1256 1257 Coronary blood flow normally parallels myocardial metabolic demand. In the average adult man, coronary blood flow is approximately 250 mL/min at rest. The myocardium regulates its own blood flow closely between perfusion pressures of 50 and 120 mm Hg. Beyond this range, blood flow becomes increasingly pressure dependent. 1258 1259 1260 1261 Under normal conditions, changes in blood flow are entirely due to variations in coronary arterial tone (resistance) in response to metabolic demand. Hypoxia—either directly or indirectly through the release of adenosine—causes coronary vasodilation. Autonomic influences are generally weak. Both α1- and β2-adrenergic receptors are present in the coronary arteries. The α1-receptors are primarily located on larger epicardial vessels, whereas the β2-receptors are mainly found on the smaller intramuscular and subendocardial vessels. Sympathetic stimulation generally increases myocardial blood flow because of an increase in metabolic demand and a predominance of β2-receptor activation. Parasympathetic effects on the coronary vasculature are generally minor and weakly vasodilatory. 1262 1263 1264 ## 3. Myocardial Oxygen Balance 1265 1266 Myocardial oxygen demand is usually the most important determinant of myocardial blood flow. Relative contributions to oxygen requirements include basal requirements (20%), electrical activity (1%), volume work (15%), and pressure work (64%). The myocardium usually extracts 65% of the oxygen in arterial blood, compared with 25% in most other tissues. Coronary sinus oxygen saturation is usually 30%. Therefore, the myocardium (unlike other tissues) cannot compensate for reductions in blood flow by extracting more oxygen from hemoglobin. Any increases in myocardial metabolic demand must be met by an increase in coronary blood flow. Table 20–5 lists the most important factors in myocardial oxygen demand and supply. Note that the heart rate and, to a lesser extent, ventricular end-diastolic pressure are important determinants of both supply and demand. 1267 1268 *TABLE 20–7 Factors affecting myocardial oxygen supply–demand 1269 balance.* 1270 1271 1272

Supply

Heart rate (diastolic filling time)

Coronary perfusion pressure

Aortic diastolic blood pressure

Ventricular end-diastolic pressure

1273 1274 1275 1276 1277

Arterial oxygen content

Arterial oxygen tension

Hemoglobin concentration

Coronary vessel diameter

Demand

Basal metabolic requirements

Heart rate

Wall tension

Preload (ventricular radius)

Afterload

Contractility

1278 1279 1280 ## EFFECTS OF ANESTHETIC AGENTS 1281 1282 Most volatile anesthetic agents are coronary vasodilators. Their effect on coronary blood flow is variable because of their direct vasodilating properties, reduction of myocardial metabolic requirements, and effects on arterial blood pressure. 1283 1284 Volatile agents exert beneficial effects in experimental myocardial ischemia and infarction. They reduce myocardial oxygen requirements and protect against reperfusion injury; these effects are mediated by the activation of ATP-sensitive K+ (KATP) channels. Some evidence also suggests that volatile anesthetics enhance recovery of the "stunned" myocardium (hypocontractile, but recoverable, myocardium after ischemia). Moreover, although volatile anesthetics decrease myocardial contractility, at moderate doses they can be potentially beneficial in patients with heart failure because most of them decrease preload and afterload. 1285 1286 1287 ## The Pathophysiology of Heart Failure [... Output truncated due to length. 2838 tokens/12355 characters removed ...]