Download determinants of cardiac output and principles of oxygen delivery

Determinants of Cardiac Output
and Principles of Oxygen
Delivery
Scott V Perryman, MD PGY-III
• Principle of Continuity:
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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
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
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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