Bod: Respiratory: Respiratory Failure

Front 1

What happens to central control of ventilation when PaCO2 increases?

Back 1

This is sensed by the chemoreceptors --> ventilation is signalled to increase (first by increases in tidal volume, then by increases in frequency)

Front 2

Disturbances in PaCO2 are sensed by what?

What else might this center sense?

Back 2

By the chemoreceptors in the medulla.

The medulla also senses the H ion concentration of the CSF

Front 3

Above what level of PaCO2 does the response to hypercapnia diminish or plateau?

Back 3

Levels above 80-100.

Front 4

Where does sensing of PaO2 occur? (2)

What are these sensors innervated by?

Which is primary for sensing changes in O2?

Back 4

1. Carotid bodies (at the bifurcation of the internal and external carotid arteries, inn by CN IX). (PRIMARY FOR SENSING CHANGES IN O2).

2. Aortic body (at the arch of the thoracic aorta, inn by CN X)

Front 5

When do the carotid bodies stimulate ventilation?

Back 5

When the PaO2 is below 70 mm Hg. With further declines there is an exponential increase in the amount firing rates to increase ventilation.

Front 6

What controls the body's main response to acidosis?

Back 6

Elevated PaCO2 levels sensed by the medulla.

Front 7

What are the three types of pulmonary mechanoreceptors?

Back 7

1. Stretch receptors in the smooth muscle of the airways (inhibit inspiration as the lung is inflated)

2. Irritant receptors in the airway epithelium (respond to noxious agents to produce cough and airway constriction).

3. J (juxtacapillary) receptors in the lung interstitium (stimulated by interstitial edema and chemical agents --> causes laryngeal closure and apnea, followed by rapid, shallow breathing)

Front 8

Resting minute ventilation is primarily determined by what?

Back 8

By PaCO2.

But hypoxia AND hypercapnia will give an even greater increase in minute ventilation.

Front 9

What will the central chemoreceptors do in response to a decreased level of PaCO2?

Back 9

They will send signals to HYPOventilate to bring the PaCO2 back up.

Don't usually see this drive causing apnea in patients that are awake. However, it can affect patients when they are asleep.

Front 10

What can cause decreased minute ventilation?

Back 10

- Normal aging
- Decreased sensitivity of the central chemoreceptors
- Athletic training
- Drug intoxications/overdoses

Front 11

What does the clinician have to think about when he or she has a patient with high or low PaCO2 problems?

Back 11

Has to think about whether it is a "effectiveness of ventilation" problem or a "drive to breathe" problem.

Front 12

How does metabolic acidosis affect ventilation?

Back 12

Metabolic acidosis --> increase in H ion concentration --> hyperventilation --> low PaCO2

Front 13

How does metabolic alkalosis affect ventilation?

Back 13

Metabolic alkalosis --> hypoventilation --> higher PaCO2

(this is relatively weak and highly variable)

Front 14

What role does hypoxemia play in determining ventilation in the normal patient?

Back 14

Very little. Only plays a role at PaO2s below 60-70 mm Hg.

Front 15

Sleep can be thought of as what two components?

Back 15

1) REM sleep
2) Non-REM sleep

Front 16

What are normal changes in ventilation during sleep?

Back 16

- Hypoventilation
- Elevated PaCO2
- Reduced PaO2

Front 17

Deprivation of REM sleep has shown to lead to what?

Back 17

- Piokilothermia (inability to regulate body temperature)
- Psychosis
- Death

Front 18

Sleep: responses to hypoxia and hypercapnia.

Back 18

The body's response to hypoxia and hypercapnia is blunted during REM sleep.

(Note that COPDers may experience a 10-35% decline in their O2 sat during sleep --> coronary ischemia, stroke)

Front 19

What is the definition of adult apnea?

Back 19

Absence of airflow and tidal volume for ≥ 10 seconds.

Front 20

What is the definition of hypopnea?

Back 20

A decline in tidal volume of 25-50% that lasts ≥ 10 seconds.

Front 21

Classification of apneas/hypopneas during sleep.

Back 21

1. Central (absences of airflow AND respiratory effort)

2. Obstructive (persistent respiratory effort during an apneic episode).

3. Mixed

Front 22

Young adults may have up to how many apneic/hypopneic episodes per night normally?

Back 22

Up to 5 episodes. Not associated with O2 desaturation.

Front 23

Obstructive sleep apnea (OSA): prevalence, demographics

Back 23

2-4% prevalence, male predominance, overweight.

Front 24

"Gold standard" test for OSA?

Back 24

Polysomnogram

Front 25

OSA: symptoms

Back 25

- Loud snoring
- Restless sleep
- Daytime somnolence
- May see PHTN in 20-60% of pts.
- Dysrrhythmias

Front 26

OSA: causes?

Back 26

- Obesity
- Hypothyroidism

Front 27

OSA: treatment

Back 27

- Weight reduction
- CPAP (produces a pneumatic "splinting" to maintain upper airway patency)

Front 28

General definition of respiratory failure?

Back 28

Disputed, but in general: if PaO2 is lower than 60 mm Hg or if PaCO2 is greater than 50 mmHg.

Front 29

What are the two types of respiratory failure?

Back 29

1. Hypoxic (usually due to a defect in the lungs themselves, e.g. ARDS)
2. Hypoxic AND hypercapnic (usually due to a failure of alveolar ventilation via a decrease in minute ventilation or from an increase in dead space, e.g. COPD exacerbation, CNS failure)

Front 30

What is a home-remedy for sleep apnea?

Back 30

Sleep apnea occurs at a higher rate when people sleep on their backs. So tape a tennis ball to the small of your back. It's uncomfortable, so you won't be able to sleep on your back.

Front 31

Failure of the lung results in what?

Failure of the "pump mechanism" of the lung results in what?

Back 31

Hypoxemia

Hypercapnia (and hypoxemia)

Front 32

What is the equation for alveolar ventilation?

Back 32

Alveolar ventilation = total minute ventilation - total dead space ventilation.

Front 33

What is the equation for minute ventilation?

Back 33

Tidal volume * respiratory rate

Front 34

What is a common feature of respiratory failure?

Back 34

Reduction in tidal volume (with subsequent increases in dead-space volume)

Front 35

What are the three ways to decrease tidal volume?

Back 35

1. Central controller modification (drug overdose)

2. Mechanical defects (flail chest, extreme hyperinflation)

3. Fatigue of respiratory muscles.

Mechanical defects and fatigue both increase the work of breathing, energy demand, and consumption.

Front 36

What are some things that can cause an increase in the production of CO2?

Back 36

1. Hyperthermia (each degree rise in temperature = 14% increase in CO2 production)

2. Shivering or increase in muscle tone --> CO2 production up as much as threefold.

3. High levels of ventilation --> excessive muscular activity --> increased CO2 production

4. Insufficient force to ventilate alveoli (CNS depression, neuromuscular weakness)

5. Shock or underlying disease, production of lactic acid.

Front 37

Acute respiratory failure due to CNS depression: causes

Back 37

- Drugs
- Brainstem stroke
- Encephalitis

Front 38

Chronic respiratory failure from CNS disease: causes

Back 38

- Chronic opiate use
- Sleep apnea syndromes
- Severe hypothyroidism (myxedema)

Front 39

What is the hallmark of failure of alveolar gas exchange?

What is seen in the early phases of these disorders?

What happens once ventilatory demand outpaces ventilatory supply?

Back 39

Hypoxemia

Respiratory alkalosis (as long as ventilatory supply can surpass ventilatory demand)

As demand exceeds supply --> respiratory muscle fatigue --> respiratory acidosis --> respiratory failure --> death.

Front 40

When supplemental O2 is required, how much do you give?

Back 40

The lowest possible FiO2 (generally less than 0.5) required to maintain a PaO2 of above 60 mm Hg (to avoid O2 toxicity)

Front 41

(extra credit)

What is the Haldane effect?

Back 41

If you give too much O2 all at once, then deoxy-Hgb will bind O2 immediately and will release tons of CO2 into the bloodstream that cannot be offloaded easily.

This can cause a "narcosis" effect that can cause a further decrease in respiratory drive.

Front 42

True or false: the point of mechanical ventilation is not to normalize blood gases.

Back 42

True!

"Respiratory acidosis is your best friend in the ICU." - Dr. Wilson

Front 43

Do you give a COPDer valium?

Back 43

Probably not. Dr. Wilson will be on you if you end up decreasing the respiratory drive of someone that could easily become hypercapnic --> respiratory failure --> death

Front 44

Do you give someone with hypercapnic respiratory failure O2?

Back 44

There is a chance that this could depress their respiratory drive.

Start on 50% O2. If you give them more of this, then you could kill them via the Haldane effect