applied respiratory physiology: part 1
DESCRIPTION
Ouchh!. Applied respiratory physiology: part 1. b y; Dr Mohd Ridhwan bin Mohd Noor Intensivist HSNZ 2013. Pre master basic science. Knowledge decay after specialist graduation. Content . Functional anatomy Deadspace / lung volumes/ shunts Ventilation/perfusion abnormalities - PowerPoint PPT PresentationTRANSCRIPT
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Applied respiratory physiology: part 1
by;
Dr Mohd Ridhwan bin Mohd Noor
Intensivist
HSNZ 2013
Pre master basic science
Ouchh!
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Knowledge decay after specialist graduation
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Content 1. Functional anatomy
2. Deadspace/ lung volumes/ shunts
3. Ventilation/perfusion abnormalities
4. Control of respiration
5. Non respiratory functions of lungs
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Functional anatomy• Nose, mouth & pharynx humidify & filter the air gases
• Larynx is 18 mm in diameter & 11 cm in length
• Trachea divides to main stem bronchus at carina (T4)
• Bronchi divides 23 times (generations) & the first 16 are
termed conducting zone & forms anatomical deadspace
• Generation 17-23 where gas exchange occurs with 300
million alveoli & about 2-3 litres in volume
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• Consists of 3 type of cells;
1. Type 1
• Provide thin layer of cytoplasm & cover 80% of gas
exchange zone
2. Type 2
• Formation of surfactant & other enzymes
3. Type 3
• Maintain lungs defense system – alveolar macrophages
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Weibels classification of airways
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Clinical points
• ETT should be 1-2 cm above carina or at T3
• Right main bronchus divides from trachea at less acute
angle, therefore prone to endobronchial intubation
• ® upper lobe bronchus arises few cm from carina,
therefore for one lung ventilation (L) double lumen
ETT is favored to avoid risk of ® upper lobe collapse
with ® double lumen tube
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Dead space
• Def; lung volume that does not participate in gas exchange
(wasted ventilation) or ventilation without perfusion
• Types:
1. Anatomical deadspace
2. Physiological deadspace
3. Alveolar deadspace
4. Apparatus deadspace
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Anatomical deadspace
• Volume of conducting airways (150 mls in
adults)
• Mostly atmospheric gas & it’s exhaled gas
before CO2 flowing to the alveoli & expired
• Influenced by age, position, height,
hypoventilation, atropine, hypothermia
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Fowler’s methods (anatomical deadspace)
• Subject breathing to
pneumatachograph &
rapid nitrogen analyser
• Subject breaths 100%
of O2 & N2
concentration plotted
against time & volume
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Alveolar deadspace
• Part of inspired gas that enter the alveoli BUT
does not participate in gas exchange
• Represents ventilated but underperfused alveoli
• Can be measured by comparing PAO2 & PaCO2
• Negligible in healthy adult & PACO2 almost
equal PaCO2
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Causes ETCO2 < PaCO2
1. Low cardiac output or hypotension
2. High inspiratory pressure esp high PEEP
3. Pulmonary embolus
4. Posture changes – leading to changes in
regional perfusion
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Physiological deadspace
• Alveoli + anatomical deadspace
• Part of tidal volume not participate in gas exchange
• Calculated using Bohr equation;
Vd = PaCO2 – PECO2
Vt PaCO2
• Normally ~ 30% of tidal volume
• Clinical: increase in physio deadspace cause alveolar ventilation
reduced unless compensatory increase in minute volume e.g. COPD
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Lung volumes
Spirometry Tacing in adult male
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Lung volumes
The volume (per kg)
• Residual volume 15-20 mls
• Expiratory reserve volume
15 mls
• Tidal volume 6-8 mls
• Inspiratory reserve volume
45 mls
The capacities (per kg)
• Total lung capacity 75-80
mls
• Vital capacity 60-70 mls
• Inspiratory capacity 50 mls
• Funtional residual capacity
30 mls
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Which volumes & capacities can’t be measured by spirometry?
1. Residual volume
2. Any capacities which contain residual
volumes
– FRC
– Total Lung Capacity (TLC)
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Functional residual capacity (FRC)
• Def: volume of gas which remains at the end
of normal expiration (FRC = RV + ERV)
• It is a balance point between tendency of
the chest wall to move outward & tendency
of the lungs to collapse
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Forces exerted on the thorax
The tendency of the chest wall and diaphragm to separate from the lungs is the reason why intrapleural pressure is negative
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Functions of FRC
1. Oxygen store
2. Buffer to maintain a steady arterial pO2
3. Prevent atelectasis
4. Minimise work of breathing (by keeping the lungs on
the steep part of the compliance curve)
5. Minimise pulmonary vascular resistance
6. Minimise V/Q mismatch
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1. FRC as oxygen store
• At room air PAO2 of 100 mmHg & FRC of 2200 mls,
the lungs contain 290 mls of O2.
• Pre-oxygenation with 100%, it can increase up to
1800 mls of O2 in the lungs
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2. Buffer for arterial PO2
• Continuous presence of gas containing in the
lungs converts the intermittent tidal delivery
into continuous availability of O2 for gas
exchange.
• Prevent large swings in PaO2 during
ventilatory cycle
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3. Prevent atelectasis
• FRC maintain partial state of partial inflation
in the lungs & prevent atelectasis
• At a balance point between the tendency of
the chest wall to move outward & the
tendency of the lung to collapse
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4. Minimize work of breathing
– At FRC, the lung work at the steep part of
compliance curve
5. Minimise pulmonary vascular resistance
– PVR varies with lung volume, high at both high
and small lung volume
– PVR lowest at FRC
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PVR & lung volume
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6. Minimize V/Q mismatch
– FRC prevent lung closure at tidal ventilation &
minimize ventilation abnormality
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Measurement of FRC
1. Gas dilution methods (nitrogen
washout/helium washin)
– Subject rebreathing from closed circuit that contain
initial volume (V1) & concentration of helium (He1)
– After period of rebreathing final helium (He2)
measured
V1 x (He1) = (V1 + FRC) x (He2)
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Factors affecting FRC
Increase
• Height
• Changing from supine to
erect position
• Decreased lung elastic
recoil (e.g. emphysema)
• PEEP
Decrease
• Obesity
• Muscle paralysis
• Changing from erect to supine
• Pregnancy
• Anaesthesia
• Pulmonary ds causing increased
elastic recoil of the lungs
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2. Body plethysmography
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Closing capacity
• Lung volume at which airways start to close in
expiration ( CC = CV + RV)
• Factors increasing CC;
– Increasing age
– Smoking/asthma/emphysema/bronchitis
– Prolonged recumbency
– Increase left atrial pressure
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Closing volume measurement
Single breath Nitrogen washout
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Relationship between FRC and closing capacity
66 yrs
44 yrs
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Ventilation-perfusion abnormalities
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Describe West’ zones of the lung
• Describe relationships of pulmonary arterial, venous
& alveolar pressure in zones from apex to the base
• Changes occur due to gravity that cause distension
of vessels at the upright lung base & compression at
the apex
• PAP decrease by 1 cmH2O per cm vertical distance
of the lung
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• At the base PAP 10 cmH2O (16 26) & PVP
fr 11-21 cmH2O
• At the apex PAP 15 cmH2O (16 1) &
venous pressure fr. 11 to -4 cmH20
# need to put head down position to avoid air embolism
during CVC insertion#
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West’s zones
• Zone 1: alveolar
pressure exceed
arterial pressure.
Creating no flow in
apex and deadspace
# Contribute to deadspace. Rarely occur in healthy subject but in hypotension, hemorrhage or use of PEEP will increase zone 1.#
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West’s zones
• Zone 2; Pa exceeds PA
but PA still above PV on
expiration. The flow or
perfusion depends on
difference ( Pa – PA) &
called waterfall effect
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West’s zones• Zone 3; Pv more than PA in
inspiration & expiration.
Flow depend on (Pa –Pv).
• Pulmonary blood flow is
constant in this region &
provide optimal condition
for gas exchange
#Swan-Ganz should float here posteriorly in supine position#
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West’s zone
• Zone 4: the lung has
positive interstitial
pressure (PE, mitral
stenosis, pulmonary
edema)
• Flow depends on difference
between Pa and Pi
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What the 7 differences between apex and base of lungs?
• Alveoli at the top of the lungs;
– Larger at end-expiration
– Have lower ventilation
– Have lower perfusion
– Have higher V/Q ratio (3.3 vs 0.63)
– Higher pO2 (132 at apex, 89 at base)
– Lower pCO2 (28 at apex, 42 at base)
– Higher pH (7.51 vs 7.39)
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Shunts
• True shunts is perfusion without ventilation (V/Q = 0)
• Refers to blood that enter arterial system without
passing ventilated areas of the lungs
• Effects;
– Reduce PaO2
– Increase A-a gradient
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Venous admixture
• Amount of mixed venous blood has to be
added to pulmonary end capillary blood to
see drop in arterial PaO2
• Sometimes used interchangeably with shunts
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2 main sources of blood contribute to venous
admixture
1. True shunts – 2 sources
– Bronchial vein
– Thebesian vein
2. Blood from alveoli with V/Q less than 1 e.g.
atelectasis, consolidated area, edema
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Recollection
V/Q = 1
V/Q < 1V/Q > 1
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Shunts vs Venous admixture
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Shunt equation
Total flow = Qt
Shunted flow = Qs
Flow thro lungs = Qt - Qs
Shunt O2 content =
CvO2
Total O2 delivery = O2 delivery from ventilated lungs + O2 delivery from shunt
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O2 flux/delivery = cardiac output x O2 content
Qt x Ca = (Qt – Qs) x CcO2 + (Qs x CvO2)
Qs = (CcO2 – CaO2)
Qt (CcO2 – CvO2
Total O2 delivery = O2 delivery from ventilated lungs + O2 delivery from shunt
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Finally what we get…..
V/Q = ∞
V/Q = 0
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What methods used to measure V/Q inequalities?
1. A-a oxygen gradient (normal 5-15 mmHg)
– Need alveolar gas equation PAO2= FiO2 x (760-47) –
(PaCO2/R) R = 0.8
– Increased in V/Q mismatch, shunting, diffusion
abnormalities
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Measurement V/Q abnormalities (2)……
2. Shunt equation
– For low V/Q unit
3. Bohr equation
– For high V/Q unit
4. PaCO2 – ETCO2 difference
– ETCO2 normally 2-5 mmHg lower than PaCO2
– Increase in high alveolar deadspace (PE, low cardiac
output, venous air embolism)
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Pulmonary blood flow & resistance
• Mixed venous blood frm RV main PA branches
of PA with bronchi/bronchioles central acinar
arterioles pulm capillaries small peripheral
acinar pulm veins pulm vein with
bronci/bronchioles 4 main pulm vein LA
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Difference between pulmonary and systemic circuit
• Pulmonary is low pressure conduit (mean PAP 15 mmHg) (25/8)
• More pulsatile than systemic circuit
• Vessel much thinner
• Not all vessel are open at resting CO, increase flow recruitment & distension
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Factors affecting pulmonary vessels
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Pulmonary vascular resistance
1. Lung volume
– Both low and high lung volume with increase
PVR
2. Hypoxic pulmonary vasoconstriction
3. Metabolic substance
PVR = 80 x (MPAP –PCWP)/CO
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Hypoxic pulmonary vasoconstriction
• Reflex vasoconstrictive effect of low alveolar PO2
• When alveoli are not ventilated HPV will effectively
shunt the blood away frm this alveoli to a better
ventilated unit
• Will reduce V/Q in equalities in the lungs &
improving oxygenation esp. in condition like LVF,
pulmonary edema
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HPV…so what?
• Particular interest for anesthetist;
1. Effect of volatile agent on HPV
2. Role of HPV during one lung anaesthesia
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Etiology of hypoxemia…..anyone?
1. Low inspired FiO2
2. Hypoventilation
3. Deadspace
4. Shunts
5. Increase diffusion capacity
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Control of respiration
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• Control of breathing is about supply and
demand
• Resp. system as supplier of oxygen &
provide the blood (road system) to the cells
(consumer) to perform aerobic metabolism
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2 levels of control
Local control
• Location: alveoli, capillaries &
bronchioles
• Role; ensure gas & blood go to
appropriate part of lungs for
efficient gas exchange
• When: changes in CO2 and O2
• Mechanism: local adjustment to
blood flow (perfusion) & oxygen
delivery (alveolar ventilation) to
alveolar
Central control
• Location: RC located in medulla
oblongata & pons and modified by
sensory neuron (peripheral & CSF)
and higher centre
• Role: adjust the depth & rate of
ventilation
• When: during normal breathing &
during larger demand
• Mechanism: involuntary reflex via
sensory feedback and voluntary
control via RC
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Local control of lung perfusion
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Local control of alveolar ventilation
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Local control tries to reduce V/Q imbalance………..
• Common value for V/Q ratio is 0.8• Local control aims at maintaining optimal V/Q
ratio
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Central controlInvoluntary control
• Direct the depth & rate of
breathing via output from
respiratory centre
• Modified by influence from
receptors from the lungs and
CSF to ensure appropriate
levels of ventilation
Voluntary control
• Influenced indirectly from
cerebral cortex & affect the
output of respiratory centres in
the medulla oblongata
• Influential factors include
emotion, anticipation of
exertion & activities requiring
alteration to normal breathing.
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Respiratory centers and breathing
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• DRG is part of NTS which obtain info from
mechano & chemoreceptors, and project to
neuron of phrenic nerve which supply
diaphragm.
– Involves inspiratory process & timing
• VRG resides in nucleus ambiguus &
concerned with amplitude of respiration
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Respiratory control reflexes1. Sensors
– Peripheral & central chemoreceptors
– Muscle proprioceptors
– Lung, upper airway & pharyngeal receptors
2. Contoller
– Cortex (voluntary control)
– Brainstem (automatic control)
– Spinal cord (integration)
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3. Effectors
– Muscle of respiration (via spinal respiratory
motor efferents
– Lungs, pharynxs, laryngx (via cranial nerve
respiratory motor efferent)
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Hering-Breuer reflex
• Inflation & deflation reflexes occur during
forced breathing.
• With the cooperation of two reflexes, the
volume and stretch of the lungs is controlled
to avoid over expansion or over deflation
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Respiratory functions1. Non gas exchange functions
2. Gas exchange
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Non gas exchange functions
1. Blood reservoir functions
– Contain ~ 450 mls of blood
– Increase PAP will increase pulmonary blood volume in 2
mechanisms
• Recruitment (more vessel open up)
• Distension (open vessel got bigger)
– “Central blood volume” defined as volume in the lungs
(450 mls) and heart (350 mls) = 800 mls
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Intra-thoracic blood volume
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2. Elimination of volatile substance
– Alcohol, acetones, volatile anesthetics
3. Blood filter – thrombi, microaggregates etc.
4. Metabolic activity
– Activation of AT 1 to AT 2 (maintaining sodium balance)
– Inactivation of noradrenaline, bradykinin, serotonin & prostatglandin
5. Immunological – IgA secretion into bronchial mucus
6. Miscellaneous
– Protein syntesis (collagen, elastin)
– Surfactant (DPPC) synthesis
– CHO metabolism (mucin & proteoglycan synthesis)