Pathophysiology and general management of failure of arterial oxygenation
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Pathophysiology and General Management of Failure of Arterial Oxygenation. Dong Soo Kim, M.D. [email protected] www.nopain365.com. 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

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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]

www.nopain365.com


Pathophysiology and general management of failure of arterial oxygenation

  • 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)


Relationship of pao 2 and sao 2

Relationship of PaO2 and SaO2


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)


Tracheobronchial tree

Tracheobronchial Tree


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


Pathophysiology and general management of failure of arterial oxygenation

Oxygen Transport Cascade


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


Pathophysiology and general management of failure of arterial oxygenation

Oxygen Transport


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 ↑

Hyperdynamic

45

Normal

35

Compromised

PvO2

27

Metabolic disruption

20

Death


Pathophysiology and general management of failure of arterial oxygenation

Critical level of PvO2

20

18

16

Blood lactate (mEq/L)

14

Survivors

12

Nonsurvivors

10

8

6

Upper limit of

normal lactate conc.

4

2

0

20

22

24

26

28

30

32

34

36

38

40

PvO2(mm Hg)

Relation between blood lactate and PvO2

JAMA 1976;236:570


Cellular metabolism

Aerobic

Glucose

Pyruvate

CO2 + H2O + ATP

Anaerobic

Glucose

Pyruvate

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


Pathophysiology and general management of failure of arterial oxygenation

Oxyhemoglobin Dissociation Curve


Pathophysiology and general management of failure of arterial oxygenation

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

Diffusion

Hypoxia


Theoretical respiratory unit

Theoretical Respiratory Unit


Theoretical respiratory unit1

Theoretical Respiratory Unit


Subdivisions of physiological shunt

Subdivisions of Physiological Shunt


Pathophysiology and general management of failure of arterial oxygenation

Normal Shunts


Pathophysiology and general management of failure of arterial oxygenation

Increased A – a Oxygen Gradient

Abnormal

Shunts


Pathophysiology and general management of failure of arterial oxygenation

Increased A – a Oxygen Gradient

Endobronchial

Intubation


Pathophysiology and general management of failure of arterial oxygenation

Increased A – a Oxygen Gradient

V/Q

Mismatch

Shunt

↓V/Q ratio(shunt effect)


Pathophysiology and general management of failure of arterial oxygenation

Increased A – a Oxygen Gradient

V/Q

Mismatch

↑V/Q ratio

Deadspace


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

Hypoxemia

Total plugging

Absorption atelectasis

Lung compliance ↓

Stasis pneumonia

Fever


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

  • 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 PaO2

Snyder JV. Oxygen transport in the critical ill. 1995


Classification of hypoxia

Classification of Hypoxia


Pathophysiology and general management of failure of arterial oxygenation

“삼순이 없는 세상

살아서 뭐하나……”


Pathophysiology and general management of failure of arterial oxygenation

“누굴 놀리나……”


General management of hypoxemia

General Management of Hypoxemia

  • 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 O2 Therapy on Variable Types of Hypoxemia


Effect of hypoventilation on oxygen therapy

Effect of Hypoventilation 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

Braun HA. Introduction to Respiratory Physiology. 1990


Effect of varying amounts of shunt on arterial oxygen tension

Effect of Varying Amounts of Shunt on Arterial Oxygen Tension

Br J Anaesth 1973;45:711


Hypoxemia and oxygen therapy

Hypoxemia and Oxygen Therapy

  • Refractory hypoxemia;

    Secondary to true shunt mechanism

  • Responsive hypoxemia ;

    Secondary to shunt effect


Diagnostic approach of refractory hypoxemia

Diagnostic Approach of Refractory Hypoxemia

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

Shapiro BA. Clinical application of blood gases. 1982


Indices of virtual shunt

Indices of Virtual Shunt

* 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

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

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

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

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 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 FiO2

  • 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 ofLow FiO2 Therapy System

  • LowFiO2therapy is adequate if ;


Relationship between respiratory rate and fio 2 during oxygen administration

Relationship between Respiratory Rate and FiO2 during Oxygen Administration

Nasal cannula

O2 flow = 6 L/min

Vt = 500 mL

0.60

0.6

0.44

FiO2

0.4

0.32

0.2

0

20

30

40

10

Respiratory rate (breaths/min)

O’Connor. Crit Care Clin. 1995


Pathophysiology and general management of failure of arterial oxygenation

In a low - flow system,

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 FiO2

  • 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 High - flow Oxygen Systems

  • Maintenance of Consistent and

  • predictable FiO2

  • Maintenance of adequate

  • temperature and humidity


Pathophysiology and general management of failure of arterial oxygenation

In the presence of severe shunt,

no amount of O2will fully oxygenate

the blood. This a common setting for

O2 toxicity.


Complications associated with excessive high fio 2

Complications associated with Excessive HighFiO2

  • Pulmonary oxygen toxicity

  • Atelectasis

  • Convulsions


Pathophysiology and general management of failure of arterial oxygenation

Oxygenmust 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

End-Exp

PEEP 12cmH2O

0

+12

A

-5

0

PAP

0

B

+12

-5

+5

PAP ;Proximal airway pressure

A : Unstable lung

B : Normal lung


Pulmonary effects of peep

Pulmonary Effects of PEEP

  • Increased FRC

  • Increased alveolar volumes

  • Alveolar recruitment

  • Redistribution of lung extravascular water

  • Decreased intrapulmonary shunting

  • Decreased dead space ventilation


Chest physiotherapy

Chest Physiotherapy

  • Improve distribution of ventilation

  • Mobilize secretions

  • Improve efficiency of ventilation

  • Improve cardiopulmonary work capacity


Postural drainage post basal seg lower lobe

Postural Drainage post. basal seg., lower lobe


Chest percussion

Chest Percussion

  • 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

  • Shaking pressure applied to the chest wall only during exhalation

  • Facilitate excretion of dislodged mucus from the airways

  • Inducing cough


Pathophysiology and general management of failure of arterial oxygenation

Thank you for your attention!


Physiologic function of the lung

Physiologic Function of the Lung

  • Respiratory :

    - Oxygenation

    - Ventilation

  • Non-respiratory :

    - Regulation of acid-base balance

    - Activation of circulating precursors of vasoactive substances

    - Inactivation of circulating vasoactive substances


Pathophysiology and general management of failure of arterial oxygenation

Inactivation of Circulating Vasoactive Substances


Pathophysiology and general management of failure of arterial oxygenation

Activation of Circulating Precursors

of Vasoactive Substances


Pathophysiology and general management of failure of arterial oxygenation

Intrapulmonary Conversion of Angiotensin


Pathophysiology and general management of failure of arterial oxygenation

Role of Lungs and Kidneys in

Regulation of Acid-Base Balance


Pathophysiology and general management of failure of arterial oxygenation

Role of Lungs in Regulation

of Acid-Base Balance

Respiratory compensation in metabolic acidosis


Pathophysiology and general management of failure of arterial oxygenation

Role of Kidneys in Regulation

of Acid-Base Balance

Renal compensation in respiratory acidosis


Normal ventilation

Normal Ventilation


Alveolar hypoventilation

Alveolar Hypoventilation


Relationship of ventilation pattern and alveolar ventilation

Relationship of Ventilation Pattern and 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


Pathophysiology and general management of failure of arterial oxygenation

Calculation of Ideal Alveolar O2 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)


Pathophysiology and general management of failure of arterial oxygenation

Alveolar to Arterial Oxygen Gradients

  • 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 / AlveolarPO2 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

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

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

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 in relation to hemoglobin and oxygen tension

Oxygen Content in relation to Hemoglobin and Oxygen Tension


Oxygen content

Oxygen Content

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 andHemoglobin Saturation


Relationship of cardiac output to oxygen extraction

Relationship of Cardiac Output to Oxygen Extraction

VO2 ; oxygen consumption

CO ; cardiac output

OE ; oxygen extraction (CaO2 – CvO2)

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


Pathophysiology and general management of failure of arterial oxygenation

Effect of Surgery on Vital Capacity

Upper abd op

Lower abd op

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


Goals of oxygen therapy

Goals of Oxygen Therapy

  • Reverse or prevent hypoxia

  • Treat hypoxemia

  • Decrease work of breathing

  • Decrease myocardial work


Pathophysiology and general management of failure of arterial oxygenation

6

Low Q

Hypoxemia

Lactate (mM/L)

4

Low Q + hypoxemia

Threshold

2

0

-2

60

10

20

30

40

50

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

  • Acute lung injury

  • Pulmonary edema

  • Physiologic PEEP

  • Postoperative thoracotomy bleeding

  • Prophylactic PEEP


Cardiac effects of peep

Cardiac Effects of PEEP

  • 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 PO2 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 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


Pathophysiology and general management of failure of arterial oxygenation

The primary compensatory mechanism

for hypoxemia secondary to true shunt

mechanism is anincrease in cardiac

output.


Pathophysiology and general management of failure of arterial oxygenation

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.


Pathophysiology and general management of failure of arterial oxygenation

Methods for Increasing

Oxygen Transport

  • Increasing Hb concentration

  • CV considerations

  • Synthetic O2 carriers

  • Hyperbaric oxygenation

  • Extracorporeal membraneoxygenation (ECMO)


Pathophysiology and general management of failure of arterial oxygenation

Tissue oxygenation may be considered the primary purpose ofinternal 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

Superoxide radical

Hydroxyl radical

Cell membrane and

Mitochondria damage

ARDS-like edema

Absorption atelectasis

Lung stiffness

Marino PL. The ICU Book. 1998


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