Pulmonary artery pressure, reduction

Diuretics have become the cornerstone of all treatment regimens of CHF (III—II3). They can reheve symptoms of pulmonary and peripheral edema. In mild CHF, the thia2ide-type diuretics are adequate unless the GFR falls below 30 ml,/min, as compared to 120 ml,/min in normal subjects. Diuretics improve left ventricular function in CHF due in part to decrease of preload. Indapamide has been shown to cause reduction of pulmonary arterial pressure and pulmonary wedge pressure. 

There is a dose-dependent decrease in systemic blood pressure during isoflurane anaesthesia. This is mainly the result of a marked reduction in peripheral vascular resistance. In contrast, the decrease in arterial blood pressure during halothane anaesthesia appears to be mainly the result of a reduction in myocardial contractility. Isoflurane, in common with other volatile agents, has little effect on pulmonary artery pressure or pulmonary vascular resistance. 

Injection into the left ventricle or the proximal aorta is likely to produce more marked effects. Cardiac rate, stroke volume, and cardiac output increase. There is a rise in right and left atrial pressures and left ventricular end-diastolic pressure. The pulmonary arterial pressure is also increased. The blood volume expands and peripheral blood flow increases and then decreases as systemic resistance falls. The hematocrit falls and venous pressure gradually rises. As the systemic arterial pressure falls, the heart rate increases. These responses are largely due to the injection of strongly hypertonic solutions, which promote a rapid expansion of the plasma volume water shifts from the extravascular fluid spaces to the blood and moves out of the erythrocytes, which shrink and become crenated. Blood viscosity rises, but plasma viscosity does not increase significantly. The erythrocytes give up potassium to the plasma and this might contribute to the observed reduction in peripheral vascular resistance. 

Milrinone is a phosphodiesterase type III/IV inhibitor that has vasodilatory properties and increases the force of contraction and velocity of relaxation of cardiac muscle. Milrinone has not been evaluated fully in the equine clinical setting. It produces a dose-dependent increase in heart rate, cardiac output, arterial blood pressure and ejection fraction and a reduction in right atrial, pulmonary artery pressures and systemic vascular resistance in normal anesthetized horses (Muir 1995). These changes persisted for 30 min after the termination of a constant i.v. infusion of milrinone. 

Direct vascular smooth-muscle relaxants evaluated in primary pulmonary hypertension include hydralazine, isosorbide dinitrate, and diazoxide. In general, the hemodynamic effects of these drugs include modest reduction in mean pulmonary artery pressure, which parallels a significant reduction in systemic arterial pressure, decreased pulmonary vascular resistance, and increased cardiac output. 

During endogenous release of thromboxane hi, after provoking the heparin-protamine reaction in awake sheep, Fratacci et a/. (1991) confirmed that inhaled NO can act as a selective pulmonary vasodilator. Significant reduction of the peak pulmonary artery pressure (PAP) required an inhaled NO dose of 180 ppm in this study. Furthermore, after indomethacin blockade of arachidonic acid metabolite production, it was shown that inhaled NO still dilated the lung vasculature (Fratacci etal., 1991). Thus, the vasodilatory effect of NO in sheep is independent of prostacyclin release. 

We challenged 12 patients with congenital heart disease and pulmonary hypertension preoperatively in the cardiac catheterization laboratory and nine postoperative patients (after cardiopulmonary bypass) with a 2-min infusion of 10 M acetylcholine into the pulmonary artery. The nine postoperative patients received a 15-min trial of inhaled nitric oxide following the infusion of acetylcholine. The results are shown in Figs. 4 and 5. The decrease in pulmonary artery pressure and resistance in the preoperative patients in response to acetylcholine was markedly attenuated postoperatively. The percentage reductions in pulmonary artery pressure preoperatively were 27% 4% and 9% 2% P < 0.003) postoperatively. Similarly, pulmonary vascular resistance decreased by 46% 5% compared to 11% 4% P < 0.002). However, the response to inhaled nitric oxide in the postoperative patients was marked vasodilation contrasted with the blunted effect of acetylcholine. Mean pulmonary artery pressure (34.4 2.6 versus... 

FIGURE 6 Bedside monitor recording of systemic artery pressure (SAP) and pulmonary artery pressure (PAP) in a 7-month-old child with postoperative pulmonary hypertension refractory to treatment, including hyperventilation with oxygen, anesthesia, alkalosis, nitroprus-side, prostaglandin E, and acetylcholine. Administration of 80-ppm inhaled nitric oxide produced an immediate reduction in PAP, with little effect on SAP. 

These reports are similar to another, in which the tolazoline-induced reduction in pulmonary arterial pressure in a child was reversed when cime-tidine was given, for acute gastrointestinal haemorrhage. Another study in 12 children found that intravenous ranitidine 3 mg/kg abolished the tolazoline-induced reduction in pulmonary and systemic vascular. ... 

Pharmacology The principal pharmacological action of nitrates is relaxation of the vascular smooth muscle and consequent dilation of peripheral arteries and especially the veins. Dilation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload). Dilation of the coronary arteries also occurs. The relative importance of preload reduction, afterload reduction, and coronary dilation remains undefined. 

It is characterized by severe, persisting pain, shock and hypotension with possible development of arrhythmias and is due to severe depression of systolic cardiac performance, systolic arterial pressure is below 80 mm Hg, low cardiac index, ventricular filling pressure is elevated and pulmonary edema may or may not be evident. The most frequent cause is infarction involving more than fourty percent of the left ventricular myocardiam, leading to a severe reduction in left ventricular contractility contradictively and failure of the left ventricular pump. 

Continuous hemodynamic monitoring is essential during all phases of hypothermia. Cardiac monitoring is necessary because of the increased risk of arrhythmias. Cardiac output is decreased 5% for every 1°C of body temperature reduction. This is thought to be secondary to bradycardia, which has been shown to occur with hypothermia (3). A pulmonary artery catheter may be placed if there is any question of hemodynamic instability. Arterial catheters are used for continuous blood pressure measurement, as well as for access to arterial blood for blood gas and electrolyte analysis. 

Nesiritide is a human B-type natriuretic peptide, which binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells, leading to dose-dependent reductions in pulmonary capillary wedge pressure and systemic arterial pressure in patients with heart failure. It is indicated in the treatment of patients with acutely decompensated CHF who have dyspnea at rest or with minimal activity. 

FIGURE 10 Effects of nitric oxide (NO) inhalation on pulmonary artery (PA) pressure (PAp) and trapulmonary shunt fraction (Qs/Qt) in one patient during the first 36 hr after lung transplantation. PAp and Qs/Qt improved with NO and deteriorated during reductions in the NO dose. [Reproduced with permission from Adatia et al. (77).]... 

In 9 healthy subjects, oral indometacin 50 mg every 6 hours for 4 doses abolished the hypotensive response to intravenous hydralazine 150 mierograms/kg, and the subjects only responded when given another dose of hydralazine 30 minutes later. A study in 7 patients with pulmonary hypertension given indometacin 50 mg and hydralazine 350 mierograms/kg, both intravenously, either alone, or concurrently, also found that the effects of hydralazine (reduction in systemic arterial pressure, heart rate, cardiac index) were reduced by indometacin. In contrast, another study in 9 healthy subjects found that oral indometacin 25 mg four times daily for 2.5 days did not affect the hypotensive response to a single 200-mierogram/kg intravenous dose of hydralazine. 

The most common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases, or abnormalities in the blood oncotic pressure. Salt and water retention with edema formation often occurs when diminished blood delivery to the kidney is sensed as insufficient "effective" arterial blood volume. Judicious use of diuretics can mobilize interstitial edema fluid without significant reductions in plasma volume. However, excessive diuretic therapy in this setting may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying condition. 

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