Respiration 16 Respiratory Failure

Respiratory Failure

Definition • Respiratory failure is defined as respiratory dysfunction resulting in abnormalities of oxygenation or ventilation (CO2 elimination) severe enough to threaten the function of vital organs • Arterial blood gas criteria for respiratory failure are not absolute but may be arbitrarily established as a PO2 under 60 mm Hg or a PCO2 over 50 mm Hg

Causes of Respiratory failure • Airway disorders    Asthma,  Acute exacerbation of chronic bronchitis or emphysema,  Obstruction of pharynx, larynx, trachea, mainstem bronchus, or lobar bronchus by edema, mucus, mass, or foreign body • Pulmonary edema    Increased hydrostatic pressure, Left ventricular dysfunction (eg, myocardial ischemia, heart failure), Mitral regurgitation, Left atrial outflow obstruction (eg, mitral stenosis), Volume overload states, Increased pulmonary capillary permeability, Acute respiratory distress syndrome, Acute lung injury, Unclear etiology, Neurogenic, Negative pressure (inspiratory airway obstruction), Reexpansion, Tocolytic-associated

• Parenchymal lung disorders    Pneumonia  Interstitial lung diseases  Diffuse alveolar hemorrhage syndromes  Aspiration  Lung contusion • Pulmonary vascular disorders    Thromboembolism  Air embolism  Amniotic fluid embolism • Chest wall, diaphragm, and pleural disorders Rib fracture   Flail chest   Pneumothorax   Pleural effusion   Massive ascites   Abdominal distention and abdominal compartment syndrome

• Neuromuscular and related disorders    Primary neuromuscular diseases     Guillain-Barré syndrome     Myastheniagravis     Poliomyelitis     Polymyositis   Drug- or toxin induced     Botulism     Organophosphates     Neuromuscular blocking agents     Aminoglycosides   Spinal cord injury   Phrenic nerve injury or dysfunction   Electrolyte disturbances: hypokalemia, hypophosphatemia   Myxedema • Central nervous system disorders    Drugs: sedative, hypnotic, opioid, anesthetics   Brain stem respiratory center disorders: trauma, tumor, vascular disorders, hypothyroidism   Intracranial hypertension   Central nervous system infections • Increased CO2 production Fever   Infection   Hyperalimentation with excess caloric and carbohydrate intake   Hyperthyroidism  Seizures   Rigors   Drugs

Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting

Classification Hypoxemic respiratory failure (type I) • It is characterized by a PaO2 of less than 60 mm Hg with a normal or low PaCO2 • This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units • Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage

Hypercapnic respiratory failure (type II) • It is characterized by a PaCO2 of more than 50 mm Hg • Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air • The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia • Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma, chronic obstructive pulmonary disease [COPD])

Pathophysiology Hypoxemic respiratory failure

• Ventilation-perfusion (V/Q) mismatch and shunt are mechanisms responsible for Type I failure

• With V/Q mismatch, the areas of low ventilation relative to perfusion (low V/Q units) contribute to hypoxemia • An intrapulmonary or intracardiac shunt causes mixed venous (deoxygenated) blood to bypass ventilated alveoli and results in venous admixture • These 2 mechanisms lead to widening of the alveolar-arterial oxygen difference, which normally is less than 15 mm Hg • The distinction between V/Q mismatch and shunt can be made by assessing the response to oxygen supplementation or calculating the shunt fraction following inhalation of 100% oxygen. • In most patients these 2 mechanisms coexist

Common causes of type I (hypoxemic) respiratory failure – – – – – – – – – – – – – – – –

Chronic bronchitis and emphysema (COPD) Pneumonia Pulmonary edema Pulmonary fibrosis Asthma Pneumothorax Pulmonary embolism Pulmonary arterial hypertension Pneumoconiosis Granulomatous lung diseases Cyanotic congenital heart disease Bronchiectasis Adult respiratory distress syndrome Fat embolism syndrome Kyphoscoliosis Obesity

Pathophysiology Hypercapnic respiratory failure

• At a constant rate of carbon dioxide production, PaCO2 is determined by the level of alveolar ventilation • A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression • In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy

• Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue • Ventilatory demand is the spontaneous minute ventilation that results in a stable PaCO2 • Normally, ventilatory capacity greatly exceeds ventilatory demand • Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both) • Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller • Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing.

Common causes of type II (hypercapnic) respiratory failure – – – – – – – – – – – – – – – – –

Chronic bronchitis and emphysema (COPD) Severe asthma Drug overdose Poisonings Myasthenia gravis Polyneuropathy Poliomyelitis Primary muscle disorders Porphyria Cervical cordotomy Head and cervical cord injury Primary alveolar hypoventilation Obesity hypoventilation syndrome Pulmonary edema Adult respiratory distress syndrome Myxedema Tetanus

Distinctions between acute and chronic respiratory failure • Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3 • Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased. • The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a longstanding disorder

Pathophysiologic causes of acute respiratory failure • Hypoventilation • V/Q mismatch • Shunt These are the most common pathophysiologic causes of acute respiratory failure

Clinical Findings • The symptoms and signs of acute respiratory failure are both insensitive and nonspecific; therefore, the physician must maintain a high index of suspicion and obtain arterial blood gas analysis if respiratory failure is suspected • Symptoms and signs of acute respiratory failure are those of the underlying disease combined with those of hypoxemia or hypercapnia

• The chief symptom of hypoxemia is dyspnea • Signs of hypoxemia include cyanosis, restlessness, confusion, anxiety, delirium, tachypnea, bradycardia or tachycardia, hypertension, cardiac dysrhythmias, and tremor • Dyspnea and headache are the cardinal symptoms of hypercapnia • Signs of hypercapnia include peripheral and conjunctival hyperemia, hypertension, tachycardia, tachypnea, impaired consciousness, papilledema, and asterixis

Treatment • Treatment of the patient with acute respiratory failure consists of • (1) specific therapy directed toward the underlying disease • (2) respiratory supportive care directed toward the maintenance of adequate gas exchange • (3) general supportive care

Management of Respiratory Failure Principles • Hypoxemia may cause death in RF • Primary objective is to reverse and prevent hypoxemia • Secondary objective is to control PaCO2 and respiratory acidosis • Treatment of underlying disease • Patient’s CNS and CVS must be monitored and treated

Respiratory Support • Respiratory support has both nonventilatory and ventilatory aspects Nonventilatory aspects • The main therapeutic goal in acute hypoxemic respiratory failure is to ensure adequate oxygenation of vital organs • Inspired oxygen concentration should be the lowest value that results in an arterial hemoglobin saturation of 90% (PO2 60 mm Hg) • Higher arterial oxygen tensions are of no proven benefit • Hypoxemia in patients with obstructive airway disease is usually easily corrected by administering low-flow oxygen by nasal cannula (1–3 L/min) or Venturi mask (24–28%) • Higher concentrations of oxygen are necessary to correct hypoxemia in patients with ARDS, pneumonia, and other parenchymal lung diseases

Ventilatory aspects • Ventilatory support consists of maintaining patency of the airway and ensuring adequate alveolar ventilation • Noninvasive positive-pressure ventilation • NPPV delivered via a full face mask or nasal mask has become first-line therapy in COPD patients with hypercapnic respiratory failure who can protect and maintain the patency of their airway, handle their own secretions, and tolerate the mask apparatus • Patients with acute lung injury or ARDS or those who suffer from severely impaired oxygenation do not benefit and should be intubated if they require mechanical ventilation.

Headgear and full face mask commonly are used as the interface for noninvasive ventilatory support

A Bilevel positive airway pressure support machine is shown here. This could be used in spontaneous mode or timed mode

• Tracheal intubation • Indications for tracheal intubation include • (1) hypoxemia despite supplemental oxygen • (2) upper airway obstruction • (3) impaired airway protection • (4) inability to clear secretions • (5) respiratory acidosis • (6) progressive general fatigue, tachypnea, use of accessory respiratory muscles, or mental status deterioration • (7) apnea

• Mechanical ventilation • Indications for mechanical ventilation include • (1) apnea • (2) acute hypercapnia that is not quickly reversed by appropriate specific therapy • (3) severe hypoxemia • (4) progressive patient fatigue despite appropriate treatment. • Several modes of positive-pressure ventilation are available • PEEP is useful in improving oxygenation in patients with diffuse parenchymal lung disease such as ARDS. It should be used cautiously in patients with localized parenchymal disease, hyperinflation, or very high airway pressure requirements during mechanical ventilation

General Supportive Care • Maintenance of adequate nutrition is vital;. Overfeeding, especially with carbohydrate-rich formulas, should be avoided, because it can increase CO2 production and may potentially worsen or induce hypercapnia • Hypokalemia and hypophosphatemia may worsen hypoventilation due to respiratory muscle weakness • Sedative-hypnotics and opioid analgesics should be titrated carefully to avoid oversedation, leading to prolongation of intubation • Temporary paralysis with a neuromuscular blocking agent is occasionally used to facilitate mechanical ventilation and to lower oxygen consumption. Prolonged muscle weakness due to an acute myopathy is a potential complication of these agents

• Psychological and emotional support of the patient and family • Skin care to avoid decubitus ulcers • Meticulous avoidance of nosocomial infection and complications of tracheal tubes are vital aspects of comprehensive care for patients with acute respiratory failure • Stress gastritis and ulcers may be avoided by administering sucralfate, histamine H2-receptor antagonists, or proton pump inhibitors but many clinicians therefore prefer sucralfate • The risk of DVT and pulmonary embolism may be reduced by subcutaneous administration of heparin (5000 units every 12 hours), the use of LMW heparin or placement of a sequential compression device on an extremity