Pulmonary artery pressure

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. 

Primary pulmonary hypertension is a disease of unclear etiology that is characterized by abnormally high mean pulmonary arterial pressures, in the absence of a demonstrable cause. A wide variety of pulmonary and cardiac diseases can lead to secondary pulmonary hypertension. 

A pulmonary artery (Swan-Ganz) catheter can be used to determine central venous pressure (CVP) pulmonary artery pressure CO and pulmonary artery occlusive pressure (PAOP), an approximate measure of the left ventricular end-diastolic volume and a major determinant of left ventricular preload. 

Vasopressin causes vasoconstrictive effects that, unlike adrenergic receptor agonists, are preserved during hypoxia and severe acidosis. It also causes vasodilation in the pulmonary, coronary, and selected renal vascular beds that may reduce pulmonary artery pressure and preserve cardiac and renal function. However, based on available evidence, vasopressin is not recommended as a replacement for norepinephrine or dopamine in patients with septic shock but may be considered in patients who are refractory to catecholamine vasopressors despite adequate fluid resuscitation. If used, the dose should not exceed 0.01 to 0.04 units/min. 

Chronic theophylline use in COPD has been shown to produce improvements in lung function, including vital capacity and FEVj. Subjectively, theophylline has been shown to reduce dyspnea, increase exercise tolerance, and improve respiratory drive. Nonpulmonary effects that may contribute to better functional capacity include improved cardiac function and decreased pulmonary artery pressure. 

Fig. 6.3 Hemodynamic profile of CAS 1609 on anesthetised dog (0.3mgkg 1 i.v.) systolic blood pressure (BPs), diastolic blood pressure (BPd), left ventricular end diastolic pressure (LVEDP), diastolic pulmonary artery pressure (PAPd), heart rate (HR), left ventricular...

Respiratory System. Tidal volume, bronchial resistance, compliance, pulmonary arterial pressure, blood gases. 

Hemodynamic effects - Digoxin produces hemodynamic improvement in patients with heart failure. Short- and long-term therapy with the drug increases cardiac output and lowers pulmonary artery pressure, pulmonary capillary wedge pressure, and systemic vascular resistance. 

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. 

Ibutilide has no significant effects on cardiac output, mean pulmonary arterial pressure, or pulmonary capillary wedge pressure in patients with or without compromised ventricular function. 

Assess for a fherapeuf ic response as evidenced by decreased chest pain, dyspnea on exertion, fatigue, pulmonary arterial pressure, pulmonary vascular resistance, and syncope, and improved pulmonary function... 

Report signs of increased pulmonary artery pressure, such as dyspnea, cough, or chest pain... 

Carvedilol significantly reduces systemic blood pressure, pulmonary artery pressure, right atrial pressure, systemic vascular resistance, and heart rate, while stroke volume index is increased. 

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. 

Butorphanol tartrate is a weak partial p-receptor agonist, 3.5-5 times as potent as morphine. The incidence of psychotomimetic effects is relatively low. The recommended doses are 1-4 mg intramuscularly every 3-4 h or 0.5-2 mg intravenously. Respiratory depression produced by butorphanol 2 mg IV is similar to that of 10 mg morphine. However, there is a ceiling effect for respiratory depression, and near-maximum depression occurs after 4 mg in normal adults. In healthy volunteers, butorphanol 0.03-0.06 mg-kg-1 produces no significant cardiovascular changes. However, in patients with cardiac disease, progressive increases in cardiac index and pulmonary artery pressure occur, and butorphanol should be avoided in patients with recent myocardial infarction. Butorphanol is metabolised mainly in the liver to inactive metabolites. The terminal half-life is 2.5-3.5 h. 

NO itself can be used therapeutically. Inhalation of NO results in reduced pulmonary artery pressure and improved perfusion of ventilated areas of the lung. Inhaled NO is used for pulmonary hypertension, acute hypoxemia, and cardiopulmonary resuscitation, and there is evidence of short-term improvements in pulmonary function. 

Initial studies of continuous intravenous prostacyclin infusion in patients with primary pulmonary hypertension have shown sustained improvement in pulmonary artery pressure, exercise capacity, and survival compared with... 

There has been a sequential comparison of inhaled nitric oxide 40 ppm with aerosolized iloprost 14— 17 micrograms in 35 adults with primary pulmonary hypertension (125). Five of the patients had minor headache and facial flushing during inhalation of iloprost, but these symptoms were short-lived and abated a few minutes after the inhalation ended. One patient had mild jaw pain after aerosolized iloprost, but again this was shortlived. There was an unexpected increase in pulmonary artery pressure in 10 patients and vascular resistance in six patients who received nitric oxide. The authors were uncertain of the cause of this increase, as nitric oxide generally behaves as a vasodilator, but they noted that... 

Ribeiro PA, al Zaibag M, Abdullah M. Pulmonary artery pressure and pulmonary vascular resistance before and after mitral balloon valvotomy in 100 patients with severe mitral valve stenosis. Am Heart J 1993 125(4) I I 10-1114. 

The activation of SIP receptors reduces renal and mesenteric blood flow in rats (Bischoff et ah, 2001), and it can be speculated that decreased blood flow and hypoxia contribute to the extreme sensitivity of rat kidneys to fumonisins. Fumonisin exposure has also been shown to decrease cardiac output, heart rate, and mean arterial pressure as well as increase pulmonary arterial pressure and pulmonary resistance in pigs (Constable et ah, 2000,2003), findings which suggest that left-sided cardiac insufficiency underlies porcine pulmonary edema. Plasma sphingoid base... 

Cardiac output, pulmonary artery pressure (PAP) and stroke volume are measured by a thermodilution technique using a Cardiac Output Computer (Gould/Statham SP 1245) and a balloon-tip triple lumen catheter (Gould SP 5105, 5F) with the thermistor positioned in the pulmonary artery via the jugular vein. 

PURPOSE AND RATIONALE Measurement of cardiac function and morphology is a key part of the preclinical evaluation of experimental medicinal compounds. Blood pressure, heart rate, and electrocardiogram evaluation are part of the core portfolio of safety pharmacology studies carried out in conscious telemetry dogs. If results from the core battery of tests raise concern then supplemental studies are conducted to measure endpoints such as left ventricular pressure, pulmonary arterial pressure, heart rate variability, baroreflex, cardiac output, ventricular contractility and vascular resistance. However, many... 

Nitric oxide, a precursor of nitrogen dioxide, occurs naturally in the human body, where it acts as endothelial derived relaxing factor (EDRF), a neurotransmitter, and in unidentified ways in the nose, sinuses, and lower airways. Up to 15 ppm can be found normally in the nose and sinuses (DuBois et al. 1998). The substrate is 1-arginine, and the enzymes consist of different forms of nitric oxide synthase, which turn arginine into citrulline. Inhaled nitric oxide gas is used at concentrations of up to 50 ppm to decrease pulmonary arterial pressure. Nitric oxide reacts in tissues to form nitrites and nitrates. 

More specific treatment to combat cardiotoxic effects is usually necessary in only a minority of instances in the series reported above (40), five patients (14%) had marked hypotension. Initial low left ventricular filling pressures were corrected within 3 hours by infusion of isotonic saline. Systemic hypotension persisted and was corrected by infusion of sympathomimetic amines. Routine insertion of a pulmonary artery catheter, with continuous monitoring of blood gases, pulmonary arterial pressure, left atrial wedge pressure, and cardiac output have been recommended (40). Volume expansion is suggested for low left atrial pressure,... 

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