Respiritory: Physiology Flashcards
Which parts of the brain are responsible for voluntary/ involuntary breathing?
Voluntary: Cortex
Involuntary: Pons, Medulla and Spinal Chord aka brain stem
What are the names of the three respiritory groups
- Pontine Respiritory Group
- Ventral Respiritory Group
- Dorsal Respiritory Group
Describe the positioning of the three main respiritory groups from a dorsal view
What are more passive, the inspiritory neurons or the expiritory neurons?
Expiritory neurons, in normal breathing the only thing they do is inhibit the inspirtory neurons
Describe the process of neuron activation during normal breathing?
By activating the inspiratory neurons this causes contraction of the inspiritory muscles. It also causes activation of the expiritory neurons which in turn inhibit the inspiritory muscles thus relaxing the muscles of inspiration allowing expiration to take place.
Normal muscles of inspiration
Diaphragm and Intercostals
Describe the prrocess of neuron activation during large respiration
In order to have a large expiration you must first take a large inpiration. This large activation of inspiration neurons has a large activation on the expiritory nuerons. When this happens the activate muscles of expiration as well as inhibiting muscles of inspiration
5 receptors which effect respiration
Which nerve carries the lung receptors
Vagus Nerve
How do the vagal nerves effect your breathing pattern?
Cutting the vagus nerve produces a reflec of slow deep breaths
Why does a normal breathing pattern look like this?
Inspiration is steep because it is active while expiration is slower because it is passive
Which of this receptors is rapidly/slowly adapting?
Slowly adapting receptors keep firing in response to a stimuus whereas rapidly adpating receptors slettle down quickly.
What are the slowly adapting receptors responsible for?
These are stretch receptors and are responsible for sensing when the airways are streched therefore activating expiration. The take a bit of time to settle down after stimulating because you want expiration to continue fully even when the airways aren’t fully stretched anymore
What are the rapidly adapting receptors responsible for?
These are irritant receptors and are responsible for sensing obnoxious substances in the airways and triggering things like the cough mechanism. Because these reactions are extreme you want them to settle quickly after the stimulus is dealth with.
What are c-fibre ending responsible for?
Stimulated by interstitial fluid and inflammatory mediators
Peripheral vs Central chemoreceptors
Peripherals sense changes in PCO2, PO2 and H+ and have a fast response. These signals are carried by the vagus nerve.
Central detects shifts in PCO2 once it has diffused over the blood brain barrier hence has a slower response.
Vagus nerve vs Phrenic nerve
Both and for breathing. Vagus is afferent, Phrenic is efferent
What are the terms for the different ammounts of oxygen and CO2 in the blood?
Why is it dangerous to give COPD patients high O2 therepy.
After chronic hypoxia and hypercapnia the central chemoreceptors become desenitised.
The drive to breath then comes from hypoxia rather than hypercapnia.
If they are given high O2 then they loose the drive to breath completely leading to further hypercapnia, CO2 narcosis and acidosis and evnetually death
Drugs that inhibit respiration
- Anaesthetics
- Opioids
- Sedatives e.g. benzos
Drugs that stimulate respiration
- Primary: these actually drive the respiritory drive e.g. doxapram. However these aren’t used due to nasty side effects
- Secondaries: these are things like bronchodialators that make breathing easier such as B2 agonists
What happen’s if control of your respiritory function is too common for example surpressing a tickly cough? And what is the name of the dissorder?
If you overide your autonomic respiritory system too often it gives up and then you rely on the cortex for breathing. This is called breathing pattern dissorder.
What is Obstructive Sleep Apnoea?
This occurs because of a loss of the tonic neural drive to maintain the upper the airways during sleep.
If you have a condition which already means your upper airways are impaired such as obesity, alcohol or anatomical abnormalities when you sleep then can get completely obstructed resulting in you waking up in order to breath therefore disrupting sleep. However you might not always fully wake up so might not know why you are so tired.
What is the tonic drive?
This is the continuous background drive that maintains our upper airways and keeps then clear.
What is tidal volume?
Tidal volume is your standard breath volume without forced respiration
What is dynamic hyperinflation in COPD?
Due to damage of lung structure the lung loses it’s elastic property and the patient loses the ability to passively deflate their lungs. Therfore without force expiration breaths stack
Quick refresher on oxygen haemoglobin dissociation curve: What is on the axis and what 4 things cause a right shift?
What does V and Q mean in a V/Q missmatch?
V = Ventilation (oxygen)
Q = Perfusion (blood flow)
Why isn’t gas diffusion in the lungs perfect?
If it were perfect equilibrium would be reached between alveolar and arterial blood and these two lines would be the same
Shunting and Dead Space
A shunt refers to blood passing through the lungs without participating in gas exchange.
Dead space is the volume of air not participating in gas exchange due to ventilation without perfusion
Normal forms of anatomical shunting?
- A small ammount of arterial blood doesn’t come form the the lung (Thebesian veins - these are tiny veins that drain blood directly from the myocardium into the heart’s chambers)
- A small amount of blood passes through the lungs without seeing gas exchange (bronchial circulation)
What are physiological shunts?
Physiological shunts are areas where there isn’t sufficient ventilation hence the blood isn’t getting oxygen as it should.
What is alveolar dead space?
This is areas of the lung with insufficient blood supply to allow for perfususion. Occurs with age and disease.
What is the natural V/Q distribution in the lungs?
In the top of the lung both Q and V are reduced however V>Q therefore V/Q is raised. PO2 is greater but there is simply less of it.
In the middle it is the average which is about 0.8 (4L Oxygen pass through the lungs for every 5L of blood)
In the bottom both Q and V are raised however Q>V therefore V/Q is reduced. PO2 is less but there is simply more blood.
It all averages out in healthy lungs.
What happens to the gas content in blood during hypoventilation and hyperventilation.
Think about the shape of the oxygen dissociation curve
In hypoventilation blood oxygen goes down due to decreased PO2 and blood CO2 goes up
In hyperventilation blood CO2 goes down but blood oxygen doesn’t really go up as the curve is already maxed out at normal ventilation
What is the main difference in presentation of type 1 and type 2 respiritory failure?
In type 1 (V/Q missmatch) only part of the lung is affected. In the part where this is occuring PaO2 is low and PaCO2 is high, high PaCO2 triggers an increased respitatory response however this fresh air will disproportionately go to the areas that have normal V/Q. Here oxygen saturation is healthy therefore no more oxygen goes in yet more CO2 goes out. This results in a low PaO2 with a normal PaCO2.
In type 2, respiration is completely affected therefore PaO2 is low and PaCO2 is high.
Causes of type 1 vs type 2 respiratory failure
What is anatomical dead space?
This is normal areas where air might go but where gas exchange doesn’t happen either because blood doens’t go there or it doesn’t conduct.
E.g. bronchus and trachia
What is physiological dead space?
This is anatomical dead space and alveolar dead space combined
Physiologically what do we need hydrogen ions (acid) for
- Energy in mitochondria
- Protein conformation/function
- Metabolism
How is hydrogen ion balance (homeostasis) acheived?
- Regulating production/excretion
- Buffering
What are the different forms of hydrogen ion production in the body?
What is a buffer solution?
A buffer solution resists changes in pH when and acid or base is added to it
Types of buffer systems in the body?
- Bicarbonate system
- Haemoglobin
- Others (don’t need ot know the details of these) : phosphate, proteins, exchange of intracellular K+ for H+
Basic equation of the bicarbonate buffering system
Priciple of the haemoglobin buffering system?
CO2 can enter an RBC causing an increase in H+. H+ can actually bind to haemoglobin encouraging it to release oxygen. At the same time the left over HCO3- is exchanged for a Cl- ion outwitht he cell. This is another way CO2 and HCO3- can effect one another.
In what way is the bicarbonate buffering system regulated?
It is open on both ends.
CO2 is excreted through the lungs and regenerated in respiration. On the other side H+ is excreted through the kidneys and HCO3- is regenerated through the kidneys.
When end of the bicarb buffering system is the fastest?
The lung side
What is the Hb buffering system an example of?
A protein buffering system
Definition of acidosis/alkalosis
Normal blood acidity (H+ concentration and pH)
What is the [H+] relationship to [CO2] and [HCO3-]
Fill in this table
Think about how each one occurs
How does respiratory acidosis occur?
Respiration is decreased
pCO2 increases
H+ increases
How does compensated respiratory acidosis occur?
In response to the acidosis more HCO3- is made resulting in a normal pH but with elevated CO2 levels
How does respiratory alkalosis occur?
Respiration increases
pCO2 decreases
H+ decreases
How does matabolic acidosis occur?
If there is a problem with your metabolism and your body is making too much H+.
You sense this acidosis and your body body responds by increasing respiration however this can only work so far.
Eventually you end up with high H+ and low pCO2
How does metabolic alkalosis occur?
The body isn’t making enough acid either kidneys excrete too much or you have consumed to much alkaline medication.
Start breathing less to compensate. Can only do this so far until you need oxygen.
If it goes this far you end up with low H+ and high pCO2
Biomarkers of acute, chronic & acute on chronic respiratory acidosis?
Biomarkers of acute and chronic alkalosis
You get a small drop in bicarb as well because renal compensation of decreased H+ excretion also includes a decrease is bicarbonate generatio
Examples of causes of matabolic acidosis
Effects of metabolic acidosis
Example causes of metabolic alkalosis
Effects of metabolic alkalosis
What’s going on here?
This is metabolic acidosis.
H+ raised but pCO2 lowered to compensate.
Think renal failure, DKA (diabetic ketone acidosis), salicylate OD (found in plants, aspirin, acidosis caused by inhibtion os citric acid cycle and ultimately lactic acidosis), lactic acidosis.
Would do a urine analysis to look for glucose, salicylate and lactate
What’s going on here?
pCO2 raised, H+ only slightly raised, pO2 low, pHCO3- raised
Chronic compensated respritory acidosis.
Most likely COPD
Acid base disturbance cheat sheet just to look at
What’s going on here?
- H+ lowered - alkalosis
- pCO2 lowered - correlates therefore cause
- HCO3- normal - no metabolic compensation
Acute respiratory alkalosis
What’s going on here?
Any changes you might expect over the next few days?
- H+ raised - acidosis
- pCO2 raised - correlated therefore cause
- HCO3- normal - no metabolic response
Acute respiratory acidosis
After a couple days you would expect the HCO3- to increase as metabolic compensation. However in accidents it is common to also have renal impairement leading to further acidosis.
What is going on here?
- H+ lowered - alkalosis
- pCO2 raised - opposite so respiratory compensation
- HCO3- raised - metabolic cause
Chronic metabolic alkalosis with respiratory compensation
The vomitting leads to a loss of acid in the system thus lowering overall H+. In order to replenish this stomach acid you end up with HCO3- getting pumped into the blood further increasing the alkalosis.
What’s going on here?
- H+ raised - acidosis
- pCO2 lowered - respiratory response
- HCO3- lowered - metabolic cause
- AG (anion gap) raised - anions taken up by H+
Metabolic acidosis with respiratory compensation
DKA - diabetic ketone acidosis.
Without insulin the liver begins to break down fats for fuel resulting in a build up of acidic ketones
What’s going on here?
- H+ raised - acidosis
- pCO2 lowered - respiratory response
- HCO3- lowered - metabolic cause
- AG (anion gap) raised - anions taken up by H+
Metabolic acidosis with full respiratory compensation
Aspirin is broken down into salicylic acid
What’s going on here?
- H+ raised - acidosis
- pCO2 lowered - respiratory response
- HCO3- lowered - metabolic cause
- AG (anion gap) raised - anions taken up by H+
Metabolic acidosis with respiratory compensation
Carbon monoxide poisoning. CO bind to haemoglobin blocking oxygen and causing a left shift of the oxygen dissociation curve reducing haemoglobin’s ability to give up the oxygen it does have. This reduces delivery to tissues causing them to produce lactic acid from anaerobic respiration resulting in acidosis
