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Respiratory disturbances

II Measurable but not life-threatening symptoms Cutaneous signs, hypotension, tachycardia Respiratory disturbance cough, difficulty to inflate... [Pg.183]

Respiratory acidosis and alkalosis result from primary disturbances in the arterial carbon dioxide (C02) levels. Metabolic compensation of respiratory disturbances is a slow process, often requiring days for the serum HC03 to reach the steady state. [Pg.419]

RDP respiratory disturbance index treatment of restless legs syndrome and periodic limb move-... [Pg.631]

Respiratory disturbance index A summary measure that quantifies the number of apneas, hypopneas, and respiratory effort-related arousals per hour of sleep. [Pg.1575]

Psychiatric Behavior problems hysteria psychosis suicidal tendencies. Respiratory Nasal congestion respiratory disturbances. [Pg.1022]

Decreased appetite, respiratory disturbance (such as increased cough) (6%) anxiety, nervousness (5%) flatulence, paresthesia, yawning (4%) decreased libido, sexual dysfunction, abdominal discomfort (3%)... [Pg.942]

While correlation may not be the optimal measure of the usefulness of the Epworth scale for discrimination or prediction (32), there also appears to be no categorical association between ESS score and sleep latency (30,33,34). Thus, although the ESS may be predictive of other variables such as general health status (16) or respiratory disturbance index (12), most of the evidence suggests that its association with sleep latency is tenuous. Similar results emerge from studies comparing ESS with the other (newer) objective measure of EDS, the maintenance of wakefulness test (MWT). In a large narcolepsy sample, the correlation between ESS and MWT was weak (r = -0.29, p <. 001) (35). [Pg.7]

The lack of association, or weak correlation, between subjective scales and objective measures suggests that subjective and objective measures evaluate different aspects of sleepiness. This is the prevailing view (15,30,31,35,36), and it is supported by the association between the ESS, nocturnal sleep latency (on polysomnogram), and respiratory disturbance index (12). [Pg.7]

Some of the respiratory disturbances experienced by Parkinson s patients are similar in nature to that experienced by non-Parkinson s patients with sleep-related respiratory disturbances. Hence the same treatments may be used in both patient groups, depending on the stage of the Parkinson s. Continuous positive airway pressure (CPAP) can improve sleep in Parkinson s patients, but is not suitable during the advanced stages of Parkinson s. Alternatively, upper-airway surgery may provide some relief. Neither of these measures, however, alleviates the respiratory disturbance that may be due to the muscle rigidity associated directly with Parkinson s disease. [Pg.98]

Ristannovic RA, Black J, Mamelak M, Montplaisir J (2002) Effect of increasing doses of sodium oxybate on nocturnal respiratory disturbances. Sleep 25 A473-A474... [Pg.60]

Respiratory disturbances Tachypnea awake or sleep apnea... [Pg.83]

Etomidate produced activation of epileptiform activity, and electrographic seizures during craniotomy in epileptic patients (8). Generalized seizures were noted after etomidate induction in 20% of 30 patients without a history of epilepsy (9). Cerebral excitation can also occur after recovery from etomidate anesthesia, with potential respiratory disturbance (10,11). Caution should be exercised when giving etomidate to patients with a history of seizures (SEDA-18,113). [Pg.1303]

Parker CJ. Respiratory disturbance during recovery from etomidate anaesthesia. Anaesthesia 1988 43(1) 16-17. [Pg.1304]

De Keyser J, Vincken W. L-dopa-induced respiratory disturbance in Parkinson s disease suppressed by tiapride. Neurology 1985 35(2) 235-7. [Pg.2046]

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. [Pg.996]

Bureau MA, Lamarche J, Foulon P, Dalle D. Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs. J Appl Physiol 1985 59 869-874. Bureau MA, Lamarche J, Foulon P, Dalle D. The ventilatory response to h poxia in the newborn lamb after carotid body denervation. Respir Physiol 1985 60 109-119. Hofer MA. Sleep-wake state organization in infant rats with episodic respiratory disturbance following sinoaortic denervation. Sleep 1985 8 40 8. [Pg.246]


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