DR. M. A. Sofi MD; FRCP; FRCPEdin; FRCSEdin Al Maarefa College of Science & Technology

 Definition Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O 2 from atmosphere to blood and remove CO 2 from blood.  Clinically Respiratory failure is defined as PaO 2 50 mmHg.

Respiratory failure may be acute or chronic:  Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually therefore less than 7.3.  Chronic respiratory failure develops over several days or longer. There is sufficient time for renal compensation and an increase in bicarbonate so the pH is usually only slightly decreased.  Clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale.

Respiratory failure is Classifieds into type I or type II relates to the absence or presence of hypercapnia respectively. PaO2PaO2 decreased (< 60 mmHg (8.0 kPa)) P a CO 2 normal or decreased (<50 mmHg (6.7 kPa)) P A-a O 2 increased Type 1 respiratory failure is defined as hypoxemia without hypercapnia, and indeed the P a CO 2 may be normal or low. It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. The basic defect in Type 1 respiratory failure is failure of oxygenation characterized by:

1. Low ambient oxygen (e.g. at high altitude). 2. Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism. 3. Alveolar hypoventilation (decreased minute volume due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease); this form can also cause type 2 respiratory failure if severe. 3. Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g.in pneumonia or ARDS). 4. Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right-to-left shunt). Type I: caused by conditions that affect oxygenation

 Chronic obstructive pulmonary disease (COPD).  Pneumonia.  Pulmonary oedema.  Pulmonary fibrosis.  Asthma.  Pneumothorax.  Pulmonary embolism.  Pulmonary hypertension.  Cyanotic congenital heart disease.  Bronchiectasis.  Acute respiratory distress syndrome.  Kyphoscoliosis.  Obesity. Common causes of type I respiratory failure

Type 2 Hypoxemia (PaO2 6.0kPa). The basic defect in type 2 respiratory failure is characterized by: PaO2PaO2 decreased (< 60 mmHg (8.0 kPa)) P a CO 2 increased (> 50 mmHg (6.7 kPa)) P A-a O 2 normal pHdecreased Type 2 respiratory failure is caused by: Inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the build up of carbon dioxide levels (P a CO 2 ) that has been generated by the body but cannot be eliminated.

A.Increase airway resistance (Chronic obstructive pulmonary disease, asthma, suffocation) B.Reduced breathing effort (drug effects, brain stem lesion, extreme obesity). C.A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis). D.Neuromuscular problems (Guillain-Barré syndrome, myasthenia gravis, motor neurone disease). E.Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest. Type II respiratory failure caused by:

 COPD.  Severe asthma.  Drug overdose poisoning.  Myasthenia gravis.  Polyneuropathy.  Poliomyelitis.  Muscle disorders  Head injuries and neck injuries.  Obesity.  Pulmonary oedema.  Adult respiratory distress syndrome.  Hypothyroidism. Common causes of type II respiratory failure

Symptoms  The history may indicate the underlying cause, e.g. paroxysmal nocturnal dyspnoea, and orthopnoea in pulmonary oedema.  Both confusion and reduced consciousness may occur. Signs  Localised pulmonary findings are determined by the underlying cause.  Neurological features may include restlessness, anxiety, confusion, seizures, or coma.  Tachycardia and cardiac arrhythmia may result from hypoxaemia and acidosis.  Cyanosis.  Polycythaemia is a complication of long- standing hypoxaemia.  Cor pulmonale: pulmonary hypertension is frequently present and may induce right ventricular failure, leading to hepatomegaly and peripheral oedema. Signs & Symptoms:

 Sudden or gradual onset  Severe morning headache ◦ Rapid, shallow breathing pattern ◦ Tripod position  Cyanosis ◦ Late sign  Tachycardia and mild hypertension ◦ Early signs  A sudden decrease in PaO 2 or rapid increase in PaCO 2 indicates a serious condition

 Respiratory failure is a common and a life-threatening condition that demands prompt diagnosis and assessment and appropriate management.  Failure to visualize an obvious abnormality on chest radiographs in hypoxemic respiratory failure suggests the possibility of right-to- left shunting.  The vast majority of patients in acute respiratory failure due to cardiogenic pulmonary edema respond to measures to reduce preload and afterload.  Those with acute respiratory distress syndrome (ARDS) require early elective intubation because the duration of respiratory failure is longer.  Hypercapnic respiratory failure occurs secondary to a variety of causes:  Increased respiratory muscle load.  Impaired neuromuscular function.  Decreased respiratory drive caused by central nervous system (CNS) depression. Diagnostic considerations

 Acute Respiratory Distress Syndrome  Sleep Apnea  Asthma  Atelectasis  Cardiogenic Shock  Cardiomyopathy, Dilated  Cardiomyopathy, Hypertrophic  Cor Pulmonale  Diaphragmatic Paralysis  Emphysema  Myocardial Infarction  Pneumonia, Aspiration  Pneumonia, Bacterial  Pneumonia, Community-Acquired  Pneumonia, Viral  Pneumothorax  Pulmonary Edema  Cardiogenic Shock  Pulmonary Edema, Neurogenic  Pulmonary Embolism  Pulmonary Fibrosis, Idiopathic  Pulmonary Fibrosis, Interstitial  Primary Pulmonary Hypertension  Secondary Pulmonary Hypertension  Respiratory Acidosis  Restrictive Lung Disease  Shock, Distributive  Ventilation, Mechanical  Ventilation, Noninvasive Differential Diagnoses

 Arterial blood gas analysis: Confirmation of diagnosis  CXR: often identifies the cause of respiratory failure.  FBC: anemia can contribute to tissue hypoxia; polycythaemia may indicate chronic hypoxaemic respiratory failure.  Renal function tests and LFTs: may provide clues to the aetiology or identify complications associated with respiratory failure.  Serum creatine kinase and troponin I: to help exclude recent myocardial infarction.  Elevated creatine kinase may also indicate myositis. Investigations:

 TFTs (hypothyroidism may cause chronic hypercapnic respiratory failure).  Spirometry: useful in the evaluation of chronic respiratory failure.  Echocardiography: if a cardiac cause is suspected for ARF.  Pulmonary function tests in the evaluation of CRF.  ECG: to evaluate a cardiovascular cause.  Right heart catheterization: if there is uncertainty about cardiac function, adequacy of volume replacement, and systemic oxygen delivery.  Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic oedema. Investigations:

 A patient with acute respiratory failure generally needs prompt hospital admission in an intensive care unit.  Many patients with chronic respiratory failure can be treated at home, depending on the severity of respiratory failure, underlying cause, comorbidities and social circumstances.  Immediate resuscitation may be required.  Appropriate management of the underlying cause. Hypoxemia  Ensure adequate oxygen delivery to tissues, generally achieved with a PaO 2 of 60 mm Hg or an arterial oxygen saturation (SaO 2 ) of greater than 90%.  Beware the prolonged use of high- concentration oxygen in chronic sufferers who have become reliant on their hypoxic drive to maintain an adequate ventilation rate.  Elevating the PaO 2 too much may reduce the respiratory rate so that the PaCO 2 may rise to dangerously high levels. Management:

Assisted ventilation:  Mechanical ventilation is used to increase PaO 2 and to lower PaCO 2.  Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue.  Weaning patients with chronic respiratory failure off of mechanical ventilation may be very difficult.  Non-invasive ventilation (NIV) has been increasingly used as an alternative to intubation.  NIV improves survival and reduces complications for selected patients with acute respiratory failure.  The main indications are exacerbation of COPD, cardiogenic pulmonary oedema, pulmonary infiltrates in immunocompromised patients, and weaning of previously intubated stable patients with COPD. Management:

 Pulmonary: PE, pulmonary fibrosis, and complications secondary to the use of mechanical ventilation.  CVS: Cor pulmonale, hypotension, reduced cardiac output, arrhythmias, pericarditis, and acute MI.  Gastrointestinal: Gastric distension, haemorrhage, ileus, pneumoperitoneum. diarrhoea, and duodenal ulceration caused by stress is common in patients with acute respiratory failure.  Polycythaemia.  Hospital-acquired infection: pneumonia, UTI, and catheter-related sepsis, are frequent  Renal: acute kidney injury (ARF) and abnormalities of electrolytes and acid-base balance are common.  Nutritional: Malnutrition and complications related to administration of enteral or parenteral nutrition.  Complications associated with nasogastric tubes, e.g. abdominal distention and diarrhea. Complications:

Adult Respiratory Distress Syndrome Pulmonary Edema Acute respiratory failure