L21. Causes and Consequences of Respiratory Centre Depression and Hypoventilation Flashcards Preview

03. Respiratory > L21. Causes and Consequences of Respiratory Centre Depression and Hypoventilation > Flashcards

Flashcards in L21. Causes and Consequences of Respiratory Centre Depression and Hypoventilation Deck (25):

What is the oxygen delivery and carbon dioxide clearance of the respiratory system at rest?

200 mL/min O2
250 mL/min CO2
and the body uses only aerobic metabolism at this rate


What is the oxygen delivery and carbon dioxide clearance of the respiratory system during exercise?

>4L/min O2
>4L/min CO2
and the body uses both aerobic and anaerobic metabolism


What are two major consequences of failure of the respiratory system?

Hypercapnoea (and respiratory acidosis)


What are the three major components of the respiratory system?

1. Controller (brainstem)
2. Pump (Respiratory muscle and airways)
3. The Gas exchangers (AC membrane)


What are the sensors of the respiratory system and what do they measure?

Chemoreceptors in the medulla and they respond to changes to PaCO2 (via CSF H measurements)

Peripheral receptors in the aorta and carotid and they respond to changes in PaO2, PaCO2 and pH


What is the ventilatory response to hypercapnoea (draw the graph)

It is a linear relationship that shows the higher the CO2 the higher the minute ventilation


What is the ventilatory response to hypoxia (draw the graph)

As PaO2 decreases, there is little to no change in minute ventilation until the PaO2 reaches about 50mmHg (which corresponds to about 90% saturation). At this point the minute ventilation rises with increasing hypoxia


What is minute ventilation?

The amount of air going in and out of the lungs in one minute


What is the minute ventilation dependent on? What is it analogous to in the cardiovascular system?

It is analogous to cardiac output
VE = RR x TV


Ventilation increases with work. Why is this?

Increasing work, increases the use (demand) of O2 and for CO2 clearance. Ventilation increases to match these demands and thus keep the arterial levels at baseline


What is the anerobic threshold? What happens to minute ventilation when this point is reached?

Anaerobic threshold is when the body begins to use anaerobic mechanisms (pyruvate--> lactic acid) as a source of energy. Thus generating more acid.

The ventilation increases more steeply (graph) with increasing work past this point. And the ventilation begins to fail in keeping the CO2 and pH at baseline (as CO2 decreases slightly to compensate for higher lactic acid - decrease in pH also seen)


What are the causes of hypoventilation? [6]

1. Reduced activity in the respiratory centre (reduced drive, drugs, trauma, stroke)
2. Neuromuscular diseases (nerve paralysis, muscle weakness)
3. Chest wall deformities
4. Obesity (gross)
5. Sleep disordered breathing
6. Secondary to respiratory failure


What are the three types of sleep disordered breathing?

1. Obstructive sleep apnoea
2. Central sleep apnoea
3. Obesity hypoventilation syndrome


Describe obstructive sleep apnoea

A transient obstruction of the throat during sleep which prevents breathing (oxygenation and clearance of CO2) and disturbs sleep


Why does airway obstruction occur in sleep apnoea?

Airway muscle relaxation (especially during REM sleep)
Narrowing of the throat (obesity, tonsils, etc)
Tongue falls backwards (especially in supine position)


What are the main stages of OSA? [5]

1. Snoring in light sleep
2. REM sleep: complete obstruction (apnoea) occurs
3. Reduced O2 and increased CO2 and other stimuli cause the brain to 'wake' into a lighter sleep: arousal
4. Muscles contract (tense) and airways open and breathing recommences
5. Person falls back into a deep sleep and apnoea occurs again


Is there any other dysfunction of the respiratory system in OSA (apart from the apnoea causing obstruction)?

No. The respiratory mechanisms and control centre are still fully functional (the person is trying to breath). So during the apnoea, the respiratory centre becomes progressively more active until arousal.


Why is there a delay between the onset of apnoea and arousal?

Because during deep sleep, the brain is relatively non-receptive to messages coming from the periphery. Thus it takes about 30-60 seconds in order to wake the brain.


When should you suspect OSA?

Witnessed apnoeas
Symptoms of disturbed sleep
Difficult to treat hypertension, unexplained respiratory failure


What are the main measurements taken in a polysomnogram?

1. Breathing (expiration detected as hot air)
2. Saturation (oximetry)
3. Chest wall and abdominal wall expansion (tests whether it is obstructive vs. central sleep apnoea)


What is the best way to describe the oximetry of people with sleep apnoea during REM sleep?

Cyclical desaturation


What is the management of OSA?

Continuous Positive Airways Pressure: CPAP delivered through a mask (4-20cm H20 pressure) which is solely to provide a pressure stent to the airways and keep them open.
Others include mandibular advancement splint (brings jaw and tongue forward), sometimes surgery and mainly lying on the side.


What is obesity hypertension apnoea?

Extra weight on the diaphragm from the abdomen increasing work on the muscle for respiration. And extra weight on the chest meaning extra work of respiration.


What is a major consequence of chronic sleep apnoea?

The respiratory centre will sometimes accept some degree of hypoxia and hypercapnoea in order to achieve some level of sleep by setting up a new set point to allow for sleep and can eventually ignore signals for hypoxia and hypercapnoea.


Why is it detrimental to give people with chronic hypercapnoea supplemental oxygen?

These people rely on the HYPOXIC DRIVE to keep them alive.
They're body has adapted to maximise its respiration in response to decreased levels of oxygen. By providing them with supplemental oxygen removes the stimulus on the respiratory sensors and their compensatory mechanisms fail and they can enter respiratory failure very quickly.