Arterial Blood Gases & Control of Respiration Flashcards
Hypoxaemia
abnormally low concentration of O2 in the blood
Hypercapnoea (hypercarbia)
abnormally high concentration of CO2 in the blood
Nuclei in the brain
cluster of neurons, which co-operate for a shared function
Minute Ventilation (VE) is determined by
the respiratory rate x the tidal volume
VE = (RR)(TV)
Dysponea
shortness of breath, trouble breathing
Sleep apnoea
interruption of breathing during sleep
Pulmonary Emboli
blood clot in the pulmonary arteries
Respiratory center in brain is
the medulla and the pons
Cortex can affect breathing?
Can think about things that cause anxiety eg:
shortness of breath
Chemoreceptors are only in brain.
True or False?
False
Central and Peripheral
control of breathing
Central chemoreceptors are divided into
dorsal respiratory group and ventral respiratory group
Breathing is conducted through —— and ——- —— in the —– and the ——- ——
inspiratory
expiratory
neurones
pons
medulla oblongata
Inputs from the cerberal cortex and hypothalamus occur via —— can change RR (respiratory rate) via ——- ——- ——-, which stimulates or suppresses breathing by affecting the medulla
CN 9 & 10 (vagus nerve)
pontine respiratory center
Dorsal Respiratory Group location and controls?
neurones controlling inspiration
Medulla
Ventral Respiratory Group location and controls?
neurones controlling inspiration and expiration during active breathing
medulla
Pacemaker for lungs
central pattern generator in the Pre-Botzinger Complex of the ventral respiratory group initiates breathing
Pons, pneumotaxic center, apneustic center
- pontine respiratory centers inhibit and excite inspiration, acts as a balance
- pneumotaxic center inhibits inspiration to allow expiration
- apneustic center excites inspiration to enhance breathing in gasps or pants
medulla and pons are located in which part of the brain
hindbrain
the cortex and the hypothalamus can —– into the medulla and the pons to ——
input
alter your breathing
Where is central pattern generator located?
Pre- Botzinger complex of the ventral respiratory group, therefor in the medulla
What is an area in the pons referred to as?
pontine
pons diagram
chemical control of breathing diagram
Central chemoreceptors detect
PCO2 and pH
Central chemoreceptors do not respond to oxygen (hypoxemia).
True or False?
True
Peripheral chemoreceptors detect
PCO2, pH and PO2
Central chemoreceptors lie near which surface of the medulla? Structures nearby?
venterolateral
exit of cranial nerves 9&10
What is the blood brain barrier?
a tight endothelial layer which separates the CSF (cerebrospinal fluid) from blood
Which ions are the blood brain barrier relatively impermeable to?
H+ & HCO3-
The blood brain barrier is impermeable to CO2.
True or False?
False
BBB is permeable to CO2
How much time taken for CO2 to cross from the blood to cerebrospinal fluid in?
20 seconds
What is the pH of cerebrospinal fluid determined by?
Arterial pCO2
In cerebrospinal fluid CO2
?
Is the pH of cerebrospinal fluid directly affected by changes in blood pH?
No, indirectly.
Cerebrospinal fluid contains relatively little protein concentration, so
has a low buffering capacity (unlike blood), which means a small change in arterial PCO2 can result in a large change in pH in CSF.
CO2 in CSF equation
CO2 dissociates into H2CO3 + H+.
Carbonic acid dissociates into HCO3- + H+
Respiratory acidosis caused by high CO2 will increase ventilation rate quicker than metabolic acidosis.
True or False?
True
Because metabolic acidosis increase concentration of H+ ions in blood, which is less permeable to BBB than CO2 and hence CO2 can change the pH of CSF
What causes buffering in blood?
protein
Is the brain sensitive to hypoxaemia?
Not unless is hypoxic hypoxemia
(lack of O2)
Increase of CO2 in the blood causes an increase of CO2 in the CSF causes and increase in minute ventilation in a very —– way
linear
Responsibility of central chemoreceptors and peripheral chemoreceptors for overall response to CO2 rising.
central chemoreceptors: 80%
peripheral chemoreceptors: 20%
Considerable variation between individuals in their sensitivity to CO2 rise for example (2):
- athletes; very sensitive to high levels of CO2??
- chronic lung disease; insensitive to high levels of CO2
If PCO2 is larger than ——, there is a ——- —– of central chemoreceptors, which has what effect on minute ventilation?
- 10kPa
- direct suppression
- decreases minute ventilation
What effect does metabolic acidosis have on CO2-ventilation curve?
Shifts the curve to the left
What effect does metabolic alkalosis have on a CO2-ventilation curve?
Shifts the curve to the right
Metabolic acidosis is caused by
non-respiratory causes like renal failures, DKA
Where are peripheral chemoreceptors found?
- carotid body
- aortic body
Peripheral chemoreceptors: carotid body:
- where
- location and structures nearby
- contains
- innervation
- common carotid artery
- 2 mg structure located at the bifurcation of the common carotid artery just above the carotid sinus
- contains type 1 glomus cells (containing granules of neurotransmitters) and Type 2 Sheath Cells
- innervated by Carotid Sinus Nerve aka Glossopharyngeal nerve (cranial nerve 9)
graph from response of CC to PCO2
On X axis is concentration of H+ ions in CSF
On Y axis is ventilation
As concentration of H+ increases, ventilation increase…
Peripheral Chemoreceptors: Aortic body:
- where
- innervation
- distributed around aortic arch T4/T5
- innervated by Vagus Nerve (cranial nerve 10)
Which is more sensitive; carotid or aortic body chemoreceptors?
Not much difference but possibly carotid
Peripheral chemoreceptors receive ————– and respond within —— to small changes in ——–.
Describe increases causing other increase/decreases of minute ventilation.
- high blood flow
- seconds
- PCO2, pH, PO2
Increase in PCO2, increase in H+ conc, decrease in pH, decrease in PO2 causes an increase in minute ventilation
Body’s sensitivity to oxygen is altered by
CO2
Chronically high levels of CO2 ( eg: in COPD), because you are undergoing hypoventilation what happens to the respiratory response?
Blunting of respiratory response
Blunting of respiratory response results in:
- chronic respiratory acidosis with metabolic compensation
- hypoxaemia due to hypoventilation
graph of adaptation of central chemoreceptors to hypercapnoea
CO2 insensitivity in ppl with chronically high CO2 levels
COPD leading to hypoventilation leading to prolonged hypercapnoea
- what happens to CSF pH?
- CSF pH gradually (weeks/months) returns to normal due to adaptive and compensatory processes even thought PCO2 remains high.
- the drive to breathe in this situation is mainly controlled by response to hypoxia = hypoxic drive
If hypoxic drive is suppressed by giving too much oxygen, what can occur
Minute ventilation decreases
Patient can stop breathing
Two receptors in the lung:
- stretch receptors
- irritant receptors
Stretch receptors
Found in the smooth muscle of bronchial walls, triggered by the distention of lungs. Receive and send signals through the Vagi (cranial nerve 10) leading to shallower inspiration, delaying the next cycle of inspiration (Hering - Breuer reflex); dont need to know reflex
Irritant Receptors:
- location
- cough reflex
- innervation
in smooth muscle, stimulated by smoke, dust, noxious gas particles, cold air and histamine.
Receptors in trachea lead to a cough reflex.
Receive parasympathetic bronchoconstrictor nerve supply via Vagi (cranial nerve 10)which act via Ach and M3 receptors, when stimulated result in deep yawns/signs, to prevent lungs from collapsing when inflate, and only slightly deflate
Juxtapulmonary (J) receptors:
- location
- stimulated by
- innervation
- stimulation results in
- located on alveolar and bronchial walls, close to capillaries
- stimulated by pulmonary congestion, pulmonary oedema, microemboli and inflammatory mediator.
- afferents are small, unmyelinated C fibres or Vagus nerve (cranial nerve 10)
- stimulation results in apnoea, rapid shallow breathing, a decrease in heart rate and BP
Proprioreceptors
- in Golgi tendon organs, muscle spindles and joints of respiratory muscles, go through spinal cord
- stimulated by the shortening of the respiratory muscles
- decreases respiratory rate by affecting respiratory center
Impact of opiods on control of breathing
- naturally occurring peptides used as analgesics (pain control)
- opioids decrease sensitivity of peripheral and central chemoreceptors leading to respiratory depression and possibly fatal
Are proprioreceptors found in the diaphragm?
No
How to treat opioid overdoes?
- naxalone
- opioid receptor antagonist
Arterial blood gas measurement taken from?
a peripheral artery: radial,brachial,femoral
Arterial Blood Gas measurement gives information on
respiratory and metabolic activity
Normal pH:
Normal PaO2:
Normal PaCo2:
Normal HCO3-:
Normal base excess:
Normal Lactate:
Normal Anion Gap:
Normal pH: 7.35-7.45
Normal PaO2: 10.3-13.3kPa (80-100mmHg)
Normal PaCo2: 4.5-6.0kPa(35-45mmHg)
Normal HCO3-: 22-28mmol/L
Normal base excess: -2-+2
Normal Lactate: 0.6-2.0mmol/L
Normal Anion Gap: 10-18mmol/L
respiratory failure = —- = —–
hypoxaemia = PaO2 < 8kPa (60mmHg)
Type 2 respiratory failure when (2)
- hypoxaemia (PaO2<8kPa)
- hypercapnoea (PaCO2>6.5kPa)
Type 1 respiratory failures when (2)
- hypoxaemia
- normal or low PaCO2
Respiratory acidosis:
- normal pH of blood?
- regulation
- buffers
- increase sequence
- results
- type of respiratory failure
- normal pH of arterial blood is 7.4 with H+ conc of 40nmol/L
- transport of CO2 in plasma is critical in acid base regulation
- bicarbonate and deoxygenated Hb are important buffers, which bind and release CO2 according to the pH
- As CO2 increase, H2CO£ increases, H+ and HCO3- increases.
- increase in H+ results in central and peripheral chemoreceptors increasing ventilation and increases respiratory rate, resulting in more CO2 expired.
- in type 2 respiratory failure
If type 2 respiratory failure, is it acidotic pH?
suggest acute type 2 respiratory failure
If HCO3- is higher than normal in type 2 respiratory failures, then
chronic type 2 respiratory failure
High lactate suggests
metabolic acidosis
Approach to ABG interpretation
- is PaO2 < 8kPa? If yes = respiratory failure
- is PaCO2 normal or low? If yes = type 1 respiratory failure
- is PaCO2 high (>6.5kPa)? If yes = type 2 respiratory failure
- If type 2 respiratory failure, is pH acidic? If yes, suggests acute type 2 respiratory failure
- If type 2 respiratory failure, is HCO3- higher than normal? If yes then chronic type 2 respiratory failure
How many more times greater is acid expired daily as CO2, than the amount of acid excreted by the kidneys?
100x
If hypercapnoea then what range is oxygen prescribed at? What would be the normal oxygen saturation?
- 88-92%
- 94-98%
Type 1 and type 2 RF table
5 causes of Type 1 Respiratory Failure
- low inspired O2 (FIO2): high altitude, asphyxia
- Hypoventilation: COPD
- Diffusion Impairment: pulmonary fibrosis
- VQ mismatch: pulmonary emboli, pneumonia
- R-L shunt: includes congenital causes
Additional causes of Type 2 Respiratory Failure
- failures of ventilation = alveolar hypoventilation
- chronic lung disease: COPD, severe chronic asthma, cystic fibrosis
- musculoskeletal abnormalities: obesity, kyphosis, thoracic surgery, chest wall trauma
- neuromuscular surgery: diaphragmatic palsy, phrenic nerve palsy, myopathies, muscular dystrophy, Guillian - Barre, myasthenia Gravis, Botulism
- Central Nervous System: anesthetics, respiratory depressants, sedatives, head injury, CVA, central sleep apnoea
Acute Type 2 RF vs Chronic Type 2 RF:
- time?
- mechanisms
- HCO3-
- pH
- hours vs days to weeks
- not active vs activated hence kidneys retain HCO3-
- HCO3- remains normal vs HCO3- high because retained by kidneys
- H+ increases so pH decreases for both
Acute Exacerbation of COPD is acute or chronic?
acute on chronic type 2 RF
Compensatory Mechanisms:
If pH decreases then ventilation,o2, h2co3, h+, pH and over how much time
If pH decreases, ventilation increases, co2 decreases, h2co3 decreases, H+ decreases, pH increases
Minutes
Anion Gap equation, normal range and used to measure
- (Na+ + K+) - (Cl- + HCO3-)
- 7-16 mEq/L
- metabolic acidosis
Compensatory mechanisms: adjustments in absorption/excretion and how long
If pH decreases, kidneys retain HCO3-, excrete H+ and pH increases
Over days
Metabolic acidosis
Results in an increase in H+ and reduced pH due to a non-respiratory cause
PaCO2 will be normal, pH will be low
High anion gap occurs because
- another anion in the blood increases the anion gap
- lactic acidosis (sepsis, MI, trauma)
- diabetic ketoacidosis
- acute renal failure
- ingestion of acids
- the neurones in the respiratory centre are stimulated to increase the respiratory rate in an effort to decrease CO2 to counter the acidosis, but this is only partially successful
Normal Anion Gap Metabolic Acidosis
- normal amount of acid in blood
- but loss of HCO3-
- diarrhoea
- renal tubular acidosis
- excessive chloride administration
What is another measure of metabolic disturbance?
- base excess
- BE - dose of acid that would be needed to return blood to the normal pH under standard conditions
- base deficit is the dose of alkali needed to return blood to normal pH
Complete later
GOLDMARK
glycols, l lactate, d lactate, methanol, aspirin, renal failure, ketoacidosis
ROME for ABG
Respiratory = Opposite:
- low pH + high PaCO2 = resp acidosis
- high pH + low PaCO2 = resp alkalosis
Metabolic = Equal:
- low pH + low bicarb = metabolic acidosis
- high pH + high bicarb = metabolic alkalosis
