Transcript RESPIRATORY FAILURE

University of Medicine and Pharmacy, Iasi
School of Medicine
ANESTHESIA and INTENSIVE CARE
Conf. Dr. Ioana Grigoras
MEDICINE
4th year
English Program
Suport de curs
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 always means 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 thoracicpulmonary 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.;
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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 ventilationperfusion 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:
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aspiration of gastric content
smoke or toxic gases inhalation
pulmonary contusion
atelectasis
bacterial or viral pneumonia
– systemic causes:
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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 alveolocapilary 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):
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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”
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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 (positive end expiratory pressure)
Advantages
Disadvantages
• Prevention of end-expiratory
alveolar colapse
• Opening of distal airways
• Increase of lung volumes
(mainly FRC)
• Reduction of intrapulmonary
shunt
• Facilitation of FiO2 decrease
• Prevention of biotrauma
• Risk of barotrauma
• Hemodynamic instability
(increased intrathoracic
pressure decreases venous
return and decreases cardiac
output)
• Increased dead space by
distension of normal alveoli
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:
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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
 Respiratory signs:
– hypoventilation – low breathing rate/volume
 Cardio-circulatory signs:
– Adrenergic response: tachycardia, increased myocardial
contractility
– Peripheral vasodilation
– Pulmonary vasoconstriction
– Acidemia may result in decreased myocardial contractility
 CNS signs:
– Progresive loss of conciousness (hypercapnic coma)
– Cerebral vasodilation
DIAGNOSIS OF RF
1.clinical examination
may be difficult to be performed at the critically ill patient because:
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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:
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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
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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
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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 – fiberoptic view
LEFT HEMOTHORAX
TENSION PNEUMOTHORAX
CHEST TRAUMA
RIGHT PNEUMOTHORAX
LEFT LUNG ATELECTASIS
TREATMENT OF RESPIRATORY
FAILURE
• OXYGENTHERAPY
• MAINTENANCE OF AIRWAY PATENCY
• VENTILATORY SUPPORT
OXYGENTHERAPY
• mechanism: increased FiO2 → PAO2 →PaO2
• may be delivered during spontaneous or
artificial ventilation
OXYGENTHERAPY
• Side effects of FiO2> 50%
– drying and irritation of upper airway mucosa
(tracheo-bronchitis, muco-cilliary dysfunction)
– pulmonary injury by reactive oxygen species
– resoption atelectasis (by replacement of alveolar
nitrogen, which stabilizes alveolar volume)
MAINTENANCE OF
AIRWAY PATENCY
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Suction of bronhial secretions
Fiberbronchoscopy
Physiotherapy
Endotracheal intubation
VENTILATORY SUPPORT
Clasification:
• invasive ventilation (by endotracheal intubation)
• non-invasive ventilation (by mask)
• Controlled ventilation
• Assisted ventilation
• Assist-controlled ventilation
VENTILATORY SUPPORT
Indications of endotracheal intubation
• Airway patency in case of obstruction
• Prevention of gastric content aspiration (coma,
drug overdose)
• Removal of abundant bronchial secretions
• Mechanical ventilation
VENTILATORY SUPPORT
Indications of mechanical ventilation:
• ARF type I or II
– Severe hypoxemia PaO2<60mmHg despite oxygentherapy
– Severe hypercapnia with acidemia
– Internal stabilization in case of flail chest
• General anesthesia
• Treatment of cerebral edema by hyperventilation
(hypocapnia -PaCO2 30mmHg- results in cerebral
vasoconstriction)
• Acute circulatory failure (shock)
VENTILATORY SUPPORT
NON-INVASIVE VENTILATION
within hours potentially reversible RF :
• Decompensated COPD
• Cardiogenic pulmonary edema
• Acute hypoxemic RF
VENTILATORY SUPPORT
NON-INVASIVE VENTILATION
Alert and cooperative pacient
Able to maintain spontaneous ventilation
Preserved conciousness
Hemodynamically stability
Absence of facial trauma
Absence of abundant bronchial secretions
VENTILATORY SUPPORT
VOLUME SUPPORT VENTILATIONIPPV/CPPV, SIMV
SETTINGS OF THE MECHANICAL VENTILATOR
• tidal volume Vt=8-10ml/kg
• assissted/controlled
• breathing rate =12/min
• inspiration/expiration ratio I:E=1:2(33%)
• airway pressure - derived (chest compliance, airway
resistance) – alarm limit
• PEEP 5 cmH20
VENTILATORY SUPPORT
PRESSURE SUPPORT VENTILATION
PCV, BIPAP, PS
SETTINGS OF THE MECHANICAL VENTILATOR
• inspiratory pressure 15-35cm H2O
• assissted/controlled
• breathing rate (12/min )
• I:E ratio I:E =1:2(33%)
• tidal volume - derived (chest compliance, airway
resistance) – alarm limit
• PEEP 5 cmH20 ( “physiologic” PEEP )