Lynchak R.M., Dogadova Т.В., Zhirova L.G., Frolov D.N.

Federal State Public Institution „National Medical and Surgical Center named after N.I. Pirogov” of the Ministry of Healthcare of the Russian Federation

Only in the last three decades, clinical medicine has come to a correct understanding of the essence of the syndrome of obstructive sleep apnea (SOSA) — a condition characterized by the presence of snoring, repeated episodes of upper airway obstruction at the pharyngeal level and cessation of pulmonary ventilation with persistent respiratory effort, a decrease in blood oxygen level, fragmentation of sleep and excessive daytime sleepiness [2]. The prevalence of SOSA is 5-7% of the total population over 30 years old. [1].

The main criterion for diagnosis of SOSA is the index of apneagipopnea (the number of episodes of apnea and hypopnea in 1 hour). The term apnea refers to the incidence of episodes of complete cessation of the nose/mouth air flow for 10 seconds or more with persistent respiratory effort. Hypopnea — incomplete obstruction of the airways, accompanied by a drop in oxygen saturation of blood by at least 3%.

Normally, the apnea-hypopnea index should not exceed 10.

The main method of treatment of SOSA, which is able to improve the prognosis of such patients, is long-term non-invasive assisted ventilation of the lungs with a constant positive pressure during night sleep (CPAP-therapy) [3]. The principle of the medicamentous effects of CPAP therapy and the appearance of the patient during this type of treatment are presented in Figures 1 and 2.

Mechanism of action of CPAP-therapy

Fig.1. The mechanism of action of the CPAP therapy is: a — the upper respiratory tract is normally open; b — collapse of the upper respiratory tract walls under SOSA; c — positive pressure prevents the walls of the upper respiratory tract from falling.

(1 изображение „Внешний вид больной во время проведения СИПАП-терапии” -> „Appearance of the patient during the course of CPAP therapy”)

Appearance of the patient during the course of CPAP therapy

Fig.2. Appearance of the patient during the course of CPAP therapy

Frequently, SOSA can hide under the „masks” of various cardiac diseases, in particular severe rhythm disturbances and conduction of the heart, as exemplified by the following clinical observation.

Patient M., 54 years old, entered the cardiology department for patients with heart rhythm disorders on May 13, 2009 with a diagnosis „Syndrome of weakness of the sinus node with pauses of ventricular asystole up to 6 seconds” with the aim of implanting a permanent electric cardiac pacemaker (Fig. 3).

Fragment of Holter ECG Patient M. with a pause of ventricular asystole up to 5.9 seconds recorded at night

Fig.3. Fragment of Holter ECG Patient M. with a pause of ventricular asystole up to 5.9 seconds recorded at night

The patient complained of intermittent sleep, snoring, increased daytime sleepiness, decreased performance, episodes of rapid heart rate.

From the anamnesis it was found out that within 10 years the patient had episodes of increase of a BP with the maximum values ​​up to 240/150 mm Hg. With a constant 3-component antihypertensive therapy (arifon-retard, monopril, nifecard), blood pressure was reached 130/90 mmHg. During the last few months, the patient had complaints about the heartbeat, which led to the implementation of Holter ECG, according to which the transient SA blockade was recorded with a maximum pause of about 6 sec at night, paroxysms of atrial tachycardia with a maximum heart rate of 116 per min. In connection with this, the cardiologist of the polyclinic at the place of residence of the patient recommended surgical treatment — the implantation of a permanent electric cardiac pacemaker.

On examination, a Pickwick constitutional type of patient, a short neck, obesity of the 2nd degree attracted attention.

Considering the fact that episodes of ventricular asystole were recorded only at night, in conjunction with obesity and hypertension, it was impossible to exclude the presence of obstructive sleep apnea syndrome in the patient as a cause of all of the above.

The patient underwent a polysomnographic study involving the recording of snoring, a nose/mouth air flow, ECG, chest and abdominal wall movements and pulse oximetry during sleep to verify the SOSA, (Fig. 4).

Appearance of the patient during the polysomnography study

Fig. 4. Appearance of the patient during the polysomnography study

As a result of this study, the patient was diagnosed with a syndrome of sleep-induced sleep apnea of ​​moderate severity (apneagipopnea index was 32, a drop in the average oxygen saturation of the blood in the night before 89% was recorded) (Fig. 5).

Fragment of a polysomnographic study

Fig.5. Fragment of a polysomnographic study

In connection with this, the patient had 3 sessions of CPAP therapy, after those positive dynamics was noted. With a control polysomnographic study on the background of CPAP therapy, the apneagipopnea index decreased to 1.5 (which corresponds to the norm), the average oxygen saturation of the blood increased to 94% per night, and in the Holter ECG, no pauses of asystole were recorded.

Thus, the causal relationship between cardiac conduction abnormalities and obstructive sleep apnea syndrome and the high efficacy of CPAP therapy has been demonstrated.

The patient was explained the inexpediency of implantation of a constant pacemaker and was recommended to continue CPAP therapy. However, the patient refused a new method for treating cardiac conduction abnormalities, preferred to him a traditional and, in her opinion, a more reliable method of treatment — implantation of electric cardiac pacemaker.

This clinical observation is consonant with the statement of the English neurologist John Hewlingas Jackson (1836-1911): „To expel a false idea from medicine, you need 50 years, and to confirm the right — one hundred.”

Literature

  1. Ерошина В.А., Р.В. Бузунов, Зимин Ю.В., Чевокина С.А. Кардиологические проявления среднетяжелого обструктивного апноэ сна: артериальная гипертония, аритмии сердца, ишемия миокарда//Кремлевская медицина.- 1988.- N 2.- С. 38-42.
  2. Guilleminault C., Tilkian A., Dement W.C. The sleep apnea syndromes // Am. Rev. Med.- 1976.- Vol. 27.- P. 465 — 484.
  3. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study// LANCET, 2005; 16; 365 (9464): 1046-53/