta Tempr-t, TI and near-infrared spectroscopy of the brain (SinvosO2)) was only slightly better than basal monitoring (r = 0.76, P < 0.001). However, adding arterial base excess (BE), TI, and peripheral temperature (Tempt) to the recommendation for major surgery resulted in a correlation of 0.87 (P < 0.001), while adding BE and TI to the recommendation for extensive surgery raised correlation to only 0.88 (P < 0.001). CONCLUSION: When the recommendations were followed the correlation to the blood loss ranged from 0.74-0.84. However, with the recording of MAP, HR, CVP, delta Tempr-t, BE and TI a correlation of 0.87 was achieved, indicating that a pulmonary artery catheter may not be in need for patients undergoing surgical procedures with expected haemorrhage.     

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.     

Hemodynamic changes during laparoscopic cholecystectomy

Hemodynamics during laparoscopic cholecystectomy under general anesthesia (isoflurane in N2O/O2 (50%)) were investigated in 15 nonobese ASA Class I patients by using invasive hemodynamic monitoring including a flow-directed pulmonary artery catheter. During surgery, intraabdominal pressure was maintained automatically at 14 mm Hg by a CO2 insufflator, and minute ventilation was controlled and adjusted to avoid hypercapnia. Hemodynamics were measured before anesthesia, after the induction of anesthesia, after tilting into 10 degrees head-up position, 5 min, 15 min, and 30 min after peritoneal insufflation, and 30 min after exsufflation. Induction of anesthesia decreased significantly mean arterial pressure and cardiac index (CI). Tilting the patient to the head-up position reduced cardiac preload and caused further reduction of CI. Peritoneal insufflation resulted in a significant increase (+/- 35%) of mean arterial pressure, a significant reduction (+/- 20%) of CI, and a significant increase of systemic (+/- 65%) and pulmonary (+/- 90%) vascular resistances. The combined effect of anesthesia, head-up tilt, and peritoneal insufflation produced a 50% decrease in CI. Administration of increasing concentrations of isoflurane, via its vasodilatory activity, may have partially blunted these hemodynamic changes. These results demonstrate that laparoscopy for cholecystectomy in head-up position results in significant hemodynamic changes in healthy patients, particularly at the induction of pneumoperitoneum.     

Pulmonary metastasectomy for soft tissue sarcomas: is it justified?

beta-blocker therapy for mitral stenosis is controversial. This study compares right and left heart hemodynamics at rest and supine submaximal exercise in patients (n = 7) receiving chronic beta-antagonists with untreated patients (n = 17) matched for age (mean +/- SD = 51 +/- 12 years) and valve area (0.7 +/- 0.2 cm2/m2). Little benefit was observed with treatment at rest. Although pulmonary capillary wedge pressures (PCWP) were lower during exercise in the beta-blocker group (22 +/- 4 vs. 31 +/- 9 mmHg; P < 0.05), exercise performance was not enhanced and cardiac output response during exercise was reduced (control = 41% increase vs. 12% for beta-blockade). PCWP rose rapidly when diastolic filling periods were < 300 msec in both groups. Pulmonary capillary wedge pressure was found to be a nonlinear functions (P < 0.001) of diastolic filling period (PCWP = 15.9 + 5.84 x 10(5)/dfp2). These data suggest that there is a critical heart rate in patients with mitral stenosis above which hemodynamic compromise rapidly occurs.     

Hemodynamic effect of inhaled nitric oxide in dilated cardiomyopathy patients on LVAD support

Recently it has been shown that inhaled nitric oxide (NO), which has been proven to contribute to improvement in critical pulmonary hypertension, may provide a favorable effect early after left ventricular assist device (LVAD) support. To improve right ventricular function, inhalation of NO was added to treatment with conventional catecholamines for four consecutive dilated cardiomyopathy (DCM) patients following institution of LVAD. In two patients 1 hr after inhalation of NO, central venous pressure (CVP), mean pulmonary arterial pressure (PAm), and pulmonary vascular resistance (PVR) were improved. These results led to better LVAD output and resulted in an adequate cardiac index. On the other hand, a right VAD (RVAD) was implemented in one patient whose high CVP, PAm, and PVR continued; he was weaned after 8 days of RVAD support. Another patient who had a high CVP but normal PAm and PVR before and after inhalation of NO had no improvement in his hemodynamic state. These data suggest that inhaled NO may improve systemic circulation by reducing right ventricular afterload and may become a promising and convenient therapy before placing RVAD in DCM patients under LVAD support. RVAD should be conducted in patients with right ventricular failure or when pulmonary hypertension is associated with impaired right ventricular reserve, even after inhalation of NO.     

Mechanism of adenosine-induced elevation of pulmonary capillary wedge pressure in humans

BACKGROUND: Continuous intravenous administration of adenosine to humans often results in a paradoxical rise in pulmonary capillary wedge pressure (PCWP), whereas arterial resistance is lowered and cardiac output and heart rate increase. This is believed to be due to diastolic stiffening of the ventricle or to a negative inotropic effect. In the present study, we tested these and other mechanisms by using pressure-volume (PV) analysis and echocardiography. METHODS AND RESULTS: Fifteen patients with normal rest left ventricular function underwent cardiac catheterization and received adenosine at a rate of 140 micrograms/kg per minute IV for 6 to 10 minutes. PV relations were measured in 9 patients (without coronary artery disease) using the conductance catheter method. In 6 additional patients with coronary artery disease, echocardiograms were used to assess wall thickness and function, and aortic and coronary sinus blood, lactate, oxygen, and adenosine levels were measured. Adenosine increased PCWP by 19% (+2.6 mm Hg) in both patient groups while lowering arterial load by 30% and increasing cardiac output by 45% (all P < .001). There was no significant effect of adenosine on mean linear chamber compliance or monoexponential elastic stiffness, as the diastolic PV relation was unchanged in most patients. Diastolic wall thickness also was unaltered. Thus, the PCWP rise did not appear to be due to diastolic stiffening. Adenosine induced a rightward shift of the end-systolic PV relation (ESPVR) (+12.7 +/- 3.7 mL) without a slope change. This shift likely reflected effects of afterload reduction, as other indexes (stroke work-end-diastolic volume relation and dP/dtmax at matched preload) were either unchanged or increased. Furthermore, this modest shift in ESPVR was more than compensated for by vasodilation and tachycardia, so reduced systolic function could not explain the increase in PCWP. There also was no net lactate production to suggest ischemia. Rather than arising from direct myocardial effects, PCWP elevation was most easily explained by a change in vascular loading, as both left ventricular end-diastolic volume and right atrial pressure increased (P < .05). This suggests that adenosine induced a redistribution of blood volume toward the central thorax. CONCLUSIONS: PCWP elevation in response to adenosine primarily results from changes in vascular loading rather than from direct effects on cardiac diastolic or systolic function.