Medullary respiratory center

Compare and contrast functions of the dorsal and ventral respiratory groups in the medullary respiratory center... 

Aggregates of cell bodies within the medulla of the brainstem form the medullary respiratory center, which has two distinct functional areas ... 

In summary, the regulation of ventilation by the medullary respiratory center determines the ... 

The medullary respiratory center receives excitatory and inhibitory inputs from many areas of the brain and peripheral nervous system, including ... 

Pulmonary stretch receptors are responsible for initiating the Hering-Breuer reflex. These stretch receptors are located within the smooth muscle of large and small airways. They are stimulated when the tidal volume exceeds 1 1. Nerve impulses are transmitted by the vagus nerve to the medullary respiratory center and inhibit the inspiratory neurons. The primary function of these receptors and the Hering-Breuer reflex is to prevent overinflation of the lungs. 

Pain receptors also influence the medullary respiratory center. Pain may cause a reflex increase in ventilation in the form of a "gasp." Somatic pain typically causes hyperpnea and visceral pain typically causes apnea, or decreased ventilation. 

Chemoreceptors provide the most important input to the medullary respiratory center in terms of regulating ventilation to meet the metabolic requirements of the body. Chemoreceptors are sensitive to changes in P02, PC02, and pH. The two types of chemoreceptors are ... 

Chemoreceptor response to decreased arterial P02. Hypoxia has a direct depressant effect on central chemoreceptors as well as on the medullary respiratory center. In fact, hypoxia tends to inhibit activity in all regions of the brain. Therefore, the ventilatory response to hypoxemia is elicited only by the peripheral chemoreceptors. 

Conversely, a decrease in the arterial PCOz due to hyperventilation results in a decrease in the H+ ion concentration in the ECF of the brain. Decreased stimulation of the central chemoreceptors (and therefore a decrease in the excitatory input to the medullary respiratory center) causes... 

Proprioceptors originating in muscles and joints of the exercising limbs provide substantial input to the medullary respiratory center. In fact, even passive movement of the limbs causes an increase in ventilation. Therefore, the mechanical aspects of exercise also contribute to the ventilatory response. The increased metabolism associated with exercise increases body temperature, which further contributes to the increase in ventilation during exercise. (Not surprisingly, ventilation is also enhanced in response to a fever.) Exercise is associated with a mass sympathetic discharge. As a result, epinephrine release from the adrenal medulla is markedly increased. Epinephrine is believed to stimulate ventilation. 

Although opioid anesthesia is particularly useful in patients with compromised myocardial function, the opioids depress respiration by inhibiting the responsiveness of the medullary respiratory center to PCO2 and alter the rhythm of breathing. Consequently, it is necessary to assist ventilation intraoperatively. Since respiratory depression may extend into the postoperative period as a result of drug accumulation in the tissues, the use of opioids whose clearances are slow, remain most appropriate for patients who are expected to require postoperative ventilatory care. 

At hypnotic doses in healthy patients, the effects of sedative-hypnotics on respiration are comparable to changes during natural sleep. However, even at therapeutic doses, sedative-hypnotics can produce significant respiratory depression in patients with pulmonary disease. Effects on respiration are dose-related, and depression of the medullary respiratory center is the usual cause of death due to overdose of sedative-hypnotics. 

With large doses, thiopental causes dose-dependent decreases in arterial blood pressure, stroke volume, and cardiac output. This is due primarily to its myocardial depressant effect and increased venous capacitance there is little change in total peripheral resistance. Thiopental is also a potent respiratory depressant, lowering the sensitivity of the medullary respiratory center to carbon dioxide. 

Death from cocaine often occurs within 2-3 minutes, suggesting direct cardiac toxicity, fatal dysrhythmias, and depression of medullary respiratory centers as common causes of death (11,12). Thus, cocaine s local anesthetic properties can contribute additional hazards when high doses are used, reminiscent of deaths reported in the era when it was used as a mucous membrane paste for nasopharyngeal surgery (13). 

Fentanyl stimulates mu-opioid receptors in the central nervous system (CNS), altering the body s response to pain. Fentanyl may alter the release of different neurotransmitters, such as jS-endorphin, sensitive to pain. Fentanyl can produce profound CNS and respiratory depression through mechanisms common to other opioids. Respiratory depression is mediated through action on the medullary respiratory center. Fentanyl is 50-100 times more potent... 

The existence of areas in the brain which are highly sensitive to changes in C02 tension was established from extensive studies over many decades (4). Initially it was thought that these sensitive areas were located in the respiratory center of the medulla. More recent studies have shown the existence of such cell groups exterior to the medullary respiratory center (2). 

What physiologic effects are manifested with opiate-induced depression of medullary respiratory centers ... 

Kappa receptor activation does not appear to be responsible for dependence, euphoria, or effects on smooth muscle. Increases in cerebral blood flow and (possibly) increased intracranial pressure result from the respiratory depressant actions of opioid analgesics. The latter effects are due to increased arterial PrOj, which results from mu receptor inhibition of the medullary respiratory center. However, the activation of kappa receptors contributes to analgesia at the spinal level and is probably responsible for sedative actions of the opioids. The answer is (D). Codeine and possibly nalbuphine could decrease gastrointestinal peristalsis but not without marked side effects (and a prescription). Dextromethorphan is a cough suppressant. The other two drugs listed are opioids with antidiarrheal actions. Diphenoxylate is not available over-the-counter since it is a constituent of a proprietary combination that includes atropine sulfate (Lomotil). Loperamide is available over-the-counter. The answer is (D). 

The respiratory centers arc neuronal groups found primarily in the medulla and pons of the brain stem. The medullary respiratory center comprises a dorsal and ventral group, located in the reticular formation of the medulla below the fourth ventricle. They are believed to be central targets for OP toxicity through an unknown mechanism. Damage to these neuronal control centers will affect inspiration and expiration. 

Airway. Airway protection in stroke patients may require immediate intervention. An impaired level of consciousness combined with emesis can occur in patients with increased intracranial pressure (ICP) and posterior circulation stroke. Vertebrobasilar ischemia may affect medullary respiratory centers and cause apnea, or more commonly, paralysis of pharyngeal and tongue musculature leading to obstruction of the airway. The patient may require gastric suction and intubation to protect the airway from aspiration of gastric contents. An oral airway or nasal trumpet can be helpful if the patient has an upper airway obstruction. 

In caffeine-naive subjects, a dose of 4mgkg increases the mean respiratory rate. This effect is not found in chronic caffeine ingestion. Several mechanisms have been suggested, such as an increase in pulmonary blood flow, an increased supply of air to the lungs due to the relaxation of bronchiolar and alveolar smooth muscle, an increase in sensitivity of the medullary respiratory center to carbon dioxide, stimulation of the central respiratory drive, an improved skeletal muscle contraction, and an increase in cardiac output. 

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