Ventilatory failure and

A Assessment Ventilatory failure has multiple causes, including failure of the ventilatory muscles, central depression of respiratory drive, and severe pneumonia or pulmonary edema. Examples of drugs and toxins that cause ventilatory failure and the causative mechanisms are listed in Table 1-1. 

Roussos C. Ventilatory failure and respiratory muscles. In Roussos C, Macklem PT, eds. The Thorax. New York Marcel Dekker, 1985 884-888. 

A large number of conditions can result in chronic ventilatory failure and patients with these conditions may benefit from home ventilation. Typically, patients with restrictive disorders have decreased compliance of the chest wall, resulting from a thoracic cage deformity or from respiratory muscle involvement (1). In patients with severe obstructive pulmonary disorders, respiratory muscle fatigue and alveolar hypoventilation, especially during sleep, are thought to contribute to respiratory failure (2,3) (Table 1). 

The term analeptics refers to convulsants and respiratory stimulants (i.e. central nervous system stimulants). They comprise a reverse group of agents (for example amphifrnazole and doxapram (respiratory stimulants) and strychnine, biculline and picrotoxin). Analeptics are mainly experimental drugs. Only amphifrnazole and doxapram are occasionally used for the treatment of acute ventilatory failure. 

Respiratory acidosis is characterized by a reduced arterial pH, a primary increase in the arterial PaC02 and, when present for sufficient time, a compensatory rise in the HCOf concentration. Because increased C02 is a potent respiratory stimulus, respiratory acidosis represents ventilatory failure or impaired central control of ventilation as opposed to an increase in C02 production. As such, most patients will have hypoxemia in addition to hypercapnia. The most common etiologies of respiratory acidosis are listed in Table 25-6. 

In order to effectively treat respiratory acidosis, the causative process must be identified and treated. If a cause is identified, specific therapy should be started. This may include naloxone for opiate-induced hypoventilation or bronchodilator therapy for acute bronchospasm. Because respiratory acidosis represents ventilatory failure, an increase in... 

Phase II begins 60 minutes into the seizure, and the patient begins to decompensate. The patient may become hypotensive, and cerebral blood flow may be compromised. Glucose may be normal or decreased, and hyperthermia, respiratory deterioration, hypoxia, and ventilatory failure may develop. 

Emergency use Nalmefene is not the primary treatment for ventilatory failure. In most emergency settings, treatment with nalmefene should follow, not precede, the establishment of a patent airway, ventilatory assistance, administration of oxygen, and establishment of circulatory access. 

In critically ill patients who have ventilatory failure from various causes (eg, severe bronchospasm, pneumonia, chronic obstructive airway disease), it may be necessary to control ventilation to provide adequate gas exchange and to prevent atelectasis. In the ICU, neuromuscular blocking drugs are frequently administered to reduce chest wall resistance (ie, improve thoracic compliance) and ineffective spontaneous ventilation in intubated patients. 

A 42-year-old woman who presented with a change in mental status and rapidly decompensated into respiratory failure and required ventilatory assistance for 2 months had not taken an overdose—her lithium concentration had increased slowly (567). 

A severely poisoned casualty becomes totally apneic and will die as a result of ventilatory failure, which precedes collapse of the circulatory sys-... 

The seven serotypes of botulinum toxin produced by Clostridium botulinum are the most toxic substances known. They are associated with lethal food poisoning after the consumption of canned foods. This family of toxins was evaluated by the United States as a potential biological weapon in the 1960s and is believed to be an agent that could be used against our troops. Unlike other threat toxins, botulinum neurotoxin appears to cause the same disease after inhalation, oral ingestion, or injection. Death results from skeletal muscle paralysis and resultant ventilatory failure. Because of its extreme toxicity, the toxin typically cannot be identified in body fluids, other than nasal... 

Along with airaray problems, breathing difficulties are the major cause of morbidity and death in patients with poisoning or drug overdose. Patients may have one or more of the following complications ventilatory failure, hypoxia, or bronchospasm. 

B. Complications. Severe bronchospasm may result in hypoxia and ventilatory failure. 

Sidi A, Kaplan RB, Davis RB. Prolongedneuromuscularblockade and ventilatory failure after renal transplantation and cyclosporine. Can JAnaesth (1990) 37,543-8. 

Metabolic acidosis can result in stimulation of chemoreceptors, leading to increased ventilatory rate and depth and Kussmaul breathing in an attempt to decrease CO to compensate for the excess acid in the body. If the hyperventilation is prolonged, fatigue could result, leading to respiratory failure. 

Santiago RM, Scharnhorst D, Ratkin G, et al. Respiratory muscle weakness and ventilatory failure in AL amyloidosis with muscular pseudohypertrophy. Am J Med 1987 83(1) 175-178. 

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