Hypoventilation

Hypoventilation is the opposite of hyperventilation and is eharaeterized by an inability to exerete CO9 rapidly enough to meet physioiogieai needs. Hypoventilation ean be eaused by nar-eoties, sedatives, anestheties, and depressant drugs diseases of the lung also lead to hypoventilation. Hypoventilation results in respiratory acidosis, as C09(g) aeeumulates, giving rise to H9CO3, whieh dissoeiates to form H and HCOa. ... 

Respiratory—hypoventilation, apnea, respiratory depression, bronchospasm, laryngospasm... 

MONITORING AND MANAGING RESPIRATORY DEPRESSION These drugs depress the CNS and can cause respiratory depression. The nurse carefully assesses respiratory function (rate, depth, and quality) before administering a sedative, Vs, to 1 hour after administering the drug, and frequently thereafter. Toxic reaction of the barbiturates can cause severe respiratory depression, hypoventilation, and circulatory collapse. 

The most common adverse reaction associated with phenobarbital is sedation, which can range from mild sleepiness or drowsiness to somnolence. These dru > may also cause nausea, vomiting, constipation, bradycardia, hypoventilation, skin rash, headache fever, and diarrhea Agitation, rather than sedation, may occur in some patients. Some of these adverse effects may be reduced or eliminated as therapy continues. Occasionally, a slight dosage reduction, without reducing the ability of the drug to control the seizures, will reduce or eliminate some of these adverse reactions. 

If present In addition to hypoventilation, P02 will be lowered further. 

To properly calculate the extent of a shunt, however, requires the patient to breathe 100% oxygen for 15-20 minutes. Table III illustrates that the low P 02 in hypoventilation, diffusion defect, and V/Q inequality is corrected by breathing 100% oxygen whereas in a true veno-arterial shunt it is not. 

General Alveolar Hypoventilation A Syndrome of Respiratory and Cardiac Failure in Patients with Normal Lungs. Quart. J. Med. (1966), 35, 261 - 275. 

Arterial blood gases for evaluating partial arterial pressure of carbon dioxide (Pco2) should be considered for patients in severe distress, suspected hypoventilation, or when PEF or FEYT, is less than or equal to 30% after initial treatment. 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

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... 

H26. Holiday, J. W and Faden, A. I Naloxone acts at central opiate receptors to reverse hypotension, hypothermia, and hypoventilation in spinal shock. Brain Res. 19,295-299 (1980). 

Hypoventilation is defined as a reduction in the rate and depth of breathing. Inadequate ventilation results in hypoxemia, or a decrease in the concentration of oxygen in the arterial blood. Hypoventilation may be induced inadvertently by various pharmacological agents, including opioid analgesics such as morphine. These medications cause hypoventilation by way of their effects on the respiratory centers in the brainstem. Doses of... 

As cellular metabolism increases, the rate of production of carbon dioxide also increases. Typically, increased activity is associated with an increase in ventilation so that the increased amounts of carbon dioxide delivered to the lungs are eliminated. Hypoventilation impairs the elimination of carbon dioxide and causes an increase in alveolar PC02. 

It is important to note that a decrease in P02 is not the primary factor in the minute-to-minute regulation of ventilation. This is because the peripheral chemoreceptors are not stimulated until the P02 falls to life-threatening levels. A decrease of this magnitude would likely be associated with abnormal conditions, such as pulmonary disease, hypoventilation, or ascent to extreme altitude. 

Hypoventilating (breathing too slowly) increases the pC02 (numerator of the magic equation), and, as long as [HCO 3] remains constant, the [H+] must increase (pH decreases). 

The respiratory response to metabolic alkalosis is to increase PaC02 by hypoventilation. 

Some patients lose the ability to increase the rate or depth or respiration in response to persistent hypoxemia. This decreased ventilatory drive may be due to abnormal peripheral or central respiratory receptor responses. This relative hypoventilation leads to hypercapnia in this situation the central respiratory response to a chronically increased PaC02 can be blunted. Because these changes in Pa02 and PaC02 are subtle and progress over many years, the pH is usually near normal because the kidneys compensate by retaining bicarbonate. 

AGC Line AG represents a metabolic alkalosis with a rise in HC03 to 35 mmol.l-1. Compensation occurs by hypoventilation along line GC. 

Breathing-Reiated Sieep Disorders. The breathing-related sleep disorders include obstructive sleep apnea, central sleep apnea, and alveolar hypoventilation. Of these three, obstructive sleep apnea is by far the most common. The patient with sleep apnea usually breathes normally when awake and only stops breathing while asleep. Occasional episodes of apnea are normal, but five or more episodes of apnea per hour are usually considered diagnostic of the disorder. 

The pH value is kept constant by buffer systems that cushion minor disturbances in the acid-base balance (C). In the longer term, the decisive aspect is maintaining a balanced equilibrium between H" production and uptake and H" release. If the blood s buffering capacity is not suf cient, or if the acid-base balance is not in equilibrium—e.g., in kidney disease or during hypoventilation or hyperventilation-shifts in the plasma pH value can occur. A reduction by more than 0.03 units is known as acidosis, and an increase is called alkalosis. 

Hypoventilation Monitor patients who have received flumazenil for the reversal of benzodiazepine effects (after conscious sedation or general anesthesia) for resedation, respiratory depression or other residual benzodiazepine effects for an appropriate period (120 minutes or less) based on the dose and duration of effect of the benzodiazepine employed, because flumazenil has not been established as an effective treatment for hypoventilation due to benzodiazepine administration. Flumazenil may not fully reverse postoperative airway problems or ventilatory insufficiency induced by benzodiazepines. In addition, even if flumazenil is initially effective, such problems may recur because the effects of flumazenil wear off before the effects of many benzodiazepines. 

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