Flashcards in Respiratory Control & Pathophysiology Deck (25)
Where are the primary respiratory centers (dorsal and ventral respiratory groups) located? Where are the secondary respiratory centers (apneustic and pneumotaxic centers) located?
The primary respiratory centers (dorsal and ventral respiratory groups) are located in the medulla of the brainstem. Secondary respiratory centers (apneustic and pneumotaxic centers) are located in the pons of the brainstem.
Identify the anatomic site where opioids produce respiratory depression.
All opioids cause dose-dependent depression of respiration through direct mu2-receptor stimulation at the brainstem respiratory centers located superficially in the floor of the 4th ventricle (i.e., medulla and pons).
What is the single most important factor responsible for directly stimulating central chemoreceptors?
Hydrogen ions (H+) in the cerebrospinal fluid directly stimulate central chemoreceptors.
How are hydrogen ions (H+) generated in CSF?
CO2 that diffuses into the CSF is converted by carbonic anhydrase first to carbonic acid (H2CO3) and then to H+ and bicarbonate ions (HCO3-).
To what 3 physiologic parameters do peripheral (carotid and aortic) chemoreceptors respond? Which stimulates the peripheral chemoreceptors most?
Peripheral chemoreceptors (carotid body and aortic body) respond to PaO2, PaCO2, and pH. Peripheral chemoreceptors are most sensitive to PaO2, but not until Pa02 < 50 mmHg.
In addition to PaO2, PaCO2, and pH what 3 exogenous (i.e., drugs, toxins) substances also stimulate peripheral chemoreceptors?
Peripheral chemoreceptors are also stimulated by cyanide, doxapram, and nicotine.
How much of the ventilatory response to an increase in PaCO2 is mediated by the central chemoreceptors? Peripheral chemoreceptors?
The ventilatory response to an increased PaCO2 is mediated primarily by central chemoreceptors. The effect of CO2 on central chemoreceptors is seven times more powerful than it is on peripheral chemoreceptors. Point: central chemoreceptors are normally more important than peripheral chemoreceptors in controlling ventilation.
What normally drives ventilation?
C02 normally drives ventilation. CO2 is the physiological respiratory stimulant. The single most important regulator of alveolar ventilation is PaCO2.
What are pathological respiratory stimulants?
Pathological stimulants are low PaO2 or acids (hydrogen ions).
Which of the following two changes will increase ventilation the most: an increase in PaCO2 or a decrease in arterial blood pH (increase in H+)?
An increase in PaCO2 produces a far greater increase in
ventilation than does a decrease in arterial blood pH. An increase in PaCO2 from 40 to 60 or from 40 to 90 mm Hg
produces a six-fold or 10-fold increase in ventilation, respectively. In contrast, a decrease in blood pH from 7.4 to
7.0 produces a four-fold increase in ventilation.
What are four causes of hypocapnia? What is the most
common cause of hypocapnia?
Four causes of hypocapnia are:
(1) voluntary hyperventilation
(2) iatrogenic hyperventilation (mechanical ventilation)
(3) decreased C02 production (hypothermia, deep anesthesia, hypotension)
(4) decreased dead space ventilation (change from mask airway to endotracheal tube airway, decreased PEEP, decreased rebreathing)
**By far the most common cause of hypocapnia is hyperventilation by mechanical means.
What happens if a gas mixture with 3-7% CO2 were inhaled?
The partial pressure of the inspired CO2 is 23-53 mmHg if one breathes 3-7% C02 (0.3% x 760 = 0.03 x 760 = 22.80 = 23 mmHg; 7% x 760 = 0.07 x 760 = 53.20 = 53 mmHg). Thus, hypercapnia (increased PaCO2) will occur. Ventilation will increase dramatically in an attempt to compensate.
What triggers the Hering-Breuer reflex? What happens when the Hering-Breuer reflex is triggered? What role does the Hering-Breuer reflex play in normal ventilation of the adult?
Lung inflation triggers the Hering-Breuer reflex. When the Hering-Breuer reflex is triggered by lung inflation, inspiration is inhibited. The Hering-Breuer reflex plays a minor role in normal ventilation in the adult. It is mainly a protective mechanism that is probably not activated until the tidal volume increases to greater than 1.5 liters.
Pulmonary stretch receptors within the smooth muscle of small airways involved in the Hering-Breuer reflex trigger sensory (afferent) impulses that travel along which nerve?
The vagus nerve carries sensory (afferent) impulses of the Hering-Breuer reflex.
**What are pulmonary J-receptors?
Juxtapulmonary-capillary receptors (J receptors) are located in the walls of the pulmonary capillaries or in the interstitium, hence the name. J receptors appear to be stimulated by pulmonary vascular congestion or an increase in pulmonary vascular congestion or an increase in pulmonary interstitial fluid volume, leading to tachypnea. The J receptors may also be responsible for the dyspnea encountered during pulmonary vascular congestion and edema secondary to left ventricular failure.
**Which nerve fiber type innervates pulmonary J-receptors?
C-fibers lie in close relationship to the pulmonary microcirculation and appear to innervate the pulmonary J receptors. The afferent pathway from the J receptors is the slow conducting non-myelinated (C) fibers in the vagal nerves.
What are four causes of hypercapnia?
1: hypoventilation (depression of ventilation by drugs such as opioids)
2: increased dead space ventilation
3: inadvertently switching off CO2 absorber
4: increased CO2 production
What nerve innervates the diaphragm? What would happen to respiratory pattern if either the right or left branch was damaged?
-diaphragm normally descends with inspiration--> but if damage to right or left phrenic occurs, then the ipsilateral half-diaphragm innervated by the damaged phrenic nerve would ascend paradoxically during inspiration.
What is a type of cell that can cause bronchoconstriction? Why?
-human cutaneous mast cells can degranulate and release histamine--> histamine can trigger bronchoconstriction
What happens to PaO2 and PaCO2 during one lung ventilation? What happens to PaO2 once a diseased lung is removed?
-PaO2 generally decreases b\c of presence of an intrapulmonary shunt during one lung ventilation (if FiO2 1.0, PaO2 may fall from 400 to 150mmHg)
PaCO2 can be prevented from increasing by increasing ventilation, UNLESS there is a severe shunt
-PaO2 increases after the excision of the diseased lung b\c the shunt decreases (blood flow has no where to go except the remaining lung)
**What is the primary mechanism of hypoxemia in the patient with COPD?
For any obstructive pulmonary disease, the hypoxemia is d\t regional mismatch of ventilation and perfusion--> V/Q mismatch
Does a patient with severe COPD leading to respiratory acidosis rely more on central or peripheral chemoreceptors for oxygen drive for breathing?
**Normal people rely on central chemoreceptors, but chronic respiratory acidosis (increased H+) causes COPD patients to rely on peripheral chemoreceptor oxygen drive
**The chronic bronchitis patient (COPD, "bluebloater") requires oxygen therapy. What is your concern and what PaO2 should not be exceeded?
-PaO2 > 60mmHg can cause respiratory failure in these patients
-oxygen therapy can elevate PaCO2 to dangerous levels in patients with CO2 retention
**patients with chronic elevation of PaCO2 have increased bicarbonate levels in the CSF--> the elevated CSF bicarb ions reset the central medullary chemoreceptors and decrease the central respiratory drive sensitivity to CO2
**If PaO2 >60, peripheral chemoreceptor respiratory drive diminishes and the patient will hypoventilate
UNDERSTAND THESE CONCEPTS
Name 2 factors that would indicate that your patient with COPD has increased risk of postop complications.
1: FEV-1 <50%
2: CO2 retention