Disease relevance of Pulmonary Wedge Pressure

• Endpoints for the administration of verapamil were the following: reversion to sinus rhythm; a ventricular rate slower than 100/min; hypotension; a pulmonary capillary wedge pressure rising above 15 mm Hg; signs of intolerance; a maximum dose of 20 mg [1].
• The major mechanisms of the preserved exercise capacity in these patients were chronotropic competence, ability to tolerate elevated wedge pressures (33 +/- 3 mm Hg) without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise [2].
• Compared with patients with sinus rhythm, patients with atrial fibrillation did not differ in etiology of heart failure, mean pulmonary capillary wedge pressure on therapy, or embolic events but were more likely to be receiving warfarin and antiarrhythmic drugs and had a slightly higher left ventricular ejection fraction [3].
• In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit [4].
• The dopamine-dobutamine combination increased mean arterial pressure (p less than 0.05 vs dobutamine), maintained pulmonary capillary wedge pressure within normal limits (p less than vs dopamine), and prevented the worsening of hypoxemia induced by dopamine (p less than 0.05) [5].

High impact information on Pulmonary Wedge Pressure

• A linear relation was found between right atrial pressure and right atrial peptide concentration (r = 0.835, P less than 0.001) and between pulmonary wedge pressure and the systemic arterial peptide concentration (r = 0.866, P less than 0.001) [6].
• In CHF, ANF induced changes in aldosterone and pulmonary wedge pressure, cardiac index, and systemic vascular resistance (all P less than 0.05); however, responses of renin and renal excretion were attenuated [7].
• 2 h after OA, triple indicator-dilution lung liquid volume and pulmonary shunt (Qs/Qt) doubled despite normal pulmonary capillary wedge pressure in 16 dogs compared with dogs not given OA in which no variable change during the same time [8].
• Application of pyruvate resulted in a 23% increase in cardiac index (p<0.05), a 38% increase in stroke-volume index (p<0.05), and a 36% decrease in pulmonary capillary wedge pressure (p<0.05) [9].
• Pulmonary capillary wedge pressure decreased more from baseline to 12 months with metoprolol than with placebo (5 vs 2 mm Hg, p = 0.06) [10].

Chemical compound and disease context of Pulmonary Wedge Pressure

• The hemodynamic responses to esmolol, an ultrashort-acting (t1/2 = 9 min) beta 1-adrenergic receptor antagonist, were examined in 16 patients with myocardial ischemia and compromised left ventricular function as evidenced by a mean pulmonary capillary wedge pressure of 15 to 25 mm Hg [11].
• However, wedge pressure was maintained with isradipine and there was no tachycardia [12].
• In 13 patients with acutely decompensated chronic left ventricular failure, we infused nitroprusside to reduce pulmonary wedge pressure to normal without inducing hypotension [13].
• To determine the mechanism of pulmonary edema, we serially measured in each patient the lung clearance of technetium 99m-diethylenetriamine pentaacetic acid (DTPA) 99mTc-DTPA), the plasma levels of Von Willebrand factor antigen, and the pulmonary capillary wedge pressure (PCWP) [14].
• Pulmonary artery wedge pressure may fail to reflect left ventricular end-diastolic pressure in dogs with oleic acid-induced pulmonary edema [15].

Biological context of Pulmonary Wedge Pressure

• At the highest dose of nitroprusside (66 +/- 41 micrograms/min), cardiac output was significantly improved, whereas PA mean and wedge pressure, resistance, impedance at the first harmonic, characteristic impedance, and wave reflection amplitude were all reduced [16].
• Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently [4].
• The lack of peak flow velocity change during nitroprusside infusion could be explained by either the associated decrease in left ventricular minimal pressure or downward shift of left ventricular diastolic pressure by the same amount as the decrease in pulmonary capillary wedge pressure [17].
• The preservation of cardiac output, with markedly reduced pulmonary wedge pressure, indicated that nicardipine improved ventricular performance in response to reversal of vasoconstriction [18].
• To explore the mechanisms of change of left ventricular diastolic filling associated with preload and afterload reduction, the influence of nitroprusside on the transmitral flow velocity pattern, pulmonary capillary wedge pressure and left ventricular pressure interaction was studied in 11 patients with end-stage heart failure [17].

Anatomical context of Pulmonary Wedge Pressure

• Isradipine produced no significant decreases in pulmonary artery occlusion wedge pressure compared with nitroprusside [19].
• In patients in whom pulmonary vein stents were implanted, mean pressure gradients fell from 11 to 0.3 mm Hg (P = .03), and mean pulmonary capillary wedge pressure fell from 17 to 6.3 mm Hg (P = .03) immediately after stenting [20].
• In addition to red blood cell replacement, either RL or PL was infused (1) to maintain the cardiac output (CO) equal to or greater than the preoperative value, (2) to maintain the pulmonary capillary wedge pressure (PCWP) plus or minus 2 mmHg of preoperative values, and (3) to keep the urinary output greater than or equal to 30 cc/hr [21].
• Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable [22].
• At the same level of pulmonary capillary wedge pressure and similar arterial oxygen tensions extravascular lung water was significantly greater in the group with chronic congestive cardiomyopathy (p less than .05) [23].

Associations of Pulmonary Wedge Pressure with chemical compounds

• In patients receiving a 100-micrograms bolus and a 100-micrograms/h infusion, heart rate, cardiac index, and systemic vascular resistance showed no significant changes, whereas right atrial pressure, pulmonary capillary wedge pressure, and inferior vena cava pressure decreased significantly after octreotide infusion compared with basal values [24].
• After placebo administration, nitroglycerin plasma levels and pulmonary wedge pressure remained unchanged [25].
• Creatine phosphokinase-MB bands, troponin levels, and pulmonary wedge pressure were not elevated [26].
• The increase in stroke volume index was greater with milrinone than with captopril (28 +/- 7 vs 24 +/- 7 ml/m2; p less than .05), while pulmonary capillary wedge pressures fell similarly (19 +/- 10 vs 21 +/- 7 mm Hg) [27].
• Among plasma levels of ANP, BNP, cGMP, and norepinephrine and clinical and hemodynamic parameters, only high levels of plasma BNP (P<.0001) and pulmonary capillary wedge pressure (P=.003) were significant independent predictors of the mortality in patients with CHF by Cox proportional hazard analysis [28].

Gene context of Pulmonary Wedge Pressure

• Both the driving pressure obtained as pulmonary arterial pressure minus wedge pressure and the PaO2 under room air were significantly correlated with the concentrations of IL-6 and TNF-alpha in the BALF [29].
• Cardiac output and pulmonary capillary wedge pressure had a linear correlation with plasma endothelin-1 levels [30].
• In group B, significant correlations were found between the peak of MCP-1 and the peak of C-reactive protein levels (r = 0.55, p < 0.02) as well as wedge pressure (r = 0.40, p < 0.05) [31].
• If this were so, then (1) tachypnea alone, without exercise, should cause the FRC and intracardiac pressures to increase in patients with COPD, (2) there should be an increase in FRC associated with the rise in wedge pressure on exercise, and (3) these changes should not occur in patients without COPD [32].
• RESULTS: There were positive correlations between peak MMP-1 level, and peak creatine kinase value and pulmonary capillary wedge pressure and peak IL-6 level (r = 0.43, r = 0.70, and r = 0.60, respectively) in all patients [33].

Analytical, diagnostic and therapeutic context of Pulmonary Wedge Pressure

• Cardiac catheterization in the 6 patients with CHF revealed severe PHT, increased pulmonary resistance (PVR), and normal capillary wedge pressure [34].
• Hepatic wedge pressures before and after treatment with propranolol were 13 and 7 mm Hg, respectively [35].
• Before and after each fenoldopam dose, thermodilution cardiac output, right atrial pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure (PCWP) were measured with a balloon-tipped pulmonary artery catheter, and heart rates and blood pressures were recorded with an automated sphygmomanometer [36].
• In the atrial fibrillation control group, passive leg elevation increased the mean pulmonary artery wedge pressure (P < 0.01), the mean right atrial pressure (P < 0.05) and plasma concentrations of ANP (139.9 +/- 85.8 vs 168.1 +/- 108.2, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)[37]
• An additional criterion for inclusion in the study was vasopressor support and high-output circulatory failure with a cardiac index of >4 L/min/m2 after fluid resuscitation (pulmonary capillary wedge pressure: 12-15 mm Hg) and without the use of positive inotropes such as dobutamine or dopexamine [38].

References