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Hemodynamic parameters

Hemodynamic parameters should be routinely monitored to assess drug tolerance. Assess blood pressure at baseline, after drug initiation and dose titration, then periodically thereafter in patients treated with fk-blockers, CCBs, nitrates, ACE inhibitors, and/or ARBs. [Pg.81]

Pulmonary artery catheter An invasive device used to measure hemodynamic parameters directly, including cardiac output and pulmonary artery occlusion pressure calculated parameters include stroke volume and systemic vascular resistance. [Pg.1575]

When fluid resuscitation is insufficient to maintain tissue perfusion, the use of inotropes and vasoactive drugs is necessary. Selection and dosage are based on the pharmacologic properties of various catecholamines and how they influence hemodynamic parameters (Table 45-5). [Pg.505]

The major difficulty in any functional brain studies is inter-subject comparisons. Essentially, all NIR functional brain studies report high variability between subjects. No true comparison can be made due to relative nature of hemodynamic data. Since path length is unknown under MBLL, it is not possible to assess absolute levels of hemodynamic parameters. Instead, each subject is compared with their own baseline measurements. However, generally speaking, the shape of the time evolution of the signals are similar between subjects and thus can be analyzed using qualitative comparisons. [Pg.363]

In humans, sepsis can follow pulmonary and nonpulmonary infections, and ARDS can occur in either clinical setting (reviewed in ref. 5). Sepsis is defined as the systemic response to a definite or probable tissue infection, and typically includes changes in body temperature, blood leukocyte counts, hemodynamic parameters, and organ function (6). There is an important distinction to be made between bacteremia, defined simply by a positive blood culture, and sepsis, which includes a specific systemic response. Most cases of bacteremia are not associated with clinical evidence of sepsis, and bacteremia by itself is rarely associated with ARDS (7). Rather, it appears that a primary tissue infection is an important requirement for the onset of sepsis in humans, and an important antecedent for ARDS whether or not bacteremia is detectable (8). [Pg.319]

Besides the different directly measured hemodynamic parameters, the following data are calculated according to the respective formulae... [Pg.90]

In each dog, either LVED or LVID is measured together with the other hemodynamic parameters. [Pg.91]

Hemodynamic parameters are recorded continuously during the whole experiment. [Pg.91]

No fatalities agitation, insomnia, increase in hemodynamic parameters... [Pg.314]

During the first two episodes of preconditioning (PC) no change in the hemodynamic parameters of the heart was observed. In some hearts, at the end of the third episode a drop of up to 7% (and an increase in EDP 0.4-0.7 mmHg) was observ ed. Nevertheless, complete recovery was recorded when the perfusion of these hearts was extended beyond 3 min. to -10 min. [Pg.50]

Hemodynamic parameters of hearts subjected to ischemia with and without PC... [Pg.51]

Table 1 depicts the values of several hemodynamic parameters at the end of 20 min reperfusion (as % of the pre-ischemic value), after ischemia of increasing duration (18-60 min). A time-dependent decrease in these parameters was observed for both group I and III (PC+ischemia and the ischemia without PC). Group III hearts, after 35 min ischemia, lost most (60-80%) of their function, while after 45 min the loss was complete. [Pg.51]

PC hearts of group I demonstrated a marked and clear protection of their function against injury following prolonged ischemia (when compared to group III). The residual function after 35 min ischemia was 56-78%, and 21-A9% after 45 min, as indicated by the various hemodynamic parameters. [Pg.51]

Table 1. The hemodynamic parameters of hearts following ischemia and reperflision with or without cardiac preconditioning (PC). The data represent the recovery values (% of the pre-ischemic value). Table 1. The hemodynamic parameters of hearts following ischemia and reperflision with or without cardiac preconditioning (PC). The data represent the recovery values (% of the pre-ischemic value).
Likewise, the hemodynamic effects of DCLHb (an intramolecularly cross-linked human Hb Baxter) in 14 critically ill patients were evaluated in a prospective, observational study. All of the subjects required vasopressor therapy to maintain adequate MAP and had secondary organ dysfunction prior to DCLHb treatment. Following a decision by the investigator to infuse, boluses (100 ml) of DCLHb were given up to a maximum of 500 ml. Each infusion was separated by 60-90 min. Hemodynamic parameters, norepinephrine and inotropic requirements, arterial and mixed venous blood gases, and urine output were monitored, and biochemical and hematological analyses were made before DCLHb administration and at multiple times up to 72 h postadministration. The main end-point employed to assess the efficacy of DCLHb as a vasopressor was maintenance of the MAP at approximately pre-infusion values concomitant with a reduction in norepinephrine requirements. This objective was met, and reductions in norepinephrine requirements were maintained at 24, 48, and 72h p < 0.01 at all time points). Thus, even in these critically ill patients, whose prognosis of survival was very poor, DCLHb seemed to have a beneficial effect. [Pg.362]

Heintz-Bamberg D, Muller H, Dick W, Reiter G. Vergleichende Klinische Untersuchungen zum Verhalten hamodynamischer Parameter be kombinationsnarkosen mit Nalbuphin (Nubain) und Fentanyl. [Comparative clinical studies of the hemodynamic parameters by anesthesia combination with nalbuphine (Nubain) and fentanyl.] Anaesthesist 1987 36(5) 217-22. [Pg.2417]

Table 1. Effect of amphotericin B infusions (0.05 mg/kg/min i.a.) on systemic glomerular hemodynamic parameters. Table 1. Effect of amphotericin B infusions (0.05 mg/kg/min i.a.) on systemic glomerular hemodynamic parameters.
Fig. 6. Extremely high levels of p2-ARs in the heart determine maximal activation of P-AR signaling in basal conditions. Mice overexpressing at very high levels of P2-ARs (TG4, open circle O) and corresponding WT controls (control, closed circle ) were anesthetized, and their hemodynamic parameters were invasively studied (A) dp/ dt max (B) heart rate (C) aortic mean pressure. (Reprinted with permission from ref. 98 1994 A A AS.)... Fig. 6. Extremely high levels of p2-ARs in the heart determine maximal activation of P-AR signaling in basal conditions. Mice overexpressing at very high levels of P2-ARs (TG4, open circle O) and corresponding WT controls (control, closed circle ) were anesthetized, and their hemodynamic parameters were invasively studied (A) dp/ dt max (B) heart rate (C) aortic mean pressure. (Reprinted with permission from ref. 98 1994 A A AS.)...
Measurement of hemodynamic parameters by catheterization. Acute or chronic effects of ischemia/reperfusion or ischemia alone can be studied. The contribution of blood components and neurohormonal changes is considered. Experimental model close to clinical conditions but many confounding factors may be involved when investigating mechanisms. Arrthythmias, hypotension or pulmonary edema can occur during the experimental procedure. [Pg.60]


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See also in sourсe #XX -- [ Pg.48 ]




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Hemodynamics

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