News about Health (Part 4)

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Clinical Implications

Thus, it may be that proximal pulmonary arterial changes leading to increased Zc and RF are predominantly the passive consequences of increased mean distending pressure, and that “fixed” proximal pulmonary arterial remodeling plays a minor role in determining RV hydraulic load. Dobutamine therapy increased cardiac output and decreased PVR, without a change in the pattern of PVZ spectrum. This observation is in keeping with experimental observations that dobutamine administration up to 10 ^g/kg/min has no flow-independent pulmonary vascular effect. A dobutamine-induced decrease in PVR probably reflects the flow dependency of this composite variable rather than structural or tone-related changes in the resistive arterioles. zithromax online

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Effects of Pharmacologic Interventions

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Effects of Pharmacologic InterventionsHowever, PVR is known to be insufficient for the evaluation of all the forces that oppose RV ejection, which result from a dynamic interplay among resistance, elastance, and wave reflection. This information is contained in Ppa and flow waves, and can be quantified by a PVZ spectrum calculation. The method provides a measure of hydraulic load by a low-frequency impedance determination (Z1), and by an estimate of compliance and wave reflection using a high-frequency Zc determination, together with the measurement of Fmin and the frequency of phase angle zero crossing. An index of wave RF can be calculated from Z0 and Zc determinations.

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Pharmacologic Interventions

Inhaled NO therapy decreased Ppa and PVR, while Q, HR, and Psa remained unaffected. Z0, Z1; and Zc decreased, while Fmin, phase indexes, and RF were unchanged (Table 2). Epoprostenol therapy decreased PVR and Psa, increased Q, while HR remained unaffected, and decreased Z0, Z1, and Zc, while Fmin, phases indexes, and RF were unchanged (Table 2). Dobutamine therapy increased Q, HR, and Ppa, did not affect Psa, and decreased PVR and Z0, while Z1, Zc, Fmin, and phase indexes remained unaffected (Table 2). Figures 1 to 3 illustrate the typical PVZ spectra modifications observed with each intervention. Source

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Statistical Analysis

The dose of NO had been selected on the basis of findings from previous reports that 10 to 20 ppm allows the maximum possible pulmonary vasodilation in PAH patients. NO was supplied from a pure NO source tank (Oxhydrique; Machelen, Belgium) and was delivered through a tight facemask. The inspired fraction of NO was monitored by chemiluminescence after calibration against a standard NO concentration (42 chemi-luminescence NO-NO2-Nox analyser; Thermo Environmental Instruments Inc; Franklin, MA). The dose of epoprostenol conformed to standard practice at the initiation of long-term continuous IV epoprostenol therapy. The dose of dobutamine was selected on the basis of experimental data showing that this inotropic drug is without flow-independent pulmonary vascular effects at doses of up to 10 ^g/kg/min. natural breast enlargement cream

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Protocol

Ppa and flow signals were recorded after the pulmonary catheter was then carefully withdrawn to position its tip just above the pulmonary valve, as close as possible to the pulsed Doppler pulmonary artery flow-velocity sampling site. The signals were visually checked for quality, and then were synchronized by an ECG artifact and recorded on paper at a speed of 100 mm/s using the built-in printing system of the echocardiograph. Pressure and flow-velocity tracings were scanned (Scanjet 4470c; Hewlett Packard), digitized at a sampling rate of 200 Hz, and analyzed on a personal computer. Between three and five heartbeats were used for the analysis during each data collection period. For each patient, a series of thermodilution cardiac outputs and concomitant average Doppler flow velocities were used to calculate a conversion factor for the flow-velocity tracings into volume flow. Link

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Right Heart Catheterization

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Right Heart CatheterizationRight heart catheterization was performed without premedication, with the patient lying supine and breathing room air. A balloon-tipped, flow-directed thermodilution 7F Swan-Ganz catheter (131HF7; Baxter Healthcare Corp; Irvine, CA) was inserted under local anesthesia into an internal jugular vein and was floated under continuous pressure-wave monitoring into a pulmonary artery to measure Ppa, pulmonary artery occluded pressure (Ppao), right atrial pressure (Pra), and cardiac output (Q). Systemic arterial pressure (Psa) was determined intermittently by an automated BP cuff. Heart rate (HR) was determined from a continuously monitored ECG lead. Pulmonary vascular pressures were measured using disposable transducers (TruWave; Baxter Healthcare Corp) connected to a bedside hemodynamic and ECG monitoring system (Sirecust 404; Siemens; Erlangen, Germany). The pressure transducers were zero-referenced at midchest, and vascular pressures were obtained at end-expiration. The static calibration was checked against a water column, and the dynamic response of the catheter-manometer system was checked using the “fast flush” test. Cardiac output was measured using the thermodilution technique as a mean of at least three successive measurements (COM-2; Baxter Healthcare Corp). The pulmonary vascular pressure signals were sampled at 200 Hz using an analog/digital converter (DAS 8-PGA; Keithley-Metrabyte; Taunton, MA), and were stored and analyzed on a personal computer.

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension: Materials and Methods

There are only a few previous studies, on PVZ in PAH patients. This is to be explained by the technical difficulties of instantaneous pressure and flow measurements requiring high-fidelity, manometer-tipped catheters and flowmeters. It has been generally assumed that the frequency response of the fluid-filled thermodilution Swan-Ganz catheters that are used for routine right heart catheterizations would be insufficient for instantaneous pressure measurements but would be acceptable for mean pressure estimations. On the other hand, flow measured by thermodilution using these catheters necessarily covers several cardiac cycles, imposing the steady flow hemodynamic approach. However, the natural frequency of commercially available Swan-Ganz catheters is around 30 Hz, decreasing to only 18 to 20 Hz for the external manometer-tubing-pulmonary catheter system, which actually may be adequate for valid and clinically relevant pressure wave measurements. Instantaneous pulmonary artery flow velocities can be measured by transthoracic pulsed Doppler echocardiography. type two diabetes medications

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary Hypertension

Feasibility of Routine Pulmonary Arterial Impedance Measurements in Pulmonary HypertensionRight heart catheterization with measurements of pulmonary vascular pressures and cardiac output, and the calculation of pulmonary vascular resistance (PVR) is an essential step in the diagnosis of pulmonary arterial hypertension (PAH). These hemodynamic measurements are of prognostic value, with, however, survival being more closely related to flow (cardiac output) than to pressure (ie, pulmonary artery pressure [Ppa]). The clinical state of PAH patients, as assessed by functional class and exercise capacity, also appears to be more related to cardiac output than to Ppa. Clinical signs of right heart failure are often not clearly related to the progression of pulmonary hypertension, as assessed by Ppa and PVR. These observations may be explained by the fact that heart failure in patients with PAH is the consequence of increased right ventricular (RV) afterload, which is not accurately measured by routine hemodynamic evaluations. fully
Ventricular afterload can be defined either by maximum wall tension or by hydraulic load. The measurement of RV wall tension is problematic because of particular geometry and associated volume measurement uncertainties. However, hydraulic load can be assessed from the morphology of Ppa and flow waves. At a given level of PVR, RV hydraulic load may be increased by a decrease in pulmonary arterial compliance and an increase in wave reflection. These changes affect pressure waves by an increased pulse pressure and late systolic peaking, and they affect flow waves by a shortened acceleration time and by late or midsystolic deceleration. There are data indicating that Ppa and wave qualitative morphology analysis may be of diagnostic and prognostic value in patients with pulmonary hyper-tension.

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Summary

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: SummaryAn abnormality in alveolar repair would also preclude the necessity of continued superimposed inflammation to drive alveolar remodeling; the lack of an essential role for inflammation in the pathogenesis has been proposed by Selman et al. The ultrastructural findings in feline IPF suggest that the propagation of the disease may be the result of an underlying defect in type II pneumocyte biology. Whether this is due to inherent genetic defect(s) in the affected feline type II cells is currently under investigation. so

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Human disease

The distribution of myofibroblasts in feline IPF are similar to that of the human disease. While myofibroblasts are found in rodent models of pulmonary fibrosis, because of the lack of honeycombing, they lack the relationship with the metaplastic epithelium that is important in the progressive fibrosis of IPF. Uhal et al showed that in human IPF lung there is an increase in the apoptosis of the metaplastic epithelial cells overlying foci of myofibroblast metaplasia. This apoptosis may be mediated by local conversion of native angiotensinogen into angiotensin II, which goes on to mediate apoptosis through the angiotensin receptor subtype AT-i.- Induction of myofibroblasts subjacent to the metaplastic epithelial cells in cats with IPF may create a similar environment of epithelial cell loss. The finding of attenuated epithelial cells overlying the sites of myofibroblast metaplasia implies repair after previous cell loss, the pathogenesis of which may involve the above process. read

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