Determinants of Cardiac Output and Principles of Oxygen Delivery Scott V Perryman, MD PGY-III
Principle of Continuity: Conservation of mass in a closed hydraulic system Blood is an incompressible fluid Vascular system is a closed hydraulic loop Vol ejected from left heart = vol received in R heart
Preload Preload: load imposed on a muscle before the onset of contraction Muscle stretches to new length Stretch in cardiac muscle determined by end diastolic volume
Preload This curve is known as the Frank-Starling curve. On the Y-axis we have the pressure changes within the ventricle. On the X-axis, we have the diastolic volume. The upper curve represents systolic performance and the lower curve, diastolic performance. This graph demonstrates several important changes. We note that with small changes in diastolic volume, there are large consequent changes in systolic pressure. The area under the curve A, B, C and D represents the stroke work.
Preload At bedside, use EDP as surrogate for ventricular preload i.e. assume EDV = EDP
Preload How can we measure EDP? Pulmonary Capillary Wedge Pressure
PCWP How does wedge pressure work? A balloon catheter is advanced into PA Balloon at the tip is inflated Creates static column of blood between catheter tip and left atrium Thus, pressure at tip = pressure in LA
PCWP Only valid in Zone 3 of lung where: Pc > PA Catheter tip should be above left atrium Not usually a problem since most flow in Zone 3 Can check with lateral x-ray Will get high respiratory variation if in Zone 1 or 2
Preload Ventricular function is mostly determined by the diastolic volume Relationship between EDV/EDP and stroke volume illustrated by ventricular function curves
Ventricular Compliance Cardiac muscle stretch determined by EDV Also determined by the wall compliance. EDP may overestimate the actual EDV or true preload
Cardiac Output and EDV
Effect of Heart Rate With increased heart rate, we get increased C.O….to a point. Increased HR also decreases filling time
Contractility The ability of the cardiac muscle to contract (i.e. the contractile state) Reflected in ventricular function curves
Afterload Afterload: Load imposed on a muscle at the onset of contraction Wall tension in ventricles during systole Determined by several forces Pleural Pressure Vascular compliance Vascular resistance
Pleural Pressure Pleural pressures are transmitted across the outer surface of the heart Negative pressure increases wall tension. Increases afterload Positive pressure Decreases wall tension. Decreases afterload
Impedence Impedence = total force opposing flow Made up of compliance and resistance Compliance measurement is impractical in the ICU Rely on resistance
Vascular Resistance Equations stem from Ohm’s law: V=IR Voltage represented by change in pressure Intensity is the cardiac output SVR = (MABP – CVP)/CO PVR = (MPAP – LAP)/CO
Oxygen Transport Whole blood oxygen content based on: hemoglobin content and, dissolved O2 Described by the equation: CaO2 = (1.34 x Hb x SaO2) + (0.003 x PaO2)
Oxygen Content Assuming 15 g/100ml Hb concentration O2 sat of 99% Hb O2 = 1.34 x 15 x 0.99 = 19.9 ml/dL For a PaO2 of 100 Dissolved O2 = 0.003 x 100 = 0.3 ml/dL
Oxygen Content Thus, most of blood O2 content is contained in the Hb PO2 is only important if there is an accompanying change in O2 sat. Therefore O2 sat more reliable than PO2 for assessment of arterial oxygenation
Oxygen Delivery O2 delivery = DO2 = CO x CaO2 Usually = 520-570 ml/min/m2
Oxygen Uptake A function of: Cardiac output Difference in oxygen content b/w arterial and venous blood VO2 = CO x 1.34 x Hb (SaO2 – SvO2) 10
Oxygen Extraction Ratio VO2/DO2 x 100 Ratio of oxygen uptake to delivery Usually 20-30% Uptake is kept constant by increasing extraction when delivery drops.
Critical Oxygen Delivery Maximal extraction ~ 0.5-0.6 Once this is reached a decrease in delivery = decrease in uptake Known as ‘critical oxygen delivery’ O2 uptake and aerobic energy production is now supply dependent = dysoxia
Tissue Oxygenation In order for tissues to engage in aerobic metabolism they need oxygen. Allows conversion of glucose to ATP Get 36 moles ATP per mole glucose
Tissue Oxygenation If not enough oxygen, have anaerobic metabolism Get 2 moles ATP per mole glucose and production of lactate Can follow VO2 or lactate levels