Fundamentals of Cardiac Anesthesia: Anatomy, Physiology, and Pharmacology
Core physiology
The cardiac anesthesiologist manipulates three levers-preload, afterload, and contractility-but must predict how drugs and ventilation change all three at once. Understand the pressure-volume loop: end-diastolic volume sets stroke volume via Frank-Starling; the end-systolic pressure-volume relationship indexes contractility; stroke work is loop area. Wall stress follows Laplace (σ = Pr/2h), so dilation raises afterload and oxygen demand, while hypertrophy lowers wall stress but impairs relaxation. Coronary perfusion occurs mainly in diastole and equals diastolic aortic pressure minus LV end-diastolic pressure; tachycardia shortens diastole and raises demand. Cardiac output is heart rate × stroke volume, and MAP is CO × SVR, but these equations do not specify which variable is abnormal-examine filling pressures, waveform, and echocardiography.
Pharmacology
Know receptor effects cold: α1 vasoconstriction; β1 inotropy and chronotropy; β2 vasodilation and bronchodilation; muscarinic vagal tone. Phenylephrine raises SVR and may cause reflex bradycardia and reduced CO; epinephrine adds β1 and arrhythmogenicity; norepinephrine balances α and β1; vasopressin acts via V1 and is useful in vasoplegia; milrinone is an inodilator with vasodilation and renal clearance; calcium sensitizers improve contractility without increasing intracellular calcium. Anesthetics depress contractility and blunt baroreflexes.
Traps
A common trap is treating hypotension with a pure vasoconstrictor when the problem is hypovolemia or pump failure. Worked example: after induction, a patient is hypotensive with a narrow pulse pressure and high SVR; phenylephrine may worsen CO. If echo shows a small, underfilled LV, give volume; if the LV is dilated and hypocontractile, use inotropy and reduce afterload. Rule of thumb: interpret every vasoactive drug by its net effect on CO, MAP, HR, and myocardial oxygen supply-demand.