Without intervention, both may lead to decreased oxygen in the blood (hypoxemia), elevated carbon dioxide level in the blood (hypercapnia), inadequate oxygen perfusion to tissue (hypoxia), and may be fatal. Respiratory arrest is also different from cardiac arrest, the failure of heart muscle contraction. If untreated, one may lead to the other. Signs and symptoms
One common symptom of respiratory arrest is cyanosis, a bluish discoloration of the skin resulting from an inadequate amount of oxygen in the blood. If respiratory arrest remains without any treatment, cardiac arrest will occur within minutes of hypoxemia, hypercapnia or both. At this point, patients will be unconscious or about to become unconscious.Symptoms of respiratory compromise can differ with each patient. Complications from respiratory compromise are increasing rapidly across the clinical spectrum, partly due to expanded use of opioids combined with the lack of standardized guidelines among medical specialties. While respiratory compromise creates problems that are often serious and potentially life-threatening, they may be prevented with the proper tools and approach. Appropriate patient monitoring and therapeutic strategies are necessary for early recognition, intervention and treatment. Causes
Airway obstruction: Obstruction may occur in the upper and lower airway. Upper airway: Obstruction of the upper airway is common in infants less than 3 months old because they are nose breathers. Nasal blockage may easily lead to upper airway obstruction in infants. For other ages, upper airway obstruction may occur from a foreign body or edema of the pharynx, larynx, or trachea.
Ectopic ACTH syndrome describes conditions leading to excess production of adrenocorticotropic hormone (ACTH) subsequently leading to mineralocorticoid production. This can arise in ectopic forms of Cushings syndrome associated with small-cell lung cancers and other ACTH-producing tumors. The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects. Metabolic and dietary forms
Metabolic causes include conditions of glucocorticoid resistance and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy. Dietary causes include overconsumption of licorice-containing products. Glycyrrhetinic acid in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the mineralocorticoid receptor by cortisol leading to aldosterone-like effects. Diagnosis
In patients with hypertension, diagnostic clues pointing to pseudohyperaldosteronism can be found on routine labwork. These include low serum potassium (hypokalemia), elevated serum sodium (hypernatremia), and elevated serum bicarbonate (metabolic alkalosis). Urine studies may show elevated urine potassium (kaliuresis). To further differentiate between hyperaldosteronism and pseudohyperaldosteronism, studies including plasma renin activity (PRA) and plasma aldosterone concentration (PAC) can be obtained. Pseudohyperaldosteronism will exhibit low levels of both PRA and PAC while hyperaldosteronism will demonstrate elevated PAC. Confirmatory tests to diagnose the specific forms of pseudohyperaldosteronism vary depending on the cause. The genetic conditions such as Liddles syndrome and CAH can be confirmed with genetic tests for the affected genes. CAH can also be confirmed by analyzing enzyme levels following ACTH stimulation testing. AME can be diagnosed with a 24 hour urine collection exhibiting an increased ratio of urinary cortisol to urinary cortisone.