respiratory failure

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Respiratory Failure

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男性 , 50 岁 , 患喘息性支气管炎 30 年 ,

三年来常下肢浮肿 . 三天前因受凉发烧 , 咳嗽加重 , 咳黄痰 . 当日上午患者神志恍惚 , 嗜睡 . 查 : T 38 , ℃ 颈静脉充盈 , 肝大 , 双下肢凹陷性水肿 . 血气分析 : pH7.29, PaCO2

10.7kPa(80mmHg), PaO2 7.33kPa(55mmHg). BE

-5mmol/L 血清钾 5.5mmol/L.

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RESPIRATION

4 distinct mechanisms:

Ventilation

Gas exchange External respiration

Transport of oxygen and carbon dioxide in the blood

Internal respiration

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The Process of External Respiration

Pulmonary gas exchange

PiO2 159mmHg

PAO2 102mmHgPACO2 40mmHg

Pulmonaryventilation

PaO2 40mmHgPaCO2 46mmHg

PvO2 100mmHgPvCO2 40mmHg

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Definition of RF Disorders of external respiratory function

PaO2 <60 mmHg (8.0kpa) while breathing air at rest, with or without PaCO2 >50 mmHg(6.67kpa).

judgment standard: PaO2 <60 mmHg , PaCO2 >50 mmHg

hypotonic hypoxia with (or without) respiratory acidosis

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respiratory insufficiency: It is a condition in which respiratory function is inadequate to meet body’s needs during exertion. However, respiratory failure does so in rest.

a kind of respiratory insufficiency

a severe respiratory insufficiency

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Classification1. According to blood gas:

1) type (hypoxemic RF) :Ⅰ

PaO2 <60 mmHg (8.0kpa)

2) type (hypercapnic RF) : Ⅱ PaO2 <60 mmHg (8.0kpa) ,

with PaCO2 >50 mmHg(6.67kpa)

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2. According to primary site

central

peripheral

3. According to duration

acute

chronic

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Section 1 Causes and pathogenesis of

respiratory failure

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Chest WallChest Wall(muscle, ribs)(muscle, ribs)

ConductingConductingAirwaysAirways

DiaphragmDiaphragm(muscle)(muscle)

LungsLungsGas ExchangeGas Exchange

Pe

Pi

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• Pathogenesis of RF:

Disorders of external respiratory function

pulmonary ventilation disturbance

pulmonary gas exchange disturbance

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• Causes of RF

Disorders of:

Central Nervous System

Spinal Cord

Neuromuscular System

the chest wall and pleura

the airway

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Ⅰ.pulmonary ventilation disturbance

i. Types and Causes

restrictive hypoventilation

obstructive hypoventilation

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Mechanisms of Breathing:Mechanisms of Breathing:

• DiaphragmDiaphragm

Rib CageRib Cage

ContractContract

DiaphragmDiaphragmVolumeVolume

• External Intercostal Muscles External Intercostal Muscles IntercostalsIntercostals

ContractContractto Liftto Lift

RibRibSpineSpine

RibsRibs VolumeVolume

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component elements causing ventilation disturbance

Lung elastic resistance increased

High spinal cord damaged

Anterior angle cell damaged

Inhibition of R. center

phrenic nerve damaged

weakness of R. M

thorax wall damaged

Airway straitness or block

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Causes and mechanisms: impaired activity of respiratory muscle (dysfunction of

CNS, neural, muscle etc.) decreased compliance of thorax (chest malformation ,

pleura fibrosis) decreased compliance of lungs (pulmonary edema ,

inflammation , fibrosis, insufficient surfactant) thorax fluidify or pneumothorax

1. Restrictive hypoventilation:

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2. Obstructive hypoventilation :

central airway obstruction

peripheral airway obstruction

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above the forfication (between the glottis and the carina)

obstruction locates out of thorax （ paralysis, edema or inflammation of vocal cords ） inspiratory dyspnea

obstruction locates within thorax

expiratory dyspnea

why?

1) central airway obstruction:

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Phase of expiration

(Ptr > Patm)

Phase of inspiration(Ptr <Patm)

Phase of inspiration(Ptr>Ppl)

Phase of expiration(Ptr<Ppl)

The effects on the phase of respiration on an extrathoracic variable obstruction

The effects on the phase of respiration on an intrathoracic variable obstruction

Ptr—intratrachel pressure Ppl—pleural pressurePatm—atmospheric pressure

PtrPatm

PtrPatm

PtrPtr

Ppl Ppl

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peripheral airway character：

Wall: thin,without cartilage support；

Diameter changes with respiration ；

keep tight connection to

surrounding alveoli

2) peripheral airway obstruction (diameter <2mm ） :

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causes and mechanism: chronic obstructive pulmonary disease

(chronic bronchitis ， emphysema), severe pneumonia, atelectasis ,etc.

→ equal pressure point is moved up expiratory dyspnea

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Equal pressure point

normal person makes forced expiration

Emphysema patients makes forced expiration

point thatIntra-airway pressure

= extra-airway pressure

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Mechanism of chronic obstructive pulmonary disease (COPD)

1. inflammation stimulation, airway wall became thickening

2. Airway smooth muscle contraction

3. Retention of inflammatory secretion in airway

→inelastic resistance ↑

→ a great amount of gas keep in alveoli

4. Alveolar wall was damaged → elastic pull to peripheral airway ↓ ， collapse occur in forced expiration.

→expiratory dyspnea

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ii. Alteration of PaO2 ， PaCO2 in

pulmonary ventilation disturbance

PaO2↓

PaCO2↑ （ type II RF ）

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Ⅱ . Pulmonary gas exchange disturbance

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Respiratory Membrane Respiratory Membrane (Air-Blood Barrier)(Air-Blood Barrier)

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Pulmonary gas exchange disturbance

diffusion impairment VA / Q mismatch

anatomic shunt

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i. Diffusion impairment

Causes: area of R-M thickness of R-M diffusion time

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1. Area of R-M

Normal adult R-M: 80 m2

At rest, used R-M:35~40 m2

area of R-M : atelectasis ， pulmonary consolidation ， lobar resection, emphysema

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2. Thickness of R-M : pulmonary edema, fibrosis, formation of pulmonary hyaline membrane, hydremia

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Alteration of PaO2 , PaCO2

PaO2↓

PaCO2 : N or ↓

according to compensatory ventilation

why?

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Oxygenation of Blood

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PO2

13.33

10.67

8.00

5.33

2.67

0 0.25 0.50 0.75 s

PCO2( kPa )

6.13PvCO2

PvO2

PaO2

PaCO2

Blood gas change when blood circulating through lungs

Real line stands for normal person;

broken line stands for patients with increased thickness of R-M

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• CO2 O2 CO2/ O2

• Solubility 51.5 2.14 24• Molecular weight 44 32• square root of MW 6.63 5.66 1.17• Diffuse coefficient ratio 20/1

CO2 diffusivity is higher than O2

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At restAt rest ：：

（（ VVAA)) ： ： ~ ~ 4L4L

（（ Q) Q) ： ： ~ ~ 5L5L

VVAA/Q /Q ： ： 0.80.8

ii. ii. Ventilation-Perfusion Mismatch

ratio

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• Ventilation-Perfusion Coupling

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1.Types and Causes1) Hypoventilation of Partial alveoli （ VA/Q↓ ）

functional shunt or

venous admixture

• Causes ： Disorders of trachea or alveolus

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functional shunt : alveolar Ventilation （ VA ） ，

alveolar Perfusion (Q) have not VA / Q

accordingly , even due to inflammation

venous blood flowing through these units have not been totally arterialized and mixes into arterial blood, this process is called as functional shunt, also as venous admixture.

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O 2 CO 2

V 血 A 血

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O 2↓ CO 2

V 血 V 血

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2) Low perfusion of Partial alveoli （ VA/Q↑ ） dead space like ventilation:

alveoli at diseased region have low perfusion,while ventilation is not decreased,

alveolar ventilation can not be fully used.

• causes ： Disorders of pulmonary vessel(vessel inflammation, occlusion ， spasm ）

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O 2 CO 2

V 血 A 血

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O 2 CO 2

V 血 A 血

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2. Alteration of PaO2 ,PaCO2

N

PaCO2

PaO2 ？

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1) blood gas change in functional shunt Asthma C.bronchitis VA / Q functional shunt

PaO2 ,PaCO2

compensatory

respiration ventilation

health region diseased region VA / Q VA / Q PaO2 ↑ ， CaO2+ ， PaO2 ↓ ，

CaO2 ↓ PaCO2 ↓ CaCO2 ↓ PaCO2 ↑ ， CaCO2 ↑

PaO2 ↓ ， PaCO2 ?

PO2 and PCO2

Dissociation curve of O2 and CO2

C . O

2 an

d C

O2 (m

l/dl)

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2) blood gas change in dead space like ventilation p. embolism P. arteritis, DIC VA / Q dead space like ventilation

other region Q

functional shunt health region diseased region VA / Q VA / Q

PaO2 ↓ ， CaO2 ↓ PaO2 ↑ ， CaO2 + PaCO2 ↑ ， CaCO2 ↑ PaCO2 ↓ CaCO2 ↓

PaO2 ↓ ， PaCO2 ?

PO2 and PCO2

Dissociation curve of O2 and CO2

C . O

2 an

d C

O2 (m

l/dl)

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iii. anatomic shunt(true shunt)1 、 Under physiological conditionanatomic shunt: bronchia vein

venous blood pulmonary vein

A-V communicating branch

true shunt: there are totally no gas exchange in the blood flowing through anatomic shunt, so anatomic shunt also called as true shunt.

N ： 2% － 3%

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2 、 Under pathological conditionbronchiectasis flow of bronchial vein

shock flow of A-V shunt 

true shunt

atelectasis

Consolidation like true shunt

of lung

PaO2 PaCO2

± or or

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Ventilation disturbance （ PaO2↓

PaCO2↑ ）

Gas exchange disturbancePaO2↓

PaCO2↑ ↓N ）

restrictive

obstructive

diffusion impairment

V/Q mismatch

true shunt↑ （ V/Q=0 ）

Hypoven-tilation

summary

RF

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Section 2 The functional and metabolic

changes in RF

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Total change direction

Dysf. of external R.

hypoxemia hypercapnia

Dist. of acid-base electrolyte

Effects on organ system

Com

p.

Discom

.

PaO2 ＜ 60mmHgPaCO2 ＞ 50mmHg

PaO2 ＜ 30mmHg

PaCO2 ＞ 80mmHg

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Ⅰ. Acid-base Disorders and Electrolytes Disorders

i. Respiratory Acidosis——type Ⅱ RF : CO2 retention

Hyperkalemia: H+-K+ exchange Secretion from distal

renal tubules ↓hydrogen ion dissociate from H2CO3

carbonic acid

ii. Metabolic Acidosis ——Hypoxia →

production of lactic acid↑

excretion ↓

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iii.Respiratory Alkalosis ----type I RFHypoxia compensation hyperventilation

→ PaCO2 ↓ Hypokalemia

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Ⅱ . Respiratory system 1 、 Effects of PaO2↓and PaCO2↑

（ 1 ） PaO2↓

PaO2 ↓  stimulate peripheral inhibit respiratory center

chemoreceptor  excite respiration inhibit respiration

30mmHg<PaO2<60mmHg ： excite respiration

PaO2<30mmHg ： inhibit respiration

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(2) PaCO2↑

• PaCO2 ↑ （ <80mmHg ）→ stimulate center

chemoreceptor→respiratory center was excited→ventilation ↑

• PaCO2>80mmHg ： respiratory center was

depressed

inhaling 30% O2

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PaO2↓30~60mmHg

<30mmHg

peripheralchemoreceptor

Respiratory center

+

PaCO2↑>50mmHg

>80mmHg

-

The effects of PaO2↓and PaCO2 ↑ on R

centerchemoreceptor

+

-

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2. Primary disorders of respiratory system1) pulmonary compliance↓

pulmonary juxtapulmonary-capillary extend reflex receptor

rapid light R. 2) obstructive hypoventilation→ins/exp dyspnea3) respiratory M. fatigue → contractibility of R.M. ↓ → rapid light R. 4) central RF: slow light R.,R. rhythm disturbance e.g.: tide-like R.

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Tide-like R.(Cheyne-Stokes

Breathing)

Over low central excitability → R.pause→ PaCO2 ↑ → R.

center was stimulated →R occur→CO2was expelled out →

R. central excitability became very low

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Ⅲ. cardiovascular system

cardiovascular center

Severe PaO2 ↓and PaCO2 ↑can inhibit

mild PaO2 ↓and PaCO2 ↑can excite

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1 、 vasoconstriction and vasodilatation -blood redistribution ：

• mild PaO2 ↓and PaCO2 ↑→ cardiovascular center → sympathetic nerve →norepinephrine → α-receptor

→ vasoconstriction• local metabolite(adenosine) → vasodilatation(heart)• direct effect → vasodilatation

→ blood redistribution skin, kidney, stomach-intestine: vasoconstriction brain, heart: vasodilatation

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2 、 Heart ： mild ： heart rate ↑, myocardium contraction

force ↑,CO↑

severe: heart rate ↓, myocardium contraction,

force ↓, CO↓ ,blood pressure↓

right heart failure

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3. Cor pulmonale• concept: Cor pulmonale is right heart

hypertrophy and even failure, which is caused by RF.

• Mechanism of Cor pulmonale :

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1) pulmonary hypertension ：• pulmonary arteriole contraction ： hypoxemia ， hypercapnia →blood hydrogen ion [H+ ] ↑ →chemoreceptor → pulmonary artery contraction

• Pulmonary vessel becomes sclerosis, stegnosis ： chronic RF → pulmonary arteriole contracts long-standing and

oxygen deficit long-term → pulmonary vessel’s smooth muscle cell and fibroblast become hypertrophy and proliferation.

• Some pulmonary disorders effects:

pneumonia ， pulmonary fibrosis → pulmonary vessel became twist

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2) cardiac diastole and contraction were confined ： intrathoracic pressure ↑; hypoxemia, acidosis 3) resistance of blood flow is increased ：Hypoxemia compensation RBC increased →blood became ropiness

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Ⅳ. CNS1. PaO2 ↓ ：• PaO2 decreased to 60mmHg →intelligence and

eyesight slight impairment

• PaO2 decreased to below 40~50 mmHg

→a series symptom of nerve and consciousness.

• PaO2 decreased to 20mmHg → nerve cell will become irreversible damaged

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2. PaCO2 ↑ ： PaCO2 is higher than 80mmHg→ carbon dioxide narcosis ： headache, dizziness, dysphoria, flapping tremor, mental disorder , drowsiness, hyperspasmia, respiratory depression ,coma, even death

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3.pulmonary encephalopathy:a kind of brain dysfunction caused by RF.

Mechanism:1) brain vessel ：• hypoxia→ brain vessel dilation, blood flow↑ →brain

congestion• acidosis → blood vessel endothelium(BVE)

permeability↑ → brain interstitial tissue edema → intracranial pressure ↑, to oppress brain vessel

→ischemia, hypoxia, acidosis became severe

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2) brain cell ：• hypoxia → ATP↓,Na+-K+-ATPase↓→ brain cell edema• acidosis → glutamic acid decarboxylase (GAD ) activity ↑ → GABA↑ • acidosis → phospholipase ↑ → lysosome enzyme release → nerve cell and tissue damage

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Ⅴ. kidney ：

PaO2 sympathetic nervous system

renal blood vessel contract

renal blood flow

functional renal failure (oliguria, azotemia, metabolic acidosis)

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Ⅵ . gastrointestinal tract ： hypoxia and acidosis → excitation of sympathetic nerve → gastrointestinal tract wall vessel contraction (large amount of receptor) → ischemia CO2 retention→↑activity of carbonic anhydrase (CA) in acid cell in stomach →secrete more acid → pH of gastric juice ↓

→ gastrointestinal mucous membrane erosion,necrosis, bleeding ulcer

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Section 3 Treatment Principle

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1. Etiology treatmentCorrecting the cause and relieving the hypoxia

and hypercapniae.g. use of bronchodilators, antibiotics for respiratory infections,

establishment of airway (using endotracheal tube )

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1) General Oxygen Therapy （ typeⅠ ）： <50%O2

2) Controlled Oxygen Therapy （ typeⅡ ） :

Continuous low concentration (<30%O2 )

Low flux (1~2L/min)

2. Oxygen therapy

PaO2 =50 ~60mmHg

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3. To decrease PaCO2

1) To unblock airway2) To strengthen respiratory driving force3) Artificial assisted respiration(mechanical ventilator) 4) To add nutrition

4. Treating the consequences of hypoxemia and hypercapnia

e.g. acidosis, heart failure.

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Case analysisA man, fifty years old, has had bronchitis for thirty years. His lower limb often became swollen the latest three years. He caught a cold three days before and coughed aggravatly with yellow sputum. He became wandering and drowsiness in the morning of the day going to hospital.

P.E.: T 38 (centi-degree ), jugular vein engorged ℃ , liver swelling, double lower limb spitting edema.Blood gas: pH7.29, PaCO2 10.7kPa (80mmHg), PaO2 7.33kPa (55mmHg),BE -5mmol/L,serum K+ 6.5mmol/L.

Please answer the following questions:

1) What pathological processes are there existing in the patient? What are the pathogenesis?

2) What should we pay attention to when the patient inhaled oxygen?

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DemandsTo grasp1. the concept and pathogenesis of RF2. the concept and pathogenesis of Cor pulmonale, and pulmonary

encephalopathy

To be familiar with1. The functional and metabolic changes in RF2. principle of inhaling Oxygen for type II RF

To learnTreatment Principle of RF