For a male client with suspected increased intracranial pressure (ICP), a most appropriate respiratory goal is to:
a- prevent respiratory alkalosis.
b- lower arterial pH.
c- promote carbon dioxide elimination.
d- maintain partial pressure of arterial oxygen (PaO2) above 80 mm Hg.
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Respiratory alkalosis is a primitive decrease in carbon dioxide partial pressure (Pco2) with or without a compensating decrease in HCO3-; the pH can be high or close to normal. The cause is an increase in respiratory rate and / or minute volume (hyperventilation). Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form causes lipothymia, confusion, paraesthesia, cramps and syncope. Symptoms include hyperpnea or tachypnea and carpopedal spasm. Diagnosis is clinical and biological by arterial blood gases and blood ionogram. The treatment is directed against the cause.
Etiology:
Respiratory alkalosis consists of a primary decrease of Pco2 (hypocapnia) caused by an increase in respiratory rate and / or minute volume (hyperventilation). An increase in ventilation is most often the physiological response to hypoxia (eg, high altitude), metabolic acidosis, and increased metabolic requirements (eg, fever), it occurs in many serious diseases. In addition, pain, anxiety, and certain CNS pathologies (eg, stroke, post-crisis epileptic seizures) may increase breathing without physiological need.
pathophysiology:
Respiratory alkalosis can be:
- Acute
- Chronicle
The distinction is based on the degree of metabolic compensation. Excess HCO3- is buffered by extracellular hydrogen (H +) ions within minutes, but greater compensation occurs within 2-3 days as the kidneys decrease H + removal.
Pseudo-respiratory alkalosis:
Pseudo-respiratory alkalosis is low blood pressure and high pH in patients with severe metabolic acidosis caused by insufficient tissue perfusion (eg, cardiogenic shock, cardiopulmonary resuscitation). Pseudo-respiratory alkalosis occurs when mechanical ventilation (often with hyperventilation) removes larger than normal amounts of alveolar carbon dioxide (CO2). The expiry of large amounts of alveolar CO2 causes apparent respiratory alkalosis (on arterial blood gases), but insufficient tissue perfusion and cellular ischemia promote cellular acidosis, resulting in venous blood acidosis. The diagnosis is based on the demonstration of marked differences in arterial and venous Pco2 and pH, and on a high lactate concentration in a patient whose arterial blood gases indicate respiratory alkalosis; the treatment consists in improving the systemic hemodynamic parameters.
Symptomatology:
The symptomatology is a function of the speed and amplitude of the fall of Pco2. Acute respiratory alkalosis causes lipothymia, confusion, perioral and peripheral paresthesia, cramps and syncope. The likely mechanism is a change in cerebral blood flow and pH. A tachypnea or hyperpnea is often the only sign; Carpopedal spasm can occur in severe cases due to decreased levels of ionized Ca in the blood (which enters cells by hydrogen ion exchange [H +]).
Chronic respiratory alkalosis is usually asymptomatic and has no characteristic symptoms.
Diagnostic:
Arterial blood gas and blood ionogram
If hypoxia is present, the cause must be vigorously sought
Recognition of respiratory alkalosis and renal clearing (Acid-Base Balance Disorders: Diagnosis) requires the measurement of arterial blood gases and blood ionogram. Minor hypophosphatemia and hypokalemia caused by intracellular transfer and decreased ionized Ca ++ caused by increased protein binding may be present.
The presence of hypoxia or an increase in the alveolo- arterial gradient in O2 (A-a) (Po2-inspired [Ar2 + arterial 5/4 Pco2 arterial]) requires the search for the cause. The causes are often apparent from the history and results of the clinical examination. However, since pulmonary embolism often occurs without hypoxia, embolism should be strongly considered in hyperventilation patients before the diagnosis of anxiety alone.
a- prevent respiratory alkalosis.
b- lower arterial pH.
c- promote carbon dioxide elimination.
d- maintain partial pressure of arterial oxygen (PaO2) above 80 mm Hg.
----------------------
Respiratory alkalosis is a primitive decrease in carbon dioxide partial pressure (Pco2) with or without a compensating decrease in HCO3-; the pH can be high or close to normal. The cause is an increase in respiratory rate and / or minute volume (hyperventilation). Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form causes lipothymia, confusion, paraesthesia, cramps and syncope. Symptoms include hyperpnea or tachypnea and carpopedal spasm. Diagnosis is clinical and biological by arterial blood gases and blood ionogram. The treatment is directed against the cause.
Etiology:
Respiratory alkalosis consists of a primary decrease of Pco2 (hypocapnia) caused by an increase in respiratory rate and / or minute volume (hyperventilation). An increase in ventilation is most often the physiological response to hypoxia (eg, high altitude), metabolic acidosis, and increased metabolic requirements (eg, fever), it occurs in many serious diseases. In addition, pain, anxiety, and certain CNS pathologies (eg, stroke, post-crisis epileptic seizures) may increase breathing without physiological need.
pathophysiology:
Respiratory alkalosis can be:
- Acute
- Chronicle
The distinction is based on the degree of metabolic compensation. Excess HCO3- is buffered by extracellular hydrogen (H +) ions within minutes, but greater compensation occurs within 2-3 days as the kidneys decrease H + removal.
Pseudo-respiratory alkalosis:
Pseudo-respiratory alkalosis is low blood pressure and high pH in patients with severe metabolic acidosis caused by insufficient tissue perfusion (eg, cardiogenic shock, cardiopulmonary resuscitation). Pseudo-respiratory alkalosis occurs when mechanical ventilation (often with hyperventilation) removes larger than normal amounts of alveolar carbon dioxide (CO2). The expiry of large amounts of alveolar CO2 causes apparent respiratory alkalosis (on arterial blood gases), but insufficient tissue perfusion and cellular ischemia promote cellular acidosis, resulting in venous blood acidosis. The diagnosis is based on the demonstration of marked differences in arterial and venous Pco2 and pH, and on a high lactate concentration in a patient whose arterial blood gases indicate respiratory alkalosis; the treatment consists in improving the systemic hemodynamic parameters.
Symptomatology:
The symptomatology is a function of the speed and amplitude of the fall of Pco2. Acute respiratory alkalosis causes lipothymia, confusion, perioral and peripheral paresthesia, cramps and syncope. The likely mechanism is a change in cerebral blood flow and pH. A tachypnea or hyperpnea is often the only sign; Carpopedal spasm can occur in severe cases due to decreased levels of ionized Ca in the blood (which enters cells by hydrogen ion exchange [H +]).
Chronic respiratory alkalosis is usually asymptomatic and has no characteristic symptoms.
Diagnostic:
Arterial blood gas and blood ionogram
If hypoxia is present, the cause must be vigorously sought
Recognition of respiratory alkalosis and renal clearing (Acid-Base Balance Disorders: Diagnosis) requires the measurement of arterial blood gases and blood ionogram. Minor hypophosphatemia and hypokalemia caused by intracellular transfer and decreased ionized Ca ++ caused by increased protein binding may be present.
The presence of hypoxia or an increase in the alveolo- arterial gradient in O2 (A-a) (Po2-inspired [Ar2 + arterial 5/4 Pco2 arterial]) requires the search for the cause. The causes are often apparent from the history and results of the clinical examination. However, since pulmonary embolism often occurs without hypoxia, embolism should be strongly considered in hyperventilation patients before the diagnosis of anxiety alone.
Treatment:
Treatment of the underlying disorder:
The treatment is that of the underlying disorder. Respiratory alkalosis is not life-threatening, so no intervention to lower the pH is necessary. Inspired CO2 rebreathing (such as breathing in a paper bag) is a common practice but can be dangerous in at least some patients with CNS disorders in which the CSF pH may already be below normal.
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Neurologic Practice