Respiration Flashcards
(142 cards)
1
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the components of the respiratory system
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- Respiratory Tract Thorax: Thoracic wall and thoracic cavity
2
Q
the major function of the respiratory tract (and other functions)
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- Major function: Air distribution (all parts except alveoli), Gaseous exchange (alveoli) 2. Other Functions: Filters, Warms and humidifies the air, Resonance of voice, Regulation of CO2-O2 levels in the body, Smell
3
Q
Gross anatomy of the respiratory tract
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Subdivisions of Respiratory Tract: Upper respiratory tract: Components outside the thorax: 1. Nose 2. Paranasal sinuses 3. Pharynx: Nasopharynx, Oropharynx, Laryngopharynx 4. Larynx Lower Respiratory Tract: Components located almost entirely within the thorax 1. Bronchial tree Lungs
4
Q
Nose (Ala)
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each side of the nostril
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Q
Nose (Nasal septum)
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divides nose into left and right cavities
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Nose (Turbinates)
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bony projections on the lateral wall of nasal cavity (superior, middle, inferior- has rich blood supply)
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Nose (anterior nares)
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external openings of nose
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Nose (posterior nares)
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openings into pharynx; allows air to pass from nose to pharynx
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Q
Vestibule
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area just inside the nasal cavity- contains vibrissae (hairs), glands
10
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Nasal muscosa components
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- Respiratory mucosa Olfactory mucosa: special sensory for smell.
11
Q
Define paranasal sinuses
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hollow spaces in skull bones and facial bones; all of these are connected to the nasal cavity
12
Q
4 pairs of paranasal sinuses
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Frontal, Maxillary, Ethmoid, Sphenoid
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Functions of paranasal sinuses
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- Airway passageway 2. Warms, moistens, filters air Sinuses, provide resonance for voice
14
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define Pharynx
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muscular tube, lined with mucous membrane extending from base of skull to esophagus
15
Q
3 subdivisions of the pharynx
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- Nasopharynx: from posterior nares to soft palate 2. Oropharynx: from soft palate to hyoid bone in neck 3. Laryngopharynx: from hyoid bone to esophagus
16
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function of the pharynx
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Common passageway for respiratory and digestive tracts, Role in speech (laryngopharynx)
17
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define Larynx
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Voice box: Lies between root of tongue and upper end of trachea.
18
Q
Location of the larynx
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against bodies of cervical vertebrae 3 to 6 (related to thyroid gland).
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Q
functions of the Larynx
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Air passageway, Voice production, Protects airway against entrance of solids or liquids.
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Q
Organisation of the larynx
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• Cartilage framework • Held by muscles and ligaments • Intrinsic and extrinsic muscles Contains: true vocal cords (Glottis) and rima glottidis
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Trachea
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• Windpipe • Extends from larynx to principal bronchi: 2.5cm in diameter, 15-20 C-shaped rings- hyaline cartilage, posterior surface (trachealis) • Lines by ciliated pseudostratified columnar epithelium
22
Q
the two functional subdivisions of the respiratory tract
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- Conducting Zone: passageways for air: nasal cavity to terminal bronchioles 2. Respiratory Zone: gaseous exchange: respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli
23
Q
components of the thoracic wall and thoracic cavity
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- Ribs and Rib cage 2. Joints- ribs with sternum, ribs with vertebrae 3. Phases- events of respiration 4. Alteration in capacity of thorax Movements of ribs and mechanics of rib movements
24
Q
what are the factors facilitating changes in the diameter
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oints of sternum, joints at vertebral column, obliquity of ribs
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What are the two phases of respiration
inspiration and expiration
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three events of respiration
1. alteration in capacity of the thoracic cavity 2. alternation in thoracic capacity: intrathoracic pressure falls 3. changes in lung size and recoil: lung acitivity controlled by ANS (sympathetic and parasympathetic)
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Arteries in the respiratory system
1. Internal thoracic artery: musculophrenic, pericardiophrenic 2. Thoracic and abdominal aorta, respectively: superior phrenic and inferior phrenic.
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Relation of lungs with mediastinal structures in the thoracic cavity. Left lungs is narrower due to presence of heart.
• Mediasatinum • Heart • Trachea • Great Vessels • Thymus Gland • Nerves Lymph Nodes and Vessels
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Two major divisions of the trachea
1. Lobar Bronchi 2. Bronchioles:
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divisions of bronchioles
Primary, Secondary, Tertiary (segmental bronchus)-terminal bronchiole, respiratory bronchiole (BP segments), alveoli
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divisions of the lung
1. Lobes: major divisions of lungs 2. Segments bronchopulmonary (BP): minor divisions of lungs Lobules: minor divisions of BP segments
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segments of the superior lobe BP
Apical segment, Posterior segment, Anterior segment
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segments of the middle lobe BP
Lateral segment, Medical segment
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segments of the inferior lobe BP
Superior, Posterior basal, Anterior basal, Medial and Lateral basal
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alveoli define
Thin walled, spherical hollow cavities; increase surface are for gaseous exchange
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define capillaries
Extensively cover alveoli to ensure gaseous exchange in alveoli
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Pleura organisation in the thoracic cavity
• Parietal pleura: lines thoracic cavity • Visceral pleura: covers outer surfaces of lungs • Pleural space: potential space b/w parietal & visceral pleura, contains tiny amount of pleural fluid Pleural recesses:
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Parietal pleura: parts and innervation
1. Parts: Cervical, Costal, Mediastinal, Diaphragmatic 2. Innervation: Intercostal nerves- Costal pleura- segmental (T1-T11) Phrenic nerve- Mediastinal pleura + diaphragmatic pleura Parts of the Parietal Pleura: Mediastinal pleura forms a sleeve of pleura around lung root (in which the two pleura layers become adherent): the pulmonary ligaments
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Blood supply of lungs and pleura
Lungs: Pulmonary circulation, Bronchial circulation. Rt bronchial 3rd post I/C artery, Lt bronchial-descending aorta Pleura: -Ant. And post intercostal arteries, -Azygos veins and internal thoracic veins to SVC
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lymphatic drainage
-Mediastinal -Parasternal -Tracheobronchial
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innervation of the lungs
Pulmonary plexus: mix of vagus and branchus of the sympathetic chain. Anterior and posterior- to bifurcation of trachea.
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innervation of the pleura
Visceral-autonomic (sensitive to stretch only), Parietal-somatic (sensitive)
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physiology of the respiratory system
Ventilation, Gas exchange (O2 and CO2), pH regulation (CO2 acidic), smell, Sound production
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anatomy of the respiratory system
Nasal passages, Pharynx, Larynx, Trachea: Cartilage, Bronchi branching into bronchioles, Alveoli (air sacs in the lungs (squamous epithelium)
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ventilation
movement of air in and out of the lungs (breathing)
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respiration
gas exchange, involves the respiratory and circulatory systems working together
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external respiration
exchange of O2 and CO2 between external environment and tissues
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cellular respiration
metabolism of nutrients in cells consuming O2 and releasing CO2.
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breathing in vs breathing out
Breathe in- O2 in external intercostal muscles expand outwards, diaphragm expands downward allowing ‘fresh’ air into the chest cavity Breathe out –CO2 intercostal muscles contract passively and diaphragm contracts upwards passively allowing the ‘stale’ air out of the chest cavity unless you force the expiration engaging the internal intercostal muscles
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inspiratory muscles
1. Diaphragm contract (75% change in volume) 2. External intercostal: bucket-handle 3. Sternum 4. Accessory muscles (Forced inspiration): Sternomastoid (upper neck), Scalenus (Lower neck)
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inspiration mechanism
1. Contraction of inspiratory muscles (Diaphragm and external intercostals) increases intra-thoracic volume 2. This causes a decrease in intra-pleural pressure 3. Lungs expand, increasing volume and the air moves in, then pressure in the airways becomes lower (negative usually 2.506mmHg) 4. Air moves in (Patm\>Palv) 5. At end of inspiration pressures are equal Recoil of lungs and chest chest wall then occur
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boyles law
Pressure exerted by gas (in this case O2) in a closed container (in this case the lungs), is inversely proportional to the volume of gas in the container. Remember that this must occur at a constant temperature.
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3 ventilation factors
Pressure gradients, Airway resistance, Lung compliance
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Patm vs Palv
• Atmospheric pressure (P atm) at sea level =760 mmHg (This is the environment pressure around us) • Intra- alveolar (intrapulmonary) pressure (P alv)
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inspiration and expiration pressures
Inspiration \<760 mmHg Expiration \>760 mmHg
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intrapleural
(Pleural space surrounding the lungs) pressure (Ppl) • This does not equilibrate with the atmosphere, it is closed and fluid filled, it keeps lungs attached to thoracic cavity, as the muscles move the thoracic cavity \>756 mmHg (Neg) The chest wall exerts a distending pressure on the pleural space, which is transmitted to the alveoli to increase its volume, lower its pressure, and generate airflow inwards
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transmural pulmonary pressure
• This distending pressure is called the transmural pulmonary pressure (Ptp).
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pressures under physiological conditions (Ptp, Ppl, Palv)
• The P tp is always positive. • The P pl is always negative. • The P alv moves from slightly negative to slightly positive as we breathe. • For a given lung volume, the transpulmonary pressure is equal and opposite to the elastic recoil pressure of the lung • So it sucks the lungs out and sucks the lungs back in, ensuring the lungs don’t collapse
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what is airway resistance dependent on
It is dependent on the radius of the conducting airways, bronchiole smooth muscle contraction and relaxation
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airway resistance
the pressure difference between the alveoli and mouth, divided by the flow rate -originates from friction between air and mucosa
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resistance formula
Pressure1-Pressure2/ Flow
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Ohms Law
R=V/I
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Factors in Ariway Resistance. Bronchioconstriction and bronchiodilation
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laminar flow
Laminar flow is smooth flow
Resistance generated is proportional to the radius (r4).
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turbulent flow
Turbulent flow is irregular, chaotic, with Eddie currents.
It’s good for transferring heat (radiators try to enhance turbulent flow), but the resistance is high
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lung compliance
Refers to the ability of the lungs to stretch and recoil during ventilation
Elastic fibres- lung connective tissue allowing stretch and recoil
Water on surface of the alveoli- creating surface tension, enhancing recoil but opposing alveolar expansion
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Pulmonary Surfactant
Fluid secreted by the type II alveolar cells, which counteracts and balances the effect of water.
- decreases alveolar surface tension
- increases compliance
- softens recoil
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Surface Tension:
Liquid surface area becomes as small as possible, i.e., sphere
Tends to collapse the alveolus
Surface tension increase with -emphysema -age
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how does surfactant reduce surface tension
Type II alveolar cells extract fatty acids from blood and synthesis surfactant
Major component is dipalmitoyl phosphatidylcholine (DPPC)
Hydrophilic and hydrophobic ends repel each other and interfere with liquid molecule attraction
Lowers surface tension
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Why is surfactant important?
Increases lung compliance because surface forces are reduced.
Promotes alveolar stability
Prevents alveolar collapse: small alveoli are prevented from getting smaller, large alveoli are prevented from getting bigger
Surface tension tends to suck fluid from capillaries into alveoli: reduction of surface tension reduces hydrostatic pressure in tissue outside capillaries and keep lungs dry
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forces in/on the lung
keeps the alveoli stretch (open): transmural pressure gradient, pulmonary surfactant
Promote alveoli recoil (collapse): Elasticity of stretched pulmonary tissue fibers, alveolar surface tension
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Elastic vs non-elastic work
elastic work: respiratory muscles, length tension realtionships, fatigue
non-elastic work: viscous resistance, airway resistance (airway diseases, rapid respiration-turbulent flow, greater energy required)
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functions of circulation
Transport of O2 from lungs to tissues
Transport of CO2 from tissues to lungs
Transport metabolic waste from tissues to liver and kidney
Distribution of nutrients from gut and liver
Distribution of body water and electrolytes between compartments
Transport of immunogenically active substances
Transport of hormones
Assisting in thermoregulation by redistribution from core to skin
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structure of circulation
Arterial system 15%
Venous system 65%
Pulmonary circulation 10%
Cardiac chambers 5%
Capillaries 5%
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systemic vs pulmonary circulation in capillaries and veins
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systemic vs pulmonary circulation in arteries
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velocity formula for circulation
velocity=blood flow/area
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systemic capillary function (filtration and reabsorption)
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peripheral oedema causes
increased pressures (venous stasis), leaky capillaries or low oncotic pressure
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pulmonary oedema causes
1. pulmonary venous congestion (left heart failure) -\> raised hydrostatic pressure -cardiogenic pulmonary oedema
2. tight junction breakdown- non-cardiogenic pulmonary oedema (ARDS- acute respiratory distress syndrome)
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different valves in the heart
right- tricuspid valve
left- bicuspid valve (mitral valve)
aortic valve
pulmonary valve
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renin-angiotensin system
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Antidiuretic hormone
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GFR vs BP
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Different types of hypoxia
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circulation in different regions: brain and autoregulation
Brain:
- 2% body mass but 14% cardiac output.
- Grey matter very high rate oxidative metabolism (20% body total at rest)
- Cerebral blood flow protected at expense of other organs by sympathetic tone and CO2
Autoregulation:
-MAP 60-150mmHg autoregulation
- As PaCO2 increases so autoregulation disappears and CBF is determines by MAP
- As PaO2 falls below 50mmHg, then CBF increases
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circulation in different regions: renal and autoregulation
Renal blood flow:
- Kidneys 1% total body weight but 20% cardiac output reflecting filtration activity
- Too high a blood flow may lead to damage and insufficient reabsorption
- Two low a blood flow leads to ischaemia and a build up toxic metabolites (acute kidney injury)
Autoregulation:
-Constriction of afferent or efferent arteriole increases overall resistance & ¯ RBF
- Constriction of afferent decreases GFR
- Constriction of efferent increases GFR
- Myogenic & tubuloglomerular feedback both act to increase renal blood flow automatically when a decreased renal perfusion pressure is detected
- The renn-angiotensin system also regulates renal blood flow
Renin-angiotensin-aldosterone axis:
- Decreased blood pressure leads to deceased tubular flow which leads to the JG cells secreting renin which causes the production of angiotensin which is converted to angiotensin II
- Angiotensin II has effects on the kidney, vascular system, adrenal gland and brain to increase blood pressure
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circulation in the skin
Skin
Skin has no local metabolic control for its blood flow but is altered by ambient temperature effects on skin heat receptors and the sympathetic nervous system at AV anastomoses
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circulation in the skeletal muscle
Skeletal muscle mass 40% of body mass.Circulatory flow can increase up to 100 fold during exercise
- Control of flow is a complex interaction between the sympathetic n. system & locally derived vasodilatory metabolites
- Oxygen extraction increases 2-3X and mixed venous oxygenation can fall from 75% to 25%
- Adrenaline & the sympathetic nervous system enhance cardiac output & cerebral blood flow is maintained. Blood flow to the kidneys and GI tract is reduced
- The muscle pumps in the calf enhance the venous return to the heart
- During exercise the local regulatory factors (CO2, K+, H+, lactate, NO) override the sympathetic vasoconstrictor influences -FUNCTIONAL SYMPATHOLYSIS
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Sphlanic circulation
At rest 25% cardiac output to liver, spleen, stomach, pancreas & small & large bowel
-Splanchnic blood flow is altered by a large number of competing controls: myogenic & local factors (intrinsic) sympathetic/parasympathetic nervous system and hormones (extrinsic) leading to great variation
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liver blood flow
Hepatic circulation:70% portal vein and rest hepatic artery
Hepatic artery 15% cardiac output
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Portal systems
A part of the circulation that begins and ends in capillaries
-Examples include the hepatic portal system (left) where nutrients are transported from the intestines to the liver and the hypophyseal portal system where hormones are rapidly transported & exchanged between the hypothalamus and the anterior pituitary gland
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PaCO2
arterial partial pressure of CO2
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PaO2
pressure of O2 in the alveoli
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PvCO2
venous partial pressure of CO2
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Hypoxaemia
reduced PaO2 (arterial partial pressure of O2)
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SaO2
Saturation of haemoglobin with O2
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CoHb
Carboxyhaemoglobin which is Hb with CO bound to it
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O2 and CO2 Exchange
O2 brought in from the lungs to alveoli then diffuses into pulmonary capillaries
O2 then delivered to tissues, which use up the O2 and produce CO2 waste
CO2 is then diffused from the tissues to the pulomnary capillaries moving to the alveoli and removed into the lungs
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Interstitium
Microscopic space where the alveoli contact the blood capillaries
Alveoli has thin simple squamous epithelial wall
Pulmonary capillary also has a thin simple squamous epithelial wall
Interstitial space 0.5um
Red blood cell (erythrocytes) has the CO2
Alveoli has O2
Alveoli macrophages (phagocytose debris in the lungs)
Type II alveolar cells (secretes surfactant)
Type I cells (simple squamous epithelium)
500 million alveoli
Premature babies don’t produce enough surfactant, to keep air sacs open
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Partial pressure
Partial pressure is a measure of the concentration of the individual components in a mixture of gases, in this case O2 and CO2. The total pressure exerted by the mixture is the sum of the partial pressures of the components in the mixture
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O2 and CO2 partial pressure
The exchange of O2 and CO2 happens at the interstitium in the lungs and at the tissues
It moves like concentration (from higher to lower gradients)
There are known as partial pressure gradients (for gases) or diffusion gradients
Partial pressure can be replaced for the word ‘concentration’ of gas in a gas mixture
REMEMBER: Partial pressure gradients are not the same as Ventilation gradients!! (Total air in atmosphere and air) they are like a diffusion gradient of the gases.
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Oxygen Saturation SaO2
Blood -\> Red Blood cells (Erythrocytes) -\> Special protein that carries O2 -\> Haemoglobin
Haemoglobin varies according to gender, race and age O2. Measures in grams per deciliter (g/dL). Adult male: 13.8-17.2g/dL, Adult female: 12.1-15.1g/dL
Saturation 94-99% (normal range)
O2 saturation 88-92% (COPD normal range)
Below normal lower hypoxia
Conditions that can affect O2 saturation (asthma, pneumothorax, anaemie, PE, COPD, e.g., emphysema and chronic bronchitis)
O2 Saturation measures by Arterial blood gases or pulse oximetry haemoglobin (sickle cell anaemia)
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Diffusing capacity for CO (DLCO)
Test for assessment of lung function
Measures the ability of lungs to transfer gas from inhaled air to erythrocytes in the capillaries
Asthma, emphysema, pulmonary fibrosis
Breathe in CO (0.3% small amount), hold breath for 10s, exhale air.
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Respiratory Quotient (RQ):
The volume of CO2 released over the volume of O2 absorbed during respiration
It is a dimensionless number used in a calculation for basal metabolic rate when estimated from CO2 production to O2 absorption.
Uptake of O2 is a form of indirect calorimetry and is measured by a respirometer directly at the tissue or mouth.
It informs us which fuel source is being metabolised (fats, carbs, or proteins).
RQ\<1.0 excessive carbohydrate
PQ=Vol CO2/ Vol O2 absorbed
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CO2 in the blood
CO2 + H20 H2CO3 H+ + HCO3-
## Footnote
It is important to highlight the main role of CO2 in the blood: to regulate the pH of the blood.
More important than transporting CO2 to the lungs for exhalation
The conversion of carbonic acid (H2CO3) to a hydrogen and bicarbonate ion (H- + HCO3-) is almost instantaneous
A small amount of dissolved CO2 produced a small rise in hydrogen ions which alters the blood pH.
The proportion of CO2 to HCO3- is critical and explains why this occurs.
pH should be 7.4 in blood. Too high-acidosis, too low-alkalosis
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Carboxyhaemoglobin:
COHb is formed when Carbon Monoxide binds to the Ferrous Iron found in haemoglobin.
Haemoglobin's affinity for CO is 218 times greater than that for O2, which results in CO displacing O2 during competition for haemoglobin binding sites.
Low concentrations of CO in inhaled air can cause rapid formation of COHb; 0.1% CO can result in 50% of haemoglobin converting to COHb and notable clinical symptoms will arise within one hour.
Levels of 0.2% CO can lead to death within a few hours
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Methaemoglobin Low O2
Methaemaglobin (MetHb) arises when the Iron component in haemoglobin is oxidised so that it is in the ferric state (Fe3+).
MetHb is unable to bind O2 and therefore, cannot participate in respiratory function.
The main causes of pathological increase in MetHb concentration are -congenital and idiopathic methaemaglobinaemia caused by deficiency of coenzyme factor I -acquired MetHb, post exposure to chemicals (anaesthetics, nitrobenzene, specific antibiotics-dapsone and chloroquine or nitrites.
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Define resp failure
Lack of O2 exchanged from alveoli to erythrocytes, resulting in build up of CO2
Occurs due to inadequate gas exchange that lowers the O2 levels in the blood, life threatening leading to respiratory arrest with a PaO2 \<8.0 kPa.
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Respiratory Failure:
Lack of O2 exchanged from alveoli to erythrocytes, resulting in build up of CO2
Occurs due to inadequate gas exchange that lowers the O2 levels in the blood, life threatening leading to respiratory arrest with a PaO2 \<8.0 kPa.
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Type I resp failure-Hypoxaemia
Occurs due to ventilation-perfusion failure (V-Q), mismatch in the lungs that result in a lower gas exchange.
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Type I Pulmonary Embolism:
Lack of O2 exchanged from alveoli to erythrocytes, resulting in build up of CO2
Occurs due to inadequate gas exchange that lowers the O2 levels in the blood, life threatening leading to respiratory arrest with a PaO2 \<8.0 kPa.
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Type II Resp failure-Hypoxaemia and Hypercapnoea:
Occurs due to failure of ventilation, resulting in alveolar hypoventilation, patients will present symptoms and be unwell
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acute type II resp failure
can develop within minutes to hours, renal buffering does not have time to act, so HCO3- remains normal and pH lowers
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chronic type II resp failure
can develop over several days to weeks, to months when the kidneys excrete H2CO3 reabsorb HCO3- increasing its levels and slightly lowers pH
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hypoxia
inadequate level of O2 in tissue for cellular metabolism (asthma, emphysema)
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hypoxaemia
abnormally low arterial O2 (PaO2) in the blood (ARDS, PE)
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Causes of type I resp failure
Obstructive airways disease: severe asthma, COPD, bronchiectasis
Parenchymal disease: pulmonary fibrosis, ARDS, pulmonary oedema, pneumonia
Vascular disease: pulmonary hypertension, pulmonary emboli
Other: pneumothorax, right to left shunt
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type II resp failure causes
Chronic: COPD, severe chronic asthma, bronchiectasis, CF
Chest wall deformity: kyphoscoliosis, thoracoplasty, extensive pleural calcification, chest wall trauma obesity
Neuromuscular and peripheral nerve disorders: myopathies, muscular dystrophy, motor neurone disease, spinal cord injury, poliomyelities, Guillain-Barre syndrome, phrenic nerve injury, damage to diaphragm
Neuromuscular lung disorder: myasthenia gravis, botulism
Disorders of the respiratory centre: anaesthetitcs, respiratory depressants, sedatives, head injuries, central sleep apnoea, ms, cerebrovascular accident
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different types of hypoxia
Cytotoxic or Histotoxic hypoxia (Cyanide poisoning) Reduced ability to utilise O2
Circulatory or Stagnant hypoxia (heart failure) Reduced ability to deliver O2
Anaemic hypoxia (CO poisoning) Reduced ability to deliver O2
Hypoxaemic or hypoxic hypoxia (PaO2) Reduced ability to deliver O2
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five mechanisms of hypoxaemia
Hypoventilation
Low FiO2
Diffusion impairment
Shunt
V/Q mismatch
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5 mechanisms of hypoxaemia
Hypoventilation
Low FiO2
Diffusion impairment
Shunt
V/Q mismatch
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hypoventilation
When the tidal volume is lower so O2 lowers and CO2 increases
Low FiO2 partial pressure of inspired O2
A-a gradient, where PA-alveolar pressure and Pa= arterial pressure
PAO2-PaO2 ideally perfectly balanced
Tidal volume: breathing in and out normally 500ml of air.
Calulation of alveolar-arterial O2 gradient
e.g., Low FiO2 partial pressure of inspired O2
Normal person breathing room air, FIO2 = 21, PaCO2 = 4 kPa, PaO2 = 13 kPa
A- a gradient = 21 – (???
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low FiO2 high altitude
Fi Partial pressure of inspired O2, decreases as altitude increases. How do we know how much O2 diffuses into our blood?
Patm=760mmHg (101kPa) at sea level, the saturated vapour pressure is 47mmHg (6.3kPa) at sea level, the saturated vapour pressure is 47mmHg (6.3kPa) where O2 is 21% of the whole i.e., 0.21% O2)
Patm=760-46mmHg) x 0.21 = 0.21 150mmHg FiO2 at sea level
Or
Patm=101-6.3kPa x 0.21 ~ 20kPa FiO2 at sea level
Fi Partial pressure of inspired O2, decreases as altitude increases
P13000 ft= 420mmHg at 13,000ft, the saturated vapour pressure is 47mmHg where O2 is 21% of the whole i.e., (0.21% O2)
P13000ft= 420-46mmHg x 0.21 ~ 78mmHg FiO2 at 13,000ft
Or
P13000ft = 56-6.3kPa) x 0.21 ~ 10.4 kPa FiO2 at 13,000ft
What do we do? Give patient 80% high flow O2, they respond so FiO2 increases
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diffusion impairment
Diffusion between alveoli and capillary hindered due to blockage in the interstitial space (0.5m) in the interstitium
Responds to O2 etiher 80% of high flowing O2 90% using CPAP
Pulmonary fibrosis/exercising because the erythrocytes are moving faster through the blood (from 0.75s to higher speeds)
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shunting
Venous blood mixes with arterial blood
Extra pulmonary- (Cardiac) pediatric condition bypassess the lungs completely
Intrapulmonary- blood transported through the lungs without gas exchange. May occur due to alveoli filled with pus e.g., pneumonia
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V/Q mismatch
Where ventilation (V), is the air flow into and out of the alveoli and perfusion (Q) is the flow of blood to alveolar capillaries.
V/Q=0.8 ratio
Auto regulation in the Pulmonary blood vessels cause low O2 to constrict the blood vessels –vasoconstriction
BUT Auto regulation in the Systemic blood vessels cause low O2 to dilate the blood vessels –vasodilation
Flow = Delta P/ resistance
Ventilation (V) refers to the volume of gas inhaled and exhaled over a given time period (e..g, 1min)
V=Alevolar ventilation rate (AVR) x Respiration Rate (RR)
AVR= Tidal volume- Alveolar dead space
e..g, TV=500ml, Alveolar dead space=150ml and RR=12/min
500ml/breath-150ml/breath) x (12 breaths/min)
350ml x 12 min
AVR=4200ml/min
Ventilation and perfusion happen simultaneously
Perfusion (Q) refers to the total volume of blood reaching the pulmonary capillaries in a given time period
Perfusion= Cardiac output (CO) =5000ml/min
CO=HR x SV
If V/Q=4200ml/min, divided by 5000ml/min
So V/Q=0.84
V/Q mismatch leads to a low O2 saturation clinical conditions: pneumonia vs pulmonary embolism
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regional difference in pleural pressure
the apices of the lungs are relatively over ventilated and the bases are relatively over perfused
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physiologic dead space
Dead space is the fraction of tidal volume which does not participate in gas exchange
Conducting zone (mouth, pharynx, bronchi)-anatomical dead space
Respiratory zone- alveolar duct, terminal bronchioles, alveolus
Physiological dead space- ventilation increases in the alveoli but no or or decreased perfusion
Wasted ventilation
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management and treatment of resp failure I
Treatment of underlying conditions, e.g., asthma
Correcting hypoxaemia by maintaining O2 saturation between 94-98%
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management and treatment for resp II failure
Treatment of underlying conditions e.g., COPD
Administering controlled O2 aiming to keep saturation between 88-92%
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further management to initial resp failure treatment
noninvasive ventilation is administered (NIV) through a nasal cannula, simple face mask
High flow O2 is administered through a reservoir or re-breathe mask
Extremely hypoxic patients will be treated with pressure controlled ventilation such as CPAP, which delivers 90% of O2 via contiuous positive pressure, used in HDU
Non invasive ventilation for palliative care
Intubation and ventilation
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