A number of clinical conclusions should be drawn from this table. First, increased heart rate (tachycardia) is harmful because it both decreases oxygen supply and increases oxygen demand. Second, severe anemia or severe hypoxemia is harmful because of reduced supply. Third, increases in LVEDV and LVEDP, which often (but not always) occur together, are harmful because of both decreased supply (decreased CPP) and increased demand (afterload). Fourth, the ideal blood pressure is patient-dependent, but severe hypotension is likely to reduce supply (DBP) more than its beneficial effect on demand (SBP). But, conversely, severe hypertension typically increases demand (afterload) more than it improves supply (DBP).
Left ventricular (LV) afterload is best defined as LV systolic wall stress. Based on Laplace's law, LV systolic wall stress = (LV systolic pressure × LV end-diastolic radius) / 2 × LV wall thickness. Therefore, factors that increase LV afterload include increased SBP and/or increased LV radius or LVEDV. Note that the normal (chronic) compensatory response to these hemodynamic changes is for the LV walls to thicken or hypertrophy, which works to normalize systolic wall stress, but requires months or years for change to occur. Therefore, of the hemodynamic variables that often change during the perioperative period, increases in SBP or LVEDV are harmful, owing to their deleterious effects on LV afterload.
O2: oxygen; SaO2: oxygen saturation of arterial blood; LV: left ventricular; SBP: systolic blood pressure. * Affects both supply and demand.
Original figure modified for this publication. Royster RL, Butterworth JF IV, Groban L, et al. Cardiovascular Pharmacology. In: Essentials of Cardiac Anesthesia. Kaplan JA (Ed), Saunders Elsevier, Philadelphia 2008. Illustration used with the permission of Elsevier Inc. All rights reserved.
