RESPIRATORY FAILURE University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4 th year

RESPIRATORY FAILURE

University of Medicine and Pharmacy, IasiSchool of MedicineANESTHESIA and INTENSIVE CAREConf. Dr. Ioana Grigoras

MEDICINE4th year

English ProgramSuport de curs

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 mmHgWhile 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 mmHgSynonyms: 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 FAILUREAlveolar hypoventilationThe 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


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.


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.


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


4. alteration of the thoracic cage– thoracic trauma (flail chest) – thoracic cage deformities (scoliosis, kyphosis)


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 ...)


6. extensive lung tissue diseases, which alter gas exchange

pulmonary edemapneumonia,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.


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).


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.


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.


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)


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


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.


Acute respiratory distress syndrome (ARDS)

acute lung injury (ALI)ARDS

severity of intrapulmonary shunt:PaO2/ FiO2: 500 normal

< 300 ALI < 200 ARDS


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


PATHOPHISYOLOGYnoncardiogenic 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



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.



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


PEEP (positive end expiratory pressure)

Advantages• 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

Disadvantages• 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 hypoxiaSimptoms 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 hypercapniaRespiratory 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 examinationmay 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 – 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

• 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 VENTILATIONAlert and cooperative pacient Able to maintain spontaneous ventilationPreserved conciousnessHemodynamically stabilityAbsence of facial traumaAbsence of abundant bronchial secretions

VENTILATORY SUPPORT

VOLUME SUPPORT VENTILATION- IPPV/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, PSSETTINGS 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 )

Documents

RESPIRATORY FAILURE University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4 th year