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Pathophysiology and General Management of Failure of Arterial Oxygenation. Dong Soo Kim, M.D. [email protected] Respiration ; exchange of oxygen and carbon dioxide between humans and the atmosphere Human respiration ; - Ventilation - Arterial oxygenation

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Pathophysiology and general management of failure of arterial oxygenation

Pathophysiology and General Managementof Failure of Arterial Oxygenation

Dong Soo Kim, M.D.

[email protected]

  • Respiration ; exchange of oxygen and carbon dioxide between humans and the atmosphere

  • Human respiration ;

    - Ventilation

    - Arterial oxygenation

    - Oxygen transport

    - Oxygen extraction and utilization

  • Respiratory failure ;

    BGA abnormalities of high PaCO2 and low PaO2 or both

Standards for basic anesthetic monitoring
Standards for Basic Anesthetic Monitoring

  • Standard IQualified anesthesia personnel shall be present in the room throughout the conduct of all general anesthetics, regional anesthetics and monitored anesthesia care.(Approved by the ASA House of Delegates on Oct. 15, 2003)

Standards for basic anesthetic monitoring1
Standards for Basic Anesthetic Monitoring

  • Standard IIDuring all anesthetics, the patient’s oxygenation, ventilation, circulation, and temperature shall be continually evaluated.(Approved by the ASA House of Delegates on Oct. 15, 2003)

Definition of hypoxemia
Definition of Hypoxemia

  • PaO2 = 105 – Age / 2

    - PaO2 of 50 year-old man ; 80 mm Hg

    - PaO2 of 80 year-old man ; 65 mm Hg

  • Defining Hypoxemia

    - Harrison’s (1998) :PaO2< 80 mm Hg

    -Shapiro BA (1998): relative deficiency of oxygen tension in the arterial blood

    -Morgan GE(2006): PaO2< 60 mm Hg

Objective and methods for oxygenation monitoring
Objective and Methods for Oxygenation Monitoring

  • Objective ;To ensure adequate O2 concentration in the inspired gas and the blood during all anesthetics

  • Methods ;

    - Inspired gas : During every administration of general anesthesia using an anesthesia machine, theconcentration of O2 in the breathing system shall be measured by an O2 analyzer with a low O2concentration limit alarm in use.(Approved by the ASA House of Delegates on Oct. 15, 2003)

Objective and methods for oxygenation monitoring1
Objective and Methods for Oxygenation Monitoring

  • Objective ;To ensure adequate O2 concentration in the inspired gas and the blood during all anesthetics

  • Methods ;

    - Blood oxygenation : During all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed. Adequate illumination and exposure of the patient are necessary to assess color.(Approved by the ASA House of Delegates on Oct. 15, 2003)

Monitoring during anesthesia
Monitoring during Anesthesia

  • BP, heart rate

  • ECG

  • CVP

  • Pulse oximetry

  • Capnography

  • Urine output

  • Temperature

  • BIS (bispectral index)

  • Cardiac output

  • Cerebral metabolic rate of oxygen (CMRO2)

Subdivisions and structure of intrapulmonary airways
Subdivisions and Structure of Intrapulmonary Airways

Pathways of o 2 and co 2 diffusion
Pathways of O2 and CO2 Diffusion

Ultrastructure of pulmonary alveoli and capillaries
Ultrastructure of Pulmonary Alveoli and Capillaries

Transfer of o 2 and co 2 between alveolar air and capillary blood
Transfer of O2 and CO2 Between Alveolar Air and Capillary Blood

Process of oxygenation
Process of Oxygenation

  • External respiration

  • Blood oxygen transport

  • Internal respiration

External respiration
External Respiration

  • Transfer of oxygen molecules from atmosphere to blood

  • Alveolar oxygen tension (PAO2) is the major limiting factor in the oxygenation of desaturated blood

  • Major factors involved in determining the PAO2

    - Fraction of inspired oxygen (FiO2)

    - Alveolar gas exchange

    - Mixed venous oxygen content

    - Distribution of ventilation

Mixed venous po 2 as an indicator
Mixed Venous PO2 as an Indicator

  • The most reliable single physiologic indicator for monitoring the overall balance between oxygen supply and demand

  • PvO2 < 28 mm Hg ; - anaerobic metabolic state

    - blood lactate levels ↑








Metabolic disruption



Critical level of PvO2




Blood lactate (mEq/L)








Upper limit of

normal lactate conc.















PvO2(mm Hg)

Relation between blood lactate and PvO2

JAMA 1976;236:570

Cellular metabolism




CO2 + H2O + ATP




Lactate + ATP

Cellular Metabolism

Pathophysiology of impaired tissue oxygenation
Pathophysiology of Impaired Tissue Oxygenation

  • Failure of arterial oxygenation

  • Failure of oxygen transport

  • Failure of tissue oxygen extraction

Mechanisms of Hypoxemia

  • Low alveolar O2 tension

  • - Low inspired O2 tension

  • - Alveolar hypoventilation

  • - Third gas effect (diffusion hypoxia)

  • - Increased O2 consumption

  • Increased alveolar - arterial O2 gradient

  • - Shunting

  • - Ventilation / perfusion mismatch

  • - Low mixed venous O2 tension

  • - Decreased cardiac output

  • - Increased O2 consumption

  • - Decreased Hb concentration

Common factors causing intraoperative and or postoperative hypoxemia
Common Factors Causing Intraoperative and/or Postoperative Hypoxemia

  • Low inspired O2 concentration

  • Hypoventilation

  • Ventilation / perfusion mismatch

  • Increased intrapulmonary Rt to Lt shunt

    - Atelectasis ; main contributor

  • Pneumothorax

  • Pulmonary edema

  • Pulmonary embolism

Low alveolar oxygen tension
Low Alveolar Oxygen Tension



Increased A – a Oxygen Gradient



Increased A – a Oxygen Gradient




↓V/Q ratio(shunt effect)

Increased A – a Oxygen Gradient



↑V/Q ratio


Effect of anesthesia on gas exchange
Effect of Anesthesia on Gas Exchange

  • During anesthesia,

    - Deadspace (normal ventilation, no perfusion) ↑

    - Alveolar ventilation ↓ (rate and/or tidal volume)

    - intrapulmonary shunting ↑

    (5-10% ↑, as a result of atelectasis, airway obstruction)

  • Prolonged administration of high concentration of O2(> 50%) may be associated with increases in absolute shunt(absorption atelectasis)

  • Inhalation anestheticsinhibithypoxic pulmonary vasoconstriction(ED50 ; 2 MAC)

Mucociliary blanket
Mucociliary Blanket

  • Normal defense mechanism of the pulmonary tree

  • Submucosal gland ;

    mucus produce (100 mL/d)

  • Mucus ; water (95%), glycoprotein (2%), carbohydrate (1%)

  • Mucus blanket moves mucus and foreign bodies toward the larynx (2 cm/min)

  • Inhalation anesthetics, smoke ; ciliary movement ↓

Potential results of retained secretions
Potential Results of Retained Secretions

Inflammation and partial plugging

Airflow resistance ↑

Work of breathing ↑

Uneven distribution of ventilation

Shunt effect


Total plugging

Absorption atelectasis

Lung compliance ↓

Stasis pneumonia


Various factors as causes of clinically detectable atelectasis following major surgery
Various Factors as Causes of Clinically Detectable Atelectasis following Major Surgery

Bendixen HH. Respiratory care. 1974

Consequences of hypoxemia
Consequences of Hypoxemia Atelectasis following Major Surgery

  • CNS ; cerebral vasodilation, confusion, convulsion, unconsciousness, coma

  • CV ; myocardial depression, coronary vasodilation, bradycardia, dysrhythmia, heart failure, shock

  • Resp ; hypoxic pulmonary vasoconstriction

  • Renal ; dec RBF and tubular function

Events associated with decreased pao 2
Events Associated with Decreased PaO Atelectasis following Major Surgery2

Snyder JV. Oxygen transport in the critical ill. 1995

Classification of hypoxia
Classification of Hypoxia Atelectasis following Major Surgery

Atelectasis following Major Surgery삼순이 없는 세상

살아서 뭐하나……”

Atelectasis following Major Surgery누굴 놀리나……”

General management of hypoxemia
General Management of Hypoxemia Atelectasis following Major Surgery

  • Directed at the cause

  • O2 therapy

  • Reserve normal CV function

  • PEEP

  • Chest physical therapy

Effect of o 2 therapy on variable types of hypoxemia
Effect of O Atelectasis following Major Surgery2 Therapy on Variable Types of Hypoxemia

Effect of hypoventilation on oxygen therapy
Effect of Hypoventilation Atelectasis following Major Surgery on Oxygen Therapy

Braun HA. Introduction to Respiratory Physiology. 1990

Effect of ventilation perfusion mismatching on oxygen therapy
Effect of Ventilation / Perfusion Mismatching on Oxygen Therapy

Braun HA. Introduction to Respiratory Physiology. 1990

Effect of shunt on oxygen therapy
Effect of Shunt on Oxygen Therapy Therapy

Braun HA. Introduction to Respiratory Physiology. 1990

Effect of varying amounts of shunt on arterial oxygen tension
Effect of Varying Amounts of Therapy Shunt on Arterial Oxygen Tension

Br J Anaesth 1973;45:711

Hypoxemia and oxygen therapy
Hypoxemia and Oxygen Therapy Therapy

  • Refractory hypoxemia;

    Secondary to true shunt mechanism

  • Responsive hypoxemia ;

    Secondary to shunt effect

Diagnostic approach of refractory hypoxemia
Diagnostic Approach of Refractory Hypoxemia Therapy

Oxygen challenge test ;

1. Increase baseline FiO2 by 0.2

2. Repeat ABG in 10 - 15 min

3. If PaO2 increases less than 10 mmHg,

most likely a true shunt mechanism

Oxygen challenge principle
Oxygen Challenge Principle Therapy

Shapiro BA. Clinical application of blood gases. 1982

Indices of virtual shunt
Indices of Virtual Shunt Therapy

* Assuming Hb 10 g/dL, PaCO2 25-40 mmHg, C(a-v) DO2 5 vol%

Braun HA. Introduction to Respiratory Physiology. 1990

Diagnosis of intrapulmonary shunt
Diagnosis of Intrapulmonary Shunt Therapy

100 % O2 test ;

1. 100 % O2 breathing for 20 min

2. ABG and calculate P(A - a)O2

3. P(A - a)O2 above 100 mmHg

indicates an abnormal vol of shunt

*PAO2 = (PB - PH2O)FiO2 – PaCO2/R

Estimated shunt equation
Estimated Shunt Equation Therapy

AaDO2X 0.003

Shunt (%) =

(AaDO2X 0.003) + C(a-v)DO2

AaDO2 ; alveolar - arterial O2 content difference

0.003 ; O2 solubility coefficient

C(a-v)DO2 ; arterial - mixed venous O2 content difference

Guidelines for interpreting the shunt calculation 1
Guidelines for Interpreting the Shunt Calculation - 1 Therapy

1. Calculated shunt <10% ; clinically compatible with normal lungs

2. Calculated shunt 10-19% ; intrapulmonary abnormality that is seldom of clinical significance in terms of maintaining respiratory homeostasis

Guidelines for interpreting the shunt calculation 2
Guidelines for Interpreting the Shunt Calculation - 2 Therapy

3. Calculated shunt 20-29% ; significant intrapulmonary disease. In a patient with limited CV or CNS function, this degree of shunt may be life-threatening

4. Calculated shunt > 30% ; potentially life-threatening and usually requires aggressive cardiopulmonary supportive therapy

Some requirements for normal oxygen transport
Some Requirements for Therapy Normal Oxygen Transport

  • PaO2 adequate for nearly full

  • saturation of Hb (> 150 mm Hg)

  • Adequate amount of Hb

  • Normal unloading mechanisms

  • (temp, pH, PaCO2, 2,3 - DPG)

  • CO adequate for delivery of HbO2

Therapy with low fio 2
Therapy with Low FiO Therapy2

  • Indications ;

    Hypoxemia resulting from hypoventilation or ventilation / perfusion mismatching

  • Methods of delivery ;

    -Venturi mask

    - Nasal Prongs

  • Monitoring

    - BGA

Ventilatory criteria for use of low fio 2 therapy system
Ventilatory Criteria for Use of TherapyLow FiO2 Therapy System

  • LowFiO2therapy is adequate if ;

Relationship between respiratory rate and fio 2 during oxygen administration
Relationship between Respiratory Rate and FiO Therapy2 during Oxygen Administration

Nasal cannula

O2 flow = 6 L/min

Vt = 500 mL













Respiratory rate (breaths/min)

O’Connor. Crit Care Clin. 1995

In a low - flow system, Therapy

the larger the tidal volume, or the faster the respiratory rate,

the lower the FiO2.

increasing MV, lower FiO2

decreasing MV, higher FiO2

Therapy with high fio 2
Therapy with High FiO Therapy2

  • Indications ;

    Hypoxemia primarily due to shunt

  • Methods of delivery ;

    - Tightly fitting face masks

    - Endotracheal intubation

  • Monitoring

    - Oxygen toxicity (if continued > 24-48 hours)

Major advantages of high flow oxygen systems
Major Advantages of Therapy High - flow Oxygen Systems

  • Maintenance of Consistent and

  • predictable FiO2

  • Maintenance of adequate

  • temperature and humidity

In the presence of severe shunt, Therapy

no amount of O2will fully oxygenate

the blood. This a common setting for

O2 toxicity.

Complications associated with excessive high fio 2
Complications associated Therapy with Excessive HighFiO2

  • Pulmonary oxygen toxicity

  • Atelectasis

  • Convulsions

Oxygen Therapymust be considered

a biomedicaldouble-edged sword ;

it not only promotes life

but also destroys life.

Lavoisier A(1785)

Positive end expiratory pressure
Positive End - Expiratory Pressure Therapy


PEEP 12cmH2O












PAP ;Proximal airway pressure

A : Unstable lung

B : Normal lung

Pulmonary effects of peep
Pulmonary Effects of PEEP Therapy

  • Increased FRC

  • Increased alveolar volumes

  • Alveolar recruitment

  • Redistribution of lung extravascular water

  • Decreased intrapulmonary shunting

  • Decreased dead space ventilation

Chest physiotherapy
Chest Physiotherapy Therapy

  • Improve distribution of ventilation

  • Mobilize secretions

  • Improve efficiency of ventilation

  • Improve cardiopulmonary work capacity

Postural drainage post basal seg lower lobe
Postural Drainage Therapypost. basal seg., lower lobe

Chest percussion
Chest Percussion Therapy

  • Mucus ; gel that can become fluid when shaken or vibrated.

  • Change the nature of sputum and decrease its adherence to airway walls

  • Increase tracheal transport velocity

  • 3-4 times/day

  • 5 minutes in a time

Chest vibration
Chest Vibration Therapy

  • Shaking pressure applied to the chest wall only during exhalation

  • Facilitate excretion of dislodged mucus from the airways

  • Inducing cough

Physiologic function of the lung
Physiologic Function of the Lung Therapy

  • Respiratory :

    - Oxygenation

    - Ventilation

  • Non-respiratory :

    - Regulation of acid-base balance

    - Activation of circulating precursors of vasoactive substances

    - Inactivation of circulating vasoactive substances

Inactivation of TherapyCirculating Vasoactive Substances

Activation of Circulating Precursors Therapy

of Vasoactive Substances

Role of Lungs and Kidneys in Therapy

Regulation of Acid-Base Balance

Role of Lungs in Regulation Therapy

of Acid-Base Balance

Respiratory compensation in metabolic acidosis

Role of Kidneys in Regulation Therapy

of Acid-Base Balance

Renal compensation in respiratory acidosis

Relationship of ventilation pattern and alveolar ventilation
Relationship of Ventilation Pattern Therapyand Alveolar Ventilation

VT 250 mL X RR 40/min = MV 10 L

VT 500 mL X RR 20/min = MV 10 L

VT 1,000 mL X RR 10/min = MV 10 L

Calculation of Ideal Alveolar O Therapy2 Tension

PAO2 = (PB-PH2O)FiO2 – PaCO2/RQ

PAO2 ; alveolar O2 tension

PB ; barometric pressure (760 mm Hg at sea level)

PH2O ; water vapor pressure (47 mm Hg)

FiO2 ; fraction of inspired O2

RQ ; respiratory quotient (0.8)

Alveolar to Arterial Oxygen Gradients Therapy

  • Difference between PAO2 and PaO2

  • -At room air,

  • A-a gradient ; < 10 mm Hg

  • - FiO2 1.0,

  • A-a gradient ; < 100 mm Hg

  • Mechanisms of increasing A-a gradient

  • - Ventilation / perfusion mismatch

  • - Shunt

  • - Diffusion impairment

Arterial alveolar po 2 ratio
Arterial / Alveolar TherapyPO2 Ratio

  • Method of analyzing the efficiency of lung as an O2 exchanger during O2 supply

  • PaO2 / PAO2(a / A ratio) Lower limit ; 0.75

Oxygen flux
Oxygen Flux Therapy

Amount of O2 delivered to the tissues per unit time

= CaO2X cardiac output

In normal person breathing air,

O2 flux = 20 X 50 = 1,000 (mL/min)

Oxygen consumption
Oxygen Consumption Therapy

Amount of O2 consumed by the tissues per unit time (VO2)

= (CaO2 – CvO2) X Cardiac output

In normal person breathing air,

VO2 = 5 X 50 = 250 (mL/min)

Oxygen extraction ratio
Oxygen Extraction Ratio Therapy

Ratio of amount of O2 consumed by the tissues per unit time to amount of O2 delivered to the tissues per unit time

OER=(CaO2– CvO2) / CaO2

In normal person breathing air,

OER = 5 / 20 = 25 (%)

Oxygen content
Oxygen Content Tension

Amount of O2 in 100 mL of arterial (CaO2 ) or venous blood (CVO2)

= O2 combined with Hb+dissolved O2

= (Hb x 1.34 x SO2) + (PO2 x 0.003)

In normal person breathing air,

CaO2 = 19.7 + 0.3 = 20 (mL/100 mL blood)

CVO2 = 14.9 + 0.1 = 15 (mL/100 mL blood)

Oxygen content and hemoglobin saturation
Oxygen Content and TensionHemoglobin Saturation

Relationship of cardiac output to oxygen extraction
Relationship of Cardiac Output to Oxygen Extraction Tension

VO2 ; oxygen consumption

CO ; cardiac output

OE ; oxygen extraction (CaO2 – CvO2)

Pontoppidan H. N Eng J Med. 287:743,1972

Effect of Surgery on Vital Capacity Tension

Upper abd op

Lower abd op

Craig DB. A & A. 1981;60:46

Goals of oxygen therapy
Goals of Oxygen Therapy Tension

  • Reverse or prevent hypoxia

  • Treat hypoxemia

  • Decrease work of breathing

  • Decrease myocardial work

6 Tension

Low Q


Lactate (mM/L)


Low Q + hypoxemia











PvO2 (mm Hg)

Relation between PvO2 and changes in blood lactate concentration

in dogs with hypoxemia or low cardiac output

Simmons DH. J Appl Physiol 1978;45:195

Indications for cpap peep
Indications for CPAP / PEEP Tension

  • Acute lung injury

  • Pulmonary edema

  • Physiologic PEEP

  • Postoperative thoracotomy bleeding

  • Prophylactic PEEP

Cardiac effects of peep
Cardiac Effects of PEEP Tension

  • Decreased venous return

  • Right ventricular dysfunction

  • Altered left ventricular distensibility

  • Negative inotropic humoral factors ?

Effect of cardiac output on the a a po 2 difference with varying degrees of shunting
Effect of Cardiac Output on the A-a PO Tension2 Difference with Varying Degrees of Shunting

Nunn JF. Applied Resp Physiology. 5th ed. 2000

Influence of cardiac output on hypoxemia due to shunt
Influence of Cardiac Output Tension on Hypoxemia due to Shunt

  • Normal cardiac output ;

    - Shunted vol ; mod unsaturated

    - Moderate arterial unsaturation

  • Low cardiac output ;

    - Shunted vol ; markedly unsaturated

    - Disastrous arterial unsaturation

The primary compensatory mechanism Tension

for hypoxemia secondary to true shunt

mechanism is anincrease in cardiac


Adequate ventilation does not insure adequate tissue oxygenation. Poor ventilation may cause inadequate tissue oxygenation; however tissue oxygenation is often adequate in spite of poor ventilation.

Methods for Increasing oxygenation.

Oxygen Transport

  • Increasing Hb concentration

  • CV considerations

  • Synthetic O2 carriers

  • Hyperbaric oxygenation

  • Extracorporeal membraneoxygenation (ECMO)

Tissue oxygenation may be considered the primary purpose of oxygenation.internal respiration–the process of molecular gas exchange at the blood – tissue interface.Internal respirationis essential for normal cellular metabolism, O2 is consumed and CO2 is produced.

Metabolism of molecular oxygen to water
Metabolism of Molecular Oxygen to Water oxygenation.

Superoxide radical

Hydroxyl radical

Cell membrane and

Mitochondria damage

ARDS-like edema

Absorption atelectasis

Lung stiffness

Marino PL. The ICU Book. 1998