11 respiratory failure

Dept. of PathologyDept. of Pathology

Medical CollegeMedical College

Hunan Normal UniversityHunan Normal University

(( 湖南师范大学医学院病理学教研室湖南师范大学医学院病理学教研室 )) 1

Chapter 11Chapter 11

Respiratory FailureRespiratory Failure（呼吸衰竭）（呼吸衰竭）

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Respiratory FailureRespiratory Failure

①① IntroductionIntroduction

②② Etiology and Classification Etiology and Classification

③③ Pathogenesis Pathogenesis

④④ Alterations of Metabolism and Alterations of Metabolism and

Function Function

⑤⑤ Pathophysiological Basis of Prevention Pathophysiological Basis of Prevention

and Treatmentand Treatment

Normal Process of Respiration

Air Lungs Blood Tissue

External respiration

Internal respiration

Transportation

Ventilation Diffusion Perfusion

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Respiratory Failure: Definition

Respiratory failure (RF) is a syndrome in which the

respiratory system fails to adequately oxygenate the

venous blood w/ or w/o retention of carbon dioxide.

PaO2: 60 mmHg (when breathing room air)

PaCO2: Normal (type I) or 50 mmHg (type II)7

Running a race at 12,000 feet

Is This Respiratory Failure?

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Function Function



Common Causes of Respiratory Failure

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EtiologyRespiratory pump damage

Brain disease (trauma or tumor)

Cephalitis

Pleural Effusion

Pneumothorax ( 气胸 )

Lung solid lesionPneumonia

Emphysema ( 肺气肿 )

Atelectasis ( 肺不张 )

Airway obstructionLaryngeal edema

Chronic bronchitis

Foreign body (or tumor)

Gas-exchanging problemPulmonary edema

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(气胸 )(胸腔积液 ) Pleural Effusion Pneumothorax

Emphysema (肺气肿 ) 12

Classification According to blood gas changes

Type I:

PaO2 60 mmHg

Type II:

PaO2 60 mmHg + PaCO2 50 mmHg

According to pathogenesisVentilation

Gas-exchanging

According to durationAcute

Chronic

According to primary site

Central

Peripheral13

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Function Function



Pathogenesis of Respiratory Failure

①① Dysfunction in ventilationDysfunction in ventilation

Restrictive hypoventilation Restrictive hypoventilation

Obstructive hypoventilationObstructive hypoventilation

②② Gas-exchange dysfunctionGas-exchange dysfunction

Diffusion impairmentDiffusion impairment

Ventilation/perfusion imbalanceVentilation/perfusion imbalance

Increase of anatomic shuntIncrease of anatomic shunt



a)a) Dysfunction of respiratory pump activityDysfunction of respiratory pump activity

b)b) Decrease of lung compliance (solid lesions)Decrease of lung compliance (solid lesions)

Pathogenesis









Causes:

Asthma

Chronic Obstructive Pulmonary Disease (COPD)

(Chronic bronchitis)

Types:

Central airway obstruction

Peripheral airway obstruction

Obstructive Hypoventilation

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Outside of chest

Inside of chest

Central Airway Obstruction

Trachea crotch

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Inspiration

Obstruction Located Outside the Chest

Inspiratory dyspnea

Expiration

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http://www.dabaoku.com/gif/154/imagepage/image376.htm




ExpirationInspiration

Expiratory dyspnea

Obstruction Located Inside the Chest

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Alveolus

Inspiration

Bronchiole

Elastic tissue

Expiration

Expiratory dyspnea

Alveolus

Bronchiole

Elastic tissue

Peripheral airway obstruction

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Pathogenesis

Diffusion Impairment Diffusion Impairment

a)a) Increase of thicknessIncrease of thickness

b)b) Decrease of gas-exchange areaDecrease of gas-exchange area

c)c) Shortening of diffusion timeShortening of diffusion time

Structure of Alveolar-Capillary Membrane(Diffusion Membrane)

Diffusion Speed∝ Surface Area

Thickness

Alveolus

RBC

Capillary

Normal:

Thickness ： ~1µm

Surface area: 80 m2

O2

CO2

Epithelium

Surfactant

Endothelium

Normal Gas Exchange

Blood

Total blood flow time from the arteriole end to the venule end:

0.75 s

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Prolonged Time for Gas Exchange

PO2

100

80

60

40

20

0s 0.25s 0.50s 0.75 s

PCO2

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PaO2

PaCO2

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Time of Blood Flow Through Capillary

Dotted lines showing thickened diffusion membrane.

CO

2

Epithelium

Surfactant

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Increase of Thickness of Diffusion Membrane

Normal Edema

CO

2

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Decrease of Gas Exchange Area

Atelectasis (肺不张 ) of the whole left lung caused by cancer

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Normal Ventilation/Blood Flow Balance

V: Alveolar ventilation (N: 4 L/min)

Q: Pulmonary blood flow (N: 5 L/min)

Normal V/Q : 0.8 (bottom)

V/Q ratio = Ventilation (V)

Blood flow (Q)

Pathological V/Q Imbalance

Hypoventilation (↓V)

- V /Q? (< 0.8)

- Also called “Functional shunt” or

“Venous admixture”

Hypoperfution (↓Q)

- V /Q ? (> 0.8)

- Also called “Dead space-like ventilation”40

Normal

Functional Shunt

Hypoventilation (functional shunt) ： V/Q ↓

Seen in asthma, COPD, edema, fibrosis

Pathological V/Q Imbalance

Hypoventilation (↓V)

- V /Q? (< 0.8)

- Also called “Functional shunt” or

“Venous admixture”

Hypoperfution (↓Q)

- V /Q ? (> 0.8)

- Also called “Dead space-like ventilation”42

Normal

Dead Space-like

Hypoperfusion (dead space-like ventilation) ：V/Q ↑Seen in pulmonary artery embolism, pulmonary vasoconstriction, pulmonary DIC


Anatomic Shunt (True Shunt) Part of venous blood directly flows into the pulmonary vein through the bronchial vein or arterio-venous fistula.

Airway

Capillary

Alveolus

vein

Artery

Arterio-venous fistulas

Functional vs. Anatomical Shunt?Distinquish：

Inspire Pure O2

PaOPaO2 2 ↑ ↑ ↑↑ ↑ ↑

PaOPaO2 2 ↑↑ Anatomical

Functional

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Summary of Pathogenesis of RF

Caused by dysfunction of external respiration.

Dysfunction Dysfunction in in

ventilativentilationon

Restrictive

ObstructiveType Ⅱ RF

Dysfunction in gas-

exchange

Diffusion V/Q RatioAnatomic shunt

TypeⅠRF

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Function Function



Alterations of Metabolism and Function

①① Acid-base imbalanceAcid-base imbalance

②② Electrolyte disturbanceElectrolyte disturbance

③③ Organ system dysfunctionOrgan system dysfunction

Pulmonary systemPulmonary system

Circulatory systemCirculatory system

Central nervous systemCentral nervous system

Urinary and digestive systemUrinary and digestive system

Acid-Base Imbalance

Metabolic acidosis (seen in both types)

Respiratory acidosis

Respiratory alkalosis

Metabolic alkalosis (Iatrogenic)Mixed acid-base disturbances

Type Ⅰ RF accompanied with hyperventilation: Metabolic acidosis + Respiratory alkalosis

Type Ⅱ RF: Metabolic acidosis + Respiratory acidosis

Simple acid-base disturbances

Hyperkalemia (↑ K+)

Acidosis

Increased tissue catabolism

Hypochloremia (↓ Cl-) or Hyperchloremia (↑ Cl-)

Depending on types of acid-base disturbance

RAc: Hypochloremia

RAl: Hyperchloremia

Electrolyte Disturbance

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Cl--HCO3- Exchange

+ H ＋Hb(O2)-HHb(O2)

RBC

HCO3-

CO2 H2CO3＋ H2O

Cl-

Cl- HCO3-

CO2

H2CO3

+

H2O

Hypochloremia Occurring in Type II RF

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Alterations of Respiratory System

PaO2

<60 mmHg: ↑ respiratory movement

<30 mmHg:↓respiratory center

PaCO2

>50 mmHg: ↑ respiratory movement

>80 mmHg:↓respiratory center

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Alterations of Circulatory System

Compensatory responses

Hypoxia and hypercapnia → ↑ vasomotor center

Increase HR, CO, myocardial contraction, BP; blood redistribution

Injurious responses

Hypoxia and hypercapnia → ↓vasomotor center

decrease HR, CO, myocardial contraction, BP;cor pulmonale

Pulmonary Heart Disease (cor pulmonale)

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Alterations of central nervous system

CNS is the most sensitive organ to hypoxia.

PO2<60 mmHg: gentle impairment of intelligence and vision

PaCO2>80 mmHg: CO2 narcosis

PO2<50 mmHg: appearance of nervous and psychiatric symptoms

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Alterations of urinary and digestive system

Functional acute renal insufficiency:

Excitement of sympathetic nerve leads to renal vessel constriction and RBF and GFR reduction.

Gastro-intestinal insufficiency:

Excitement of sympathetic nerve leads to GI organ vessel constriction → erosion, necrosis, hemorrhage, ulcer.

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Function Function



Prevention and Treatment

1. Remove the factors that cause RF

2. Raise PaO2 via oxygen therapy

3. Reduce PaCO2 through improving ventilation

4. Others:

Correct acid-base imbalance

Correct electrolyte disturbance

Protect against heart and brain failure

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Type II RF:

Low concentration (30% O2)

Low flow (1 - 2 L/min)

- Avoid too rapid correction of hypoxia

Oxygen Therapy

Type I RF:

High concentration (40% O2)

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Introduction

Etiology and Pathogenesis

ARDS

Alterations of Metabolism and Function

Principle for Treatment

Contents

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Acute Respiratory Distress Syndrome

Definition Clinical concept

defined it as a spectrum of ALI

- Acute onset

- bilateral infiltrates on CXR (“White lung”)

- PCWP =< 18 mmHg

- Hypoxia and PaO2/FiO2 =< 200

( ALI if P/F ratio =< 300 )

-No cardiovascular lesion 67

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ARDS is a severe lung syndrome (not a disease) caused by a variety of direct and indirect issues. It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange

Pathophysiological concept

Alveolar-capillary membrane injury

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Acute respiratory distress syndrome

Normal

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ARDS

Acute lung injury

Diffuse alveolar damage (DAD)/Acute respiratory distress syndrome

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ARDS

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White lung75

Causes

Sepsis and Shock

Severe multiple trauma

Aspiration of gastric contents

Inhalation of toxic gases and fumes

etc.

Insults involved in alveolar capillary membrane injury

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Pathogenesis

A-Cm injury

Pathogenic factors

PMN activation

Protease release ROS generation Inflammatory mediators

Plt activation aggregation

Thrombosis

Pulmonary edemaBleeding

hyaline membrane

Atelectasis Bronchial spasm

Vaso-constriction

Diffusion dysfunction

ShuntDead space

Hypoxemia 77

11 respiratory failure

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