RESPIRATORY FAILURE

RESPIRATORY FAILURE

Respiration is a fundamental cellular process.

Definition
= respiratory failure is the incapacity of the
body to maintain normal gas exchange at
the cellular level as well as the incapacity
of maintaining the aerobic metabolism.
 RESPIRATORY FAILURE
Mechanisms of respiratory failure:
- the incapacity of the thoracic-pulmonary system to
achieve a normal gas exchange at the pulmonary level
(pulmonary respiratory failure);
- the incapacity of the cardio-vascular system to
maintain an optimal tissue perfusion
(e.g. referring to the shock states);
- the incapacity of tissues to use the oxygen brought by
the arterial blood at the cellular level
(e.g. septic shock, cyanide poisoning);
 RESPIRATORY FAILURE
Respiration is
a function of the respiratory system

Definition
= the incapacity of the lung to maintain
normal levels of oxygen and carbon
dioxide in arterial blood.
 RESPIRATORY FAILURE
- partial pressure of oxygen in arterial blood
PaO2 < 60 mmHg
Hypoxemia is the mandatory consequence
of respiratory failure.

- partial pressure of CO2 in arterial blood

PaCO2 > 44 mmHg
While respiratory failure means always the decrease of PaO2,
the alteration of PaCO2 is not the rule.
 RESPIRATORY FAILURE
PaO2
• 60 mm Hg - threshold of hypoxemia is a relative
value.
• PaO2 which defines respiratory failure is
specific to each patient.
• It depends on:
– the inspiratory fraction of O2 – FiO2
– the patient age
– the chronic level of the blood gases
 RESPIRATORY FAILURE
PaO2
Inspiratory fraction of O2:
• FiO2 = 0,21 → PaO2 = 100mm Hg
• FiO2 = 0,4 → PaO2 = 200mm Hg
• FiO2 = 0,6 → PaO2 = 300mm Hg
• FiO2 = 1 → PaO2 = 500mm Hg

respiratory dysfunction / respiratory failure

 CLASSIFICATION
OF RESPIRATORY FAILURE
= pathophysiological classification:
- hypoxemic RF
PaO2 < 60mmHg
PaCO2 </= 40mmHg
Synonyms: Type I RF
Partial RF
Nonventilatory RF
- hypoxemic-hypercapnic RF
PaO2 < 60mmHg
PaCO2 > 45 mmHg
Synonyms: Type II RF
Global RF
Ventilatory failure
 CLASSIFICATION
OF RESPIRATORY FAILURE

• classification according to
the duration of the evolution:
- acute RF
- chronic RF
 RESPIRATORY FAILURE

Common features of acute RF:

- appears within minutes, hours or days;
- is associated with
- hypoxemia
- imbalance of the acid-base status (acidemia or alkalemia);
- is a immediate life threatening condition.
 RESPIRATORY FAILURE

Common features of chronic RF:

- appears after months/years of evolution;
- is associated with
- hypoxemia
- hypercapnia;
- is a potential life threatening condition;
- results after a chronic disease or a sequel of an
acute/chronic process.
 RESPIRATORY FAILURE

Clinical classification
- manifest RF
- hypoxemia and hypercapnia at rest
- compensated RF
a low level of exercise is possible, but results in homeostatic
alterations: hypoxemia and respiratory acidosis with metabolic
compensation
- decompensated RF
severe alterations of blood gases, accompanied by alterations of the
normal functions of the different tissues (e.g. the brain - respiratory
encefalopathy).
- latent RF
- no signs of RF at rest;
- RF is manifest in case of different levels of exercise.
 RESPIRATORY FAILURE
Mechanisms of hypoxemia (RF):
- decreased FiO2
- alveolar hypoventilation
- ventilation-perfusion mismatch
- diffusion alteration
- intrapulmonary shunt
In clinical practice RF is rarely the result of a single
pathophysiological mechanism (e.g. acute obstruction of
upper airways). Usually more than one mechanism are
associated and are responsible for RF generation.
 RESPIRATORY FAILURE

Decreased oxygen inspiratory concentration:

• high altitude
• closed spaces
• combustion in closed spaces, etc.
rare
The pulmonary system is normal. RF is a result of external factors.

Treatment - removal from the abnormal environment

 RESPIRATORY FAILURE
Alveolar hypoventilation
The normal pulmonary gas exchange requires a constant, normal
composition of the alveolar gas. The aim of the external
ventilation is to preserve this normal composition of the alveolar
gas.

Alveolar hypoventilation (AH) is the result of alterations in

external ventilation (abnormal composition or abnormal
volume of the air at the alveolar level)
AH concerns evenly all the alveolar spaces.

Type II RF (hypoxemia + hypercapnia)

 ALVEOLAR HYPOVENTILATION

Mechanisms of the AH:

-restriction of the movements of the thoracic-
pulmonary system (amplitude and/or frequency);
-obstruction of the airways;
-coexistence of the restrictive and obstructive
mechanisms.
RESTRICTIVE ALVEOLAR HYPOVENTILATION

CAUSES:
1.disorders envolving the respiratory center
2. disorders envolving the respiratory neural pathways
3. muscle disorders
4. alteration of the thoracic cage
5. alterations of the thoracic cage content
6. extensive lung tissue diseases, which alter gas exchange
RESTRICTIVE ALVEOLAR HYPOVENTILATION

1.disorders envolving the respiratory center

– drug overdose
• opioids, anaethetics, CO, barbiturates, benzodiazepines, tricyclic antidepresives,
etc.;
– endogenous or exogenous coma
– infections (meningitis, encephalitis);
– tumors;
– head trauma and increased intracranial pressure
– stroke

All these conditions may alter the respiratory drive initiated by the
respiratory center and cause RF.
RESTRICTIVE ALVEOLAR HYPOVENTILATION

2. disorders envolving the respiratory neural

pathways:
– medullar disorders (trauma, bulbar polio)
– intercostal/phrenic nerves damages (trauma, polio)
– neuro-muscular junction alterations (myasthenia gravis,
neuro-muscular relaxants)

All these conditions may alter the transmission of the neural

command (stimulus) to the respiratory muscles and cause failure
of the external ventilation.
RESTRICTIVE ALVEOLAR HYPOVENTILATION
3. muscle disorders
– respiratory muscles atrophy ( decreased mass of respiratory muscle)
• starvation, cachexia
• congenital or acquired muscle dystrophies, miopathies
– respiratory muscles weakness ( steady decreased force of contraction)
• congenital or acquired muscle dystrophies,
• miopathies, hypoKmia, steroid therapy, chronic renal failure
– respiratory muscles fatigue ( decreasing force of contraction due to
persistent increased respiratory work overload)
• the final pathway of any type of RF

All patients who die due to RF, die due to type II

RF,
no matter the initial form (type I or type II) RF
RESTRICTIVE ALVEOLAR HYPOVENTILATION

4. alteration of the thoracic cage

– thoracic trauma (flail chest)
– thoracic cage deformities (scoliosis, kyphosis)
RESTRICTIVE ALVEOLAR HYPOVENTILATION

5. alterations of the thoracic cage content

– pleural interposition (pneumothorax, massive
pleural effusion, tumors)
– intrathoracic tumors
– elevated diaphragms (massive ascitis, intestinal
occlusion, large abdominal tumors ...)
RESTRICTIVE ALVEOLAR HYPOVENTILATION

6. extensive lung tissue diseases, which alter gas

exchange
pulmonary edema
pneumonia,etc.

Only late stage or severe parenchimal diseases

may result in AH
OBSTRUCTIVE VENTILATORY FAILURE

CAUSES:
– upper airway obstruction (nasopharinx, larynx, trachea)
• airway obstruction by the tongue
– coma, anaesthesia, head trauma, etc.
• foreign bodies, fluids
– blood, aspirated gastric content, drowning
• neck and facial trauma
• laryngeal or tracheal tumors
• infections
– laryngitis, epiglotytis
– obstruction of bronchi
• aspiration of gastric content, drowning
OBSTRUCTIVE VENTILATORY FAILURE

The obstruction of the most distal airways

does not result in alveolar hypoventilation,
but in ventilation-perfusion mismatch
because of uneven obstruction
of the very numerous small airways.

Type II RF (hypoxemia + hypercapnia)

 ALVEOLAR HYPOVENTILATION
Principles of treatment in ventilatory failure:
- oxygen therapy
- combined with endotracheal intubation and ventilatory
support, whenneeded
- airways management
- mandatory treatment in case of obstructive ventilatory
failure
- often the procedures are life-saving;
- mechanical ventilatory support
- substitute of spontaneous respiratory mechanical activity
until restauration of normal alveolar ventilation.
VENTILATION-PERFUSSION MISMATCH
Normal status of the lung is defined
by a matching of ventilation and perfusion.

Uneven intrapulmonary distibution of the inspired

air and/or of the pulmonary blood
Zones of hypo/hyperventilation are uneven
coupled with zones of hypo/hyperperfusion.
The consequence of this imbalance is the
impairment of gas exchange.
VENTILATION-PERFUSSION MISMATCH

Consequences of ventilation-perfusion mismatch:

- hypoxemia + normocapnia (CO2 has a great diffusibility;
the normally ventilated areas compensate for CO2
elimination in hypoventilated zones).
- hypoxemia + hypocapnia (hypoxemia results in
hyperventilation with an increased elimination of CO2)
- hypoxemia + hypercapnia (highly severe ventilation-
perfusion mismatch; may be accompanied by alveolar
hypoventilation).
VENTILATION-PERFUSSION MISMATCH

CAUSES:
- pulmonary diseases which affect the airways leading to an
uneven distribution of the inspiratory air into the lungs;
e.g. chronic bronchitis.
- pulmonary diseases with functional or organic impairment
of pulmonary vasculature (vasospasm, vascular
thrombosis, pulmonary capillary bed distruction, etc.)
e.g.: pulmonary embolism, emphysema.

In COPD the bronchial and vascular impairment coexist.

VENTILATION-PERFUSSION MISMATCH
PRINCIPLES OF TREATMENT:
- oxygen therapy is efficient. The increased FiO2 leads to
improvement of the gas exchange in the hypoventilated areas and
to the partial or total correction of hypoxemia.
In the chronic RF O2 therapy can withdraw the hypoxic stimulus of ventilation and
can cause the worsening of hypoxemia and hypercapnia.
- the establishment of airways pattency can contribute to a more
even distribution of the inspired flow (aerosols, nebulization,
bronhodilators, etc;)
- the improvement of the pulmonary blood flow distribution is
difficult to achieve; alleviation of pulmonary hypertension,
prophylaxis and treatment of pulmonary embolism, etc.
- ventilatory support should be initiated in type II RF
 DIFFUSION IMPAIRMENT

Mechanism:
The concentration of the O2 in the alveolar air is
normal.
The hypoxemia is a consequence of an increased
oxygen alveolo-arterial gradient.
This increased gradient is caused by the
impairment of the oxygen diffusion through
the alveolo-capillar membrane.
 DIFFUSION IMPAIRMENT
CAUSES:
- alterations of the structure and/or thickness of
the alveolo-capillary membrane (interstitial
edema, alveolar edema, pulmonary fibrosis)
- the decrease of the contact time of the arterial
blood with the alveolar air (e.g. in
pneumonectomy the contact time is decreased
because the whole cardiac output passes
through the single lung per time unit)
 DIFFUSION IMPAIRMENT

Consequences:
- hypoxemia + hypo/normocapnia
- CO2 has a 20 fold greater diffusibility compared to
O2;
- CO2 elimination remains normal even in cases with
severe alterations of O2 diffusion
 DIFFUSION IMPAIRMENT

Principles of treatment :
- O2 therapy may ameliorate hypoxemia
(increased alveolar O2 partial pressure, but the
O2 alveolo-arterial gradient remains the same)
- the causative treatment is the most important
-whenever possible (e.g. the treatment of the
pulmonary edema, etc.)
 INTRAPULMONARY SHUNT
Normally there is a small amount of venous blood which contaminates the
arterial blood through extrapulmonary pathways (e.g. Tebesius vein) or
through intrapulmonary pathways (anastomosis between bronchial and
pulmonary circulations) (1% of the cardiac output)

The increased shunt fraction is generated by the

presence of numerous areas of nonventilated but
perfused alveoli.
The shunt fraction is measured as percents of cardiac
output. When it is more than 15% the hypoxemia is
highly severe, even if the pulmonary gas exchange is
normal.
 INTRAPULMONARY SHUNT
Acute respiratory distress syndrome (ARDS)

acute lung injury (ALI)

ARDS

severity of intrapulmonary shunt:

PaO2/ FiO2: 500 normal
< 300 ALI
< 200 ARDS
 INTRAPULMONARY SHUNT
Acute respiratory distress syndrome (ARDS)
CAUSES:
– pulmonary causes:
• aspiration of gastric content
• smoke or toxic gases inhalation
• pulmonary contusion
• atelectasis
• bacterial or viral pneumonia
– systemic causes:
• all types of shock
• massive transfusion TRALI
• acute pancreatitis
• polytrauma
• extracorporeal circulation
 Acute respiratory distress syndrome (ARDS)
PATHOPHISYOLOGY
noncardiogenic pulmonary edema
permeability edema
• pulmonary or systemic aggresion → ↑permeability of alveolo-capilary
membrane (“pulmonary capillary leak syndrome”)
• ↑ extravascular lung water (interstitial and alveolar space) (“wet lung”)
∀ ↓ alveoli volume → alveolar collaps (perfused, but unventilated alveoli)
→↑ intrapulmonar shunt
∀ ↓ lung volumes (“baby lung”)
∀ ↓ lung compliance
• ↑ pulmonary vascular pressure
• hypoxemia + hypocapnia (type I RF) – ventilated alveoli compensate for
the CO2 removal
Acute respiratory distress syndrome (ARDS)
 Acute respiratory distress syndrome (ARDS)

DIAGNOSIS:
American European Consesus Conference on ARDS
(1994):
• acute onset;
• pulmonary or systemic condition associated with ARDS;
• PaO2/FiO2 <200 at any PEEP level;
• bilateral infiltrates on chest X-ray;
• pulmonary capillary wedge pressure ≤ 18mmHg or absence of
clinical/radiological signs of increased left atrial pressure.
Acute respiratory distress syndrome (ARDS)
 Acute respiratory distress syndrome (ARDS)
TREATMENT:
• treatment of the causative disease
• supportive treatment
– ventilatory support
• PEEP (positive end expiratory pressure)
• “open lung strategy”
– pressure or volume support
– tidal volume 5-6ml/kg
– peak airway pressure < 30-35 cmH2O;
– respiratory rate 20-22/min;
– permisive hypercapnia;
– PEEP to correct hypoxemia (usually 10-15 cmH2O);
– low FiO2 (preferable <0,6) to maintain SpO2 > 90%;
– prone position ventilation;
– nonventilatory therapy
 Acute respiratory distress syndrome (ARDS)

PEEP
 Acute respiratory distress syndrome
(ARDS)
PEEP (positive end expiratory pressure)

Avantaje
• previne colapsul alveolar la
sfarsitul expirului
• deschide caile aeriene distale
• creste volumele pulmonare (in
special CRF)
• reduce suntul intrapulmonar
• permite scaderea FiO2
• previne aparitia biotraumei
Dezavantaje
• risc de barotrauma
• instabilitate hemodinamica
cresterea presiunii
intratoracice scade returul
venos - scade debitul
cardiac)
• creste spatiul mort prin
distensia alveolelor normale
 CLINICAL SIGNS OF RESPIRATORY
FAILURE
• clinical signs of hypoxemia and hypoxia
• clinical signs of hypo/hypercapnia

Clinical signs of hypoxemia and hypoxia

Simptoms depend on:
– rapidity of hypoxemia development,
– the degree of hypoxia,
– the duration of hypoxia,
– the associated alterations of PaCO2.
 Clinical signs of hypoxemia and hypoxia
• respiratory signs:
• hyperventilation with tachypnea
• hyperventilation may lead to hypocapnia
• cardio-circulatory signs:
• ↑ adrenergic response:
– ↑ cardiac output + tachycardia
– cold extremities + profuse diaphoresis
– the arterial pressure increases (initially)
• cyanosis
• cardio-circulatory deterioration:
– bradycardia , decreased cardiac output, decreased arterial
pressure and cardiac arrest.
• central nervous system signs:
– fatigue and decreased mental capacity
– impressive restlessness, then stupor and coma
Clinical signs of hypercapnia:
- central nervous system signs
 DIAGNOSIS OF RF
1.clinical examination
may be difficult to be performed at the critically ill patient because:
– the patient can be restless, stuporous or comatous
– it may be difficult to take the history of the disease when the patient is
dyspneic
– physical examination may be tiresome to the patient
– physical examination may be difficult because of monitoring devices, i.v.
lines, etc.
Clinical examination is of the main importance in the RF diagnosis
because:
– can be performed at once during the first contact with the patient
– a presumptive diagn. may be evoked before laboratory
– it allows the assessment of other organs and systems, producing important
keys to final diagnosis
– it allows to start emergency treatment
 DIAGNOSIS OF RF
2. blood gas analysis
It allows the measurement of PaO2, PaCO2, pH and other
parameters useful in the interpretation of the acid-base status.

Blood gas analysis is very important in the RF diagnosis because

– proves the existence of hypoxemia
– differentiates the forms of RF(type I and II)
– assessment of the severity degree of hypoxemia
– assessment of the presence of the metabolic compensations,
– allowing to differentiate between acute and chronic RF
– it allows the assessment of evolving RF before the moment of
– time when the clinical signs are diagnostic.
 DIAGNOSIS OF RF

3. radiology and laboratory

– Radiological methods of examination offer data on the
morphology and not on functional status of the respiratory
system. Are contributive to the etiologic diagnosis, but are
irrelevant in the diagnosis of RF.
– Laboratory is orientative for the etiologic diagnosis and for
the assessment of functional and organic involvement of
other organs.
PULMONARY EMBOLISM
PNEUMONIA – bronchofiberoptic view
LEFT HEMOTHORAX
TENSION PNEUMOTHORAX
CHEST TRAUMA
RIGHT PNEUMOTHORAX
LEFT LUNG ATELECTASIS
 TRATAMENTUL
INSUFICIENTEI RESPIRATORII

• OXIGENOTERAPIE

• ELIBERAREA CAILOR AERIENE

• SUPORT VENTILATOR
 OXIGENOTERAPIA

• mecanism: cresterea FiO2, PAO2, PaO2

• se poate realiza in ventilatie spontana
sau controlata
• dispozitive:
– flux mare
– flux mic
 OXIGENOTERAPIA

• efecte secundare FiO2> 50%

– iritarea si uscaciunea mucoasei cailor aeriene
superioare (traheobronsita, disfunctie mucociliara)
– efecte toxice pulmonare prin producerea de radicali
liberi de oxigen
– atelectazie de resorbtie (dezazotizare) - apare din
prima ora de administrare O2 100%
 ELIBERARE CAI AERIENE

• Aspirare secretii traheobronsice

• bronhofibroscopie
• kinesiterapie
• IOT
 SUPORTUL VENTILATOR

Clasificare:
• invaziv (ventilatie pe sonda de IOT)
• noninvaziv (ventilatie pe masca faciala)

• controlat
• asistat
• asistat - controlat
 SUPORTUL VENTILATOR

Indicatiile IOT:

• eliberarea cailor aeriene superioare in caz de obstructie

• prevenirea aspiratiei continutului gastric (pacientii
comatosi, intoxicatii medicamentoase)
• toaleta bronsica (secretii bronsice abundente)
• facilitarea ventilatiei mecanice
 SUPORTUL VENTILATOR

Indicatiile ventilatiei mecanice:

• IRA tip I sau II
– hipoxemie severa PaO2<60mmHg in ciuda oxigenoterapiei
– hipercapnie severa cu acidemie
– volet costal - stabilizare
• anestezie generala
• tratamentul edemului cerebral prin hiperventilatie (hipocapnia -PaCO2
30mmHg- induce vasoconstrictie cerebrala)
• insuficienta circulatorie acuta (toate formele de soc)
 SUPORTUL VENTILATOR

Ventilatia noninvaziva

IR potential reversibila in scurt timp:

• BPOC decompensat

• edem pulmonar acut hemodinamic

 SUPORTUL VENTILATOR

Ventilatia noninvaziva:
• pacient treaz si cooperant
• capabil sa sustina pe perioade scurte ventilatia spontana
• functii CAS intacte
• stabil hemodinamic
• absenta leziunilor traumatice faciale
• absenta secretiilor bronsice abundente
 VENTILATORY SUPPORT

VOLUME SUPPORT VENTILATION- IPPV/CPPV,

SIMV
• tidal volume Vt=8-10ml/kg – setted
• assissted/controlled - setted
• breathing rate Fr=12/min - setted
• inspiration/expiration ratio I:E=1:2(33%) - setted
• airway pressure - derived (chest compliance, airway resistance) –
alarm limit
• PEEP 5 cmH20
 VENTILATORY SUPPORT

PRESSURE SUPPORT VENTILATION -PCV, BIPAP,

PS
• inspiratory pressure – setted
• assissted/controlled
• breathing rate (12/min ) - setted
• I:E ratio I:E =1:2(33%) - setted
• tidal volume - derived (chest compliance, airway resistance) –
alarm limit
• PEEP 5 cmH20 ( “physiologic” PEEP )