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.