1. Dept. of PathologyDept. of Pathology
Medical CollegeMedical College
Hunan Normal UniversityHunan Normal University
(( 湖南 范大学医学院病理学教研室师湖南 范大学医学院病理学教研室师 )) 1
Chapter 11Chapter 11
Respiratory FailureRespiratory Failure
(呼吸衰竭)(呼吸衰竭)
2. 22
Respiratory FailureRespiratory Failure
a.a. IntroductionIntroduction
b.b. Etiology and ClassificationEtiology and Classification
c.c. PathogenesisPathogenesis
d.d. Alterations of Metabolism andAlterations of Metabolism and
FunctionFunction
e.e. Pathophysiological Basis ofPathophysiological Basis of
Prevention and TreatmentPrevention and Treatment
3. Normal Process of Respiration
Air Lungs Blood Tissue
External respiration
Internal respiration
Transportation
Ventilation Diffusion Perfusion
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4. 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)
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5. Running a race at 12,000 feet
Is This Respiratory Failure?
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6. 99
Respiratory FailureRespiratory Failure
a.a. IntroductionIntroduction
b.b. Etiology and ClassificationEtiology and Classification
c.c. PathogenesisPathogenesis
d.d. Alterations of Metabolism andAlterations of Metabolism and
FunctionFunction
e.e. Pathophysiological Basis ofPathophysiological Basis of
Prevention and TreatmentPrevention and Treatment
10. Classification
According to blood gas changes
Type I:
PaO2 ≤ 60 mmHg
Type II:
PaO2 ≤ 60 mmHg + PaCO2 ≥ 50 mmHg
According to pathogenesis
Ventilation
Gas-exchanging
According to duration
Acute
Chronic
According to primary site
Central
Peripheral
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11. 1414
Respiratory FailureRespiratory Failure
a.a. IntroductionIntroduction
b.b. Etiology and ClassificationEtiology and Classification
c.c. PathogenesisPathogenesis
d.d. Alterations of Metabolism andAlterations of Metabolism and
FunctionFunction
e.e. Pathophysiological Basis ofPathophysiological Basis of
Prevention and TreatmentPrevention and Treatment
12. Pathogenesis of Respiratory Failure
a.a. Dysfunction in ventilationDysfunction in ventilation
Restrictive hypoventilationRestrictive hypoventilation
Obstructive hypoventilationObstructive hypoventilation
a.a. Gas-exchange dysfunctionGas-exchange dysfunction
Diffusion impairmentDiffusion impairment
Ventilation/perfusion imbalanceVentilation/perfusion imbalance
Increase of anatomic shuntIncrease of anatomic shunt
13. a.a. Dysfunction in ventilationDysfunction in ventilation
Restrictive hypoventilationRestrictive hypoventilation
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
14. Pathogenesis of Respiratory Failure
a.a. Dysfunction in ventilationDysfunction in ventilation
Restrictive hypoventilationRestrictive hypoventilation
Obstructive hypoventilationObstructive hypoventilation
a.a. Gas-exchange dysfunctionGas-exchange dysfunction
Diffusion impairmentDiffusion impairment
Ventilation/perfusion imbalanceVentilation/perfusion imbalance
Increase of anatomic shuntIncrease of anatomic shunt
20. Pathogenesis of Respiratory Failure
a.a. Dysfunction in ventilationDysfunction in ventilation
Restrictive hypoventilationRestrictive hypoventilation
Obstructive hypoventilationObstructive hypoventilation
a.a. Gas-exchange dysfunctionGas-exchange dysfunction
Diffusion impairmentDiffusion impairment
Ventilation/perfusion imbalanceVentilation/perfusion imbalance
Increase of anatomic shuntIncrease of anatomic shunt
21. Pathogenesis
Diffusion ImpairmentDiffusion 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
22. Structure of Alveolar-Capillary Membrane
(Diffusion Membrane)
Diffusion Speed∝
Surface Area
Thickness
Alveolus
R
B
C
Capillary
Normal:
Thickness : ~1µm
Surface area: 80 m2
O2
CO2
Epithelium
Surfactant
Endothelium
24. Prolonged Time for Gas Exchange
PO2
100
80
60
40
20
0s 0.25s 0.50s 0.75 s
PCO2
46
PaO2
PaCO2
40
Time of Blood Flow Through Capillary
Dotted lines showing
thickened diffusion
membrane.
C
O
2
Epithelium
Surfactant
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29. 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”
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31. 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”
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32. Normal Dead Space-like
Hypoperfusion (dead space-like ventilation) : V/Q ↑
Seen in pulmonary artery embolism, pulmonary
vasoconstriction, pulmonary DIC
34. 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
35. Functional vs. Anatomical Shunt?
Distinquish :
Inspire Pure O2
PaOPaO22 ↑ ↑ ↑↑ ↑ ↑
PaOPaO22 ↑↑ Anatomical
Functional
37. Summary of Pathogenesis of RF
Caused by dysfunction of external respiration.
Dysfunction inDysfunction in
ventilationventilation
Restrictive
Obstructive
Type Ⅱ RF
Dysfunction in
gas-exchange
Diffusion
V/Q Ratio
Anatomic shunt
TypeⅠRF
38. 4949
Respiratory FailureRespiratory Failure
a.a. IntroductionIntroduction
b.b. Etiology and ClassificationEtiology and Classification
c.c. PathogenesisPathogenesis
d.d. Alterations of Metabolism andAlterations of Metabolism and
FunctionFunction
e.e. Pathophysiological Basis ofPathophysiological Basis of
Prevention and TreatmentPrevention and Treatment
39. Alterations of Metabolism and Function
a.a. Acid-base imbalanceAcid-base imbalance
b.b. Electrolyte disturbanceElectrolyte disturbance
c.c. Organ system dysfunctionOrgan system dysfunction
Pulmonary systemPulmonary system
Circulatory systemCirculatory system
Central nervous systemCentral nervous system
Urinary and digestive systemUrinary and digestive system
40. 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
43. 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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44. 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
46. 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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47. 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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48. 6363
Respiratory FailureRespiratory Failure
a.a. IntroductionIntroduction
b.b. Etiology and ClassificationEtiology and Classification
c.c. PathogenesisPathogenesis
d.d. Alterations of Metabolism andAlterations of Metabolism and
FunctionFunction
e.e. Pathophysiological Basis ofPathophysiological Basis of
Prevention and TreatmentPrevention and Treatment
49. 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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50. 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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52. 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
55. 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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60. 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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Respiratory failure relates to external respiration.
Acute respiratory failure can defined as a state in which the pulmonary system is no longer able to meet the metabolic demands of the body. It can be divided into hypoxaemic respiratory failure and hypercapnic respiratory failure. Hypoxaemic respiratory failure is defined as an arterial partial pressure of oxygen of less than or equal to 6.7 kPa when breathing room air and hypercapnic respiratory failure is defined as an arterial partial pressure of carbon dioxide of more than or equal to 6.7 kPa
12,000 feet = 3,780 m.
No, because the external respiratory system functions normally.
Cephalitis: 脑炎
pleural Effusion
胸腔积液; 胸膜渗出(液)
On the left is a diagram of the lungs and airways with an inset showing a detailed cross-section of normal bronchioles and alveoli. On the right is lungs damaged by COPD with an inset showing a cross-section of damaged bronchioles and alveoli
(2) A measure of the distensibility of lung using the following formula: C = ΔV / ΔP, where ΔV is the change in volume and ΔP is the change in pressure, typically expressed in L/cm HOH.
Lung compliance can be influenced by disease states. For instance, fibrosis in lungs makes the lungs stiffer, thereby, decreasing lung compliance. In Emphysema, where many alveolar walls are lost resulting in the lungs becoming loose and floppy that only a small pressure difference is necessary to maintain a large volume., there will be an increase in lung compliance.
The greater surface tension, the greater 弹性回缩力, the lower the lung compliance。
dipalmitoyl lecithin: 二棕榈酰卵磷脂(磷脂酰胆碱)
Pulmonary surfactant decreases surface tension.
The greater surface tension, the greater 弹性回缩力, the lower the lung compliance.
Obstruction mainly comes from big airways (not small airways).
Diffusion impairment = Impairment of diffusion membrane
Normal surface area of respiratory membrane is about 70-80 m^2.
Normally, only 50% (40 m^2) respiratory membrane is used under resting conditions. Respiratory membrane surface area decrease by half, respiratory failure may occur.
&lt;0.25 s is required for O2 and CO2 diffusion.
In case of shortening of diffusion time (as short as 0.25 s), only PaO2 (not PaCO2) will be affected. CO2 diffuses much faster than O2.
Normal case, PaCO2 changes from venous to arterial blood at 0.13 s.
At rest, only about half of alveolus is involved in the respiratory process, while in motion the number will increase.
V/Q at top can be as high as 3.0.
Normal: 3%
COPD: 30-50%
Normal:30%
Lung vessel disease:60%~70%
Normally, anatomic shunt accounts for 2-3% of total cardiac output.
Distinguishment of true or functional shunt by breathing 100% oxygen
Inspire pure O2 for 15-30 min to distinguish.
Patients with anatomical shunt can’t be treated with pure O2, but with mechanical ventilation.
肺泡通气与血流比例失调模式图
Why in gas-exchange dysfunction, PCO2 can be normal or down, just because 1) overventilation stimulated by low O2 level; 2) CO2 diffuses faster than O2.
Why acidosis leads to hyperkalemia? Across cells: H+-K+ interchange; Kidney: H+-Na+ exchange increase, K+-Na+ exchange decrease.
In acidosis, 1) HCO3- goes out from the cell, and Cl- goes in; 2) NH4Cl secretion is increased (therefore lower Cl).
Decrease of Cl- in type II respiratory failure because of respiratory acidosis.
Hypoxia inhibits the central respiratory center and excites peripheral respiratory center. &lt;60 mmHg: Respiration faster and deeper.
This was talked about in Hypoxia.
Cor pulmonale is a condition in which the right ventricle of the heart enlarges (with or without right-sided heart failure) as a result of diseases that affect the structure or function of the lung or its vasculature. Any disease affecting the lungs and accompanied by hypoxemia may result in cor pulmonale.
CNS is activated to control our body, so, CNS need large energy to maintain its activation status.
Too rapid correction of hypoxia will repress respiration (not good for expiration of CO2).
ARDS was defined as the ratio of arterial partial oxygen tension as fraction of inspired oxygen below 200 mmHg in the presence of bilateral infiltrates on the chest x-ray, and PAWP is less than 18 mmHg .