Pulmonary vascular resistances indices

FIGURE 9 The effects of 80-ppm nitric oxide (NO) inhalation in six patients with transient graft dysfunction after lung transplantation. Pulmonary artery pressure (PAp), pulmonary vascular resistance index (PVRI), and intrapulmonary shunt fraction (Qs/Qt) decreased significantly, while arterial oxygen pressure (PaOi increased. [Adapted and reproduced with permission from Adatia et al. (77).]... 

Administration by inhalation has been explored by Brilli [124], mentioned previously for his work with NONOates. Here he uses one of these same NONOates, DMAEP/NO (see Fig. 8.11), in aerosol form. When administered in an aerosolized state, DMAEP/NO again shows selective pulmonary vasodilation in a porcine model. This is achieved without affecting the systemic vascular resistance index (SVRI) or the cardiac index (Cl). Work from the same year by Adrie et al. [125] compared aerosolized DEA/NO with aerosolized SNP and inhaled NO, in sheep. As the NONOate has a short half-life (2.1 min), it was predicted that this would be a selective pulmonary vasodilator. However, compared with inhaled NO this was not observed, though SNP... 

Figure 2. Effect of various treatments on cardiac index (upper panel) and pulmonary vascular resistance (lower panel). Data adapted from (140).

In a comprehensive comparison of the pharmacokinetics and pharmacodynamics of dextran and etherified starch (8), the effects of etherified starch on the cardiovascnlar system have been delineated. The mean arterial pressnre, central venous pressure, wedge pressure, cardiac index, left ventricular stroke work index, and stroke output aU rise, whereas the pulmonary vascular resistance falls. Oxygen availability to the tissues is improved. The effects of etherified starch on blood viscosity and erythrocjde aggregation, in particular, are more pronounced than with dextran. 

On the premise that phosphodiesterase inhibitors also inhibit the production of cytokines, milrinone has been used in the treatment of nine patients with the systemic inflammatory response sjmdrome and compared with seven patients with congestive heart failure (4). In both groups mikinone significantly altered cardiac index, pulmonary capillary wedge pressure, and left ventricular stroke work index. In the patients with cardiac failure it also reduced systemic vascular resistance index, and the dose of adrenaline had to be increased substantially during milrinone infusion to counteract vasodilatation. 

A 16-year-old boy who took long-term verapamil after a Mustard operation for transposition of the great arteries developed severe congestive heart failure, which did not respond to diuretics. Systemic vascular resistance was increased by 75% and pulmonary vascular resistance by 150% the cardiac index was reduced from 3.0 to 1.8 1/minute/m. Ejection fraction and atrial pressure were unchanged and neurohormonal causes were excluded. The heart failure resolved after withdrawal of verapamil. 

Figure 12 Changes in pulmonary hemodynamic and oxygenation parameters for an ARDS patient before and after aerosolized DETA/NO administration (a) pulmonary vascular resistance (PVR) index, (b) mean pulmonary arterial pressure (PAP), (c) intrapulmonary shunting, and (d) alveolar-arterial oxygen partial pressure gradient (A-aDC>2). The 20-min period of DETA/NO aerosol administration is indicated by ( ). [Adapted from Reference 27 with permission.]...

Pulmonary hypertension is characterized by a chronically elevated pulmonary artery pressure. As described in previous sections of this chapter, under normal conditions, the pulmonary artery pressure has a systolic value of 18 to 25 mm Hg, a diastolic value of 6 to 10 mm Hg, and a mean value ranging from 12 to 16 mm Hg. Pulmonary hypertension exists when the pulmonary artery systolic and mean pressures exceed 30 and 20 mm Hg, respectively. In the disease state, the pressure in the pulmonary artery may fluctuate widely and is often so high that it equals the blood pressure in the systemic arterial bed. As would be expected, pulmonary vascular resistance is also extremely high in patients with pulmonary hypertension. In addition, patients with this disease exhibit an enlarged right ventricle and an enlargement of the main pulmonary artery and its branches. Systemic hemodynamic parameters, however, such as cardiac output, cardiac index, systemic artery pressure, and pulmonary artery wedge pressure are usually not elevated. 

FIGURE 2 Percentage changes in hemodynamic variables from baseline values during a 15-min administration of inhaled nitric oxide in 100 children with congenital heart disease. There was marked specificity for the pulmonary circulation. HR, Heart rate b, beats Cl, cardiac index BP, mean arterial blood pressure SYR, systemic vascular resistance, mPAP, mean pulmonary artery pressure PVR, pulmonary vascular resistance. 

Patients with left atrial hypertension may have an elevated pulmonary vascular resistance because the cardiac index is low, the pulmonary vasculature is constricted, or there is fixed pulmonary vascular obstructive disease with a reduction in recruitable lung vessels. Peroperative assessment may be aimed at increasing cardiac output with drugs such as dobutamine or by combining vasodilation and an increase in cardiac output with drugs such as nitroprusside or prostacyclin. The use of catecholamines or systemic vasodilators is not without risk, especially in patients with left ventricular outflow tract obstruction, as in two of our patients, or in patients with... 

The IV administration of propafenone is accompanied by an increase in right atrial, pulmonary arterial, and pulmonary artery wedge pressures in addition to an increase in vascular resistance and a decrease in the cardiac index. A significant decrease in ejection fraction may be observed in patients with preexisting left ventricular dysfunction. In the absence of cardiac abnormalities, propafenone has no significant effects on cardiac function. 

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

A 42-year-old woman suffered an acute anterior myocardial infarction, initially associated with pulmonary edema. After hemodjmamic stabilization she was given lisinopril 10 mg oraUy. Two hours later she developed circulatory failure in conjunction with acute renal insufficiency. Right heart catheterization showed markedly reduced systemic vascular resistance but a normal cardiac index. After the usual causes of cardiogenic shock had been ruled out, repeated fluid challenges and intravenous noradrenaline failed to improve her hemodynamic status. She was therefore given angiotensin II intravenously (5-7.5 pg/minute), which immediately and markedly raised the systematic vascular... 

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