Control of Breathing – Key Vocabulary

A set of vocabulary flashcards covering the anatomical structures, neural pathways, reflexes, and physiological terms involved in the control and regulation of breathing, as discussed in the lecture.

Respiratory Center

Clusters of autonomic nuclei in the brainstem (medulla oblongata and pons) that generate and regulate the rhythm and depth of breathing.

Medullary Respiratory Center

Portion of the respiratory center located in the medulla; contains the dorsal and ventral respiratory groups and the Pre-Bötzinger complex.

Dorsal Respiratory Group (DRG)

Medullary region that controls quiet (eupneic) breathing by sending 2-sec bursts to inspiratory muscles followed by 3-sec silence.

Ventral Respiratory Group (VRG)

Medullary region with neurons active mainly during forced breathing; contains the Pre-Bötzinger complex and separate neurons for forced inhalation and exhalation.

Pre-Bötzinger Complex

Cluster of VRG neurons thought to act as the rhythm generator for respiratory cycles, analogous to the heart’s SA node.

Pontine Respiratory Group (PRG)

Pons area that modulates DRG and VRG activity, smoothing the transition between inhalation and exhalation.

Eupnea

Normal, quiet breathing in which inspiration is active and expiration is passive.

Apneustic Breathing

Pathological pattern of prolonged gasping inspirations with occasional expirations, usually caused by damage to the PRG.

Quiet Breathing

Resting ventilation controlled by DRG impulses to diaphragm and external intercostals without accessory muscle involvement.

Forced Breathing

Ventilation during exercise or exertion involving accessory muscles and VRG neurons for both inhalation and exhalation.

Accessory Muscles of Inhalation

Sternocleidomastoids, scalenes, and pectoralis muscles activated during forced inspiration.

Accessory Muscles of Exhalation

Internal intercostals and abdominal muscles activated during forced expiration.

Chemoreceptors

Sensory receptors that detect changes in CO₂, H⁺, and O₂ levels to adjust respiratory activity.

Central Chemoreceptors

Receptors in the medulla that respond chiefly to pH (H⁺) changes in cerebrospinal fluid caused by CO₂ fluctuations.

Peripheral Chemoreceptors

Carotid and aortic bodies that sense blood levels of CO₂ (primary), O₂, and H⁺ and relay impulses via glossopharyngeal and vagus nerves.

Carotid Bodies

Peripheral chemoreceptors located at the bifurcation of the common carotid artery; send signals through glossopharyngeal nerves.

Aortic Bodies

Peripheral chemoreceptors in the aortic arch; transmit information via the vagus nerve.

Hypercapnia

Elevated arterial CO₂ (>40 mm Hg) that stimulates chemoreceptors and increases ventilation.

Hypocapnia

Reduced arterial CO₂ (<40 mm Hg) leading to decreased respiratory drive until CO₂ normalizes.

Hyperventilation

Increased rate and depth of breathing that lowers arterial CO₂ and raises blood pH.

Apnea

Temporary cessation of breathing; can be voluntary or reflexive (e.g., cold-shock response).

Proprioceptors

Joint and muscle sensors that increase breathing rate at the onset of exercise before chemical changes occur.

Baroreceptors (Pulmonary Stretch Receptors)

Receptors in bronchi/bronchioles that trigger the Hering-Breuer reflex to prevent over-inflation of the lungs.

Hering-Breuer Reflex

Inflation reflex: lung stretch inhibits DRG, ending inspiration and initiating expiration.

Hypoxia

General term for inadequate O₂ supply to tissues.

Hypoxic Hypoxia

Low arterial PO₂ due to high altitude, airway obstruction, or pulmonary edema.

Anemic Hypoxia

Reduced O₂ delivery because hemoglobin quantity/function is insufficient (e.g., hemorrhage, iron deficiency, CO poisoning).

Ischemic Hypoxia

Adequate O₂ content but diminished blood flow to tissues (e.g., stroke, atherosclerosis).

Histotoxic Hypoxia

Tissues cannot utilize delivered O₂ (e.g., cyanide poisoning) despite normal PO₂ and hemoglobin.

Aging and the Respiratory System

With age, lung tissues stiffen, vital capacity drops (~35% by 70 yrs), macrophage and ciliary activity decline, increasing infection risk.