respiratory 3 Flashcards
what does the lungs separate the heart from the ribcage and what are the 5 structures within teh lungs
separate heart from ribcage except at cardiac notch (at about 3rd-5th intercostal space) - feel heartbeat
- base (= diaphragmatic surface): concave surface adjacent to diaphragm
- apex: adjacent to thoracic inlet
- costal surface: convex - in contact with rib cage
- medial surface: indented by heart (region of 3rd-6th ribs) - contact with mediastinum around the heart
- root:
- composed of grouped principal bronchus, pulmonary artery, veins and nerves, wrapped together in pleural covering
- location of tracheobronchial lymph nodes
- enters lung at hilus
how many lobes in most domestic species, dogs and horses and what defines a lobe
dog: 2 left, 4 right - most domestic species
• horse: 2 left; 3 right
• defined as structures supplied by a secondary (lobar) bronchus
what does the connective tissue septa separate, what does it contain and what is the consistency in different species
- separate different lung lobes
- contain collagen, elastin (expansion and remain expanded with decrease in pressure), blood vessels
○ thick in ruminants, pig - infection less readily spread to other lobes
○ thin and incomplete in horse
○ almost non-existent in dog
what is the tracheal bronchus and what is its function
Tracheal bronchus comes straight off trachea before the primary and secondary bronchus splits
- Provides air to cranial lobe of right lung
what is the left and right lung divided into
left lung: 2 lobes 1. cranial - has cranial and caudal portions 2. caudal right lung 1. cranial lobe - ventilated by tracheal bronchus in ruminants and pigs 2. middle lobe - not present in horse 3. caudal lobe 4. accessory lobe
what are the 3 systems of vasculature for the lungs and where do they enter
1) pulmonary arteries - oxygen-depleted blood from right ventricle - pulmonary trunk - left and right arteries - lungs
2) pulmonary veins - oxygen-rich blood from lungs - left atrium, also provides venous return from bronchi
3) bronchial artery - oxygenated blood for the bronchus - arises from aorta
what are the 2 networks of lymphatic drainage
- superficial network: drains subpleural tissue into vessel at hilus of lung
- deep network: drains deeper tissues via vessels running along airways (from level of bronchioles)
where do the 2 networks of lymphatic drainage meet and what are they responsible for
both sets merge at hilus ⇒ tracheobronchial lymph nodes ⇒ cranial mediastinal nodes ⇒ tracheal lymphatic vessels or thoracic duct
• responsible for:
- removal of material phagocytosed by macrophages in airways
- mounting immune response to infectious agents
○ Very important as air breathed in isn’t sterile unlike the blood
what is the innovation for lungs and glands and reflexes
autonomic supply (sympathetic and parasympathetic) from pulmonary plexus within mediastinum:
1) efferent
- regulates activity of bronchial glands
○ Sympathetic - drying up of glands
○ Parasympathetic - secretion from glands
- smooth muscle of bronchi ⇒ broncho-constriction or dilation
2. afferent supply from:
- stretch receptors ⇒ reflex modification of respiration
- mechanoreceptors ⇒ reflex coughing
what are two processes that result in ventilation-perfusion mismatching
1) hypoventilation - insufficient airflow to lungs due to partial obstruction of upper or lower airway (pathological) or holding breath
⇓
O2 depletion and CO2 accumulation in alveoli
⇓
O2 depletion and CO2 accumulation in blood
2) Hyperventilation
• breathing more deeply or rapidly than necessary to maximally oxygenate blood flowing through lungs
- Beyond the animals needs
⇓
surplus fresh air flowing into and out of lungs
⇓
decrease in [CO2] in blood (constant removal from lungs) = hypocapnia
+
only slight increase in [O2] in blood (already almost saturated)
what are the normal mismatching with ventilation-perfusion ratios
1) generally air goes to dorsal region and blood ventral regions in standing animal due to hydrostatic pressure
2) ventilated unperfused lung = alveolar dead space, during anaesthesia of large animals in dorsal recumbancy therefore get pooling of blood in dorsal lung, need to adminster pure O2 to maintain blood PO2
what are the 4 ways in which localised ventilation-perfusion matching occurs
1) local hypoventilation in alveolar airflow - increase PCO2 results in bronchodilation - increase in airflow
2) local hyperventilation in alveolar airflow - decrease PCO2 - bronchoconstriction - decrease in airfow
3) local hypoventilation of capillary blood flow - decrease PO2 - vasoconstriction of arterioles - reduction in blood flow
4) local hyperventilation in capillary blood flow - increase in PO2 in alveolus - vasodilation - increase in blood flow
what are the two types of alveolar epithelial cells and their shape and function
1) type I alveolar epithelial cells:
- very flattened cells - squamous
- cover majority of alveolar wall
- sit on basement membrane
- terminally differentiated (cannot divide)
- allow gas diffusion across cytoplasm
2) type II alveolar epithelial cells:
- cuboidal
- cytoplasmic granules contain surfactant (secreted to coat alveolar lining and reduce surface tension)
divide to replace type I and type II cells
what are alveolar separated by and what does contain and what allows passage of O2
interalveolar septa:
- contain fibroblasts, mast cells, macrophages
- rich in capillaries:- endothelial basement membrane fused with that of alveolar epithelial cells in some places, fused with thin interstitium in others
- alveolar pores - allows O2 movement between adjacent alveoli
what are the 5 structures of the blood-air barrier
- alveolar fluid
- alveolar epithelial cell
- basement membrane of alveolar epithelium (+/- thin interstitium)
- basement membrane of capillary endothelium
- capillary endothelial cell
what are the 3 location pulmonary macrophages are present and what line are they dervied from
- intravascular: associated with endothelium (pigs, ruminants)
- Interstitial - degrade particular material
- alveolar: function to clear alveolar surface; removed via trachea (mucociliary clearance, coughing) or via interstitium ⇒ lymphatic system
• derived from haemopoietic stem cells (monocyte-macrophage lineage)
how to determine partial pressure
e.g. if O2 comprises 20% of a gas mixture with total pressure of 760 mm Hg
partial pressure of a gas is found by multiplying its percentage concentration by the total pressure
e.g. if O2 comprises 20% of a gas mixture with total pressure of 760 mm Hg: ⇒ PO2 = 0.20 X 760 mm Hg = 152 mm Hg
what makes the partial presure of O2 drop in the alveoli
water vapour added to air during inspiration ⇒ change in partial pressures of gases, although total pressure remains the same: - acts as a partial pressure
also diluted by stale air that is maintained within alveoli
what is the total alveolar air replaced with each normal breath and what is the average PAO2 and PACO2 in the alveoli
about 15% total alveolar air replaced with each normal breath
⇒ average PO2 of alveolar air (PAO2) = 100 mm Hg; PACO2 = 40 mm Hg
what determines the partial pressure of gases in liquids and what measures PO2 and PCO2 in the blood
concentration of gas dissolved in the fluid
PO2 - only O2 dissolved in plasma
PCO2 - CO2 (what we are measuring) + H2O ⇔ H2CO3 ⇔ H+ + HCO3
⇒ lowered PCO2 in the blood
does CO2 or O2 diffuse quicker, why and what does this result in
CO2 Has a lower partial pressure gradient than oxygen however has higher diffusion coefficient so diffuses quicker than O2
- factors limiting diffusion may result in hypoxia without hypercapnia - indicates disease results in problem with diffusion
rate of gas transfer in terms of blood flow and what does this result in
gas transfer in alveolar capillary bed usually completed in about 1/3 time it takes for blood to travel past alveolus ⇒ existence of enormous diffusion reserve - capacity to add more oxygen to the blood
what do fish use as gas exchange surface
make use of gills – delicate evaginations (out pocketing) of tissue protruding into surrounding water; consist of thin epidermis highly perfused by circulatory system, providing high surface area for gas exchange between water and blood - equivalent to alveoli
what is the mechanism of fish breathing
- breathing involves taking water into mouth while operculum (gill cover) is shut; the mouth is then shut and operculum opened, thus forcing water over gills and out through operculum
• flowthrough (unidirectional) system
thoracic radiograph why most common modality for evaluating respiratory disease
- readily available
- low cost
- easy to perform
- does not require GA
what are the main differences between a cat and a dog thoracic radiograph
- Cats more compressed laterally
- cardiac silhouette different
- Diaphragm more simple less complicated outline
in terms of lung opacity what do most lung diseases result in
Increase or decrease
Increase - aspiration pneumonia - more cells, tissue more dense, less X-ray hit receptor as more absorbed
decrease - pulmonary bulla (not epithelial lining)
list 5 limitations of thoracic radiography
- ability to interpret is highly dependent on radiographic quality
- limited sensitivity for detecting subtle change - especially pulmonary parenchyma
- limited specificity - often relies on signalment and clinical history to prioritise differential diagnoses list
- lesions may be obscured due to superimposition of structures
- pleural effusion will obscure lesions - underlying lung pathology
what are the advantages of thoracic computed tomography and therefore when would you use it
1) eliminates problems due to superimposition
○ more sensitive than radiographs for detecting pulmonary lesions
2) excellent at determining extent of disease and relationship to surrounding organs
3) more refined list of differential diagnoses
use
1) screening for pulmonary metastases as CT can be seen as small as 2-3mm radiograph 0.5cm
2) pleural effusion evaluation - able to see lung parenchyma
3) evulate with PTE (pulmonary thromboembolism) - generally normal radiograph
what are the two images you can get from CT and wha one is tracheobronchial lymph nodes need
can reconstruct to see
1) soft tissue - lymph node
2) lung parenchyma
generally do both
list 3 reasons why nasal computed tomography is preferred over nasal radiographs
1) more sensitive and specific - very bbvious in CT not radiograph
2) more rapid acquisition - easy to do
3) guides rhinoscopic biopsy - how many cms in from nares
disadvantages and limitations of nasal computed tomography
1) Limited availability (referral or large practices)
2) Requires general anaesthesia - especially when looking at lungs as need to inflate - additional cost
3) More expensive than radiographs
4) Requires more expertise - further study and licence
○ machine operation
○ image interpretation
5) higher ionising radiation dose
You would like to image a patient with a mammary tumour, to search for pulmonary metastases. Which imaging modality would you choose - thoracic radiographs or thoracic CT? Why?
- CT - for pulmonary metastasis as higher spacial and contrast resolution
what are the negatives of using an ultrasound for thoracic imaging
1) Does not go through bone
2) Ultrasound cannot pass through air-filled lung
- reverberation artefact = normal lung surface
- Multi reflection in surface - gives multiple lines
○ Cannot image ‘deep’ lesions in the lung
what species would you use ultrasound and what useful for
hose as generally have to take 4 different radiographs
Useful to
- assess surface of lung
- assess cranial & caudal mediastinum
- investigate cases of pleural effusion
- evaluate thoracic wall masses - solid or cysts filled can determine
- guide sampling by FNA or biopsy
In a dyspnoeic dog with dull chest sounds, which modality would you choose to use to evaluate the thorax: radiographs or ultrasound? Why?
Most often cause - lungs aren’t right on pleural surface - pleural effusion or pneumothorax - air in abdomen
- Able to be distinguished with ULTRASOUND
Generally animal may be distressed and don’t want to move it - can bring ultrasound machine to the patient
In a dyspnoeic dog with harsh chest sounds, which modality would you choose to use to evaluate the thorax: radiographs or ultrasound? Why?
Thoracic radiograph as bronchial disease so ultrasound would bounce off creating reverberation artefact
Thoracic Scintigraphy what is it used for and why not widely used
assess FUNCTION
- perfusion
- ventilation
•limited availability (referral) - only a couple institutions in Victoria
•poor anatomic resolution
•animals must be isolated after procedure - until radioactivity has to go back to normal level
what are the 3 ways to sample the respiratory system
1) Bronchoalveolar lavage - endoscopic guided
- can select a bronchus
- provides a ‘deeper’ wash of the lung
2) Transtracheal wash - fluid introduced in trachea via catheter, then rapidly aspirated
- Good to determine if inflammatory cells - cytology
- Straight forward to perform
3) cytology or culture & sensitivity from fluid - drainage o pleural effusion
what are some potential complications of sampling respiratory system and how monitor
- Pneumothorax - needle tear pleural surface - generally not too bad, & haemorrhage
- usually mild & self-limiting
- monitor patient clinically - respiratory rate and with radiographs
what percentage of oxygen in the blood is transported bound to haemoglobin and how much dissolved in plasma
98.5% - haemoglobin
rest - dissolved
oxygen-haemoglobin saturation curve when does HB load and unload O2 and what is saturation at 100mmHg
Hb loads with O2 where PO2 high, and unloads where O2 low
increasing alveolar PO2 cannot result in very great increase in binding to Hb, because already almost 100% saturated at PO2 = 100 mm Hg = 97.5% saturation
List the 3 ways the oxygen-haemoglobin saturation curve is shifted to the right
1) increased blood PCO2 or acidicity (Bohr Effect)
2) increased blood temperature
3) inncrease in 2,3-diphosphoglycerate (DPG) - present in erythrocyte
describe how the Bohr effect shifts the oxygen-haemoglobin saturation curve to the right and what results in
○ binding of CO2 to Hb ( ⇒ carbamino haemoglobin = HbCO2) or H+ to Hb alters conformation of Hb ⇒ reduced affinity for O2 - due to strenuous exercise
○ ↑ [H+] of blood during exercise results from both ↑ PCO2 and lactic acid (anaerobic glycolysis)
results in readier dissociattion of O2 from Hb at tissues, doesn’t change maximum saturation
how is CO2 transported in the blood and give percentages and what contributes to PCO2
majority (60%) transported as HCO3 -; 30% bound to Hb; 10% as dissolved CO2 (what contributes to PCO2)
what is the carbonic anhydrase equation for CO2 in blood and when driven in what direction
carbonic anhydrase
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-
○ Reaction driven to the right in peripheral circulation and to the left in the lungs
How is the carbonic anhydrase reaction driven to the right in the tissues
HCO3- removed by diffusion out of erythrocyte in exchange for Cl- ( = chloride shift), to maintain electrical neutrality.
○ This exchange of anions necessary because cations (i.e. H+) do not readily cross plasma membrane.
○ Flow of Cl- and HCO3- is reversed in pulmonary circulation.
what is the Haldane effect and what does it work in conjunction with
reduced Hb (HB without O2 bound) has greater affinity for both CO2 and H+ than does HbO2 - works in synchrony with Bohr effect to facilitate CO2 and O2 exchange in the tissues
what is the normal blood pH
7.4
what defines acidosis and what are the two types
elevated [H+] (i.e. decreased pH) in blood = acidosis
can result from increase in PCO2 in blood - respiratory acidosis
OR increase [H+] in blood relative to [HCO3-]
what are the causes of respiratory and metabolic acidosis
respiratory - resulting from inadequate ventilation
metabolic
1. during heavy excercise - lactic acid accumulation
2. ketoacidosis - accumulate in plasma or ketone bodies due to major physiological distress or diabetes
3. when [HCO3-] lost from body without concomitant loss of [H+]:
○ in severe diarrhoea HCO3- not reabsorbed ⇒ more HCO3- than H+ is lost
alkaosis what are the two types and examples of what causes them
lowered [H+] (i.e. elevated pH) in blood = alkalosis
• can result from ↓ PCO2 in blood ( = respiratory alkalosis), resulting from hyperventilation
Metabolic alkalosis:
- repeated vomiting over extended period causes excessive loss of H+
what are the 3 measurements that help you distinguish between respiratory and metabolic acidosis/alkalosis
- PaO2 - arterial PO2
- PaCO2 - arterial PCO2
- pH
- from these they calculate a number of parameters including [HCO3-]
what changes in pH and [HCO3-] result in respiratory alkalosis and metabolic alkalosis
↑ pH and ↑ [HCO3-] ⇒ metabolic alkalosis
↑ pH and ↓ [HCO3-] ⇒ respiratory alkalosis
what does low PAO2 in presence of normal PaCO2 represent
indicates diffusion defect (e.g. oedema), rather than ventilation defect (because diffusion of CO2 not limiting)
what occurs when bird fly at high altitudes
birds overventilate (not hyperventilation as it is needed) -> ↓ arterial PCO2 -> severe alkalosis (tolerated much better than in mammals)
what is the tendency of upper airways to do during inspiration and what resists this
tendency to collapse during inspiration (due to subatmospheric pressure) resisted by cartilaginous support and muscular action:
- flaring of nostrils
- tensor muscles of pharyngeal walls
- abduction of arytenoid cartilages
- tracheal cartilages
List 5 pathological disorders of structures in upper airways that restrict airflow
1) facial nerve paralysis
2) displacing soft palate (horse)
3) elongated soft palate (brachycephalic dogs)
4) laryngeal hemiplegia (horse, dog) - paralysis of part of the recurrent laryngeal nerve
5) collapsing trachea (dog)
in the lower airways what controls airway size and what can increase resistance
autonomic nervous system to meet body’s needs: bronchoconstriction (parasympathetic) and bronchodilation (sympathetic)
• increased resistance may result from:
- bronchoconstriction
- excessive production of mucus
- oedema (fluid infiltration) of bronchial walls
what prevents bronchioles from collpasing
not supported by cartilage but have transmural pressure gradient between pleural cavity and bronciolar lumen
what occurs to the transmural pressure gradient in normal inspriation and expiration, forced expiration and obstructive airway disease
- maintained during normal inspiration and expiration
- forced expiration - intrapleural pressure may rise above intraluminal resulting in collapse of small airways at end of expiration (air trapped in alveoli)
- in obstructive airway disease (which occurs as a result of increased resistance) bronchiolar pressure may drop below intrapleural pressure early in expiration ⇒ premature collapse and reduced air exchange with atmosphere - problem with emptying the lungs - occurs with asthma
what is pulmonary compliance and what does a less compliant lung mean and how reduced
a measure of the distensibility of lungs and thorax:
- the less compliant the lung, the more work required (greater transmural pressure gradient) to inflate it and get normal volume of air
- reduced by disease (fibrosis) or increased alveolar fluid surface tension - doesn’t change with rest
what is lung elasticity and how elastic do you want the lung
recoil tendency of lung conferred by elastic connective tissue and surface tension of fluid lining alveoli disease
• Don’t want it to be too elastic as want air left in alveoli so able to expand the lung during inspiration
how is surface tension, surfactant, elasticity and compliance all related
if surfactant is low surface tension will increase resulting in increase elasticity and reduced compliance
alveolar surface tension what results from and what does it result in
results from attracting forces between atoms or molecules
• at air-water interface water molecules more strongly attracted to each other than to air, and therefore resist forces that increase surface area
• in alveolus, surface tension opposes expansion of alveolus
what is a surfactant and what does pulmonary surfactant do
surfactant:
- surface-active substance for which water molecules have less attraction
- reduces surface tension
• pulmonary surfactant = phospholipoprotein:
- reduces tendency to collapse
- increases pulmonary compliance
- keeps lungs dry (without surfactant surface tension of alveolar fluid tends to pull fluid out of capillaries)
what is Laplace’s Law and what does it say about the alveoli and what stops this
P = 2T/r
P = collapsing pressure
T = surface tension
r = radius
- smaller alveolus should have greater tendency to collapse than larger alveolus with same surface tension, however:
surfactant reduces surface tension of small alveoli more than that of large alveoli - surfactant molecules closer together in deflated alveolus than in expanded alveolus, therefore when animal breaths again will be able to expand alveoli to normal size
what is interdependence in terms of alveoli
interalveolar connective tissue also helps prevent tendency to collapse of individual alveoli - elastic tissue of surrounding alveoli resists being stretched by collapsing alveolus
what does obstructive airway disease result in in terms of lung volumes
premature collapse of lower airways during forced expiration ⇒ trapping of air at end of maximal expiration
⇓
increased RV (residual volume - don’t manage to empty lungs completely) ⇒ reduced VC (vital capacity)
• reduced FEV (forced expiratory volume) due to increased airway resistance
what does restrictive lung disease result in in terms of lung volumes
diseases causing loss of lung compliance so can’t fill lungs completely
⇓
reduced TLC (total lung capacity)
where is the central control for breathing, what sensitive to and influenced by and effect of anaesthesia
- Medulla
○ Central chemoreceptors sensitive to H+ changes in the CDF
○ Mainly influenced by PaCO2 - Effect of anaesthesia
○ can depress sensitivity of respiratory control centre receptors results in higher PaCO2
○ Direct relationship between PaCO2 and ventilation
what are the other two receptors that control breathing other than central control
1) Peripheral chemoreceptors
○ Cartoid and aortic bodies - sensitive to PaCO2, pH but mainly PaO2
○ Hypoxemic - in order to change the ventilation have to get very low PaO2 (PaCO2
2) Lung receptor
○ Via vagus nerve
- Stretch receptors = inhibiting of inspiration (hering breurer reflex)
- Inhibition of expiration (deflation reflex)
what is the normal V/Q ratio and what are the two types of mismatching
- Normally ratio is V/Q(perfusion) = 0.8
1) V/Q = infinity (dead space)
2) V/Q = 0 (shunt)
what effect does dorsal recumbence have on blood pressure and lung function
Blood pressure - decrease due to compression on caudal vena cava
Lung function - abdominal viscera compress diaphragm which compress lungs - compression of alveoli - results in ventilation perfusion mismatch - results in shunt - no ventilation but perfusion present
what is the alveolar oxygen equation
PaO2 = F1O2(Patm-PH20) - (PaCO2/R)
R = constant that takes into concentration of nitrogen and other gases - between 0.8 - 1
F102 - percetnage of oxygen
PH20 - always 40 also PaCO2 generally 40 if not given values
capnograph what is it, what does it use and why is it useful
a machine that measures carbon dioxide in the expired air
- End tidal CO2 is virtually identical to the alveolar and arterial CO2
- Expired CO2 gives useful measurement of adequacy of alveolar ventilation
- End tidal carbon dioxide tells us about metabolism, ventilation and circulation
pulse oximetry what does it measure, how and where
- Gives indication of saturation of haemoglobin with oxygen and allows for detection of hypoxaemia
- Generates 2 wavelengths of red light that pass through the tissue and detected by probe
- Once have percentage of oxygen saturation can use curve below can determine the partial pressure of oxygen
list some things that may interfere with signal generated by the pulse oximeter
- Vasoconstriction
- Pigmented skin
- Hypothermia
- Hypotension
- Movement
- Ambient light
An end tidal CO2 value of 65mm Hg may result from:
- Increased metabolism
- Rebreathing carbon dioxide (exhaustion of soda lime carbon dioxide absorber)
An end tidal CO2 value of 25mm Hg may result from:
- Hypothermia
- Impending cardiac arrest
what are voluntary and involuntary modification of respiratory activity
- voluntary - speech, breath holding
- involuntary - coughing, sneezing
V/Q = infinity (dead space) what does it mean, where does it occur, how measure and what levels are an issue
nose, trachea, bronchi - no gas exchange - lots of V but low Q (perfusion)
○ Measure by measuring CO2 breathing out and compare to CO2 concentration in arterial
○ Is above <5 mmHg then an issue
V/Q = 0 (shunt) what does it mean, what does it result from, how to measure, what acceptable level and how to decrease
Q Is very high but have no V - high cause of hypoxaemia
○ Results from desaturated mixed venous blood from right heart returns to the left heart without being resaturated with O2 in the lungs
○ Measure - look level of O2 in artery vs oxygen in the lungs (alveoli) - PAO2 = 6 times Fi(O2) - percentage of oxygen that patient is breathing in
○ Difference is less than 200 acceptable
○ How to decrease:
1. Give forced expiration - put on ventilator
2. Bronchodilation - more air into the alveoli
3. Change position of the animal
List possible causes of hypoxaemia
- Low inspired oxygen concentration (FiO2) - below 80 mmHg, below 60 mmHg severe hypoxia
- Hypoventilation
- Venous admixture
○ Ventilation/perfusion mismatch
○ Shunt
○ Diffusion impairment
List the 3 main causes of hypoventilation under anaesthetic
1) decrease elimination of CO2
2) rebreathing
3) increase production of CO2
what are 7 things that may result in decrease elimination of CO2
- CNS depression due to aesthetic agents, opiates
- Respiratory muscle weakness
- Restricted air flow -(anatomic, pathologic
- Movement of ribs restricted - broken ribs, external pressure (due to surgeon, instruments on the actual chest - may place something there, lean on animal)
- Diaphragm excursion limited - Colic, GDV, obesity, pregnancy
- Movement of lungs restricted - reduce intrathoracic space, tumour
Lung disease - V/Q mismatch
what are the causes of rebreathing and increase production of CO2
Rebreathing - Exhausted soda-lime - capture CO2 - One-way valve malfunction - Excessive dead space Increase production of CO2 - Malignant hyperthermia - genetic disease - mitochondria in muscle increased - too much CO2 ○ Main trigger is anaesthesia ○ Can be common in pigs
what are 4 causes of hyperventilation under anesthetic
- Pain - most common
- Surgical stimulation
- Hypoxia
- Hypotension
why is there an increased risk of horse mortality under anesthetic and how to relieve
1) Cardiac arrest - under anaesthesia - less and less - better monitoring
2) Fracture in recovery - fight and flight response even when still out of it want to stand up and cannot get up properly
- Use padding during recovery and sedation until anaesthetic has worn out
3) Myopathy - horse large and heavy all that weight on muscle, decrease oxygen delivery to muscle - hypoxia to muscle
- Should use good padding during surgery and recovery
what are the 5 aggregations of neuronal cell bodies that make up the respiratory center
- Medullary respiratory group - 1. dorsal respiratory group (DRG), 2. ventral respiratory group (VRG) and 3. pre-Bötzinger complex within medulla oblongata
- apneustic centre and 5. pneumotaxic centre within pons
Efferent fibres from DRG (dorsal respiratory group) what stimulate, what does it cause, what is rate of firing regulated by
- stimulate inspiratory spinal motor neurons innervating diaphragm by synapsing with phrenic nerves
- rhythmic firing of DRG in response to pacemaker activity (i.e. repetitive self-induced action potentials)
- firing of DRG neurons causes inspiration; with cessation of firing expiration occurs.
- rate of rhythmic firing regulated by excitatory or inhibitory synaptic input from other brain areas or elsewhere in body
- DRG alters rate and depth of ventilation
Axons from VRG (ventral respiratory group) what do they communicate with and function
project to spinal motor neurons of both expiratory (abdominal and internal intercostal muscles) and accessory inspiratory muscles (external intercostal muscles) by synapsing with intercostal nerves
- VRG activated by DRG when demands for ventilation increased to increase rate and depth of ventilation further
List the 4 areas of input that the DRG receives
1) pneumotaxic and apneustic centres
2) stretch receptors in smooth muscle airways
3) mechanreceptors in airways
4) chemoreceptors
role of Pneumotaxic and apneustic centres
○ fine-tuning of output from medullary centres - normal smooth inspiration and expiration
○ pneumotaxic centre acts to terminate inspiration
○ apneustic centre prevents switching off of inspiratory neurons
what is the role of the stretch receptors and mechanoreceptors in smooth muscle of airways
stretch receptors
○ initiate Hering-Breuer reflex if increase stretch detected, i.e. inhibition of firing of inspiratory neurons to prevent over-inflation of lungs, protect delicate structures of the alveoli
Mechanoreceptors
○ initiate coughing/sneezing reflex to remove unwanted material
what are the two main chemoreceptors and receptors within for controlling ventilation
1) peripheral chemoreceptors located in:
1. carotid bodies - located at origin of internal carotid artery. (transmit info to DRG through CNIX)
-Supplies the brain so very important to be monitoring gas levels in the brain
2. aortic bodies - aortic arch (transmit info via CNX - vagus nerve) -
□ blood coming from directly from the lungs - useful information about oxygen saturation
2) central chemoreceptors located in ventral part of medulla oblongata
Regulation of lowered PO2 - what detects this, when and what occurs
Arterial PO2 monitored by peripheral chemoreceptors:- only sensitive to dramatic change in arterial PO2, - generally doesn’t affect ventilation
PO2< 60 mm Hg (point where %Hb saturation 90%)
-> aortic and carotid body chemoreceptors detect this - activated
-> stimulate medullary inspiratory neurons
-> increased ventilation - rate and depth
why is regulation of lowered PO2 from chemoreceptors important and why don’t they respond to anaemia
- PO2 depresses all neural function except chemoreceptors
- only respond to arterial PO2, not O2 content of blood - in cases of anaemia, O2 content may be extremely low, but no stimulus for hypoxic drive because arterial PO2 maintained at 100 mm Hg
what are the two chemoreceptors stimulated for varying arterial PCO2 levels and what occurs with increase
peripheral chemoreceptors - weak response
• central chemoreceptors: - most important, respond to [H+] generated from CO2 in brain extracellular fluid (ECF)
-elevated [H+] in brain ECF
-> stimulation of medullary respiratory centre (DRG and if necessary VRG)
-> stimulation of ventilation (increase removal of CO2 from lung, etc)
what occurs in arterial PCO2 drops below normal and what if very high
->lowered [H+] in brain ECF
-> decrease stimulation of medullary respiratory centre by central chemoreceptors
-> decrease ventilation - rate and depth- NOT HYPOVENTILATION as have a need
○ very high levels of CO2 in blood (> 75 mm Hg) directly depress neural function -> depression of ventilation -> death
Regulation by arterial [H+] what does it influence and what response from increase and decrease concentration
cannot influence central chemoreceptors ([H+] does not cross blood-brain barrier)
• does influence peripheral chemoreceptors:-
- ↑[H+] in blood (= acidosis) ↑ventilation - aortic and carotid body chemoreceptors stimulate medullary inspiratory neurons
- ↓ [H+] in blood (= alkalosis) ↓ ventilation
how does increase in ventilation help correct acidosis
- even if not caused by elevated PCO2, increased ventilation can correct acidosis by reducing arterial PCO2 below normal - drive carbonic anhydrase reaction to the left away from H+ production
what is higher control of ventilation and give some examples
conscious control of ventilation by higher (cortical) centres
1) stop breathing
2) vocalisation - modification of breathing
3) defecation and partuition - fix diaphgram, abdominal muscles push caudally not cranially
4) breath holding with diving
5) change in gait - horses when go from trotting to galloping go to 1 to 1 ventilation with step frequency
can higher control be overriden
yes by chemotactic centres with extreme change in arterial PCO2
