Acute respiratory failure

DEFINITION
ARF is a syndrome characterized by modification of blood
gases: decreasing the oxygen partial pressure less than 60
mm Hg. with/or increasing the carbon dioxide partial
pressure more than 46 mm Hg., due to the imposibility of
the respiratory system to assure adequates gases changes
between alveolar air and pulmonary capillaries.
ETIOLOGY
The disease which can produce ARF can be divided in two categories:
1.extrapulmonary diseases (with normal lung)-these affect respiratory centre, the
efferent way, respiratory muscles, thoracic cage or superior airways;
2.pulmonary diseases of inferior airways, pulmonary parenchyme or pulmonary vassels.
The most frequent causes of ARF are:
-bronchopulmonary diseases with obstructive syndrome: obstructive chronic bronchitis,
pulmonary emphysema, asthma;
- pulmonary embolism;
-acute pulmonary oedema;
-acute respiratory distress syndrome.
Extrapulmonary causes of ARF
- respiratory centers disfunctions:
-drugs (anestezics, sedatives), alcohol;
-metabolic disturbances:hyponatremia,hypocalcemia,hypoglycemia, alchalosis;
- neoplasma, infections, trauma of the nervous system,intracranial hypertension;
-central hypoventilation and sleeping apneea;
-affections of the spinal cord and peripheral nerves:
-poliomielita;
-lateral amiotrofic sclerosis;
-neoplasma, trauma, hemorrhages;
Extrapulmonary causes of ARF
-affections of the respiratory muscules:
-botulism, tetanos;
-musculary dystrophy;
-miasthenia;
- affections of the thoracic cage and pleura:
-deformations, trauma;
-ankilosant spondilitis;
-hydro-, pneumo- and fibrothorax;
- obstruction of the superior airways:
-tumors;
-laringeal oedema, acute epiglotitis.
Pulmonary causes of ARF
-affections of the inferior airways: bronchitis, asthma, bronchiectasia,neoplasia;
-affections of the pulmonary parenchyma: pneumonia, absces, atelectasis, fibrosis;
-affections of the vassels : pulmonary embolism, cardiac faillure;
-respiratory distress;
PHYSIOPATHOLOGY
Normal value of O2PaP is 95-96mmHg, and CO2PaP is 40mmHg.
Hipoxemia- could be: simple- O2 PaP=95-60mmHg
medium- O2PaP=60-45mmHg
severe- O2PaP<45mmHg.
Hypoxemia
Hypoxemia can appear by next mechanisms:
unequal fraction ventilation/ perfusion in different zones of lungs. This situation appears in asthma,
obstructive bronchitis, emphysema, fibrosis, pulmonary embolism, pulmonary stasis from left cardiac
failure.
Hypoxemia can be corrected by administration of oxygene in small concentration 24-40%.
alveolar hypoventilation appear in cases when extrapulmonary diseases produced ARF, or is associated
with unequal fraction ventilation/perfusion in cases from a. Hypoxemia is associated with
hypercapneea, and can be corrected by administration of oxygene in big concentration 100%.
alteration of gases difusion through alveolocapilary membrane, which produce isolate hypoxemia and
can be easily corrected by administratuion of small quantities of oxygene.
Intrapulmonary right-left shunt like in arteriovenous fistule, or in zones completely unventilated
(pneumonia, atelectasis). Administration of oxygene doesn’t correct the hypoxemia.
Hypercapneea
Hypercapneea can be: simple CO2PaP=45-50mmHg
medium CO2PaP=50-70mmHg
severe CO2PaP>70mmHg.
In most of the cases it appears due to alveolar hypoventilation.

ARF is divided in 2 categories depending the hypercapneea:

ARF type 1 without hypercarneea ( CO2 PaP in normal or decreased)
ARF type 2 with hipercapneea. After the compensatory mechanisms are overtaken, appear
respiratory acidosis( decompensated ARF).
 CLINICAL FINDINGS
1. Clinical manifestations of acute hypoxemia are:
- cyanosis- the most specific sign;
-dyspneea,tachypneea- with different characthers function the etiology
-cardiovasculary signs- tahycardia, hypertension;
Severe hypoxemia can produce bradycardia, hypotension and shock by miocardic distress;
-neurological signs- motor instability, confusion (like in the acute alcoholic syndrom).
2.Clinical manifestations of hypercapneea are:
-respiratory signs-dyspneea and tachypneea
In case of big values og CO2PaP appear respiratory distress cu attenuation of dyspneea
-neurological signs- hypercapnic encefalopathy-when the CO 2 PaP > 70 mm Hg. Appear drawsiness or sleeplessness, temporospatial
desorientation, tremor, asterixis;
Coma appears when CO2 PaP > 80mm Hg;
-vasculary signs (by vasodilatation)- warm extremities, sweatening, signs of intracranial hypertension: nauseea, vomitting, headache;
-cardiac signs: tachycardia,arrythmias;
 The clinical manifestations of the acute respiratory failure are a little specific and they intricate
in practice with the manifestation of the basic disease.
The essential exploration for establishing the diagnosis is the measurement of the blood gases.
Other useful determinations are:
-acidobasic parameters,
- EKG,
-chest x-rays,
- sputum exam,
- bronchoscopy,
- ventilatory tests.
TREATMENT
Principles of treatment for ARF includes:
-oxygenotherapy and assurance of ventilation
-correction of the reversible factors
-ethiological tratment
-treatment of acido-basic disturbances
 ACUTE RESPIRATORY FAILURE DUE
TO OBSTRUCTION OF AIRWAYS
Common clinical signs:
-inspiratory dyspneea and stridor
-decreased level of counsciousness: anxiety, agitation, obnubilation, hypoxemic coma
-cianosis
-other signs function the etiology of the obstruction:
1.foreign body in superior airways:
-cough
-classical sign of asphyxia by foreign body
-possitive anamnesis
 ACUTE RESPIRATORY FAILURE
DUE TO OBSTRUCTION OF
AIRWAYS
2.glotic edema
-dysphonia
-atopical reaction and suggestive anamnesis
-other manifestations of anaphylactic reaction: generalized rush, pruritus, bronchospasm, anaphylactic shock.
3.epiglotitis
-especially to the children
-high fever, in the recent history pharingitis,
-disphonia, disphagia
-intercostal thiraj and whistling
 ACUTE RESPIRATORY FAILURE
DUE TO OBSTRUCTION OF
AIRWAYS
PARACLINICAL: hypoxemia with hypercapneea.
TRATMENT
1.foreign body:
◦ consciouss patient:

-ask the patient to cough

-5 strong hits interscapulovertebral
-Heimlich manouvre
-extract the foreign body under laringoscope control
-traheostomy / cricotiroidotomy.
◦ unconsciouss patient:

-lateral decubitus- 5 toracic hits

-dorsal decubitus- Heimlich manouvre.
ACUTE RESPIRATORY FAILURE
DUE TO OBSTRUCTION OF
AIRWAYS
2.Quinke edema
-assure opened airways, oxygen, 2 i.v. lines
-Adrenaline 0,2- 0,3- 0,5mg i.v. diluted or s.c.
-Corticosteroids: 200 mg i.v.; if is needed the dose can be increased
-Antihistaminic drugs: Clorfeniramin 1 phial i.v. or Romergan 1 ph i.m.
-Gluconic calcium 1-2 ph. i.v.
-Aminophylline if is associated bronchospasm
ACUTE RESPIRATORY DISTRESS
SYNDROME - ARDS
DEFINITION
ARDS is a particullary form of acute respiratory faillure characterized by:
-clinically: severe dyspneea, tahypneea, cyanosis and hypoxemia which doesn’t correct to oxygene
administration
-radiologically: difused bilateral infiltrates.
ETIOLOGY
The most frequent causes which produce ARDS are:
-any type of the shock;
-septicemia (one fifth of the patients with septicemia have ARDS);
-politrauma;
-caloric aggression;
ARDS
-pulmonary inhalation of the gastric fluids;
-diffused pulmonary infections (and general severe infections);
-politrauma and lipids embolism;
-large burns;
-inhalation of toxic irritants gases (smoke, amonium, oxygene in high concentration);
-drug overdoses (salicilates, barbiturics, tiazidics);
- metabolic disorders (uremia, diabetic acidocetosis);
-hematological disorders (multiple transfusions, diseminate intravasculare coagulation);
-obstetric pathology ( eclampsia, amniotic embolism);
-pancreatitis.
ARDS
POSITIVE DIAGNOSIS is strictly based on:
-the presence in the near history (hours,days) of one of the etiological factor;
-brutally onset of severe acute respiratory failure with untreatable hypoxemia by oxygene
administration;
-pulmonary auscultation: crepitants crackles bilateral diseminated - lesional pulmonary oedema;
-radiologically :diffused bilateral infiltrates;
-reduced pulmonary compliance (less than 50 ml/ cm H2O)
ARDS
DIFFERENTIAL DIAGNOSIS
-acute cardiologic pulmonary oedema-which appears to the patient with cardiac history with big
size of the heart, ortopneea, opacity localized perihilar, increased pressure in pulmonary
capilaries;
- chronic pulmonary disease can produce acute respiratory faillure in the moment of infectious
acutisation.
 ARDS
TREATMENT
Includes:
1. etiological treatment;
2. respiratory support: the aim is obtaining an oxygene partial arterial pressure equal with 60 mm Hg. or more, or hemoglobin
saturation equal with 90 %.
Methods:
*oxygen via facial mask or nasal tube with moderate flow 5-10 l/min. with high concentration (100%);
*orotracheal intubation and assisted mechanical ventilation with PEEP to values 50-60 cm. H 2O. Bigger pressures have risk of
barotrauma and decreasing the cardiac output by increase intrathoracic pressure.
PEEP = positive end expiratory pressure.
3. pathogenic treatment-corticosteroids-high doses;
4. diuretics drugs – have a limitated efficiency in case of normal cappilarie pressure. If exist signs of hypovolemia, diuretics are
contraindicated.
ARDS
5. prevention the complications:
-heparinotherapy in small doses:5.000 U.I./ 8-12 h.
- H2 inhibitors for prevention the digestive haemorrhage;
If there is hypotension and oliguria, you must sustain the blood pressure with fluids and
Dopamine.
PROGNOSIS
In case of ARDS prognosis is severe, mortality is increased, around 50%.
Frequently is associated MSOF- multiple system organs failure, because exist endotelial
modifications in all teritories.