Central Venous Pressure In Patients Research Articles

Vascular pedicle width in acute lung injury: correlation with intravascular pressures and ability to discriminate fluid status

IntroductionConservative fluid management in patients with acute lung injury (ALI) increases time alive and free from mechanical ventilation. Vascular pedicle width (VPW) is a non-invasive measurement of intravascular volume status. The VPW was studied in ALI patients to determine the correlation between VPW and intravascular pressure measurements and whether VPW could predict fluid status.MethodsThis retrospective cohort study involved 152 patients with ALI enrolled in the Fluid and Catheter Treatment Trial (FACTT) from five NHLBI ARDS (Acute Respiratory Distress Syndrome) Network sites. VPW and central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) from the first four study days were correlated. The relationships between VPW, positive end-expiratory pressure (PEEP), cumulative fluid balance, and PAOP were also evaluated. Receiver operator characteristic (ROC) curves were used to determine the ability of VPW to detect PAOP <8 mmHg and PAOP ≥18 mm Hg.ResultsA total of 71 and 152 patients provided 118 and 276 paired VPW/PAOP and VPW/CVP measurements, respectively. VPW correlated with PAOP (r = 0.41; P < 0.001) and less well with CVP (r = 0.21; P = 0.001). In linear regression, VPW correlated with PAOP 1.5-fold better than cumulative fluid balance and 2.5-fold better than PEEP. VPW discriminated achievement of PAOP <8 mm Hg (AUC = 0.73; P = 0.04) with VPW ≤67 mm demonstrating 71% sensitivity (95% CI 30 to 95%) and 68% specificity (95% CI 59 to 75%). For discriminating a hydrostatic component of the edema (that is, PAOP ≥18 mm Hg), VPW ≥72 mm demonstrated 61.4% sensitivity (95% CI 47 to 74%) and 61% specificity (49 to 71%) (area under the curve (AUC) 0.69; P = 0.001).ConclusionsVPW correlates with PAOP better than CVP in patients with ALI. Due to its only moderate sensitivity and specificity, the ability of VPW to discriminate fluid status in patients with acute lung injury is limited and should only be considered when intravascular pressures are unavailable.

Effect of catheter site on the agreement of peripheral and central venous pressure measurements in neurosurgical patients

Study Objective Previous studies suggest a correlation of central venous pressure (CVP) with peripheral venous pressure (PVP) in different clinical setups. The aim of this study was to investigate the effect of measurement site on PVP and its agreement with CVP in patients undergoing general anesthesia. Design Prospective randomized study. Settings University hospital. Patients Thirty patients of American Society of Anesthesiologists physical status I and II undergoing elective craniotomy. Interventions Patients were randomly assigned into Group A (antecubital; n = 15) and Group D (dorsum hand; n = 15) for antecubital and hand dorsum catheterization sites, respectively. Central venous pressure and PVP were monitored throughout the study. A total of 1925 simultaneous measurements were recorded at 5-minute intervals. Bland-Altman assessment for agreement was used for CVP and PVP in 2 groups. Measurements Peripheral venous pressure measurements were within the range of ±2 mm Hg of CVP values, in 93.9% of the measurements in Group A, and in 91.2% of the measurements in Group D. Considering all measurements, mean bias was −0.072 mm Hg (95% CI, −0.134 to −0.010). Group A measurements showed a bias (CVP-PVP) of 0.173 ± 3.557 mm Hg, whereas the bias was −0.122 ± 4.322 mm Hg (mean ± SD corrected for repeated measurements) in Group D. All of the measurements were within mean ± 2SD of bias, which means that PVP and CVP are interchangeable in our clinical setting. Conclusion Peripheral venous pressure measurement may be a noninvasive alternative for estimating CVP in patients undergoing elective neurosurgical operations. Measuring PVP from hand dorsum does not interfere with the agreement of CVP and PVP.

Goal-Directed Therapy of Cardiac Preload in Induced Whole-Body Hyperthermia

To optimize volume therapy during induced whole-body hyperthermia (WBH) < or = 42.2 degrees C, pulmonary capillary wedge pressure (PCWP) and intrathoracic blood volume index (ITBVI) were compared as goal parameters. Prospective clinical study. ICU at university hospital. Twenty-three patients with metastatic cancers. Radiant WBH in combination with induced hyperglycemia, hyperoxemia, and chemotherapy was applied. Volume therapy was directed to the PCWP (group A, 8 to 12 mm Hg [20 treatments]), or to ITBVI (group B, 800 to 1,100 mL/m2 [19 treatments]) following a standardized protocol. Goals other than PCWP and ITBVI were cardiac index of > 3.5 L/min/m2 and mean arterial pressure of > 55 mm Hg. In addition to the primary goals PCWP and ITBVI, at defined temperatures, central venous pressure (CVP), extravascular lung water index, the number of infusions, and packed RBCs, as well as serum lactate level, norepinephrine dosage, and levels of liver enzymes, bilirubin, creatinine, and urea were measured. Patients in group A received a significantly greater mean (+/- SD) amount of crystalloids compared to those in group B (6,175 +/- 656 vs 3,947 +/- 375 mL, respectively) and required significantly lower dosages of vasoconstrictors compared with patients in group B. Except for the lower values of CVP in patients in group A during hyperthermia, all of the other hemodynamic and laboratory parameters showed no significant differences between the groups or stayed in a normal range. PCWP and ITBVI are useful parameters to assess preload in induced WBH. Differences in crystalloids and vasopressor dosages may suggest an appropriate ITBVI of > 1,100 mL/m2 for patients with good cardiopulmonary health under such extremely hypercirculatory conditions.

Effect of Body Temperature on Peripheral Venous Pressure Measurements and Its Agreement with Central Venous Pressure in Neurosurgical Patients

Previous studies suggest a correlation of central venous pressure (CVP) with peripheral venous pressure (PVP) in different clinical settings. The effect of body temperature on PVP and its agreement with CVP in patients under general anesthesia are investigated in this study. Fifteen American Society of Anesthesiologists I-II patients undergoing elective craniotomy were included in the study. CVP, PVP, and core (Tc) and peripheral (Tp) temperatures were monitored throughout the study. A total of 950 simultaneous measurements of CVP, PVP, Tc, and Tp from 15 subjects were recorded at 5-minute intervals. The measurements were divided into low- and high-Tc and -Tp groups by medians as cutoff points. Bland-Altman assessment for agreement was used for CVP and PVP in all groups. PVP measurements were within range of +/-2 mm Hg of CVP values in 94% of the measurements. Considering all measurements, mean bias was 0.064 mm Hg (95% confidence interval -0.018-0.146). Corrected bias for repeated measurements was 0.173 +/- 3.567 mm Hg (mean +/- SD(corrected)). All of the measurements were within mean +/- 2 SD of bias, which means that PVP and CVP are interchangeable in our setting. As all the measurements were within 1 SD of bias when Tc was > or = 35.8 degrees C, even a better agreement of PVP and CVP was evident. The effect of peripheral hypothermia was not as prominent as core hypothermia. PVP measurement may be a noninvasive alternative for estimating CVP. Body temperature affects the agreement of CVP and PVP, which deteriorates at lower temperatures.

Comparison of pulmonary artery and central venous pressure waveform measurements via digital and graphic measurement methods

Background: Techniques to measure pulmonary artery (PA) pressure waveforms include digital measurement, graphic measurement, and freeze-cursor measurement. Previous studies reported the inaccuracy of digital and freeze-cursor measurements. However, many of the previous studies were small and did not thoroughly examine the circumstances of when digital measurements might be inaccurate. Objectives: To compare digital measurements and graphic measurements of PA and central venous pressure (CVP) waveforms in patients with a variety of respiratory patterns, and to compare digital measurements and graphic measurements of CVPs in patients with abnormal or right ventricular waveforms. Methods: A total of 928 patients were enrolled in this study. Waveforms from the PA and CVP were collected from each patient. The monitor pressure value (digital measurement) printed on the recorded waveform was compared with the pressure value obtained by a graphic strip recording and measured by one of the primary investigators (graphic measurement). Results: Digital measurements were found to be inaccurate in measuring waveforms in all respiratory categories and in measuring right ventricular waveforms. PA diastolic values and CVP values were the most inaccurately measured waveforms. Digital errors of more than 4 mm Hg were common. Conclusion: There were instances in which the monitor’s digital measurement was substantially different from the graphically measured value. This difference has the potential to mislead interpretation of clinical situations. The monitor’s ability to occasionally give digital measurement values similar to the graphic measurements may lead to a false sense of security in clinicians. Because the accuracy of the monitor is inconsistent, the bedside clinician should interpret waveforms through use of a graphic recording rather than rely on the digital measurement on the monitor. (Heart Lung® 2001;30:26-38.)

Therapy of acute heart failure, medicamentous strategy

The leading pathophysiology of acute heart failure and cardiogenic shock is acute or subacute myocardial infarction. Reperfusion of the occluded coronary vessel accompanied by adequate support of cardiac function via assist systems, preferentially the intraaortic balloon counterpulsation, is the therapy of choice. Adjustment of preload (high pulmonary capillary pressure in-acute myocardial infarction with small heart, low pulmonary capillary wedge pressure in patients with large ventricles and chronic heart failure, high central venous pressure in patients with right heart failure, and right ventricle myocardial infarction) and afterload (peripheral arterial vasodilatation, recommended systolic arterial pressure 80-90 mm Hg) but not maximization of cardiac output play an important role. Positive inotropic drugs should be considered when these strategies fail. In acute right heart failure in pulmonary hypertension, a preferential pulmonary vasodilatation with intravenous or inhalative prostaglandins or inhalative NO are of utmost importance. Systemic hypotension is not a contraindication in this pathophysiology.

Elevation of superior vena caval pressure increases extravascular lung water after endotoxemia.

In many sheep Escherichia coli endotoxin results in pulmonary hypertension, increased microvascular permeability, pulmonary edema, and increased central venous pressure. Since lung lymph drains into the systemic veins, increases in venous pressure may impair lymph flow sufficiently to enhance the accumulation of extravascular fluid. We tested the hypothesis that, following endotoxin, elevating the venous pressure would increase extravascular fluid. Thirteen sheep were chronically instrumented with catheters to monitor left atrial pressure (LAP), pulmonary arterial pressure (PAP), and superior vena caval pressure (SVCP) as well as balloons to elevate LAP and SVCP. These sheep received 4 micrograms/kg endotoxin, and following the pulmonary hypertensive spike the left atrial balloon was inflated so that (PAP + LAP)/2 = colloid osmotic pressure. It was necessary to control PAP + LAP in this way to minimize the sheep-to-sheep differences in the pulmonary hypertension. We elevated the SVCP to 10 or 17 mmHg or allowed it to stay low (3.2 mmHg). After a 3-h period, we killed the sheep and removed the right lungs for determination of the extravascular fluid-to-blood-free dry weight ratio (EVF). Sheep with SVCP elevated to 10 or 17 mmHg had significant increases in EVF (5.2 +/- 0.1 and 5.6 +/- 1.2) compared with the sheep in which we did not elevate SVCP (EVF = 4.5 +/- 0.4). These results indicate that sustained elevation in central venous pressure in patients contributes to the amount of pulmonary edema associated with endotoxemia.

Cardiovascular function in shock. Responses to volume loading and isoproterenol infusion.

Hemodynamic responses to volume loading with infusion of dextran-40 and myocardial stimulation with isoproterenol in 23 patients in shock from hemorrhage, trauma, or sepsis, and 10 healthy controls were studied. Responses of the control were moderate to dextran and marked to isoproterenol. Shock patients were divided into three groups according to the response of the cardiac index to dextran-40: group I, &gt;50% increase; group II, 15 to 50% increase; group III, &lt;15% increase or a decrease. The central venous pressure of patients who responded to dextran (group I) generally rose moderately and that of those who failed to respond (group III) increased without improvement of cardiac index or stroke index, suggesting myocardial failure. Group II showed cardiac improvement at the expense of marked increase in venous pressure, suggesting relative cardiac insufficiency. Group I failed to respond to isoproterenol infusion, indicating that circulatory failure primarily resulted from failure of venous return. All group III patients responded markedly to isoproterenol. It is concluded that a significant number of patients in shock from hemorrhage, trauma, and sepsis exhibit signs of cardiac insufficiency. The ability of these hearts to respond to isoproterenol suggests that depletion or altered metabolism of endogenous catecholamines in part underlies this insufficiency. Further-more, it is suggested that cardiac insufficiency may contribute to the death of a significant number of patients with severe hemorrhagic and septic shock.