Respiratory Failure

Respiration
external respiration pulmonary ventilation and
gas exchange in lung
transport of gas
internal respiration

Respiratory failure
concept and classification

1. respiratory insufficiency
The condition in which the lungs can not take in
sufficient oxygen or expel sufficient carbon dioxide to
meet the needs of the cells of the body. Also called
pulmonary insufficiency.

2. respiratory failure
Respiratory failure is a syndrome in which the respiratory
system fails in one or both of its gas exchange functions:
oxygenation and carbon dioxide elimination.
In practice, respiratory failure is defined as a PaO2 value
of less than 60 mm Hg while breathing air or a PaCO2 of more
than 50 mm Hg.

normal reference values

PaO2 < 60mmHg 8kPa
with or without PaCO2 > 50mmHg 6.67kPa
RFI = PaO2/FiO2 300

3 classification
1 according to PaCO2

hypoxemic (Group ) respiratory failure

a PaO2 of less than 60 mm Hg with a normal or low PaCO2.
Cause of: Edema, Vascular disease, Chest Wall.

hypercapnic (Group ) respiratory failure

a PaO2 low 60 mm Hg and PaCO2 of more than 50 mm Hg.
Cause of: Airway obstruction, Neuromuscular disease.

 2 according to pathogenic mechanism

ventilatory disorders
gas exchange disorders

3 according to primary site

central respiratory failure

peripheral respiratory failure

4 according to duration

acute respiratory failure

chronic respiratory failure

etiology and pathogenesis

classification of respiration failure mechanism
respiratory failure
ventilatory
disorders

gas exchange
disorders

ventilation-perfusion

mismatching

diffusion disorders

obstructive ventilatory
disorders

restrictive ventilatory
disorders

. ventilatory disorders
1. restrictive ventilatory disorders
Restrictive hypoventilation is caused by the diseases that affect
the distensibility of the alveolar.

Respiratory movement

forced breathing

Disorders of the respiratory muscles

decreased lung compliance

decrease of pulmonary surfactants and increase of
surface tension force

diffuse interstitial fibrosis

decreased

thoracic compliance of lung

deformity of thorax , fracture of several ribs,

tension
pneumothorax, thickened constrictive pleural layer.

2. obstructive ventilatory disorders

obstructive ventilatory disorders are caused by the diseases which
share the common characterestic of causing enough narrowing within

the tracheobronchial tree to increase resistance to the flow of air.

etiology
asthma, emphysema, chronic bronchitis, and bronchiectasis.

1 central airway obstruction

defined as airway obstruction between the glottis and the carina

Obstruction

is located in the

airway outside the thorax

inspiratory dysnea

three
depression
Obstruction is located in the
sign
airway inside the thorax

expiratory dysnea
expire
inspire

2 peripheral airway obstruction

smaller airways less than 2 mm in diameter.

Determinants of airway closure are the intrinsic caliber of peripheral

airways.
Smooth muscle tone, thickness of the wall,
mechanical properties of the surface film,
and secretions in the lumen ,bingding
effect of attachments of the surrounding
lung parenchyma.

equal pressure point

(EPP)
In forced expiration, the point where
intrapleural pressure and alveolar
pressure are equal.

Peripheral airway obstruction may be

caused by: specific chemical
mediators (such as histamine,
leukotrienes, prostaglandins ), other
substances released during
inflammatory and allergic responses.

EPP moves distally as expiration

progresses because as air leaves the
alveolar unit, the pressure in the
alveolar decreases hence the pressure
in the airway decreases as well.

forced expiration

3. The alteration of blood gas

1 Low PaO2 PaO2 < 60mmHg
2 PaCO2 change
A. hypoventilation high PaCO2.
R=40/50 mmHg=0.8
B. part hypoventilation: Low PaO2 and normal or low PaCO2.

. gas-exchanging dysfunction
1. diffusion disorders
The diffusion impairment is characterized by
a disruption in the exchange of O2 or CO2 or
both across the alveolar-capillary membrane.
Causes:
reduction and/or thicken of alveolar-capillary
membrane or reduction of the diffuse time.

1 etiology of diffusion disorders

reduction of diffusion membrane area

Abnormalities of diffusion may not cause arterial hypoxia in
persons at rest unless they are extremely severe.
(total: 80 mm2; at rest: 30~40 mm2)
Causes: emphysema, pneumonia, lobectomy

increase of diffusion membrane thickness

edema, fibrosis, capillary vessel dilatation

decreased time of blood contacts with alveolar

2. ventilation/perfusion imbalance
The dysfunction of gas exchange can arise secondary to ventilation
/perfusion mismatching.

V
A

VA/ Q

Top

1.2L/min

0.4L/min

3.0

Middle

1.8L/min

2.0L/min

0.9

Bottom

2.1L/min

3.4L/min

0.6

1) type and cause of ventilation-perfusion-mismatching

(1) decreased ratio of VA/Q

underventilated in relation to their perfusion

asthma, chronic bronchitis, obstructive emphysema, fibrosis,

edema

VA/ Q
functional shunt>30%

part alveolar ventilatory

respiratory failure


(2) increased ratio of VA/Q
poor perfusion in relation to their ventilation with air

pulmonary artery embolization, DIC in lung, vessels contract, pulmonary

arteritis,
dead space like ventilation
respiratory failure

VA/Q

poor perfusion

3 increased of anatomical shunt

Right-to-left shunts or anatomic shunt
increased

of anatomical shunt

bronchiectasi
s
increased

of
anatomical-like shunt
pulmonary
consolidation,
Atelectasis

anatomicallike shunt

anatomic shunt
Pulmonary A-V
shunt open

true
shunt
Respiratory
failure

. Acute respiratory distress syndrome ARDS

[concept]
ARDS is a clinical description of severe lung injury
characterized by increased permeability of alveolar-capillary
membranes, development of protein-rich pulmonary edema,
marked hypoxemia refractory to increase in inspired oxygen
concentration, and the absence of left ventricular failure.

[etiology]
shock from any cause,
multisystem trauma,
infection including bacterial and nonbacterial pneumonia,
inhaled toxic substances,
overdose of some drug,
acute pancreatitis.

[ pathogenesis of ARDS]
1 direct injury of damage factor
2 indirect injury of inflammation medium

ARDS

[Mechanisms of respiratory failure]

1. diffusion disorders
damage of alveolar-capillary membrane

increased permeability

diffusion disorders

2. ventilatory disorders
edema, type alveolar epithelial cells damage

airway obstruction

obstructive ventilatory

restrictive ventilatory

disorders

disorders

inflammation medium

decreased lung volume

bronchia spasm respiratory failure

3 VA/Q mismatching

Effects of respiratory failure

1. Acid-base disturbances & disorders of electrolyte balance
2. Alteration of the respiratory system
peripheral chemoreceptor
PaO2 60mmHg

30mmHg

respiratory center(+)

respiratory movement

respiratory center (-)

respiratory movement

PaCO2

central chemoreceptor (+)

80mmHg

respiratory movement

respiratory center (-)

respiratory movement

3. Alteration of the respiratory system

compensatory

reaction

PaO2<60 mmHg PaCO2 increase

cardiovascular center(+)

increase in cardiac output : increase in stroke volume and heart

rate
redistribution of blood
injurious changes

flow

PaO2< 40 mmHg PaCO2> 80 mmHg

center(-)

rate slow, decreased blood pressure

cardiac output decrease

pulmonary hypertension

cardiovascular

co pulmonale
PaO2

Pulmonary
wall

pulmonary
vasoconstrictio
n
vascular

Stenosis

RBC blood viscosity

blood resistance

chronic pulmonary
thickening
and
hypertension
pulmonary arterial embolism, capillary
hardening
damage
afterload to right
ventricle
Hypoxia, acidosis
myocardial systolic
and diastolic function(-)
difficulty breathing
Restricted diastolic co pulmonale

4. Alteration of the nervous system

(1) Hypoxia: the nervous system is very sensible to oxygen lack.
< 40~50 mmHg, serious but reversible deterioration in cerebral
function
( orientation, arithmetic tasks, memory) occurs, and
restlessness and
confusion are common.
< 30 mmHg, loss of consciousness results.

(2) Hypercapnia: CO2 nacosis.

< 20 mmHg, irreversible damage of neural cells.

a condition of confusion, tremors, convulsions, and possible coma

that
may occur if blood levels of carbon dioxide increase to 80 mm Hg or
higher.

[pulmonary encephalopathy]
cerebrovascular

PaCO2, acidosis
hypoxia

Cerebral vasodilation

vascular endothelial damage

edema on brain cell

injury

Intracranial pressure

Brain cell injury

CSF pH 7.25

extracellular brain edema

Vascular compression
Increased cerebral anoxia

EEG slow or stop

GABA
lysosomal membrane stability

Cerebral blood flow

lysosomal enzyme release

pulmonary
encephalopath
y
nerve cell necrosis

4. Alteration of the renal function

5. Alteration of the digestive system