Cheyne-Stokes respiration is a form of periodic breathing in which central apneas and hypopneas alternate with periods of hyperventilation, producing a waxing and waning pattern of tidal volume. This review focuses on the causes and consequences of Cheyne-Stokes respiration in patients with congestive heart failure, in whom the prevalence is strikingly high and ranges from 30% to 50%. Several factors have been implicated in the genesis of Cheyne-Stokes respiration, including low cardiac output and recurrent hypoxia. The key pathophysiological mechanism triggering Cheyne-Stokes respiration is hyperventilation and low arterial CO 2 (PaCO 2 ) that when below the apneic threshold triggers a central apnea. Hyperventilation is associated with pulmonary congestion, and Cheyne-Stokes respiration is more prone to occur during sleep, when the respiratory system is mainly dependent on chemical control. It is associated with recurrent dips in oxygen saturation and arousals from sleep, with oscillations in blood pressure and heart rate, sympathetic activation and increased risk of ventricular tachycardia. Cheyne-Stokes respiration is an independent marker of poor prognosis and may participate in a vicious cycle, further stressing the failing heart.
The aim of this study was to analyze clinical aspects, hearing evolution and efficacy of clinical treatment of patients with sudden sensorineural hearing loss (SSNHL). This was a prospective clinical study of 136 consecutive patients with SSNHL divided into three groups after diagnostic evaluation: patients with defined etiology (DE, N = 13, 10%), concurrent diseases (CD, N = 63, 46.04%) and idiopathic sudden sensorineural hearing loss (ISSHL, N = 60, 43.9%). Initial treatment consisted of prednisone and pentoxifylline. Clinical aspects and hearing evolution for up to 6 months were evaluated. Group CD comprised 73% of patients with metabolic decompensation in the initial evaluation and was significantly older (53.80 years) than groups DE (41.93 years) and ISSHL (39.13 years). Comparison of the mean initial and final hearing loss of the three groups revealed a significant hearing improvement for group CD (P = 0.001) and group ISSHL (P = 0.001). Group DE did not present a significant difference in thresholds. The clinical classification for SSNHL allows the identification of significant differences regarding age, initial and final hearing impairment and likelihood of response to therapy. Elevated age and presence of coexisting disease were associated with a greater initial hearing impact and poorer hearing recovery after 6 months. Patients with defined etiology presented a much more limited response to therapy. The occurrence of decompensated metabolic and cardiovascular diseases and the possibility of first manifestation of auto-immune disease and cerebello-pontine angle tumors justify an adequate protocol for investigation of SSNHL.
During the onset of ISSHL, the following variables were correlated with a worse prognosis: dizziness, profound hearing loss, impaired hearing in the contralateral ear, and delay to start treatment. Tinnitus at the onset of ISSHL correlated with a better prognosis.
In all eight patients, the lateral sinus thrombosis was detected by imaging studies performed to evaluate complications and symptoms related to COM. Fever, headache, and cranial nerve paralysis were the main clinical manifestations associated with coexisting mastoiditis, meningitis, and cerebellar and epidural abscess. We could not identify features specific to lateral sinus thrombosis in any case. All patients underwent mastoidectomy and were given broad-spectrum antibiotics for 2 months. Four cases were anticoagulated and all eight cases experienced complete clinical recovery without sequelae.
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