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Pulmonary pressures

Pulmonary pressures. Changes in thoracic volume and lung volume cause pressures within the airways and the pleural cavity to change. These pressure changes create the pressure gradients responsible for airflow in and out of the lungs. Four pressures must be considered (see Figure 17.1) ... [Pg.244]

Vascular changes include thickening of pulmonary vessels that may lead to endothelial dysfunction of the pulmonary arteries. Later, structural changes increase pulmonary pressures, especially during exercise. In severe COPD, secondary pulmonary hypertension leads to right-sided heart failure (cor pulmonale). [Pg.935]

Aerosol Use of aerosolized ribavirin in patients requiring mechanical ventilator assistance should be undertaken only by health care providers and support staff familiar with the specific ventilator being used and this mode of administration of the drug. Pay strict attention to procedures that have been shown to minimize the accumulation of drug precipitate that can result in mechanical ventilator dysfunction and associated increased pulmonary pressures. [Pg.1771]

Both somatostatin and octreotide cause transient increases in mean arterial pressure and mean pulmonary pressure when given intravenously to patients with cirrhosis, more marked with bolus administration than with continuous infusion (5). This may be either direct or mediated by inhibition of gut vasodilatory peptides (SEDA-24, 505 6) and is not usually associated with significant clinical effects. [Pg.503]

Treatment still remains difficult, because few clinical studies are available. High doses of calcium antagonists are recommended, but their frequent side effects have to be taken into account, particularly with a cardiac output of <2 1/min. (146) In severe cases, pulmonary pressure reduction by permanent infusion of epoprostenol over several weeks or long-term administration of oxygen may be helpful. Good experience has been made with the endothelin-receptor antagonist bosentan (2 x 125 mg/day). (36) (s. p. 338 )... [Pg.736]

The elevated pulmonary artery pressures are attributed to vasoconstriction (in response to chronic hypoxemia), vascular remodeling, and loss of pulmonary capillary beds. If elevated pulmonary pressures are sustained, cor pulmonale can develop, characterized by hypertrophy of the right ventricle in response to increases in pulmonary vascular resistance. [Pg.541]

Pulmonary edema may result from the failure of any of a number of homeostatic mechanisms. The most common cause of pulmonary edema is an increase in capillary hydrostatic pressure because of left ventricular failure. Excessive fluid administration in compensated and decompensated heart failure patients is the most frequent cause of iatrogenic pulmonary edema. Besides hydrostatic forces, other homeostatic mechanisms that may be disrupted include the osmotic and oncotic pressures in the vasculature, the integrity of the alveolar epithelium, interstitial pulmonary pressure, and the interstitial lymph flow. The edema fluid in cardiogenic pulmonary edema contains a low amount of protein, whereas noncardiogenic pulmonary edema fluid has a high protein concentration. This indicates that noncardiogenic pulmonary edema results primarily from disruption of the alveolar epithehum. The reader is referred to Chap. 28 for a detailed discussion of this topic. [Pg.582]

Metaraminol is contraindicated for use in patients who have compromised renal function, a CNS dysfunction, or head trauma. It may also be contraindicated in patients who have emphysema or congestive heart failure, as constriction of the pulmonary vessels can occur, resulting in elevated pulmonary pressure and pulmonary edema. [Pg.97]

Epi increases arterial and venous pulmonary pressures. Although direct pulmonary vasoconstriction occurs, redistribution of blood from the systemic to the pulmonary circulation, due to... [Pg.153]

For further evaluation, selected compounds are submitted to a dog assay (117,118) in which the prostaglandin is administered by aerosol to an anesthetized pilocarpine bronchoconstricted dog (n=3 to 6) and the decrease in airway resistance is recorded at the same time effects on the cardiovascular system (femoral pressure, pulmonary pressure, heart rate) are noted. This experiment is allowed to proceed for one hour, which also permits an assessment of the compound s ability to produce a prolonged bronchodilation. In this assay salbutamol maintains its effect for the entire hour, whereas isoproterenol and 1-PGEi lose theirs within the first twenty minutes. At the conclusion of the study a standard dose of isoproterenol is administered to determine the animal s maximum capacity to respond. [Pg.336]

Mixed form—weakened muscle and dilated ventricular walls that are unable to relax resulting in poor ejection fraction (< 35 percent), high pulmonary pressures, and biventricular failure... [Pg.208]

Benito S, Lemaire E. Pulmonary pressure-volume relationship in acute respiratory distress syndrome in adults role of positive and expiratory pressure. J Crit Care 1990 5 27-34. [Pg.24]

Regardless of whether a ventilator uses positive pressure or negative pressure, the trans-pulmonary pressure gradient determines the tidal volume. A ventilator that is a pressure controller delivers a preset pressure and this variable is unaffected by changes in limg compliance or resistance. A positive pressure ventilator applies pressure inside the chest to expand it using a noninvasive interface, or an artificial airway. [Pg.232]

Another common problem is early right heart failure following transplantation because of elevated pulmonary resistance in the recipient. The right ventricle of the donor is not adapted to this elevated pulmonary pressure and is therefore not able to function effectively (Klima et al. 2005). [Pg.23]

Figure 4 A beagle dog was anesthetized with thyamylal sodium (Surital) and intubated. The tidal volume, pulmonary artery pressure, lung resistance, dynamic compliance, trans-pulmonary pressure, and airflow are shown before and following administration of 14 breaths of an irritant. Laurie acid was heated, in a La Mer-type condensation generator (19), the vapor was condensed in a cold trap operated below 0°C. The response was due to the small particles and any vapors that were not deposited in this trap. This aerosol-vapor was administered for 14 breaths, using a time-controlled series of soleniod valves and thus only transpulmonary pressure and arterial pressure are displayed during the challenge. Figure 4 A beagle dog was anesthetized with thyamylal sodium (Surital) and intubated. The tidal volume, pulmonary artery pressure, lung resistance, dynamic compliance, trans-pulmonary pressure, and airflow are shown before and following administration of 14 breaths of an irritant. Laurie acid was heated, in a La Mer-type condensation generator (19), the vapor was condensed in a cold trap operated below 0°C. The response was due to the small particles and any vapors that were not deposited in this trap. This aerosol-vapor was administered for 14 breaths, using a time-controlled series of soleniod valves and thus only transpulmonary pressure and arterial pressure are displayed during the challenge.

See other pages where Pulmonary pressures is mentioned: [Pg.243]    [Pg.244]    [Pg.595]    [Pg.119]    [Pg.475]    [Pg.137]    [Pg.618]    [Pg.1762]    [Pg.550]    [Pg.559]    [Pg.145]    [Pg.418]    [Pg.154]    [Pg.81]    [Pg.145]    [Pg.265]    [Pg.1528]   
See also in sourсe #XX -- [ Pg.244 ]




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