BASIC SCIENCES� �
PACU BREATHING Learning and Teaching Resource
©BARNA.2021
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Learning outcomes
By the end of this session you will understand the structure and function of respiratory system in normal health :
Purpose of respiration
To enable
We need oxygen (O2)
for oxidative metabolism
O2reacts with carbon in glucose, fats, proteins to form CO2 and energy – our physical life force
Enzymes store energy as ATP [adenone tri-phosphate] which acts like chargeable batteries
All body cells use ATP to provide electrical energy, heat and to kick start and maintain biochemical reactions
Body cells will die if deprived of O2
Metabolism : oxygen fuels energy
Failure to deliver oxygen to tissue cells
Hypoxia : Hypoxaemia
Two terms here :
Hypoxia
all or part of the body is deprived of adequate oxygen supply at the tissue level.
Hypoxaemia
denotes a drop in the level of oxygen in the blood.
May or may not be connected with an increase in carbon dioxide
Oxygen measurement �Pulse oximetry - arterial blood gas analysis
In clinical practice oxygen levels are measured by :
If the patient is hypoxic, or hypoxaemic,
both of the above values will fall
Why do we need to eliminate �Carbon Dioxide [C02]?
C02 and water are the waste products of metabolism
Hypercarbia = C02 retention�Hypocarbia = C02 elimination
Hypercarbia = raised partial pressure of C02 in the blood. Measured by ABG’s [PaC02=<6.2kPa]
Hypocarbia denotes C02 elimination caused by excessive ventilation [PaC02=>6.2kPa]
CO2 measurement : �capnography and arterial blood gas analysis
In clinical practice CO2 levels are measured by :
Capnography
this measures end tidal C02 [ETC02] the amount of C02 in the blood stream
Arterial blood gases [ABG’s]
measures the partial pressure of C02 dissolved in the plasma.
Normal range : 35-45mmHg or 5.6 kPa
ETC02 : a mark of ventilation
pH is a figure which expresses the acidity or alkalinity of a solution on a scale on which 7 is neutral.
Lower values are more acid & higher values more alkaline
pH - 7.35-7.42 are parameters for blood
C02 retention causes acidosis – pH above 7.35
C02 excessive excretion causes blood to be alkaline : pH below 7.42
If pH distorted at either end cells malfunction
Breathing is always �the 2nd priority of care after Airway�
It is essential for life that breathing is efficient, that air containing O2 is taken in [oxygenation] and CO2 is exhaled with each breath [ventilation].
If the airway is blocked breathing cannot take place.
AIRWAY IS ALWAYS THE FIRST PRIORITY
The Respiratory Cycle
External Respiration
External Respiration : at the level of the lungs.
Oxygen transfers from the atmosphere to the alveoli to the circulation.
Carbon dioxide transfers from the circulation to the alveoli for exhalation
Internal respiration
Internal Respiration : at tissue level
O2 enters the blood stream and is conveyed to the cells.
C02 is excreted from cells to the blood and returns in the circulation to the lungs for exhalation
External respiration
We will analyse how external respiration takes place in the following sub-sections:
LUNGS
Gross anatomy & physiology
Respiratory System overview
Composed of airway and lungs
BREATHING
Heart & Lungs lie proximal
Heart and lungs work as an integrated system [cardio-pulmonary circuit] to pump oxygenated blood to the body tissues and to excrete CO2.
Their proximity allows fast
transfer of gases from alveoli
to blood capillary and back.
Failure of either heart or lungs
stimulates the other to
compensate.
�Deoxygenated blood leaves the right heart for the lungs where it picks up O2 from the alveoli. CO2 diffuses to alveoli and is expired. Oyxgenated blood is delivered to the left heart from where it is pumped into the systemic circulation.
Blood supply to the lungs
The Lungs are held within the Rib Cage
The lungs are attached to
the rib cage by pleura
Pleura cushion the lungs and �attach lungs to rib cage
The pleura are 2 thin layers
of tissue.
The outer pleura [parietal]
is attached to the ribcage.
The inner layer [visceral] is
attached to the lungs.
Pleural cavity contains fluid
to allow the surfaces to slide over each other.
Intercostal muscles �activate ribs to expand on inspiration
The role of the Diaphragm
The diaphragm is a large muscle. It connects to the base of the lungs and has a vital role in breathing.
On inspiration the diaphragm
descends, the rib cage expands and lung volume increases.
The Lungs : Airway Tree
Consist of :
- Lobes
- Bronchiole tree [airways]
- Alveolar network
Bronchiole tree / lower airway
The Lower Airway consists of :
Smaller airways set up airway �resistance
The trachea and large bronchi have cartilage in their walls to stiffen them.
The smaller bronchi and bronchioles have smooth muscle and elastic tissue
in their walls. Contraction & relaxation of smooth muscle regulate airway pressure and
resistance. Signals from the sympathetic system relax smooth muscle [bronchodilation
& decreased resistance]. COPD patients have narrowed airways & increased resistance.
The terminal bronchioles give way to the Alveolar Network
These ‘bunches of grapes’ create maximum surface area for gas exchange
300,000,000 alveoli in the lungs create a surface area of around 2 tennis courts
There are many reasons for alveolar collapse in peri-anaesthesia practice. This leads to diminished surface exchange area for gas exchange and hypoxia.
The Alveolar Network
Alveolar network : �blood supply
The heart pumps around 5 litres/minute of blood to the lungs [pulmonary system]. The
lungs inhale around 5 litres of air over a minute. Ratio of blood to gas should be equal.
The
RESPIRATORY CENTRE
controls BREATHING
The Respiratory Centre [RC]
Situated in the medulla oblongata in the brain stem
the RC controls the rate, depth and timing of breaths
Chemoreceptors �are specialised cells which sense levels of O2,C02 & pH
2 types :
Peripheral chemoreceptors found in Aortic Arch & Carotid Body
Central chemorecptors found near the Respiratory Centre
Both types of receptors alert Respiratory Centre that it is
TIME TO TAKE A BREATH!
Action of Chemoreceptors
Peripheral chemoreceptors
monitor pH, pressure of C02, pressure of 02 in blood
C02 excess and lack of O2 will stimulate chemoreceptors to transmit information to respiratory centre to instigate breathing
Central chemoreceptors
in medulla monitor acid base in the blood
Acidic blood pH stimulates chemoreceptors to transmit information to respiratory centre to instigate breathing
to blow off excess C02
Respiratory centre controls breathing
Ventilation is increased by 2-4 L/min for each mmHg increase in PaC02
Clinical Reference�� Drugs used in general anasthesia - opioids, anaesthetic agents and muscle relaxants - affect the respiratory centre and the intercostal muscles. The residual effect may result in hypoventilation [slow, shallow breaths] in the PACU.
Other factors that impact on breathing
Voluntary Control
breathing can be controlled voluntarily. We can hold our breath or take deep breaths to order
Emotion
emotional factors affect breathing and result in rapid shallow breathing
Pain
like emotion pain can affect breathing and result in rapid shallow breathing
The
MECHANICS
of
BREATHING
Respiratory Centre stimulates breath
When the build up of C02 becomes too
high the respiratory centre in the
medulla stimulates the action of the
intercostal and phrenic nerves.
The intercostal nerves contract the
intercostal muscles which raise the
rib cage. The phrenic nerve contract
the diaphragm which descends.
Pleura attaches lungs to ribs
Action of intercostal muscles �elevates rib cage : diaphragm descends
Intercostal muscle action : As they tighten they lift the rib cage [like a bucket handle] upwards and out. Lungs expand.
Diaphragm action: In inspiration diaphragm descends : Lungs expand.
Clinical application : muscle relaxants are given in general anaesthesia and their residual weakening effect contributes to post operative hypoventilation.
Failure to reverse these agents causes residual paralysis, an emergency.
Air rushes into lungs on �inspiration
Lung volume increases
on inspiration.
Pressure in lungs is
lower than atmosphere.
Air rushes in
On expiration lung volume decreases. Lung pressure is higher than atmosphere.
Air rushes out
Boyles Law of Physics
Pressure in gas in closed container
is inversely
proportional to the volume in that container
As volume enlarges so pressure falls and vice versa
Inspiration, expiration affects �air pressure
On inspiration
lung volume increases and PRESSURE FALLS
Now pressure in lungs is lower than atmospheric
On expiration
lung volume decreases and PRESSURE RISES
Now pressure higher than atmospheric
Gases always diffuse from high to low pressure until equilibrium reached
This is a fundamental principle which governs respiration [external and internal]
Diffusion of gases : external respiration
Lung compliance
LUNG VOLUMES
Lung volumes of healthy adult
Healthy adult at rest takes in 500mls of air per breath =TIDAL VOLUME [TV]
Average number of Breaths per Minute [bpm] = 12
In one minute around 500 x 12 = 6000mls of air taken in = MINUTE VOLUME [MV]
Minute Volume = Tidal Volume X Breaths per Minute
MV = TV x BPM
Lung volumes
Not all fresh gas reaches alveoli for gas exchange
150mls of stale air is trapped in airway – known as ‘dead space’. This reduces the TV and MV
Effective alveolar ventilation rate per minute is therefore 500 minus 150mls = 350mls
If alveolar ventilation is less than dead space then CO2 will be retained
Anatomical ‘dead space’
Alveolar Ventilation Rate : �the amount of fresh air containing O2 �used to replenish the O2 stores in the capillary
If this is deficient the patient will become hypoxic and CO2 will not be expired
Hypoventilation : inadequate alveolar
ventilation for gas exchange is a serious complication of general anaesthesia
CLINICAL IMPLICATIONS ?
Exchange of gases
at the
Alveolar-Capillary Membrane
Exchange of gases across the alveolar-capillary membrane
The end of external respiration occurs when O2 diffuses across the alveolar-capillary membrane to enter the pulmonary blood capillary
At the same time CO2 diffuses from the pulmonary capillary across the membrane to enter the alveoli for expiration
ALVEOLAR-CAPILLARY MEMBRANE
Diffusion – molecules diffuse freely cross a semi-permeable membrane from an area of higher to an area of lower pressure until pressures on both sides of the membrane are equal
O2 and C02 diffuse across the alveolar-
capillary membrane due to a pressure gradient
External respiration : Diffusion of gases across the alveolar-capillary membrane
Pressure Gradient : gas diffusion
GAS | ALVEOLI | PULMONARY CAPILLARY [venous end] |
O2 | 100mmHg [13.3kPa] | 40mmHg [5.3kPa] |
C02 | 40mmHg [5.3kPa] | 45mmHg [5.8kPa] |
Units of measurement of partial pressures
In the USA they still use this measurement
Factors that facilitate �rapid gas exchange
See diagrams in next 2 slides
An extensive capillary network surrounds each alveoli. The venous end flows into the arterial end of each capillary
Alveolar-capillary junction
Peri-anaesthesia practice disrupts diffusion of gases
How gases behave
&
Partial Pressures explained
How gases behave
The pressure of a gas results from its molecules colliding with the walls of a container.
Pressure is determined by the frequency and force of these collisions.
Each molecule is oblivious to others – it strikes the walls as if it were alone.
Decreasing the volume that the molecules occupy increases the pressure as the confined molecules collide more frequently.
Dalton’s law of partial pressures ��‘The total pressure in a mixture of gases is the sum of the partial pressures of each gas’
This is an important concept as it explains the partial pressures of O2 and CO2
Dalton’s Law of Partial Pressures
Each gas here
exerts a unique
partial pressure
as the number of
molecules jostling
for position signifies.
The mixture below
is the sum total of
all the above gas
pressures
But within the mixture
the individual gases
exert their unique
partial pressure
Partial pressures of gases in the atmosphere
Atmospheric pressure = 760 mmHg at sea level comprises of several gases, each of which exert their own partial pressure according to their % of the whole:
Total 760 mmHg
Includes other gasses. N2 = Nitrogen
Partial pressures of 02 & C02 �in the atmosphere & in the alveoli
Atmospheric air contains
O2 = 160mmHg
C02 = 0.3mmHg
Alveoli air contains
O2 = 100mmg
C02 = 40mmHg
The air we breathe
mixes with C02 from
the ‘dead space’ in
the airway & water vapour
in the alveoli. Pressure
exerted by oxygen is lost.
The 02 in the alveoli
is reduced to 100mmHg
C02 is constantly diffusing
into the alveoli from the
pulmonary capillary.
The C02 in the alveoli
Is 40mmHg.
P02 = 100mmHg
PC02 = 40mmHg
Carriage of gases
in the blood
Gases travel by mass transport in blood to body tissues
Efficient cardio-vascular system is essential to deliver O2 to tissues and CO2 back to lungs
Any major disturbance in CVS will lead to poor tissue oxygenation
This will result in metabolism taking place without O2 : anaerobic metabolism
Anaerobic metabolism leads to build up of lactic acids - metabolic [lactic] acidosis
In post operative practice a mild degree of lactic acidosis is common with underperfusion, while patients are being warmed and filled
After diffusion from alveoli to capillary�98% of O2 attaches to Hb molecule�2% of O2 dissolves in plasma to exert a partial pressure [Pa02]
Carriage of oxygen in the blood stream
O2 does not readily dissolve so red blood cell [Hb] carries 98% of O2
It is however the 2%
of dissolved oxygen
[Pa02] that forces oxygen
onto the Hb molecule.
2% of oxygen is dissolved in plasma
2% of O2 exerts the Pa02
[partial pressure of oxygen in the blood = 13.3kPa/100mmHg]
It is this pressure that forces O2 onto the Hb molecule.
If the Pa02 is high : the O2combines strongly with the Hb
If the Pa02 is low – the O2 dissociates [drops off] from the Hb molecule
Falling Pa02 causes oxygen to dissociate from Hb
If PaO2 is diminished – the oxygen molecule will dissociate easily from Hb
[see next slide]
Relationship between Partial Pressure & Saturation of O2
Pa02 greater than 8kPa shows flat line [as oxygen is bound tightly to Hb]
PaO2 of 8kPa is the tipping point. At this level O2 rapidly dissociates from Hb
& SaO2 falls FAST below 90%
If PaO2 is not corrected patient quickly becomes hypoxic.
Cyanosis is a late sign of hypoxia [PaO2 < 6.6kPa / SaO2 < 85%]
The Oxyhaemaglobin
Dissociation curve
All O2 delivered to cells by mass transport in the blood
The oxygen carried by Hb molecule [98%] is carried in the blood stream and diffuses across into the tissue cells
Arterial Blood Gas Analysis
Arterial blood gas analysis measures partial pressures of :
Normal values
Pulse oximetry measures saturation �of Hb with oxygen - SaO2�
It is impossible to be more than
100% saturated
Normal values 98-100%
If patient has normal Hb
oxygen content will be high
as ‘full quota’ of Hb molecules
ready to receive oxygen
Anaemic patients with lowered
Hb can still be 100% as their
diminished Hb chains are all
taken up by O2
Carriage of CO2 in the blood
Capnography
The capnograph measures end tidal CO2 [ETCO2]
This reflects the level of CO2 in the alveoli at the end of expiration which is equivalent to the partial pressure of CO2 in the capillary blood vessel.
Normal values : 35-45mmHg [4.6 – 5.9kPa]
If high indicates patient hypoventilating
INTERNAL RESPIRATION
Diffusion of O2 from capillary to tissue cells
Diffusion of CO2 from the tissue cells to the blood capillary
Internal Respiration : diffusion of gases �to and from capillary to tissue cells
Pressure Gradient : gas diffusion
GAS | TISSUE CELLS | ARTERIAL CAPILLARY [arterial end] |
O2 | 45mmHg [5.3kPa] | 100 mmHg [13.3kPa] |
CO2 | 45mmHg [5.8kPa] | 40mmHg [5.3kPa] |
The PaO2 is higher in the blood capillary than in the tissue cells
O2 diffuses across until equilibrium is established
PaCO2 in the tissue cells is higher than in the blood capillary
CO2 diffuses from tissue cells to blood capillary until equilibrium is established
Summary
For efficient oxygenation and ventilation of the tissues we need
pulmonary blood flow
blood flow to tissues
Risk of respiratory complications following GA
Central Respiratory
Depression [opioids,
volatiles] : slow, shallow
breaths / delayed return
to consciousness
Residual paralysis
Failure to reverse muscle
relaxants leading to
weakness.
Other causes of hypoxia &
Hypercarbia:
Airway obstruction [upper]
In semi or unconscious
patients caused by tongue,
blood, secretions,laryngospasm,
haematoma
Limited/no feel of air, noisy
breathing …..airway manoevres
[Lower]: bronchospasm [smokers,
COPD patients at risk : wheezing
dypsnoea
Pneumothorax:
Surgical risk /
Central line placement
Diminished air entry,
Dypsnoea.
Atelactasis :
Partial lung collapse
Stasis on table, mechanical
ventilation, loss of surfactant,
VQ mismatch
References : You Tube videos
You Tube videos:
https://www.youtube.com/watch?v=AtmW_3EUydU