3.4 Levitzsky

What initiates breathing in the central nervous system?

In eupneic states, how does breathing occur?

What forms the 'final common pathway' for respiratory control in the brainstem?

What determines the depth of respiration or tidal volume?

Where are the centers that initiate breathing located?

Which area is known as the medullary center or medullary respiratory center?

What is the function of inspiratory neurons in the dorsal respiratory groups?

What happens if the brainstem is transected below the area where breathing initiation centers are located?

Where do inspiratory neurons in the dorsal respiratory groups mainly project to?

What do the dorsal respiratory groups consist mainly of?

Where is the primary projection site of visceral afferent fibers of the ninth and tenth cranial nerves?

Which neurons primarily innervate the ipsilateral laryngeal, pharyngeal, and tongue muscles for breathing?

What is the main function of the Ventral Respiratory Group (VRG) neurons?

Which population of cells in the DRG increase their activity if lung inflation is withheld?

Where are the expiratory neurons located in the ventral respiratory groups?

What is the role of I   cells if lung inflation is withheld?

Which neurons are involved in maintaining the patency of the upper airway?

What is the location of DRG within the NTS responsible for?

What is the main function of the pontine respiratory groups in the brainstem?

What is the result of apneusis when induced by the transection in the brainstem?

Where are the pontine respiratory groups located in the brainstem?

What is the likely role of pulmonary inflation afferent information in relation to the pontine respiratory groups?

Which group of neurons is suggested to be associated with the normal 'inspiratory cutoff switch'?

What is suggested to be the cause of apneusis according to the text?

'Apneusis' is a result of what according to the text?

Which receptors are activated in the Hering-Breuer inflation reflex?

What is the afferent pathway in the Hering-Breuer inflation reflex?

What is the efferent limb of the Hering-Breuer inflation reflex responsible for?

What is the threshold tidal volume range required to elicit the Hering-Breuer inflation reflex in unanesthetized humans?

What effect does abrupt deflation of the lungs have on ventilatory rate?

Which receptors might play a role in periodic spontaneous deep breaths that help prevent atelectasis?

'Sighs' consisting of slow deep inspirations followed by slow deep expirations are important for maintaining what in infants?

Where are the receptors for the paradoxical reflex of the head located?

What effect does lung inflation have on inspiratory effort according to the Hering-Breuer inflation reflex?

What is the effect of low PaO2 and high PaCO2 on arterial chemoreceptors?

What reflex is triggered by mechanical or chemical irritation of the airways?

Where are the receptors responsible for the J receptors reflex believed to be located?

Which nerve is responsible for transmitting information from the carotid body, one of the arterial chemoreceptors?

What physiological response may be caused by stimulation of J receptors?

What causes apnea or rapid shallow breathing in response to pulmonary embolism?

What is the primary stimulus to ventilation that is very powerful and surpasses minute ventilations obtained with hypercapnia?

What is the most important input to the ventilatory control system in establishing breath-to-breath levels of tidal volume and ventilatory frequency?

What happens to arterial PCO2 during severe exercise according to the text?

Which stimuli is postulated to produce dyspnea in patients with congestive heart failure?

What is the effect of stimulation of the arterial baroreceptors by elevated blood pressure?

What type of pain generally causes hyperpnea according to the text?

Which stimuli leads to bronchoconstriction based on the information provided?

How can spontaneous rhythmicity generated in the medullary respiratory center be temporarily overwhelmed?

What is the effect of stimulating the arterial chemoreceptors according to the text?

How does metabolic acidosis affect ventilation?

What is the primary mechanism responsible for the depressed ventilatory response to hypercapnia in chronic obstructive lung diseases?

How does the respiratory control system respond to increased metabolic production of carbon dioxide?

In the context of the text, what is exemplified by the negative feedback system of the respiratory control system?

Why does anemia (without acidosis) not stimulate ventilation according to the text?

What is the primary reason for ventilation increasing above oxygen consumption at high work levels during exercise?

What characterizes the ventilatory response to constant work-rate exercise?

What contributes to the immediate increase in ventilation at the beginning of exercise?

What is a possible explanation for the unexplained aspects of the ventilatory response to exercise according to the text?

How does hypoxia alone influence arterial PCO2 according to the text?

What is the 'set point' for the respiratory control system as mentioned in the text?

Where are the central chemoreceptors located, according to the text?

What is the main response of peripheral chemoreceptors to elevated PCO2, decreased PO2, or decreased pH?

What may stimulate the arterial chemoreceptors apart from elevated PCO2?

What is suggested to be the reason behind certain drugs like cyanide stimulating the carotid body?

How do peripheral and central chemoreceptors differ in terms of exposure to substances?

How does the blood-brain barrier affect the transmission of arterial PCO2 to cerebrospinal fluid?

Why does the cerebrospinal fluid have a lower buffer line compared to blood?

What is the main function of central chemoreceptors?

How do alterations in arterial pH affect the cerebrospinal fluid?

Why are the peripheral chemoreceptors considered less important in the short-term response to elevated carbon dioxide?

What is the primary buffer in the cerebrospinal fluid?

What receptors do NOT play a significant role in the initial immediate ventilatory response to exercise?

What is a probable reason for the slower increase in ventilation during constant work-rate exercise in patients who had their carotid bodies surgically removed?

What type of receptors may respond to increased carbon dioxide load in mixed venous blood during exercise?

Which receptors are believed to send information about increased muscle metabolism to the respiratory controllers?

What may stimulate the arterial chemoreceptors during exercise levels above the anaerobic threshold?

What receptors are not believed to be significant in the ventilatory response to exercise during mild or moderate levels?

Which receptors could potentially respond to the metabolites released during exercise, leading to stimulation of pain receptors?

Which group of receptors has NOT been conclusively demonstrated according to the text?

What may stimulate the arterial chemoreceptors during exercise levels above the anaerobic threshold?

What receptors are believed to send information about increased muscle metabolism to the respiratory controllers? What may stimulate the arterial chemoreceptors during exercise levels above the anaerobic threshold?

What is the role of the central chemoreceptors in monitoring the balance of arterial PCO2, cerebral blood flow, and cerebral metabolism?

What is the primary stimulus to ventilation that is influenced by alterations in hydrogen ion concentration?

Which condition results in an initial hyperpnea that mainly arises from the peripheral chemoreceptors?

What effect does acidotic stimulation of the peripheral chemoreceptors have on alveolar ventilation?

Where does the ventilatory response to hypoxia primarily arise from?

Which factor potentiates the response to hypoxia at higher arterial PCO2 levels?

What happens to ventilation with increasing degrees of hypoxia when the peripheral chemoreceptors are intact?

How does a progressive increase in hypoxia affect the central respiratory controller in the absence of peripheral chemoreceptor response?