Lecture 17 Flashcards
- What is the difference between eupnea and dyspnea?
- Eupnea – Normal, unlabored breathing at rest.
- Dyspnea – Labored breathing or shortness of breath, often due to increased ventilatory efforts.
- What triggers Biot’s breathing, and in which conditions is it observed?
Biot’s breathing is triggered by damage to the medulla and is observed in conditions such as brainstem injuries and opioid overdose.
* Biot’s Breathing – Equal-volume breaths separated by apnea.
- How does Kussmaul breathing differ from Cheyne-Stokes respiration?
- Kussmaul Breathing – Deep, rapid breathing associated with metabolic acidosis (e.g., diabetic ketoacidosis).
- Cheyne-Stokes Respiration – Cyclic pattern of increasing and decreasing tidal volume, often seen in heart failure or brain injuries.
Kussmaul (seen in metabolic acidosis).
- Which factors influence the rhythm of ventilation?
Metabolic changes, exercise, eating, mechanical conditions, and disease states.
- How does exercise impact respiratory control?
Ventilation increases in proportion to oxygen consumption and CO2 production, and anticipatory mechanisms help regulate breathing before metabolic demand rises.
- What role does the phrenic nerve play in inspiration?
It stimulates the diaphragm to contract, initiating inspiration.
- Explain the concept of the inspiratory ramp and its effect on tidal volume.
The inspiratory ramp gradually increases action potential frequency over 0.5–2 seconds, ensuring a smooth increase in tidal volume.
- What happens during the expiration phase in normal breathing?
The inspiratory ramp stops, the phrenic nerve relaxes, and the diaphragm passively returns to its resting state.
- What are the roles of the cortex and hypothalamus in respiratory regulation?
The cortex allows voluntary control, while the hypothalamus modulates breathing in response to emotions and temperature changes.
- How do the pneumotaxic and apneustic centers interact?
The pneumotaxic center inhibits the apneustic center to limit inspiration, while the apneustic center promotes prolonged inspiration.
- What functions do the Dorsal and Ventral Respiratory Groups (DRG & VRG) serve?
DRG controls normal inspiration and processes sensory input, while VRG controls forced respiration and expiratory muscles.
- Where are central chemoreceptors located, and what do they detect?
Located in the ventral medulla, they detect pH changes in cerebrospinal fluid caused by CO2 levels.
- How do peripheral chemoreceptors respond to changes in oxygen, CO2, and pH?
Carotid and aortic bodies detect low O2, high CO2, and low pH, increasing ventilation as a response.
- How does the body respond to respiratory acidosis?
It increases ventilation to remove excess CO2 and restore pH balance.
- What breathing pattern is associated with metabolic acidosis?
Kussmaul breathing, characterized by deep, rapid respiration to compensate for low pH.
- Why do COPD patients rely more on hypoxic drive for ventilation?
Chronic CO2 retention causes central chemoreceptor adaptation, making peripheral O2 receptors the primary drivers of ventilation.
- What is the Hering-Breuer reflex, and what function does it serve?
It prevents lung overinflation by inhibiting large tidal volumes via pulmonary stretch receptors.
- How do pulmonary irritant receptors contribute to airway protection?
They detect harmful substances (e.g., smoke, dust) and trigger bronchoconstriction and coughing.
- What is the function of juxtacapillary (J) receptors, and what triggers them?
Located in lung interstitium, they respond to pulmonary congestion (e.g., edema) by inducing rapid, shallow breathing and bronchoconstriction.
- Why do blood gases remain relatively stable during exercise?
Anticipatory and neurological control mechanisms regulate ventilation to match metabolic demand.
- What causes the initial increase in ventilation before metabolic demand rises?
Neural input from the motor cortex and joint/muscle receptors activate respiratory centers preemptively.
- How does ventilation change after exercise ceases, and why?
Ventilation initially decreases, but residual metabolism causes a temporary spike in CO2, increasing ventilation again before returning to baseline
