Flow-directed Pulmonary Artery Catheter Research Articles

The pulmonary artery catheter in 2008 - A (finally) maturing modality?

The first description of the flow-directed pulmonary artery catheter (PAC) was published in the 1970s by Jeremy Swan and William Ganz. Ever since its clinical debut, many controversies surrounded the use of the PAC. Regardless of these controversies, the most fundamental issues surrounding this hemodynamic monitoring device remain unresolved, including the exact indications, contraindications, identification of patients who potentially benefit from this technology, and the way we interpret and use PAC-derived parameters. Despite recent intensification of attacks against the use of the PAC by its opponents, it seems overly harsh to discount a technology that might be beneficial in appropriately selected clinical situations, especially when considering the fact that our true knowledge of this technology is somewhat limited. In fact, the PAC may still play an important role considering the resurgence of the concepts of euvolemic resuscitation and hemodynamic sufficiency.Republished with Permission from: Stawicki SP, Prosciak MP. The pulmonary artery catheter in 2008 – a (finally) maturing modality? OPUS 12 Scientist 2008;2(4):5-9.

Misplacement of a pulmonary artery catheter.

Placing a flow-directed pulmonary artery catheter (PAC) can be difficult and lead to serious complications. We present the case of an attempted PAC insertion in a patient undergoing implantation of a left ventricular assist device. Although physiologic pressure waveforms were established, plausible measurements of cardiac output and pulmonary capillary wedge pressure were not initially obtainable. Chest radiography showed that the catheter was looped in the pulmonary artery. This malposition could not be visualized intraoperatively by transesophageal echocardiography. The PAC was replaced in the operating room after the left ventricular assist device was implanted.

Intramedullary nailing of femoral shaft fractures in polytraumatized patients. a longitudinal, prospective and observational study of the procedure-related impact on cardiopulmonary- and inflammatory responses

BackgroundEarly intramedullary nailing (IMN) of long bone fractures in severely injured patients has been evaluated as beneficial, but has also been associated with increased inflammation, multi organ failure (MOF) and morbidity. This study was initiated to evaluate the impact of primary femoral IMN on coagulation-, fibrinolysis-, inflammatory- and cardiopulmonary responses in polytraumatized patients.MethodsTwelve adult polytraumatized patients with femoral shaft fractures were included. Serial blood samples were collected to evaluate coagulation-, fibrinolytic-, and cytokine activation in arterial blood. A flow-directed pulmonary artery (PA) catheter was inserted prior to IMN. Cardiopulmonary function parameters were recorded peri- and postoperatively. The clinical course of the patients and complications were monitored and recorded daily.ResultsMean Injury Severity Score (ISS) was 31 ± 2.6. No procedure-related effect of the primary IMN on coagulation- and fibrinolysis activation was evident. Tumor necrosis factor alpha (TNF-α) increased significantly from 6 hours post procedure to peak levels on the third postoperative day. Interleukin-6 (IL-6) increased from the first to the third postoperative day. Interleukin-10 (IL-10) peaked on the first postoperative day. A procedure-related transient hemodynamic response was observed on indexed pulmonary vascular resistance (PVRI) two hours post procedure. 11/12 patients developed systemic inflammatory response syndrome (SIRS), 7/12 pneumonia, 3/12 acute lung injury (ALI), 3/12 adult respiratory distress syndrome (ARDS), 3/12 sepsis, 0/12 wound infection.ConclusionIn the polytraumatized patients with femoral shaft fractures operated with primary IMN we observed a substantial response related to the initial trauma. We could not demonstrate any major additional IMN-related impact on the inflammatory responses or on the cardiopulmonary function parameters. These results have to be interpreted carefully due to the relatively few patients included.Trial RegistrationClinicalTrials.gov: NCT00981877

Stroke Volume Optimization Versus Central Venous Pressure in Fluid Management

Q What is the current evidence for using stroke volume optimization rather than central venous pressure and urine output for fluid management?A Thomas Ahrens, RN, PhD, CCNS, replies:This question is easy to answer. Little evidence supports the use of central venous pressure (CVP) and urine output to guide fluid therapy, but a large body of evidence supports use of stroke volume optimization. A little background will illustrate why stroke volume optimization should be the predominant method used when giving fluids.The assessment of volume status (eg, hypovolemia) is a major problem in the perioperative setting and in intensive care units. Because of care-givers’ inability to accurately assess the severity of hypovolemia and the patient’s response to treatment, patients are often misdiagnosed and do not receive the proper treatment. The results are delays in treatment, undertreatment, and overtreatment, all of which lead to outcomes that are less than desirable and increases complications and patients’ length of stay.The problem in assessment of hypovolemia stems from the inability to measure blood flow, specifically stroke volume, directly. Stroke volume (how much blood the heart pumps with each beat) is the first parameter to change when a patient has volume loss. Every other compensatory sign occurs because of the reduction in stroke volume; such signs include increased heart rate, decreased cardiac output, decreased urine output, increased oxygen extraction, and reduced blood pressure. Even parameters such as CVP, which purportedly measures cardiac volume (a point that will be disputed in the following paragraph), are not helpful because it is not volume that is important, but blood flow. A patient whose heart is not even beating can have adequate volume (ie, normal CVP). It is the loss of blood flow that threatens patients’ outcomes.Clinicians often like to think that they can determine volume status by using the compensatory methods listed in the preceding paragraph and other physical signs. However, multiple studies1–9 have shown that physicians and nurses cannot accurately assess volume status with the current techniques. Measuring stroke volume only recently became feasible. In the early 1970s, Drs Swan and Ganz introduced the flow-directed pulmonary artery catheter in an attempt to help position assessment of cardiac function and flow. Unfortunately, one of the main clinical tools used with the Swan-Ganz catheter was cardiac filling pressures, such as CVP and pulmonary artery occlusion pressure (PAOP) or “wedge” pressure. These pressures were designed to estimate volume status of the right and left ventricles. Unfortunately, no study of CVP and PAOP has shown that those pressures correlate well with volume or flow status.10–14 In addition, CVP and PAOP do not reveal any information about stroke volume. Marik et al15 recently recommended that CVP not even be used in intensive care units, emergency departments, and operating rooms because of its lack of accuracy.With the development of technologies to measure stroke volume, fluid requirements have moved from guesswork to precise treatments. Many technologies exist to measure stroke volume, including Doppler monitoring, bioimpedance/reactance measurements, and arterial waveform analysis. All techniques to measure blood flow and stroke volume have strengths and limitations, and the best choice often depends on the particular patient. Clinicians should evaluate the technologies to determine which is best for their patient. However, when stroke volume is used as the end point, particularly with esophageal Doppler monitoring, improved outcomes for patients have been clearly demonstrated.For example, treatment of low stroke volume is relatively easy. If a fluid bolus is administered (rapidly, not just by increasing the infusion rate on the intravenous pump) and the stroke volume increases by more than 10%, then more fluid is needed. The concept of Starling’s Law is being used at this point. Only when the stroke volume does not increase by more than 10% is the fluid stopped. This simple algorithm allows fluids to be administered precisely so that the patient is not given too much or too little fluid.Optimizing stroke volume in surgical populations has resulted in a substantial decrease in hospital length of stay and the frequency of postoperative complications.16–25 The Centers for Medicare and Medicaid Services Web site has an annotated bibliography summary of the research and the reasons why they approved one form of Doppler monitoring for reimbursement (because of the economic benefit of stroke volume optimization).26At this point in medical practice, no strong scientific reason supports use of CVP to guide fluid therapy. However, multiple studies have shown that stroke volume optimization is the best guide to fluid therapy. We can decrease our patients’ complications, length of stay, and costs by using stroke volume optimization, the more accurate technique for assessing fluid volume.

NT-proBNP as a tool to stratify disease severity in pulmonary arterial hypertension

The recent development of treatment modalities for patients with idiopathic pulmonary arterial hypertension has been based on the evaluation of many different markers such as functional capacity, addressed by NYHA classification, six-minute walk test (6MWT) and hemodynamic parameters. The aim of this study was to evaluate the correlation of N-terminal fragment (NT-proBNP) with other markers in IPAH and its potential for patient stratification. We studied 42 IPAH patients consecutively evaluated through right heart catheterization in the absence of any specific treatment for pulmonary hypertension. Blood samples, clinical evaluation and 6MWF distance were collected at baseline. The levels of NT-proBNP showed a high correlation with hemodynamic parameters, such as pulmonary vascular resistance (r=0.80, P<0.001). A significant difference was found among patients with different functional classes, addressed by NYHA classification (P< 0.02 for all groups comparison). The discriminant analysis reinforced the ability of NT-proBNP to stratify patients according to NYHA functional class. Compared to the other variables studied (hemodynamics and 6MWT), NT-proBNP had the lowest level of overlap in the stratification of IPAH patients. We conclude that NT-proBNP differs among the different functional classes and correlates with other measures of disease severity, although its role in predicting survival still needs to be addressed.

Inadvertent Placement of a Flow-Directed Pulmonary Artery Catheter in the Coronary Sinus, Detected by Transesophageal Echocardiography

We report a case in which flow-directed placement of the pulmonary artery catheter led to its inadvertent placement in the coronary sinus, in the absence of congenital anomalies. Incorrect placement was diagnosed by use of the transesophageal echocardiography. If unrecognized, the catheter might have provided misleading information and led to mismanagement of the patient.

Unusual positioning of a central venous catheter

Central venous cannulation, with or without a flow-directed pulmonary artery catheter, is commonly performed in patients undergoing cardiac surgery to measure central filling pressure and cardiac output, and to administer medications and fluids. The complications of central venous cannulation are numerous and include malposition, arterial puncture, pneumothorax, hemothorax, chylothorax, extravasation of infusate, thrombophlebitis, and infection. We describe a single-lumen catheter that was placed through the hemostatic valve of a 9F percutaneous introducer, which inadvertently entered the left internal mammary (internal thoracic) vein. The current case is unique in that it was diagnosed by visualization of the catheter during surgical dissection.

The effects of vasoactive drugs on hepatic blood flow changes induced by CO2 laparoscopy: an animal study.

Laparoscopic surgery is associated with systemic and splanchnic hemodynamic alterations. Recent data suggest that small-dose dobutamine may attenuate the reduction in splanchnic blood flow associated with increments in intraabdominal pressure. We conducted this study to analyze the effects of dopamine and dobutamine on the hepatic circulation in this setting. Twenty-one pigs were anesthetized and mechanically ventilated. A flow-directed pulmonary artery and carotid artery catheters were inserted. Perivascular flow probes were placed around the main hepatic artery and the portal vein. CO2 was insufflated into the peritoneal cavity to reach an intraabdominal pressure of 15 mm Hg. After 60 min, animals received dopamine (5 microg x kg(-1) x min(-1); n = 8), dobutamine (5 microg x kg(-1) x min(-1); n = 8), or saline (n = 5) for 30 min. Pneumoperitoneum induced significant increases in heart rate, mean arterial pressure, and systemic vascular resistance, with decreases in cardiac output and hepatic artery and portal vein blood flows. Dobutamine infusion, in contrast to dopamine, corrected, at least in part, cardiac output, systemic vascular resistance, and hepatic artery blood flow alterations, but neither drug restored total hepatic blood flow. Hepatic blood flow decreases during laparoscopic surgery. A small-dose infusion of neither dobutamine nor dopamine corrects the total hepatic blood flow impairment, but the former is able to restore the hepatic arterial blood supply in an animal model mimicking this condition.

Experimental Use of an Illuminated and Magnetic Tip, Flow-Directed Pulmonary Artery Catheter for Lung Resection

The authors performed a study to design and evaluate a device giving the surgeon added protection against pulmonary artery injury in a closed thoracic compartment. Eleven swine were used for a total of 12 lobectomies. A light-bearing, magnetic-tipped, modified Swan-Ganz catheter was passed through the jugular vein into the left pulmonary artery. By using magnetic guidance through a port site and balloon inflation, cessation of flow in the pulmonary artery was documented by Doppler. Twelve video-assisted lobectomies were performed. Nine of 12 (75%) lobectomies were completed successfully by using the magnetic-tipped, illuminated balloon catheter. In 4 cases, the catheter displaced because of the short left main pulmonary artery in swine. In one case, the balloon was recovered, and successful lobectomy was performed. The use of a magnetic-tipped, flow-directed device may provide an effective means of endovascular control during thoracoscopic pulmonary arterial dissection.

Bleeding from a pulmonary artery catheter temperature connection port

p ERIOPERATIVE MONITORING with a balloon-tipped flow-directed pulmonary artery catheter (PAC) has been used clinically since 1970.1 The use of a PAC for cardiac surgical patients has become common practice, with low morbidity and mortality. However, significant complications during the insertion and use of this monitor include hematoma, 2 carotid artery puncture, 2 arrhythmias, 3,4 Homer's syndrome, 5 pulmonary artery embolism or rupture, sepsis, pneumothorax, catheter knotting, or entrapment by sutures. 1,6-8 This report describes two unusual presentations of PAC entrapment by sutures not reported in the earlier literature.

Continuous Spinal Anesthesia for Hip Surgery in a Patient with Shy-Drager Syndrome

Continuous Spinal Anesthesia for Hip Surgery in a Patient with Shy-Drager Syndrome

Estimation of pulmonary capillary wedge pressure from M-mode mitral echograms.

We investigated whether the isovolumic relaxation time (IRT) and an interval from the start of opening to the maximal amplitude of the anterior mitral leaflet in early diastole (D-E interval) would be useful predictors of the pulmonary capillary wedge pressure (PCWP). We recorded M-mode mitral echograms and phonocardiograms in 33 patients (aged 38-70 years) with acute myocardial infarction (AMI) in the coronary care unit and in 34 patients (aged 40-75 years) with prior myocardial infarction (OMI) during cardiac catheterization. All patients underwent the insertion of a flow-directed pulmonary artery catheter to obtain the PCWP. We measured the IRT and the D-E interval from the phonocardiograms and the M-mode echograms. There was no significant correlation between the IRT and the mean PCWP (mPCWP) in patients with AMI and in patients with OMI. The D-E interval was significantly and inversely correlated with the mPCWP (r = -0.91, p <0.0001) in all patients. The regression equation was mPCWP = -0.42 x (D-E) +47.9. The D-E interval of < or = 75 ms indicated a high mPCWP (mPCWP > or = 18 mm Hg) with high sensitivity (96%) and specificity (88%). The derived equation was tested in a prospective group of 32 additional patients (aged 43-75 years). A significant correlation was observed between the predicted and measured mPCWP (r = 0.91, p <0.0001). Thus, the PCWP can be estimated by using the D-E interval derived from M-mode mitral echograms in patients in the coronary care unit and in patients with chronic heart disease.

Use of the Pulmonary Artery Catheter in Severe Preeclampsia

The use of a balloon-tipped, flow-directed pulmonary artery catheter in critically ill and surgical patients has become commonplace in the United States since its introduction into clinical medicine in 1970. The capability of acquiring continuous hemodynamic and, more recently, oxygen transport data, has led to an enhanced understanding of pathophysiologic processes in disease states and to an improved ability to guide therapeutic decision making. The purpose of this paper is to review experience with the pulmonary artery catheter in subsets of women with severe preeclampsia.

THE NEW PULMONARY ARTERIAL CATHETERS: Right Ventricular Ejection Fraction and Continuous Cardiac Output

The flow-directed pulmonary artery catheter is the mainstay of hemodynamic monitoring in critically ill and injured patients. During its 25-year history, the catheter has been modified to measure mixed venous oxygen saturation, right ventricular ejection fraction, and recently, continual thermodilution cardiac output. The clinical application of the new generations of pulmonary artery catheters is reviewed in this article.

Noninvasive cardiac index monitoring in gunshot wound victims.

To evaluate a bioimpedance device for the noninvasive measurement of cardiac index (CI) against standard thermodilution measurements in patients with gunshot wounds. A prospective open-label performance evaluation was done using a convenience sample of gunshot wound victims initially treated in the resuscitation area of a high-volume, urban ED. After initial resuscitation, patients had a flow-directed pulmonary artery catheter placed for thermodilution cardiac output (CO) measurements. The CO measurements were made in triplicate and averaged. Estimates of body surface area were used to convert these measurements to CI estimates. Electrodes for bioimpedance measurements were placed as soon as practical after ED arrival. Simultaneous measurements of CI using the bioimpedance device were made as clinically indicated during each patient's hospital course. There were 54 patients studied, with an overall mean (+/- SEM) age of 32 +/- 3 years, Revised Trauma Score of 6.7 +/- 0.4, and Injury Severity Scale score of 22 +/- 3. There were 42 survivors and 12 nonsurvivors. The CI as estimated by bioimpedance correlated well with that measured by thermodilution (r = 0.79, p < or = 0.02). The precision of the invasive and noninvasive measurements was 1.1 L/min/m2; the bias was -0.011 L/min/m2. In 24 patients with thoracic injuries requiring tube thoracostomy or thoracic surgery, the correlation of the 2 devices was r = 0.71 with precision and bias of 1.4 L/min/m2 and -0.018 L/min/m2, respectively. Cardiac index can be noninvasively estimated in acutely injured patients with gunshot wounds using a bioimpedance device. Further study of bioimpedance measurements as a guide to volume therapy is warranted.

Inhaled Nitric Oxide Improves Hepatic Tissue Oxygenation in Right Ventricular Failure

Inhaled Nitric Oxide Improves Hepatic Tissue Oxygenation in Right Ventricular Failure

Right heart function and prediction of respiratory morbidity in patients undergoing pneumonectomy with moderately severe cardiopulmonary dysfunction

Detailed hemodynamic monitoring was performed in 20 patients undergoing pneumonectomy with moderately severe chronic obstructive pulmonary disease. Flow-directed pulmonary artery catheters capable of determining thermal dilution right ventricular ejection fraction and other indexes of right ventricular performance were placed in each patient. The mean actual and percent values for forced expiratory volume in 1 second in this group were 1.8 ± 0.5 L and 66% ± 18%, respectively. Pulmonary hypertension was present in 76.5% of patients at the baseline nonintubated state. At pulmonary artery clamping, 53.8% of this subgroup had no change or a mean drop of 8 mm Hg in pressure. The remaining had a mean rise of 12 mm Hg. Mean systolic pulmonary artery pressures in this subset (41 mm Hg) did not change from the nonintubated state to pulmonary artery clamping. Patients with normal pulmonary artery pressures before intubation had an average rise of only 4 mm Hg at pulmonary artery clamping. In the immediate postoperative period, only 10.0% of the entire group had normal pulmonary artery pressures. Right ventricular ejection fraction and pulmonary vascular resistance were normal in 58.8% and 94.1%, respectively, at the baseline nonintubated state. Abnormal right ventricular ejection fraction values (<45%) were present in 70.0% of patients at pulmonary artery clamping; 25.0% fell below 35%. Pulmonary vascular resistance increased above 200 dyne · sec · cm -5 in 30.0% at pulmonary artery clamping. No correlation was found between right ventricular ejection fraction and pulmonary vascular resistance or pulmonary artery pressure during operation. No pulmonary function test or hemodynamic variable measured in this study accurately predicted the days of hospital stay or early postoperative cardiopulmonary morbidity. At the baseline nonintubated state, no parameter consistently predicted late New York Heart Association class III/IV. At the time of pulmonary artery clamping, a right ventricular ejection fraction of less than 35%, a pulmonary vascular resistance greater than or equal to 200 dyne · sec · cm-5, and a pulmonary vascular resistance/right ventricular ejection fraction ratio greater than or equal to 5.0 predicted the development of long-term cardiopulmonary disability. Thirteen patients (65.0%) in this series with abnormally low preoperative pulmonary function could have been excluded from pneumonectomy. Only five of 13 patients (38.5%) had late class III/IV symptoms. Four of these five patients had a right ventricular ejection fraction less than 35% during operation. Those patients with a right ventricular ejection fraction greater than or equal to 35% and normal pulmonary vascular resistance appear to have sufficient pulmonary vascular capacitance to tolerate pneumonectomy despite the presence of pulmonary hypertension and abnormally low pulmonary function tests. (J THORAC CARDIOVASC SURG 1994;108:169-75)

The Effect of the Pericardium on Right and Left Ventricular Diastolic Functions During Isoflurane Anesthesia

We examined the effects of the pericardium on diastolic function of the right and left ventricles during isoflurane anesthesia. The diastolic properties of the ventricles were assessed by indices of isovolumetric relaxation such as -dP/dt, -dP/dt25, and time constant for relaxation, and by end-diastolic pressure. In seven mongrel dogs, anesthesia was initially induced by the administration of pentobarbital and maintained with alpha-chloralose. Two 7F microtipped pressure transducers were inserted into the right and left ventricles, and a flow-directed pulmonary artery catheter was placed in the pulmonary artery. After a left thoracotomy, opening and closing the pericardium was performed at 0% isoflurane, 1.3% isoflurane, and 2.6% isoflurane. Isoflurane 1.3% and 2.6% produced a decrease in cardiac output in association with a decrease in -dP/dt and an increase in time constant for relaxation of both ventricles, suggesting that isoflurane may depress isovolumetric relaxation of both ventricles. Isoflurane also increased end-diastolic pressure of the left ventricle. With 0% isoflurane, pericardial opening did not significantly change the diastolic properties of either ventricle and other hemodynamics. Pericardial opening at 1.3% and 2.6% isoflurane increased cardiac output without any significant changes in -dP/dt and time constant of either ventricle, but with significant decreases in end-diastolic pressures of both ventricles. We conclude that the pericardium may have a constraining effect on the diastolic properties, especially end-diastolic pressure, but not on isovolumetric relaxation of both ventricles during isoflurane anesthesia.

The Effect of the Pericardium on Right and Left Ventricular Diastolic Functions During Isoflurane Anesthesia

We examined the effects of the pericardium on diastolic function of the right and left ventricles during isoflurane anesthesia. The diastolic properties of the ventricles were assessed by indices of isovolumetric relaxation such as −dP/dt, −dP/dt25, and time constant for relaxation, and by end-diastolic pressure. In seven mongrel dogs, anesthesia was initially induced by the administration of pentobarbital and maintained with α-chloralose. Two 7F microtipped pressure transducers were inserted into the right and left ventricles, and a flow-directed pulmonary artery catheter was placed in the pulmonary artery. After a left thoracotomy, opening and closing the pericardium was performed at 0% isoflurane, 1.3% isoflurane, and 2.6% isoflurane. Isoflurane 1.3% and 2.6% produced a decrease in cardiac output in association with a decrease in −dP / dt and an increase in time constant for relaxation of both ventricles, suggesting that isoflurane may depress isovolumetric relaxation of both ventricles. Isoflurane also increased end-diastolic pressure of the left ventricle. With 0% isoflurane, pericardial opening did not significantly change the diastolic properties of either ventricle and other hemodynamics. Pericardial opening at 1.3% and 2.6% isoflurane increased cardiac output without any significant changes in −dP / dt and time constant of either ventricle, but with significant decreases in enddiastolic pressures of both ventricles. We conclude that the pericardium may have a constraining effect on the diastolic properties, especially end-diastolic pressure, but not on isovolumetric relaxation of both ventricles during isoflurane anesthesia. (Anesth Analg 1993;76:1195-1200)

Effects of labetalol on uterine blood flow and cardiovascular hemodynamics in the hypertensive gravid baboon

The purpose of this study was to investigate the effects of labetalol on uterine blood flow and cardiovascular parameters in acutely instrumented, hypertensive gravid baboons. During the latter half of pregnancy six gravid baboons were acutely instrumented, with ultrasonic flow probes placed on ipsilateral, external iliac, and uterine arteries and a flow-directed pulmonary artery catheter in the pulmonary artery. After a stable arterial pressure baseline was obtained, norepinephrine was infused to increase mean arterial pressure by at least 20%. A 20-minute hypertensive steady state was obtained. Labetalol at 0.5 and 1.0 mg/kg was randomly infused, followed by a 2.0 mg/kg dose, each over 1 minute. A 20-minute recovery period followed every labetalol infusion, allowing the hypertensive steady state to reestablish. External iliac and uterine blood flow measurements were continuously recorded during the baseline and experimental trials. Mean arterial blood pressure, heart rate, pulmonary artery and capillary wedge pressure, central venous pressure, and cardiac output were obtained at 5, 10, and 15 minutes during each steady state and after each labetalol infusion. Labetalol at all dosages significantly reduced the mean arterial pressure and the systemic vascular resistance at 1.0 and 2.0 mg/kg. External iliac blood flow was not consistently significantly reduced; however, uterine blood flow was significantly reduced after the 1.0 and 2.0 mg/kg labetalol dosages (p < 0.05). Although uterine vascular resistance tended to increase after the 1.0 and 2.0 mg/kg doses, statistical significance was not achieved. Low-dose labetalol (0.5 mg/kg) significantly reduces the pharmacologic hypertensive gravid baboon's mean arterial blood pressure without adversely affecting uterine blood flow.