Lecture 5: Resp control Flashcards
What efferent nerves are required for inspiratory muscles?
Diaphragm(s): phrenic nerves, C3-C5
External intercostal muscles: thoracic nerves T1-T11
Accessory muscles: sternocleidomastoid (XI cranial nerve) and scalene muscles (C3-C8)
What efferent nerves are required for expiratory muscles?
Abdominal wall: T5-T12
External intercostal muscles: T1-T12
What is the role of the pons?
Not essential for respiration but exerts fine control over medullary neurons
What are the dorsal respiratory group of neurons required for?
Trigger inspiratory impulses
What are the ventral respiratory group of neurons required for?
Trigger inspiratory and expiratory impulses (during exercise or other times of active exhalation)
What is the role of the rhythm generator in the medulla?
Controls the basic, automatic pattern of breathing - the pacemaker for breathing is not a single cell but a group of neurons concentrate in the Pre-Botzinger complex
Where are the group of neutrons that act as the pacemaker for breathing?
In the Pre-Botzinger complex
What afferent inputs may impact breathing rate?
- Emotional inputs from the cerebral cortex
- Lung mechanoreceptors
- Chemoreceptors (central and peripheral)
What is the role of lung stretch receptors(vagal nerve afferent fibres)?
Sense lung stretch during breathing to terminate breath to prevent over-stretching
Sense abnormal changes in airway mechanical properties
What is the role of irritant and particulate receptors (vagal nerve afferent fibres)?
C-fibre neurons: activated by oedema and molecules such as bradykinin
Irritant receptors (sometimes called ‘cough receptors’): respond to punctate mechanical stimuli
What is detected by the central chemosensors?
[H+] in the CSF
[H+] in the CSF reflects blood [H+], PaCO2 and CSF CO2 but these are NOT directly sensed by central chemoreceptors
What area of the brain responds to input from central chemoreceptors?
Hindbrain
Where are the peripheral chemosensors?
Carotid body: bundle of cells outside the bifurcation of carotid arteries
Aortic body: bundle of cells within aortic arch
Carotid and aortic bodies are back up for each other, but normally the carotid bodies do bulk of peripheral sensing
Both respond to PO2 (hypoxaemia) and CO2. Carotid bodies also detect pH.
What is detected by carotid body?
PO2, CO2 and pH
What is detected by the aortic body?
PO2 and CO2
What is the relationship between sensitivity to PO2 and PCO2?
Sensitivity to PO2 is altered by PCO2: more sensitive to hypoxaemia in setting of hypercarbia
Give an example of a volatile acid?
CO2
What is respiratory acidosis?
The build up (retention) of CO2
What are fixed acids?
Non-volatile acids have to be physically eliminated from the body, typically via the kidneys
They are products from the oxidation of dietary substrates. Baseline production is well managed by the kidneys and liver, where lactate is converted to glucose in the liver
Increased production of acids, especially lactic acid, can outstrip normal clearance
How do the kidneys eliminate fixed acids?
Filtration and elimination of the conjugate base of acids: urate, lactate, and ketones are main types
What are the 6 steps to ABG interpretation?
Step 1: Examine the pH, PCO2 and HCO3 –
Step 2: Determine the primary process. Does the patient have an acidaemia or alkalaemia based on the pH? If so, what type is it?
Step 3: If a metabolic acidosis is present, calculate the anion gap
Step 4: Identify the compensatory process
Step 5: Determine if a mixed acid-base disorder is present
Step 6: Determine the cause
What pH is suggestive of acidaemia?
A low blood pH (< 7.38)
What pH is suggestive of alkalaemia?
A high blood pH (> 7.42)
How do you determine respiratory acidosis?
High PCO2 (> 44 mmHg / 5.9 kPa)
How do you determine metabolic acidosis?
Low HCO3- (< 22 mmHg / 2.9 kPa)
How do you determine respiratory alkalosis?
Low PCO2 (< 36 mmHg / 4.8 kPa) Metabolic alkalosis: high HCO3- (> 26 mmHg / 3.5 kPa)
How do you determine metabolic alkalosis?
High HCO3- (> 26 mmHg / 3.5 kPa)
What is metabolic acidosis?
Loss of bicarbonate or the addition of acid
What are the main causes of metabolic acidosis (loss of bicarb)?
Renal tubular acidosis (RTA)
- all types result in urinary loss of bicarbonate and a hyperchloremic acidosis
GI losses
Acetazolamide (carbonic anhydrase inhibitor)
Excessive chloride administration (intravenous fluids with NaCl)
What is the anion gap?
There are more uncounted anions than uncounted cations. The uncounted anions minus the uncounted cations is called the ANION GAP.
What are the causes of anion gap metabolic acidosis?
Glycols (ethylene and propylene), Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, and Ketoacidosis.
GOLD MARK.
What is anion gap metabolic acidosis?
If it is acidosis as a result of addition of acid (rather than loss of bicarb)
What does an anion gap of >12 mean?
There is a hidden/extra anion present
The conjugate base of fixed acids are the source of this extra anion.
What is the compensatory response to resp acidosis?
Retain HCO3
What is the compensatory response to resp alkalosis?
Reduce HCO3
What is the compensatory response to metabolic acidosis?
Reduce CO2
What is the compensatory response to metabolic alkalosis?
Retain CO2
What type of compensation is faster?
Respiratory compensation occurs quickly - the lungs are FAST (seconds)
Metabolic compensation can take days - the kidneys are SLOW (days)
What is a mixed disorder?
Two or more primary acid-base disturbances
What are the clues that a mixed disorder exists?
The anion gap should be similar in value to the reduction in bicarbonate; this calculation is called the “gap of the gap”
An anion gap is present but the pH is alkalaemic
Incomplete compensation for any primary process. Note, “complete compensation” does not result in a normal pH, but it gets close
What is a base excess?
The dose of acid that would be needed to return bloodto normal pH (7.40) under standard conditions (37C and a PCO2 of 40 mm Hg)
What is base deficit?
The dose of alkali to returnblood to normal pH
In reality, the term “base excess” is used: a metabolic acidosis is described as a “negative” base excess rather than a base deficit
What are the causes of metabolic alkalosis?
Increased aldosterone (some medications, ‘contraction alkalosis’)
Vomiting
What are the causes of respiratory acidosis?
Increased dead space (emphysema)
Weakness
Depression of respiratory centre
What are the causes of respiratory alkalosis?
Hyperventilation due to pain or anxiety
Pregnancy
Hypoxaemia
What are the causes of metabolic acidosis (anion gap and non-anion gap)?
Anion gap: GOLD MARK
Non-anion gap: RTA, GI loss
What are the results from the respiratory centre becoming less sensitive to chronic PaCO2 elevations
Respiratory responses become blunted
- Chronic respiratory acidosis with metabolic compensation
- Hypoxaemia due to hypoventilation.
What causes respiratory depression?
Opiates/narcotics (heroin, legal prescription narcotics)
Alcohol
Anaesthesia and other sedatives
Cerebral diseases: ex. cerebral vascular accident
What is caused by respiratory depression?
Hypercarbia
Hypoxaemic hypoxia
Acute respiratory acidosis
Where can you get a DVT?
Legs > pelvis > arms
What is an embolism?
Any intravascular material that migrates from its original location to occlude a distal vessel
What is a PE?
Pulmonary embolism, and the result of migration of all or part of a peripheral DVT to the lungs
What are the signs and symptoms of a PE?
Hypoxaemia Dyspnea Cough Pleuritic chest pain Pleural rub Haemoptysis Syncope Tachycardia
What are the symptoms of a DVT?
Calf pain
Leg swelling
What tests can be used to diagnose DVT or PE?
Blood D-dimer level: to screen for a possible clot (not specific for PE)
Duplex ultrasound: to diagnose DVT
Ventilation perfusion scan (V/Q scan): specific for PE
CT pulmonary angiography (not CXR): specific for PE
