- Clinical trials have shown that inhaled nitric oxide is a selective pulmonary vasodilator that is beneficial in the treatment of reversible pulmonary hypertension. By improving perfusion only in ventilated areas of the lung, inhaled nitric oxide may improve oxygenation in patients with acute respiratory distress syndrome or during one-lung ventilation.
- Acute cyanide toxicity is characterized by metabolic acidosis, cardiac arrhythmias, and increased venous oxygen content (as a result of the inability to utilize oxygen). Another early sign of cyanide toxicity is the acute resistance to the hypotensive effects of increasing doses of sodium nitroprusside (tachyphylaxis).
- By dilating pulmonary vessels, sodium nitroprusside may prevent the normal vasoconstrictive response of the pulmonary vasculature to hypoxia (hypoxic pulmonary vasoconstriction).
- Preload reduction makes nitroglycerin an excellent drug for the relief of cardiogenic pulmonary edema.
- Hydralazine relaxes arteriolar smooth muscle, causing dilatation of precapillary resistance vessels via increased cyclic guanosine 3’,5’-monophosphate.
- The body reacts to a hydralazine-induced fall in blood pressure by increasing heart rate, myocardial contractility, and cardiac output. These compensatory responses can be detrimental to patients with coronary artery disease and are minimized by the concurrent administration of a β-adrenergic antagonist.
- Fenoldopam mesylate (infusion rates studied in clinical trials range from 0.01-1.6 mcg/kg/min) reduces systolic and diastolic blood pressure in patients with malignant hypertension to an extent comparable to nitroprusside.
- Dihydropyridine calcium channel blockers preferentially dilate arterial vessels, often preserving or increasing cardiac output.
A multitude of drugs are capable of lowering blood pressure, including volatile anesthetics, sympathetic antagonists and agonists, calcium channel blockers, β-blockers, and angiotensin-converting enzyme inhibitors. This chapter examines agents that may be useful to the anesthesiologist for intraoperative control of arterial blood pressure.
Patients with an increasing “vascular age” routinely present for anesthesia and surgery. As patients chronologically age, so too does their vasculature. When a pulse wave is generated by ventricular contraction, it is propagated through the arterial system. At branch points of the aorta, the wave is reflected back toward the heart. In patients of young vascular age, the reflected wave tends to augment diastole, improving diastolic pressure. In patients with “older” vasculature, the wave arrives sooner, being conducted back by the noncompliant vasculature during late systole, which causes an increase in cardiac workload and a decrease in diastolic pressure (Figure 15-1). Thus, older patients develop increased systolic pressure and decreased diastolic pressure.
Illustration of the influence of increased vascular stiffness on peripheral (radial) and central (aortic) pressures. Note the similarity of peripheral radial pressures in individuals with normal (lower left panel) and increased (upper left panel) vascular stiffness. In young individuals with normal vascular stiffness, central aortic pressures are lower than radial pressures (lower panels). In contrast, in older individuals with increased vascular stiffness, central aortic pressures are increased and can approach or equal peripheral pressures as a result of wave reflection and central wave augmentation during systole (top panels). (Reproduced, with ...