Acute Respiratory Failure, Acute Lung Injury/Acute Respiratory Distress Syndrome, and Acute Chest Syndrome

Chapter 24 Acute Respiratory Failure, Acute Lung Injury/Acute Respiratory Distress Syndrome, and Acute Chest Syndrome



Prema R. Menon, MD , Gilman B. Allen, MD




1 What is acute respiratory failure (ARF)?


ARF is a syndrome in which the respiratory system fails in gas exchange, in either oxygenation, carbon dioxide elimination, or both. ARF can occur within minutes or over hours.



2 What are the types of ARF?


ARF can be either hypoxemic, hypercapnic, or a combination of both. Arterial blood gas analysis is the gold standard for diagnosis of respiratory failure. An arterial PO2 of less than 50 mm Hg while breathing ambient air is considered hypoxemic, and hypercapnia is defined as a PCO2 of greater than 50 mm Hg.



3 What are the mechanisms and causes of hypoxemic respiratory failure?


Mechanisms of hypoxemia are as follows:



image Low mixed venous oxygen (low cardiac output, anemia)


image Ventilation-perfusion (V/Q) mismatch


image Alveolar hypoventilation


image Shunt: physiologic (alveolar level) and anatomic (proximal to lung)


image Diffusion limitation


image Low inspired oxygen fraction


Common causes of hypoxemia and their respective primary mechanisms are as follows:



image Chronic obstructive pulmonary disease: V/Q mismatch, diffusion limitation


image Pneumonia, pulmonary edema, and acute respiratory distress syndrome: physiologic shunt


image Pulmonary embolism: V/Q mismatch (physiologic dead space)


image Pulmonary fibrosis: diffusion limitation


image Obesity: alveolar hypoventilation



4 What are the mechanisms and causes of hypercapnic respiratory failure?


Mechanisms (all related to alveolar hypoventilation) are as follows:



image Decreased central respiratory drive


image Abnormalities of the chest wall leading to excessive restriction


image Airways abnormalities leading to excessive dead space or increased work of breathing and fatigue


image Neuromuscular diseases (peripheral nervous system)


Causes are as follows:



image Severe asthma


image Drug overdose


image Myasthenia gravis


image Cervical cord injuries


image Brain stem injuries


image Obesity-hypoventilation


image Kyphoscoliosis



5 What are the most important immediate goals of therapy for ARF?


Hypoxia is the major immediate threat to organ function, and therefore initial goals should be directed toward oxygen supplementation and reversal or prevention of tissue hypoxia. Hypercapnia is generally better tolerated if not sudden or associated with severe acidosis. Supplemental oxygen should be delivered to achieve a PaO2 > 55 mm Hg. This can be achieved with nasal prongs or face mask, but in many cases mechanical ventilation is required to reverse hypoxemia. Mechanical ventilation can maximize both inspired O2 and alveolar ventilation (decrease PaCO2).



6 What are the main indications for endotracheal intubation and mechanical ventilation?


Bradypnea, apnea, or respiratory arrest; acute respiratory distress syndrome; respiratory muscle fatigue; obtundation or coma; PaO2 less than 55 mm Hg despite supplemental oxygen; PCO2 greater than 50 mm Hg with arterial pH < 7.2.



7 What are acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)?


The American-European Consensus Conference recommended the following criteria for definition of ARDS:



image Acute onset


image Bilateral infiltrates on chest radiograph


image Pulmonary artery wedge pressure ≤ 18 mm Hg or the absence of clinical evidence of left atrial hypertension


image PaO2/FiO2 ratio ≤ 200* for ARDS


image Acute lung injury is defined by all of the above except a PaO2/FiO2 ratio ≤ 300*



8 What is the pathogenesis of ARDS?


The early phase of ALI or ARDS is characterized by injury and increased permeability of the endothelial and epithelial barriers of the lung leading to the accumulation of protein-rich edema fluid in the interstitium and alveolar airspace. This fluid contains plasma proteins, inflammatory cells (mostly neutrophils), and necrotic debris that can pack down into dense eosin-staining hyaline membranes, the latter of which are pathognomonic for the pathology of ARDS, termed diffuse alveolar damage. Leukocytes, fibroblasts, and epithelial cells release cytokines that enhance the inflammatory response. Because of up-regulation of procoagulant pathways diffuse intravascular thrombi formation and fibrin deposition occur. Patients usually begin to recover in the first 5 to 14 days of disease. During the later phase of injury, type II pneumocyte hyperplasia and collagen deposition occur and can serve to repopulate the epithelium during the healing process but can also progress to fibrosis. This latter fibroproliferative phase can lead to prolonged time using the ventilator and increased mortality but can also be self-limited and resolve entirely.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Acute Respiratory Failure, Acute Lung Injury/Acute Respiratory Distress Syndrome, and Acute Chest Syndrome

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