Successful Treatment of an Infant Case of Apnea Caused by Rhinovirus Infection with High-flow Nasal Cannula / 日本プライマリ・ケア連合学会誌

The case involved a one-month-old male infant. Around two weeks after birth, cold-like symptoms were observed within the family. Over the course of approximately one month, the infant gradually developed coughing, apnea, and cyanosis, leading to a visit to a nearby medical facility. The episodes of apnea were initiated by a wet-sounding, choking cough. Respiratory pathogen multiplex screening revealed rhinovirus infection. The infant was managed in the intensive care unit and treated with a high-flow nasal cannula (HFNC), which resulted in an improvement of the recurrent episodes of apnea. We discontinued HFNC on the 7th day of hospitalization; however, the patient had recurrence of apnea. After relieving abdominal distension through rectal enema, the infant was successfully weaned off HFNC and discharged on the 14th day of hospitalization. In addition to the immaturity of the respiratory center in infants, laryngeal chemoreflex triggered by chemical receptors in the larynx is known to contribute to apnea. In the present case, we considered that the reduction of respiratory effort through HFNC, the expectorant effect of warmed and humidified air, and the decrease in gastroesophageal reflux due to alleviation of abdominal distension played roles in the successful outcome.

Effects of enriched-potassium diet on cardiorespiratory outcomes in experimental non-ischemic chronic heart failure

BACKGROUND: Chronic heart failure (CHF) is a global health problem. Increased sympathetic outflow, cardiac arrhythmogenesis and irregular breathing patterns have all been associated with poor outcomes in CHF. Several studies showed that activation of the renin-angiotensin system (RAS) play a key role in CHF pathophysiology. Interestingly, potassium (K+) supplemented diets showed promising results in normalizing RAS axis and autonomic dysfunction in vascular diseases, lowering cardiovascular risk. Whether subtle increases in dietary K+ consumption may exert similar effects in CHF has not been previously tested. Accordingly, we aimed to evaluate the effects of dietary K+ supplementation on cardiorespiratory alterations in rats with CHF. METHODS: Adult male Sprague-Dawley rats underwent volume overload to induce non-ischemic CHF. Animals were randomly allocated to normal chow diet (CHF group) or supplemented K+ diet (CHF+K+ group) for 6 weeks. Cardiac arrhythmogenesis, sympathetic outflow, baroreflex sensitivity, breathing disorders, chemoreflex function, respiratory- cardiovascular coupling and cardiac function were evaluated. RESULTS: Compared to normal chow diet, K+ supplemented diet in CHF significantly reduced arrhythmia incidence (67.8 ± 15.1 vs. 31.0 ± 3.7 events/hour, CHF vs. CHF+K+), decreased cardiac sympathetic tone (ΔHR to propranolol: - 97.4 ± 9.4 vs. - 60.8 ± 8.3 bpm, CHF vs. CHF+K+), restored baroreflex function and attenuated irregular breathing patterns. Additionally, supplementation of the diet with K+ restores normal central respiratory chemoreflex drive and abrogates pathological cardio-respiratory coupling in CHF rats being the outcome an improved cardiac function. CONCLUSION: Our findings support that dietary K+ supplementation in non-ischemic CHF alleviate cardiorespiratory dysfunction.

Effect of chronic ethanol exposure on rat ventilatory responses to hypoxia and hypercapnia

OBJECTIVE: The effect of chronic ethanol exposure on chemoreflexes has not been extensively studied in experimental animals. Therefore, this study tested the hypothesis that known ethanol-induced autonomic, neuroendocrine and cardiovascular changes coincide with increased chemoreflex sensitivity, as indicated by increased ventilatory responses to hypoxia and hypercapnia. METHODS: Male Wistar rats were subjected to increasing ethanol concentrations in their drinking water (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). At the end of each week of ethanol exposure, ventilatory parameters were measured under basal conditions and in response to hypoxia (evaluation of peripheral chemoreflex sensitivity) and hypercapnia (evaluation of central chemoreflex sensitivity). RESULTS: Decreased respiratory frequency was observed in rats exposed to ethanol from the first until the fourth week, whereas minute ventilation remained unchanged. Moreover, we observed an increased tidal volume in the second through the fourth week of exposure. The minute ventilation responses to hypoxia were attenuated in the first through the third week but remained unchanged during the last week. The respiratory frequency responses to hypoxia in ethanol-exposed rats were attenuated in the second through the third week but remained unchanged in the first and fourth weeks. There was no significant change in tidal volume responses to hypoxia. With regard to hypercapnic responses, no significant changes in ventilatory parameters were observed. CONCLUSIONS: Our data are consistent with the notion that chronic ethanol exposure does not increase peripheral or central chemoreflex sensitivity. .

The contribution of inspiratory muscles function to exercise limitation in heart failure: pathophysiological mechanisms / Contribuição da musculatura inspiratória na limitação ao exercício na insuficiência cardíaca: mecanismos fisiopatológicos

BACKGROUND: Heart failure induces histological, metabolic and functional adaptations in the inspiratory muscles. This inspiratory muscle weakness, which occurs in 30% to 50% of the heart failure patients, is associated with reduction in the functional capacity, reduction in the quality of life and with a poor prognosis in these individuals. OBJECTIVES: The objective of this review was to discuss the pathophysiological mechanisms that may explain the role of the inspiratory muscles in the exercise limitation with focus in the reflexes that control the ventilation and the circulation during the exercise. METHOD: We performed searches in the PUBMED database using the terms "inspiratory muscles", "inspiratory muscle training", "metaboreflex" and chemoreflex" and including studies published since 1980. RESULTS: Inspiratory muscle weakness is associated with exercise intolerance and with an exaggerated inspiratory chemoreflex and metaboreflex in heart failure. The inspiratory metaboreflex may be attenuated by the inspiratory muscle training or by the aerobic exercise training improving the exercise performance. CONCLUSIONS: Patients with heart failure may present changes in the inspiratory muscle function associated with inspiratory chemoreflex and metaboreflex hyperactivity, which exacerbate the exercise intolerance.

CONTEXTUALIZAÇÃO: A insuficiência cardíaca (IC) acarreta alterações histológicas, metabólicas e funcionais dos músculos inspiratórios. A fraqueza dos músculos inspiratórios, que ocorre em 30% a 50% dos pacientes com IC, associa-se com a redução da capacidade funcional, prejuízos para a qualidade de vida e piora no prognóstico desses indivíduos. OBJETIVOS: Discutir os mecanismos fisiopatológicos que potencialmente explicam o papel da musculatura inspiratória na limitação ao exercício, abordando-se os reflexos que controlam a ventilação e a circulação durante o exercício. MÉTODO: Foram realizadas pesquisas na base de dados PUBMED, utilizando os termos inspiratory muscles, inspiratory muscle training, metaborreflex e chemoreflex e incluindo estudos publicados desde 1980. RESULTADOS: A fraqueza muscular inspiratória está relacionada com intolerância ao exercício e com exacerbação do quimiorreflexo e do metaborreflexo inspiratório na IC. O metaborreflexo inspiratório pode ser atenuado pelo treinamento muscular inspiratório ou pelo treinamento aeróbico, melhorando o desempenho ao exercício. CONCLUSÕES: Os pacientes com IC podem apresentar alterações da função muscular inspiratória associadas com hiperatividade quimiorreflexa e metaborreflexa inspiratória, as quais podem agravar a intolerância ao exercício.

Central chemoreceptors and neural mechanisms of cardiorespiratory control

The arterial partial pressure (P CO2) of carbon dioxide is virtually constant because of the close match between the metabolic production of this gas and its excretion via breathing. Blood gas homeostasis does not rely solely on changes in lung ventilation, but also to a considerable extent on circulatory adjustments that regulate the transport of CO2 from its sites of production to the lungs. The neural mechanisms that coordinate circulatory and ventilatory changes to achieve blood gas homeostasis are the subject of this review. Emphasis will be placed on the control of sympathetic outflow by central chemoreceptors. High levels of CO2 exert an excitatory effect on sympathetic outflow that is mediated by specialized chemoreceptors such as the neurons located in the retrotrapezoid region. In addition, high CO2 causes an aversive awareness in conscious animals, activating wake-promoting pathways such as the noradrenergic neurons. These neuronal groups, which may also be directly activated by brain acidification, have projections that contribute to the CO2-induced rise in breathing and sympathetic outflow. However, since the level of activity of the retrotrapezoid nucleus is regulated by converging inputs from wake-promoting systems, behavior-specific inputs from higher centers and by chemical drive, the main focus of the present manuscript is to review the contribution of central chemoreceptors to the control of autonomic and respiratory mechanisms.

Experimental Study of Laryngeal Chemoreflex in Puppies / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Mechanical or chemical stimulation of the supraglottic mucosa may result in either or both of two responses: the laryngeal adductor reflex response (LAR), which causes glottic closure, and the laryngeal chemoreflex (LCR), which results in centrally mediated apnea, hemodynamic instability and swallowing. Exaggeration of this normally protective reflexes is thought to be responsible for several disorders, including the sudden infant death syndrome (SIDS). MATERIALS AND METHODS: The supraglottic laryngeal mucosa which was topically stimulated by saline, distilled water, cow's milk and acid at pH 1.0 was introduced in 14 anesthetized puppies of three different age groups. In group I, four puppies were 2-weeks-of-age, and in group II and III, five puppies were 4 and 6-weeks-of-age, respectively. RESULT: 1) Strong acid (pH 1.0) induced the LCR response.20) After stimulating, respiration was depressed initially, followed by later hyperventilation. We found strong contraction or laryngospasm of thyroarytenoid (TA) muscle after a short period of latency. 3) Respiration was not, or minimally depressed in group I. Moderate depression or apnea was elicited in group II and III. 4) After stimulating, the heart rate was reduced, but it had no statistical meaning. 5) We found 3 types of TA muscle contraction pattern. Type I showed no laryngospasm, but large contraction wave was noted by EMG. Type II showed no laryngospasm, but strong contraction was noted initially and followed by some large waves by EMG. Type III showed laryngospasm that was visible to the naked eye and by EMG. 6) Peak to peak amplitude differences of TA muscle were significantly increased statistically in all age groups. CONCLUSION: We suggest that the LCR is an age-dependent response which is absent in very young puppies before 2 weeks and appears after that age. Thus, it has important implications that postnatal neural maturation may influence laryngeal reflex to some extent.