Respiratory Failure

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Respiratory Failure

• Zhang Xiao-ming
• Dept. pathophysiology

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• ??, 50?, ????????30?, ????????. ????????,
  ????, ???. ??????????, ??. ? T 38?, ?????, ??,
  ????????. ???? pH7.29, PaCO2 10.7kPa(80mmHg),
  PaO2 7.33kPa(55mmHg). BE -5mmol/L??? 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
PiO2 159mmHg
Pulmonary ventilation
PAO2 102mmHg PACO2 40mmHg
Pulmonary gas exchange
PaO2 40mmHg PaCO2 46mmHg
PvO2 100mmHg PvCO2 40mmHg
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• Definition of RF
• Disorders of external respiratory function
• PaO2 lt60 mmHg (8.0kpa) while breathing air at
  rest, with or without PaCO2 gt50 mmHg(6.67kpa).
• judgment standard PaO2 lt60 mmHg , PaCO2
  gt50 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 bodys needs during exertion.
However, respiratory failure does so in rest.
a kind of respiratory insufficiency a
severe respiratory insufficiency
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• Classification
• 1. According to blood gas
• 1) type?(hypoxemic RF)
• PaO2 lt60 mmHg (8.0kpa)
• 2) type ? (hypercapnic RF)
• PaO2 lt60 mmHg (8.0kpa) ,
• with PaCO2 gt50 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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• Pathogenesis of RF
• Disorders of external respiratory function
  pulmonary ventilation disturbance
• pulmonary gas exchange disturbance

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• ?.pulmonary ventilation disturbance
• i. Types and Causes
• restrictive hypoventilation
• obstructive hypoventilation

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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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component elements causing ventilation disturbance
Lung elastic resistance increased
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1. Restrictive hypoventilation

• 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

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• 2. Obstructive hypoventilation
• central airway obstruction
• peripheral airway obstruction

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1) central airway obstruction

• 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?

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Phase of inspiration (Ptr ltPatm)
Phase of inspiration (PtrgtPpl)
Phase of expiration (PtrltPpl)
Phase of expiration (Ptr gt Patm)
Patm
Patm
Ptr
Ptr
Ptr
Ptr
Ppl
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
Ptrintratrachel pressure
Pplpleural pressure Patmatmospheric pressure
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2) peripheral airway obstruction (diameter lt2mm)

• peripheral airway character
• ? Wall thin,without cartilage support
• ? Diameter changes with respiration
• keep tight connection to
• surrounding alveoli

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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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point that Intra-airway pressure extra-airway
pressure
Equal pressure point
normal person makes forced expiration
Emphysema patients makes forced expiration
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• ii. Alteration of PaO2 ,PaCO2 in
• pulmonary ventilation disturbance
• PaO2?
• PaCO2? ( type II RF)

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? . Pulmonary gas exchange disturbance
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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-M3540 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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ratio
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• Ventilation-Perfusion Coupling

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• 1.Types and Causes
• 1) Hypoventilation of Partial alveoli (VA/Q?)
• functional shunt or
• venous admixture
• CausesDisorders 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
A?
V?
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O 2?
CO 2
V?
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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.
• causesDisorders of pulmonary vessel(vessel
  inflammation, occlusion, spasm)

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O 2
CO 2
A?
V?
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O 2
CO 2
A?
V?
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2. Alteration of PaO2 ,PaCO2

PaO2
?
N
PaCO2
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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 ?
C . O2 and CO2 (ml/dl)
PO2 and PCO2 Dissociation curve of O2 and CO2
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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 ?
C . O2 and CO2 (ml/dl)
PO2 and PCO2 Dissociation curve of O2 and CO2
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iii. anatomic shunt(true shunt)

• 1?Under physiological condition
• anatomic 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 condition bronchiectasis
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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summary
restrictive
Ventilation disturbance(PaO2? PaCO2?)
Hypoven- tilation
?
obstructive
RF
Gas exchange disturbance PaO2? PaCO2? ?N)
diffusion impairment
V/Q mismatch
true shunt?(V/Q0)
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Section 2 The functional and metabolic changes
in RF
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Total change direction
Comp.
hypoxemia hypercapnia
PaO2lt60mmHg PaCO2gt50mmHg
Dysf. of external R.
Effects on organ system
Dist. of acid-base electrolyte
Discom.
PaO2lt30mmHg PaCO2gt80mmHg
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?. Acid-base Disorders and Electrolytes Disorders

• i. Respiratory Acidosistype ? 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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• Respiratory Alkalosis ----
• type I RF
• Hypoxia compensation hyperventilation
• ? PaCO2 ?
• Hypokalemia

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?. Respiratory system

• 1?Effects of PaO2?and PaCO2?
• (1) PaO2?
• PaO2 ?
•  
• stimulate peripheral inhibit
  respiratory center chemoreceptor
•  
• excite respiration inhibit
  respiration
• 30mmHgltPaO2lt60mmHg excite respiration
• PaO2lt30mmHg inhibit respiration

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• (2) PaCO2?
• PaCO2 ? (lt80mmHg)?stimulate center
  chemoreceptor?respiratory center was
  excited?ventilation ?
• PaCO2gt80mmHg respiratory center was depressed
• inhaling 30 O2

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The effects of PaO2?and PaCO2 ? on R

Respiratory center
PaO2? 3060mmHg lt30mmHg

peripheral chemoreceptor
-
center chemoreceptor
PaCO2? gt50mmHg gt80mmHg

-
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• 2. Primary disorders of respiratory system
• pulmonary compliance?
• pulmonary
  juxtapulmonary-capillary
• extend reflex
  receptor
• rapid light R.
• 2) obstructive hypoventilation?ins/exp dyspnea
• 3) 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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?. cardiovascular system
mild PaO2 ?and PaCO2 ?can excite
cardiovascular center
Severe PaO2 ?and PaCO2 ?can inhibit

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• 1? vasoconstriction and vasodilatation
• -blood redistribution
• mild PaO2 ?and PaCO2 ?? cardiovascular center
  ? sympathetic nerve ?norepinephrine ?
  a-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 vessels 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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• ?. CNS
• 1. PaO2 ?
• PaO2 decreased to 60mmHg ?intelligence and
  eyesight slight impairment
• PaO2 decreased to below 4050 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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• ?. kidney

PaO2 sympathetic nervous
system


renal blood vessel contract
renal blood flow

functional renal failure
(oliguria, azotemia, metabolic acidosis)
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?. 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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• Etiology treatment
• Correcting the cause and relieving the hypoxia
  and hypercapnia
• e.g. use of bronchodilators,
• antibiotics for respiratory infections,
  establishment of airway
• (using endotracheal tube )

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2. Oxygen therapy

• 1) General Oxygen Therapy(type?)lt50O2
• 2) Controlled Oxygen Therapy (type? )
• Continuous low concentration (lt30O2 )
• Low flux (12L/min)

PaO2 50 60mmHg
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3. To decrease PaCO2

• 1) To unblock airway
• 2) To strengthen respiratory driving force
• 3) 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 analysis A 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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Demands

• To grasp
• 1. the concept and pathogenesis of RF
• 2. the concept and pathogenesis of Cor pulmonale,
  and pulmonary encephalopathy
• To be familiar with
• 1. The functional and metabolic changes in RF
• 2. principle of inhaling Oxygen for type II RF
• To learn
• Treatment Principle of RF