respiratory failure by dr. sookun rajeev kumar
TRANSCRIPT
Dr. SOOKUN RAJEEV K
(MD)
Dept of General Medicine
Anna Medical College
RESPIRATORY FAILURE
What is Respiratory Failure?
Respiratory Failure is a syndrome in
which the respiratory system fails in
one or both of its gas exchange
functions.
i.e.
(i) Oxygenation
(ii) Elimination of Carbon Dioxide.
Classification of Respiratory Failure(i) Type I or Hypoxemic
It is characterized by an arterial oxygen pressure
(PaO2) lower than 60 mm Hg with a normal or low
arterial carbon dioxide pressure (PaCO2).
Therefore, it’s a failure of Oxygen exchange.
(ii) Type II or Hypercapnic
It is characterized by a PaCO2 higher than 50
mmHg. Therefore, it’s a failure to exchange or
removal of Carbon Dioxide
Classification of Respiratory Failure (cont)
(iii) Type III. Perioperative respiratory failure.
Increased atelectasis due to low functional residual capacity in the setting of abnormal abdominal wall mechanics.
(iv) Type IV . Shock
Patients who are intubated and ventilated in the process of resuscitation for shock
Classification of Respiratory Failure (cont)
(i) Acute
develops over minutes to hours
(ii) Chronic
develops over several days or longer
(iii) Acute on Chronic
E.g. Acute exacerbation of advanced COPD
Type I Respiratory Failure
This is essentially hypoxemia without CO2 retention
Physiologic causes include:
A low inspired oxygen concentration (FIO2). E.g High
Altitude.
Mismatch of alveolar ventilation (V) to alveolar perfusion (Q)
A shunt where blood passes from the pulmonary artery to
the left heart without passing through ventilated alveoli
Type I Respiratory Failure
Pathological causes: Pneumonia
Asthma
COPD (predominantly
emphysema – ‘pink puffers’)
Acute Respiratory Distress
Syndrome and Noncardiogenic
Pulmonary Edema
Cardiogenic Shock
Tension Pneumothorax
Pulmonary Fibrosis
Pulmonary edema
Pulmonary embolism
Pulmonary arterial hypertension
Pneumoconiosis
Granulomatous lung diseases
Cyanotic congenital heart disease
Bronchiectasis
Fat embolism syndrome
Kyphoscoliosis
Obesity
Type II Respiratory FailureThe underlying cause is alveolar hypoventilation ,with or without (V/Q)
mismatch
Type II respiratory failure can be broken down anatomically as dysfunction somewhere between the brainstem and the chest wall:
Reduced central drive (e.g. sedation and brainstem disorders).
Neuromuscular disease (e.g. spinal cord lesions, poliomyelitis, myasthenia gravis and diaphragmatic palsy).
Thoracic wall abnormalities (e.g. kyphoscoliosis and obesity).
Intrinsic lung disease (e.g. asthma, COPD, pneumonia and lung fibrosis).
Type II Respiratory FailureCommon Causes:
COPD (Predominantly Chronic
Bronchitis)
Respiratory muscle failure (e.g. Bilateral
diaphragmatic palsy)
Kyphoscoliosis and other structural
thoracic disorders
Muscular dystrophy
Guillain-Barre syndrome (acute
demyelinating polyneuropathy)
Poliomyelitis
Myasthenia
Head injury
Sleep apnea
Poisonings
Myasthenia gravis
Polyneuropathy
Porphyria
Cervical cordotomy
Head and cervical cord injury
Primary alveolar hypoventilation
Obesity-hypoventilation syndrome
Pulmonary edema
ARDS
Myxedema
Tetanus
Opiate overdose
Severe asthma
Type III Respiratory Failure
Inadequate post-operative analgesia, upper abdominal incision
Obesity, ascites
Pre-operative tobacco smoking
Excessive airway secretions
Type IV Respiratory Failure
Cardiogenic shock
Septic shock
Hypovolemic shock
Physical Examination: History
Sepsis suggested by fever, chills
Pneumonia suggested by cough, sputum production, chest pain
Pulmonary embolus suggested by sudden onset of shortness of breath or chest pain
COPD exacerbation suggested by history of heavy smoking, cough, sputum production
Cardiogenic pulmonary edema suggested by chest pain, paroxysmal nocturnal dyspnea, and orthopnea
Physical Examination: History (cont.)
Noncardiogenic edema suggested by the presence of risk factors including sepsis, trauma, aspiration, and blood transfusions
Accompanying sensory abnormalities or symptoms of weakness may suggest neuromuscular respiratory failure; as would the history of an ingestion or administration of drugs or toxins.
Additional exposure history may help diagnose asthma, aspiration, inhalational injury and some interstitial lung diseases
Physical Examination: Physical FindingsHypotension usually with signs of poor perfusion
suggests severe sepsis or massive pulmonary embolus
Hypertension usually with signs of poor perfusion
suggests cardiogenic pulmonary edema
Wheezing suggests airway obstruction:
Bronchospasm
Fixed upper or lower airway pathology
Secretions
Pulmonary edema (“cardiac asthma”)
Physical Examination: Physical Findings (cont.)
Stridor suggests upper airway obstruction.
Elevated jugular venous pressure suggests
right ventricular dysfunction due to
accompanying pulmonary hypertension
Tachycardia and arrhythmias may be the
cause of cardiogenic pulmonary edema
Specific Clinical Signs of Type II Respiratory Failure
Tachycardia
Distention of the forearm veins
A flapping tremor of the outstreched hands
Clouding of consciousness
Papilledema (rare)
Investigations for Respiratory Failure
ABGQuantifies magnitude of gas exchange abnormality Identifies type and chronicity of respiratory failure
Complete blood count
Anemia may cause cardiogenic pulmonary edema
Polycythemia may suggests chronic hypoxemia
Leukocytosis, a left shift, or leukopenia suggestive of infection
Thrombocytopenia may suggest sepsis as a cause
Investigations for Respiratory Failure (cont)
Cardiac Serologic Markers
Troponin, Creatine kinase- MB fraction (CK-MB)
B-type natriuretic peptide (BNP)
Microbiology
Respiratory cultures: sputum/tracheal
aspirate/broncheoalveolar lavage (BAL)
Blood, urine and body fluid (e.g. pleural) cultures
Investigations for Respiratory Failure (cont)
Chest radiography
Identify chest wall, pleural and lung parenchymal pathology; and distinguish disorders that cause primarily V/Q mismatch (clear lungs) vs. Shunt (intra-pulmonary shunt; with opacities present)
Electrocardiogram
Identify arrhythmias, ischemia, ventricular dysfunction
Echocardiography
Identify right and/or left ventricular pathologies
Investigations for Respiratory Failure (cont)
Pulmonary function tests/bedside spirometry
Identify obstruction, restriction, gas diffusion abnormalities
May be difficult to perform if critically ill
Bronchoscopy
Obtain biopsies, brushings and BAL for histology, cytology and microbiology
Results may not be available quickly enough to avert respiratory failure
Bronchoscopy may not be safe in the critically ill
Management of Respiratory FailureABC’s
Ensure airway is adequate
Ensure adequate supplemental oxygen and assisted ventilation, if indicated
Support circulation as needed
Treatment of a specific cause when possible Infection
Antimicrobials, source control
Airway obstruction
Bronchodilators, glucocorticoids
Improve cardiac function
Positive airway pressure, diuretics, vasodilators, morphine, inotropy, revascularization
Management of Respiratory Failure (cont)
Mechanical ventilation
Non-invasive (if patient can protect airway and is
hemodynamically stable)
Mask: usually orofacial to start
Invasive
Endotracheal tube (ETT)
Tracheostomy – if upper airway is obstructed
Treatment of Type II Respiratory Failure
As in type I, the main therapeutic objective
is to ensure adequate oxygenation of vital
organs by administering oxygen therapy.
Oxygen therapy must be carefully controlled
so that sufficient oxygen is supplied, usually
24% via face mask, to prevent death from
hypoxemia but without precipitating severe
respiratory acidosis.
As a consequence of causes other than
COPD, usually is an indication for
mechanical ventilation.
Treatment of Type II Respiratory Failure
Specific therapy of the underlying cause (e.g. Antibiotics
for infective exacerbation of COPD or treatment of
myasthenia).
General supportive care as in Type I Respiratory Failure.
Chemical (respiratory stimulants e.g Doxapram) or
mechanical ventilation should be considered if other
measures fail.
Beware: Patients with Type II respiratory failure can stop
breathing if given uncontrolled high-flow oxygen. The
underlying physiology causing this is oxygen-sensitive
pulmonary vasoconstriction rather than ‘dependence on
hypoxic drive’ oxygen.