Oxygen Supply and Demand in Critical Illness

Edward M. Omron MD, MPH, FCCP

Critical Care Services

Objectives

• Is oxygen delivery adequate for the patient?

• Is cardiac output adequate for oxygen consumption?

• Is oxygen consumption adequate for oxygen demand?

Oxygen Demand, Consumption, and Delivery

Oxygen Demand: The amount of oxygen needed to satisfy the metabolic requirements of all body tissues. Determined by physiologic stress, infection, temperature, and is coupled to cardiac output and minute ventilation

Oxygen Consumption: Amount of oxygen used and made available to the body tissues

Oxygen Demand, Consumption, and Delivery

Physiologic stress states: Infection, Surgery, and Trauma Oxygen Demand exceeds delivery and occult or frank shock may be present Anaerobic metabolism Lactic acidosis Cell Injury Cell Death

Cardinal Rules of Critical Care

• Golden Hour• Early correction of oxygen debt prevents multi-

organ failure that leads to death

• Maximize oxygen delivery• The supply of oxygen to the tissues must

always exceed demand

• Minimize oxygen consumption• Shock: oxygen demand exceeds supply• Global tissue hypoxia, anaerobic metabolism,

lactic acidosis and cell death.

Cardinal Rules of Critical Care1.1. GOLDEN HOUR GOLDEN HOUR

• Time dependent functionTime dependent function

• Early correction of oxygen debt prevents multi-organ failure that leads to death

• In World War I, there was an appreciation of time between wounding and shock treatment. If the patient was treated within one hour, mortality was 10%; and, after eight hours the mortality was 75%.

Golden Hour Survival Time To Treatment• Vietnam War 97.5% 1 hours• Korean War 95.5% 5 hours• World War 2 95.5% 10 hours

• Regarding penetrating torso injuries• Medical success was attributed to helicopter evacuation, whole

blood, medical teams, and forward hospitals• Not really a “Golden Hour” but a term used to indicate urgency

of care and the crucial importance of time

Ann Emerg Med 1981; 10: 659-661

Acad Emerg Med 2001; 8: 758-760

GOLDEN HOURGOLDEN HOUR• Shoemaker, WC

– Chest 1988;94:1187-1195– Prospective trial of early goal-directed therapy

in high risk surgical patients– Marked improvement in mortality in

experimental groups that received early pre-operative and perioperative optimization of oxygen transport variables

GOLDEN HOURGOLDEN HOUR• Rivers, Emmanual

– NEJM 2001; 345: 1368-1377– Early goal-directed therapy in severe sepsis

and septic shock during the first 6 hours after presentation

– Significant reductions in mortality, morbidity in experimental group that optimized oxygen delivery and consumption variables

Components of Oxygen Delivery

• DO2 (oxygen delivery in mL O2/min)

• DO2 = CO x CaO2 x10

• DO2 = (HR x SV) x CaO2 x10

• DO2=(HR x SV)x(1.34 x Hb x SaO2)x10

Effects of PaO2, Hemoglobin, cardiac output on DO2 (oxygen delivery)

• FiO2 PaO2 SaO2 Hb (g/dL) C.O. (l/min) DO2 %

• 0.21 70 96% 13 5.3 900 0• 0.21 45 75% 7 4 288 -68• 0.60 350 98% 7 4 384 +25• 0.60 350 98% 10.5 4 568 +48• 0.60 350 98% 10.5 6 852 +50

Preload Augmentation

• DO2 (oxygen delivery in mL O2/min)

• DO2 = CO x CaO2 x 10

• DO2 = HR x SV x CaO2 x 10

• DO2 = HR x SV x Hb x SaO2 x 13.8

Stroke VolumeCardiac OutputVenous Return

RAP, Preload or RV End diastolic Volume

preload-dependence

preload-independence

Starling Curve

Volume Responsive

Volume Unresponsive

Preload Augmentations/p fluid bolus

Preload RESPONSIVE

RAP RVEDV

Car

dia

c O

utp

ut Normal

Abnormal (Cardiogenic or septic shock)

50 mL 100 mL 150 mL 200 mL

Preload Augmentations/p fluid bolus

Preload UNRESPONSIVE

RVEDV or LVEDV

Stroke Volume

Normal

Abnormal (Cardiogenic or septic shock)

50 mL 100 mL 150 mL 200 mL

.

Stroke volume

Ventricular preload

normal heart normal heart

failing heart failing heart

preload-dependencepreload-dependence

preload-independencepreload-independence

Starling Curve

Leg RaisePP VariationPCO2TTESVO2CCICEDV?

Cardinal Rules of Critical Care

2. Maximize Oxygen Delivery• Improve Cardiac Performance

– Maintain MAP > 65 mm Hg (arbitrary)» Preload Augmentation (crystalloid/colloid)» Inotropes (norepinephrine)» Peripheral vasoconstrictor (vasopressin)

• Transfuse Packed Red Blood Cells• Assume control of ventilation/oxygenation

– FIO2 factors

VO2 or Oxygen Consumption

• VO2 = Arterial O2 delivery – Venous O2 delivery

• The difference represents the amount of oxygen consumed by the tissues

• Normal = 250 mL/min or 5 mL/100 mL blood

Fick Equation for Oxygen Consumption

• VO2= Oxygen Consumption (250 mL/min)

• VO2 = 10*C.O.*(CaO2 –CvO2)

• VO2 = 10 * C.O. * (1.34*Hgn*SaO2 -1.34*Hgn*SvO2)

• VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)

• Solve for SvO2? Or the mixed venous saturation?

Four Determinants of Mixed Venous Oximetry

SvOSvO22 = SaO = SaO2 2 - (VO - (VO22 / C.O. x Hgb x 1.34) / C.O. x Hgb x 1.34)

SvO2 = Mixed venous saturation (%)

SaO2 = Arterial oxygen saturation (%)

VO2 = Oxygen consumption mL (O2/min)

Hgb = Hemoglobin concentration (g/dL)Cardiac Output (C.O.) = dL/min

Why measure SvO2?

• A decrease in SvO2 is an early indicator of a threat to tissue oxygenation

• Earlier information results in earlier diagnosis with interventions

• Normal range of SvO2 = 60-80%

• The 5th vital sign

PaO2 vs PvO2 in Cardiogenic Shock

Arterial Venous Saturation Difference

SHOCK

Master EquationMaster Equation

ScvO2ScvO2 SvO2 = SaO2 - (VO2 / C.O. x Hgb x 1.34) SvO2 = SaO2 - (VO2 / C.O. x Hgb x 1.34)

• Acute Illness or Post-op Surgery– SaO2, VO2, Cardiac Output, and Hgb are

dynamically changing concurrently

– Optimize each parameter then recheck ScvO2 to assess response to intervention

Cardinal Rules of Critical Care

3. Minimize oxygen consumption• Sedation, analgesia, rarely neuromuscular

blockade• Work of breathing• Fever• Rigors• Pain• Anxiety

Is cardiac output adequate for oxygen consumption?

• Mixed or central venous PCO2 gradient is proportional to 1/Cardiac index

• Tissue hypercarbic acidosis evolves during ischemic hypoxia or low flow states

• Oxygen utilization coefficient > 35% as well

Paradoxical Respiratory Acidosis of Cardiopulmonary Arrest

Venous Arterial CO2 Difference

Cardiogenic Shock

Central Venous-Arterial PCO2 Gradient

Fick Equation for CO2 production

• VCO2 =Carbon dioxide production (200 mL/min)

• VCO2 = 10*C.O.*(PvCO2 – PaCO2)

• If cardiac output decreases and VCO2 remains constant, what must happen to venous-arterial CO2 difference?

• VCO2 = 10* C.O.* (PvCO2 – PaCO2)

• 65 year old man presents to the ER in Shock

– BP 60/30, HR 150 bpm– Paleness– Cool Skin– Dilated Pupils– Semicomatose state– Low Urine Output

Two Possible Causes of the Low Blood Pressure were Considered

• Cardiogenic Shock

• Hemorrhagic Shock

Match the ABG VBG with the Associated Condition

(a) pH = 7.25, PCO2 = 30, PaO2 = 75, saturation = 97%, BE = -15, LA = -15(v) pH = 7.20, PCO2 = 36, PvO2 = 25, venous saturation = 45%

(a) pH = 7.30, PCO2 = 25, PaO2 50, BE = -10, saturation = 85% LA = -10(v) pH = 7.20, PCO2 = 50, PvO2 = 25, venous saturation = 45%

Endpoints of Resuscitation

• 50% of critically ill patients who present in shock who were resuscitated to normal vital signs continued to have increased lactate and low SvO2 and ScvO2

Endpoint of Resuscitation

• Conventional Endpoints are lagging indicators of inadequate oxygen delivery– Blood Pressure– Heart Rate– Urine Output– Mental Status Changes– Central Venous Pressure (poor surrogate of

filling pressures)

• More effective endpoints of resuscitation

• Continuous Cardiac Index– Pulse pressure variation– Systolic pressure variation

• SvO2 or ScvO2 • Serum lactate (Tissue hypoxia)• Venous – arterial PCO2

– Directly correlates with cardiac index

• Metabolic acid-base status (SBE)• With CVP

Resuscitation Endpoints

• A single set of data points is useless– C.I., SvO2, PaCO2-PvCO2, SBE, Lactate

• Construct multiple data points to assess trends and response to interventions!

• REAL time bedside interventions

Systolic Pressure Variation

SEPTIC SHOCK PRESENTSBP ≤ 90 mmHg or MAP ≤ 65 mmHg

ORLactate ≥ 4 mmol/L

PLUSClinical Picture c/w Infection

Fluid bolus 20 ml/kg(.9 NaCl or LR)

PLUSVasopressors if MAP is

judged to be critically low

SBP < 90 mmHg, orMAP < 65 mmHg, orLactate > 4 mmol/L

CVP < 8 mmHg

Insert CVP

Catheter

Boluses crystalloid or colloid equivalent

until CVP > 8 mmHg

CheckMAP

Assess

ScvO2

Achieve ALL

Goals?

< 70%

Dobutamine or RBCs depending

on HCT

MAP ≥ 65

Resuscitation complete. Establish

re-evaluation intervals.

YES

Benefits of EGDT

• $12,000.00 reduction in total hospital charges• 34% reduction in sepsis mortality• 3.8 reduction in hospital days

References

• Chest 2005;128:554s-560s• Chest 2006; 130: 1579-1595• Intensive Care Medicine 2004; 30:2170-2179• Crit Care Med 2003; 31:S658-S667• Current Opinion Critical Care 2001; 7: 204-211• NEJM 2001; 345: 1368-1377• Critical Care Medicine 2002; 30: 1686-1692• Circulation 1969; 40: 165• Thorax 2002; 57: 170-177• Academic Emer Med 1999; 6: 421