Systemic vascular resistance, normal value

Invasive hemodynamic monitoring usually is performed with a flow-directed pulmonary artery (PA) or Swan-Ganz catheter placed percutaneously through a central vein and advanced through the right side of the heart and into the PA. Inflation of a balloon proximal to the end port allows the catheter to wedge, yielding the PAOP, which estimates the pulmonary venous (left atrial) pressure and, in the absence of intracardiac shunt or mitral valve or pulmonary disease, left ventricular diastolic pressure. Additionally, cardiac output may be measured and systemic vascular resistance (SVR) calculated. Normal values for hemodynamic parameters are listed in Table 14—12. 

ACE Inhibitors in Hypertension ACE inhibition lowers systemic vascular resistance and mean, diastolic, and systolic blood pressures in various hypertensive states see Chapter 32). ACE inhibitors commonly lower blood pressure in hypertensive subjects, except in those with primary aldosteronism. The initial change in blood pressure is most marked in subjects with high PRA and Angll plasma levels prior to treatment. Several weeks into treatment, additional patients show sizable reductions in blood pressure that correlate poorly or not at aU with pretreatment PRA values. It is possible that increased local (tissue) production of Angll and/or increased responsiveness of tissues to normal levels of Angll in some hypertensive patients makes them sensitive to ACE inhibitors despite normal PRA. Regardless of the mechanisms, ACE inhibitors have broad clinical utility as antihypertensive agents. 

An example of this type of reflex is the baroreceptor reflex (see Figure 1.2). Baroreceptors located in some of the major systemic arteries are sensory receptors that monitor blood pressure. If blood pressure decreases, the number of sensory impulses sent from the baroreceptors to the cardiovascular control center in the brainstem also decreases. As a result of this change in baroreceptor stimulation and sensory input to the brainstem, ANS discharge to the heart and blood vessels is adjusted to increase heart rate and vascular resistance so that blood pressure increases to its normal value. 

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. 

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