Internal Respiration

Module F

Module F

• Chapter 9 – Assessment of Hypoxemia and Shunting

• Chapter 10 – Treatment of Hypoxemia and Shunting

• Chapter 11 – Hypoxia: Assessment and Intervention

ObjectivesAt the conclusion of this session the participant will:

• Still be awake! This covers 3 chapters!• Relax…most is a review and some will be covered in

Winter 09.• Define oxygen extraction.• Describe the effects of anaerobic metabolism.• State the formula for calculating RQ.• List the 5 causes of hypoxemia.• State the effect of an increase or decrease in cardiac

output on the shunt fraction.• List three methods, other than the shunt fraction, which

can be used to assess the degree of physiologic shunting.

• State three ways to treat acute hypoxemia.

Objectives• Define anemia.

• List three types of anemia and state the causes of the defect.

• Describe the effect of anemia on the presence of hypoxia.

• State the benefit, problems, and specific levels for each of the following as it relates to it being an indicator of cellular hypoxia:• Lactate

• Mixed Venous Oxygenation

• Oxygen Consumption & Utilization

• Gastric Mucosal Acidosis

Internal Respiration• Exchange of oxygen and carbon dioxide at

the cellular level.• Some control by local vasculature.

• Increased distance from capillary to tissue will result in decreased delivery.

• Some organs use more than others. • Table 7-1 (p. 188).• Note: % of blood flow is not equal to volume of

oxygen consumed.

Internal Respiration• Normal metabolism exists when O2 is

consumed and CO2 is produced.

• Normal ratio of CO2 produced : O2 consumed is 0.8:1 (200/250)

• Increased ratio with excess CHO utilization; decreased with fat & ETOH.

• When insufficient oxygen is present, anaerobic metabolism results.• Less ATP produced.• Lactic Acid is produced.

Adequacy and Efficiency of Oxygen Delivery

• Adequacy: Is there sufficient oxygen present? (Hint: Is hypoxemia present?)• Causes of Hypoxemia

• Low PIO2

• Hypoventilation• Absolute Shunts• Relative Shunts• Diffusion Defects• True or Absolute Deadspace (secondary mechanism)

• Efficiency: Is the PaO2 appropriate for the FIO2?• If not…assume a shunt is present!

Effects of Cardiac Output on PaO2

• The normal decrease in PaO2 from alveolar oxygen levels is due to the small mixing of anatomically shunted blood (5%).• This blood is venous in nature and has a PO2 the

same as the PO2.

• FourFour situations exist that can affect the PaO2:• Decreased Cardiac Output with a Normal Shunt• Increased Shunting with a Normal Cardiac Output• Decreased Cardiac Output with an Increased Shunt• Increased Cardiac Output with an Increased Shunt

The Normal Ventilation/Perfusion Relationship

• Normal PAO2

• Normal PćO2

• Normal PO2

• Normal CO• Normal Oxygen

Consumption

• Normal PaO2

Decreased Cardiac Output with a Normal Shunt

• PO2 decreases with a decrease in cardiac output because of an increased oxygen extraction (assuming

O2 doesn’t change).• Any shunted blood will

have a reduced PO2.

• Because the amount of shunted blood is so small, the decrease in PaO2 isn’t significant.

Increased Shunting with a Normal Cardiac Output

• Example: ARDS• Normal Cardiac

Output = Normal PO2

• The problem here is a significant increase in intrapulmonary shunt, meaning more PO2 “contaminated” blood entering the pulmonary vein (arterial system).

Decreased Cardiac Output with an Increased Shunt

• Similar to the first scenario, but here there is an increased intrapulmonary shunt.• Example: ARDS with

an MI• Reduced Cardiac

Output yields a reduced PO2 (higher extraction).

• More of that low PO2 blood is shunted in the lungs, resulting in a large reduction in PaO2.

Increased Cardiac Output with an Increased Shunt

• Normal physiologic response to hypoxemia is to increase heart rate (peripheral chemoreceptors) and Cardiac Output.• PO2 is increased (better

oxygen delivery).• With an increased

intrapulmonary shunt, however, there still is an increased amount of PO2 “contaminated” blood entering the system.

So What?• Don’t always assume that an improvement or

deterioration in PaO2 is occurring solely because of a change in pulmonary gas exchange.

• Suspect a change in cardiac output when an abrupt, unexplained hypoxemia is observed in critically ill patients.

• Also, consider other non-cardiac causes of reduced PO2.• Anemia• Increased metabolism (fever)• Maldistribution of systemic perfusion

Assessment of Hypoxemia

• Definition of “Hypoxemia”.• Severity?

• Causes of Hypoxemia• Differential Diagnosis of HypoxemiaAbnormality PaO2 PaCO2 RA P(A-a)O2 100% O2 P(A-a)O2

Hypoventilation N N

Absolute Shunt N or Relative Shunt N, , N

Diffusion Defect N at Rest,

w/ exercise

N or N at rest, with exercise

N

Shunt Substitutes

• P(A-a)O2

• PaO2/PAO2

• PaO2/FIO2

PAO2

• PAO2 = [(PBARO - PH2O) x FIO2] – (PaCO2/0.8)• On FIO2 of less than 60%

• PAO2 = [(PBARO - PH2O) x FIO2] – PaCO2

• On FIO2 greater than 60%

• Normal Values:• Room Air: 100 – 104 mm Hg• 100% Oxygen: 600

P(A-a)O2

• Normal values is around 10 mm Hg on room air.• Values increase with increasing age and the

supine position.

• Normal values 25-65 mm Hg on 100%• Difficult to use when FIO2 varies from 21

or 100%• Normal values differ for each FIO2

• Limited value when using supplemental oxygen.

P(A-a)O2 on Room Air

• Normal A-a gradient on 21% is seen with:• Pure hypoventilation• High altitude• Diffusion defect (patient at rest)

• Abnormal A-a gradient on 21% is seen with• Relative shunt• Absolute shunt

P(A-a)O2 on 100%

• Relative Shunt will improve• A-a gradient less than 300 mm Hg

• Absolute Shunt will not improve• A-a gradient is greater than 300 mm Hg

Using P(A-a)O2 to Estimate Shunt

• On 100% FIO2, a 1% shunt is estimated for every 10 – 15 mm Hg P(A-a)O2

• Example: A-a gradient is 140 mm Hg• 140 = 9.3% 140 = 14.0%

15 10

Using P(A-a)O2 to Estimate Shunt

• Normal Shunt is 5%

• Add 5 % to the normal 5% shunt for every 100 mm Hg gradient; Example:• 100 mm Hg – 10%• 200 mm Hg – 15%• 300 mm Hg – 20%

Shunt Equation

• Classic Shunt Equation• “Gold Standard”

• Clinical Shunt Equation• A shunt greater than or = 15% is significant• Increased shunts will correlate with

• “White out on x-ray unless its cardiac in origin.• Atelectasis, pneumonia, pulmonary edema, ARDS

Classic Shunt Equation

• Where:• CćO2= (1.34 x Hb x 1.0) + (PAO2 x .003)

• Assumes 100% saturation in the ideal alveolus

• Requires a Pulmonary Arterial Catheter (BTFDC)

100Q

Q

22

22

t

s

OvCOcC

CaOOcC

Clinical Shunt Equation

• Requires a Pulmonary Arterial Catheter (BTFDC)

• Only accurate at lower FIO2

222

2

t

s

003

003Q

QOvCCaOOaAP

OaAP

.

.

PaO2 /PAO2 (a-A ratio)

• Normal value is greater than 75% on any FIO2

• Example: 100/104 = 96%• 96% of oxygen is diffusing across the A-C

membrane

PaO2/FIO2 ratio

• Normal value is 400 – 500

• Example: 100 mm Hg/.21 = 476

• Value between 200 – 300 = ALI

• Value less than 200 = ARDS• Values less than 200 correlate with a shunt

of greater than 20%

Treatment of Hypoxemia

• Increase FIO2

• Increase MAP• PEEP, Inspiratory Time, Vt

• Body Positioning• Prone Positioning• Lateral decubitus (good lung down)

• Good bronchial hygiene• Suction, bronchodilators, CPT/Flutter/PEP

Oxygen Administration

• Treat hypoxemia/Hypoxia

• Decrease the work of breathing

• Decrease the work of the heart

Hazards of Oxygen Therapy

• Absorption atelectasis• Oxygen Toxicity• Retinopathy of prematurity• Oxygen induced hypoventilation in COPD

• Look for oxygen levels above 60 mm Hg and a rising PaCO2

• Evaluate FIO2 patient is receiving• Patient symptomatic: sleepy, lethargic

Hyperoxemia

• PaO2 greater than 100 mm Hg• Usually undesirable• Very little oxygen content is gained

• A PaO2 above 130 mm Hg indicates the patient is breathing supplemental oxygen.

• Hyperoxemia is indicated in COHb%.

Hyperoxemia

• SpO2% of 100% means the PaO2 could be between 100 mm Hg & 600 mm Hg• Very dangerous in infants

Oxygen Administration in Chronic Hypercapnia

• PaO2 will increase 3 mm Hg for each 1% increase in FIO2

• Keep PaO2 around 60 mm Hg

• FIO2 = 60 - PaO2 on room air

3

Example

• You are asked to draw an ABG on a CO2 retainer. The PaO2 is 39 mmHg on 21%

Where should the FIO2 be set?

FiO2 = 60 - 39 = 7% Add to 21%

3

• Set FIO2 at 28%

Calculating the maximal PaO2 for any given FIO2

• The PaO2 on room air during hyperventilation may go up to 130 mm Hg

• A PaO2 more than 5 times the % of oxygen is suspicious.• 30 x 5 = 150• 40 x 5 = 200• 50 x 5 = 250• 60 x 5 = 300

Problem

• pH 7.32, PaCO2 48, PaO2 200, FIO2 .30

• PAO2 = 760 – 47 x 0.30 – 48/.8

= 154 mm Hg

• Can’t have a PaO2 greater than PAO2, so…• Either the FIO2 was not recorded accurately

• Lab error (air bubble)

Evaluating FIO2

• High flow devices may not be delivering the FIO2 that is set• If the patient’s total flowrate is exceeding the

flow from the oxygen delivery device, the FIO2 will decrease

• Water in the aerosol tubing will increase FIO2

• High flow oxygen delivery systems should be analyzed

Analyze High Flow Systems

• Polarographic (battery and electrolyte solution)

• Galvanic (fuel cell)• Troubleshooting: If analyzer is not

reading the FIO2 within + 2% then:• Calibrate analyzer first• Change fuel cell (galvanic) or• Change battery/electrolyte level

(polarographic)

Correlating ABG to the Patients Condition

• A patient who looks good but has bad ABG• Suspect a lab error• Venous blood gas sample

• COPD (high PaCO2 and HCO3-)

Correlating ABG to the Patients Condition

• A patient who looks and feels bad but ABG are good.• CO poisoning, MetHB%• Tissue hypoxia

• Anemic hypoxia• Histotoxic hypoxia• Circulatory hypoxia

• Pulmonary embolism – high Vd/Vt ratio and highE

Analyzing an ABG

• On 21%, add PaCO2 and PaO2 to see if greater than 150.

• If one of the three acid base parameters is abnormal, there is an error.• pH 7.58, PaCO2 40, HCO3

- 24

• PaO2 cannot be greater than PAO2 on any FIO2.

Analyzing an ABG

• Know normal venous values and suspect when a venous sample may have been drawn

• Inaccurate FIO2

• Improperly recorded• Patients total flow exceeds flow from

delivery device

• FIO2 recorded from low flow system

• Water in the aerosol tubing

Objectives• Define anemia.• List three types of anemia and state the

causes of the defect.• Describe the effect of anemia on the

presence of hypoxia.• State the benefit, problems, and specific

levels for each of the following as it relates to it being an indicator of cellular hypoxia:• Lactate• Mixed Venous Oxygenation• Oxygen Consumption & Utilization• Gastric Mucosal Acidosis

Hypoxia• Definition: Reduced oxygen levels at the

tissue.• No “best” index for assessing tissue

oxygenation.• Begin assessment by assessing the

components of oxygen delivery:• Dissolved Oxygen• Bound Oxygen• Hemoglobin• Cardiac Output (This will be covered in RSPT 2420)

• Then look at markers of the effects of possible tissue hypoxia.

Types of Hypoxia

• Hypoxemic Hypoxia

• Circulatory (Stagnant) Hypoxia

• Anemic Hypoxia

• Histotoxic Hypoxia

Oxygenation Indices• Dissolved Oxygen as an index of hypoxia.

• Not very useful• Pretty good bet hypoxia is present with severe hypoxemia

• Be careful at extremes!

• Keep PaO2 above 60 mm Hg.

• Combined Oxygen (SaO2) as an index of hypoxia.• Make sure how you know HOW it is reported

• SaO2 with nomogram, 2-wavelength oximetry, CO-Oximetry, Pulse Oximetry

• Better than PaO2, but has its faults.• Abnormal species of hemoglobin• Insensitive in telling deterioration or at high PaO2 levels.

Anemia• RBC:

• 5 million/mm3 in men; 4.5 million/mm3 in women.

• Hemoglobin• 15 g% in men, 13 to14 g% in women.

• Anemia defined as a reduction in the amount of circulating RBC or hemoglobin.

• Hematocrit (formed elements in blood)• 47% in men, 42% in women.• Too low is bad; too high is bad.

Types of Anemia• Presence of anemia means one of two things:

• Decrease in production of RBC or Hb • Bone Marrow Failure (Aplastic Anemia)

• Usually due to chemical or physical agent (normocytic)

• Inadequate Hemoglobin synthesis• Iron deficiency 2° chronic blood loss or pregnancy (microcytic)

• Pagophagia: Ice chip craving• Thalassemias – genetic disorder (microcytic)

• Inadequate RBC formation• Folic Acid deficiency: Green vegetables & alcoholics (macrocytic)

• B12 deficiency: Pernicious anemia 2° lack of intrinsic factor (macrocytic)

• RBC & Hb are being lost or destroyed at an accelerated rate.• Blood loss

• Acute bleeding (normocytic)• Excessive hemolysis

• Sickle cell disease

Analyzing FIO2

• Always correlate ABG to patients condition.

• When drawing from an A-line, always remove all heparin from the lines – this means withdrawing 3-5 cc and discarding.

• Understand the relationship of increased metabolism with leukocytosis (leukemia).

Anemia and Hypoxia

• Mild anemia (10 g%) usually won’t cause hypoxia• 25% extraction• Cardiac output reserves (acute)• Changes in levels of 2,3 DPG (cardiac)

• Probably significant with Hb < 6 g%

• Transfuse when Hb levels fall below 7 g%

Key Indicators of Hypoxia

• Lactate

• Mixed Venous Oxygen

• Oxygen Consumption/Oxygen Extraction

• Gastric Tonometry

• Vital Organ Function

Lactate• Immediate response to a reduced oxygen

delivery is the onset of anaerobic metabolism.• Glycolysis: Pyruvate reduction to lactate.• Normal lactate is 0.9 to 1.9 mM/L or 8 to 17 mg/dL• Metabolic Acidosis + hypoxemia + CO = Hypoxia• Increase in mortality at levels above 2.5 mM/L; 90% at

levels above 8 mM/L• Problem is lactate elevation is not linear (not a good

early predictor) • Reduction is by liver. Poor perfusion/Liver failure worsens

prognosis.• Cyanide poisoning (Histotoxic hypoxia) should be

suspected with high lactates and no increase in HbCO with smoke inhalation.

Mixed Venous Oxygenation

• Requires a pulmonary artery catheter.• Assessment of oxygen supply vs. demand• SO2: Continuous vs. Spot Check

• Normal 75%• Decreased with increasedO2, decreased SaO2, decreased Hb or

decreased CO.

• PO2: Average end-capillary driving pressure.• Usefulness depends on distribution of cardiac output.• Decreases are associated with decreased supply or increased

demands.• Increases are associated with reduced utilization (NOT

ALWAYS A GOOD THING!)

Oxygen Uptake and Utilization

• Normal oxygen uptake (consumption) by the tissue remains constant despite changes in cardiac output because of huge reserve (25% normal extraction).• Hypoxia is present when O2del falls below 8 to 10

ml/kg/min.

• Covert Hypoxia: Normally, increasing oxygen delivery is not needed; in some situations (MOF secondary to ARDS, septic shock, ARF). The cause is suspected to be an altered oxygen utilization.

Gastric Tonometry

• Blood shunting to key organs occurs with reduced oxygen supply at the expense of non-vital organ systems (GI tract).

• If hypoxic crisis is present, GI involvement will be a primary source.

• The mixing of gases to a point of equilibration is called tonometry.

• Use of a specialized catheter with a balloon can measure the gastric carbon dioxide and infer gastric blood flow.

Sublingual Tissue PCO2

• Improvement on gastric tonometry.

• Uses CO2 sensor in “temperature” like probe.

• Results within 60 seconds.

Vital Organ Function

• If compensatory mechanisms are intact, the presence of these compensatory mechanisms may be an indication that hypoxia is present.• Urine output• Mental status• Skin coolness• Great toe temperature