Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Neuroanaesthesia PPT 7 Respiratoryphysiology And Acute Respiratory Failure Lecture Notes
RespiratoryPhysiology
&AcuteRespiratoryFailure
? Respiratory physiology is central to the
practice of Anaesthesia
The most commonly used anaesthetics-
the inhalational agents- depend on the
lungs for uptake and elimination.
The most important side effects of both
inhalational and intravenously
administered anaesthetics are primarily
respiratory.
FunctionsoftheRespiratory
System
? Gas Exchange
? O2, CO2
? Acid-base balance
? CO2 +H2O H2CO3 H+ + HCO3-
? Phonation
? Pulmonary defense
? Pulmonary metabolism and handling of
bioactive materials
6
Respiration
? The term respiration includes 3 separate
functions:
? Ventilation:
? Breathing.
? Gas exchange:
? Between air and capillaries in the lungs.
? Between systemic capillaries and tissues of
the body.
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? 02 utilization:
? Cellular respiration.
Ventilation
? Mechanical process that moves air
in and out of the lungs.
? [O2] of air is higher in the lungs
Insert 16.1
than in the blood, O2 diffuses from
air to the blood.
? C02 moves from the blood to the
air by diffusing down its
concentration gradient.
? Gas exchange occurs entirely by
diffusion:
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? Diffusion is rapid because of the
large surface area and the small
diffusion distance.
RespiratoryZone
? Region of gas
exchange
between air
and blood.
? Includes
respiratory
bronchioles
and alveolar
sacs.
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? Must contain
alveoli.
Alveoli
? Polyhedral in shape and clustered like units of honeycomb.
? ~ 300 million air sacs (alveoli).
? Large surface area (60?80 m2).
? Each alveolus is 1 cell layer thick.
? Total air barrier is 2 cells across (2 mm).
? 2 types of cells:
? Alveolar type I:
? Structural cells.
? Alveolar type II:
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? Secrete surfactant.
ConductingZone
? All the structures air
passes through before
reaching the respiratory
Insert fig. 16.5
zone.
? Warms and humidifies
inspired air.
? Filters and cleans:
? Mucus secreted to trap
particles in the inspired air.
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? Mucus moved by cilia to be
expectorated.
TracheobronchialTree:
a) Trachea- conduit for ventilation
? Clearance of tracheal &bronchial secretions
? Begins at the lower border of the cricoid cartilage
and extends to the level of the carina
? Average length of 10?13 cm
? The external diameters of the trachea is
approximately 2.3 cm coronally and 1.8 cm
sagitally in men and 2.0 cm & 1.4 cm,
respectively, in women
? The trachea bifurcates at the carina into the right
and left main stem bronchi
? Dichotomous division, starting with the trachea
and ending in alveolar sacs, is estimated to
involve 23 divisions.
? An estimated 300 million alveoli provide an
enormous membrane (50?100 m2 ) for gas
exchange in the average adult
? Gas exchange can occur only across the flat
epithelium, which begins to appear on
respiratory bronchioles
PulmonaryCirculation&
Lymphatics
? The lungs are supplied by two circulations,
pulmonary and bronchial
? The bronchial circulation arises from lt heart
? Along their courses, the bronchial vessels
anastomose with the pulmonary arterial
circulation and continue as far as the alveolar
duct.
? The pulmonary circulation normally receives the
total output of the right heart via the pulmonary
artery, which divides into rt and lt branches to
supply each lung
? Deoxygenated blood passes through the
pulmonary capillaries, where O2 is taken up and
CO2 is eliminated
? The oxygenated blood is then returned to the lt
heart by 4 main pulmonary veins (two from each
lung)
Innervation
? The diaphragm is innervated by the phrenic
nerves, which arise from the C3?C5 nerve roots.
? U/L phrenic nerve palsy only modestly reduces
most indices of pulmonary function (~ 25%).
? B/L phrenic nerve palsies produce more severe
impairment
? The vagus nerves provide sensory innervation to
the tracheobronchial tree
ThoracicCavity
? Diaphragm:
? Sheets of striated muscle divides anterior body cavity
into 2 parts.
? Above diaphragm: thoracic cavity:
? Contains heart, large blood vessels, trachea, esophagus,
thymus, and lungs.
? Below diaphragm: abdominopelvic cavity:
? Contains liver, pancreas, GI tract, spleen, and
genitourinary tract.
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? Intrapleural space:
? Space between visceral and parietal pleurae.
IntrapulmonaryandIntrapleural
Pressures
? Visceral and parietal pleurae are flush against each other.
? The intrapleural space contains only a film of fluid
secreted by the membranes.
? Lungs normally remain in contact with the chest walls.
? Lungs expand and contract along with the thoracic cavity.
? Intrapulmonary pressure:
? Intra-alveolar pressure (pressure in the alveoli).
? Intrapleural pressure:
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? Pressure in the intrapleural space.
? Pressure is negative, due to lack of air in the intrapleural
space.
TranspulmonaryPressure
? Pressure difference across the wall of the lung.
? Intrapulmonary pressure ? intrapleural pressure.
? Keeps the lungs against the chest wall.
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IntrapulmonaryandIntrapleural
Pressures(continued)
? During inspiration:
? Atmospheric pressure is > intrapulmonary
pressure (-3 mm Hg).
? During expiration:
? Intrapulmonary pressure (+3 mm Hg) is >
atmospheric pressure
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.
Boyle'sLaw
? Changes in intrapulmonary pressure occur as a
result of changes in lung volume.
? Pressure of gas is inversely proportional to its volume.
? Increase in lung volume decreases intrapulmonary
pressure.
? Air goes in.
? Decrease in lung volume, raises intrapulmonary
pressure above atmosphere.
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? Air goes out.
PhysicalPropertiesoftheLungs
? Ventilation occurs as a result of pressure
differences induced by changes in lung
volume.
? Physical properties that affect lung
function:
? Compliance.
? Elasticity.
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? Surface tension.
Compliance
? Distensibility (stretchability):
? Ease with which the lungs can expand.
? Change in lung volume per change in
transpulmonary pressure.
DV/DP
? 100 x more distensible than a balloon.
? Compliance is reduced by factors that produce
resistance to distension.
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Elasticity
? Tendency to return to initial size after
distension.
? High content of elastin proteins.
? Very elastic and resist distension.
? Recoil ability.
? Elastic tension increases during inspiration
and is reduced by recoil during expiration.
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SurfaceTension
? Force exerted by fluid in alveoli to resist
distension.
? Lungs secrete and absorb fluid, leaving a very thin film of fluid.
? This film of fluid causes surface tension.
? Fluid absorption is driven (osmosis) by Na+ active
transport.
? Fluid secretion is driven by the active transport of Cl- out
of the alveolar epithelial cells.
? H20 molecules at the surface are attracted to
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other H20 molecules by attractive forces.
? Force is directed inward, raising pressure in alveoli.
Surfactant
? Phospholipid produced by
alveolar type II cells.
? Lowers surface tension.
Insert fig. 16.12
? Reduces attractive forces of
hydrogen bonding by becoming
interspersed between H20
molecules.
? Surface tension in alveoli is
reduced.
? As alveoli radius decreases,
surfactant's ability to lower
surface tension increases.
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? Disorders:
? RDS.
? ARDS.
QuietInspiration
? Active process:
? Contraction of diaphragm, increases thoracic volume
vertically.
? Parasternal and external intercostals contract,
raising the ribs; increasing thoracic volume
laterally.
? Pressure changes:
? Alveolar changes from 0 to ?3 mm Hg.
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? Intrapleural changes from ?4 to ?6 mm Hg.
? Transpulmonary pressure = +3 mm Hg.
Expiration
? Quiet expiration is a passive process.
? After being stretched by contractions of the diaphragm and
thoracic muscles; the diaphragm, thoracic muscles, thorax, and
lungs recoil.
? Decrease in lung volume raises the pressure within alveoli
above atmosphere, and pushes air out.
? Pressure changes:
? Intrapulmonary pressure changes from ?3 to +3 mm Hg.
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? Intrapleural pressure changes from ?6 to ?3 mm Hg.
? Transpulmonary pressure = +6 mm Hg.
PulmonaryVentilation
Insert fig. 16.15
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Lung volumes and capacities
4 lung volumes:
tidal (~500 ml)
inspiratory reserve (~3100 ml)
expiratory reserve (~1200 ml)
residual (~1200 ml)
4 lung capacities
inspiratory (~3600 ml)
functional residual (~2400 ml)
vital (~4800 ml)
total lung (~6000 ml)
Terms Used to Describe Lung Volumes
and Capacities
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AnatomicalDeadSpace
? Not all of the inspired air reached the alveoli.
? As fresh air is inhaled it is mixed with air in anatomical
dead space.
? Conducting zone and alveoli where [02] is lower than
normal and [C02] is higher than normal.
? Alveolar ventilation = F x (TV- DS).
? F = frequency (breaths/min.).
? TV = tidal volume.
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? DS = dead space.
RestrictiveandObstructiveDisorders
? Restrictive disorder:
? Vital capacity is
reduced.
? FVC is normal.
Insert fig. 16.17
? Obstructive disorder:
? Diagnosed by tests
that measure the rate
of expiration.
? VC is normal.
? FEV1 is < 80%.
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GasExchangeintheLungs
? Dalton's Law:
? Total pressure of a gas mixture is = to the sum of the
pressures that each gas in the mixture would exert
independently.
? Partial pressure:
? The pressure that an particular gas exerts
independently.
? PATM = PN
+ P + P
2 + P02
C02
H20= 760 mm Hg.
? 02 is humidified = 105 mm Hg.
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? H20 contributes to partial pressure (47 mm Hg).
? P0 (sea level) = 150 mm Hg.
2
? PC0 = 40 mm Hg.
2
PartialPressuresofGasesinInspiredAir
andAlveolarAir
Insert fig. 16.20
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PartialPressuresofGasesinBlood
? When a liquid or gas (blood and alveolar air) are
at equilibrium:
? The amount of gas dissolved in fluid reaches a
maximum value (Henry's Law).
? Depends upon:
? Solubility of gas in the fluid.
? Temperature of the fluid.
? Partial pressure of the gas.
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? [Gas] dissolved in a fluid depends directly on its
partial pressure in the gas mixture.
SignificanceofBloodP0
2andPC02
Measurements
? At normal P0 2
arterial blood
is about 100
mm Hg.
? P0 level in
2
the systemic
veins is about
40 mm Hg.
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nPC0 is 46 mm Hg in the systemic veins.
2
nProvides a good index of lung function.
PulmonaryCirculation
? Rate of blood flow through the pulmonary
circulation is = flow rate through the systemic
circulation.
? Driving pressure is about 10 mm Hg.
? Pulmonary vascular resistance is low.
? Low pressure pathway produces less net filtration than
produced in the systemic capillaries.
? Avoids pulmonary edema.
? Autoregulation:
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? Pulmonary arterioles constrict when alveolar P02
decreases.
? Matches ventilation/perfusion ratio.
PulmonaryCirculation(continued)
? In a fetus:
? Pulmonary circulation has a higher vascular resistance,
because the lungs are partially collapsed.
? After birth, vascular resistance decreases:
? Opening the vessels as a result of subatmospheric
intrapulmonary pressure.
? Physical stretching of the lungs.
? Dilation of pulmonary arterioles in response to
increased alveolar P0 .2
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LungVentilation/PerfusionRatios
? Functionally:
Insert fig. 16.24
? Alveoli at
apex are
underperfused
(overventilated).
? Alveoli at the base are
underventilated
(overperfused).
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BrainStemRespiratoryCenters
? Neurons in the reticular
formation of the
medulla oblongata
form the rhythmicity
Insert fig. 16.25
center:
? Controls automatic
breathing.
? Consists of interacting
neurons that fire either
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during inspiration (I
neurons) or expiration
(E neurons).
BrainStemRespiratoryCenters(continued)
? I neurons project to, and stimulate spinal motor
neurons that innervate respiratory muscles.
? Expiration is a passive process that occurs when
the I neurons are inhibited.
? Activity varies in a reciprocal way.
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RhythmicityCenter
? I neurons located primarily in dorsal respiratory group
(DRG):
? Regulate activity of phrenic nerve.
? Project to and stimulate spinal interneurons that
innervate respiratory muscles.
? E neurons located in ventral respiratory group (VRG):
? Passive process.
? Controls motor neurons to the internal intercostal
muscles.
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? Activity of E neurons inhibit I neurons.
? Rhythmicity of I and E neurons may be due to
pacemaker neurons.
PonsRespiratoryCenters
? Activities of medullary rhythmicity center is
influenced by pons.
? Apneustic center:
? Promotes inspiration by stimulating the I
neurons in the medulla.
? Pneumotaxic center:
? Antagonizes the apneustic center.
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? Inhibits inspiration.
Chemoreceptors
? 2 groups of chemo-
receptors that monitor
changes in blood PC0 , P0 ,
2
2
and pH.
Insert fig. 16.27
? Central:
? Medulla.
? Peripheral:
? Carotid and aortic bodies.
? Control breathing indirectly via
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sensory nerve fibers to the
medulla (X, IX).
EffectsofBloodPC0 andpHon
2
Ventilation
? Chemoreceptor input modifies the rate and depth
of breathing.
? Oxygen content of blood decreases more slowly
because of the large "reservoir" of oxygen attached to
hemoglobin.
? Chemoreceptors are more sensitive to changes in PC0 .2
H
H
-
20 + C02 2C03 H+ + HC03
? Rate and depth of ventilation adjusted to
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maintain arterial PC02 of 40 mm Hg.
ChemoreceptorControl
? Central chemoreceptors:
? More sensitive to changes in arterial PC0 .2
H
H
20 + CO2 2C03 H+
? H+ cannot cross the blood brain barrier.
? C02 can cross the blood brain barrier and will form H2C03.
? Lowers pH of CSF.
? Directly stimulates central chemoreceptors.
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ChemoreceptorControlofBreathing
EffectsofBloodP0 onVentilation
2
? Blood PO2 affected by breathing indirectly.
? Influences chemoreceptor sensitivity to changes in PC02.
? Hypoxic drive:
? Emphysema blunts the chemoreceptor response to PC02.
? Choroid plexus secrete more HC0 -3 into CSF, buffering the
fall in CSF pH.
? Abnormally high PC02 enhances sensitivity of carotid bodies
to fall in P02.
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EffectsofPulmonaryReceptorson
Ventilation
? Lungs contain receptors that influence the brain stem
respiratory control centers via sensory fibers in vagus.
? Unmyelinated C fibers can be stimulated by:
? Capsaicin:
? Produces apnea followed by rapid, shallow breathing.
? Histamine and bradykinin:
? Released in response to noxious agents.
? Irritant receptors are rapidly adaptive receptors.
? Hering-Breuer reflex:
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? Pulmonary stretch receptors activated during inspiration.
? Inhibits respiratory centers to prevent undue tension on lungs.
Hemoglobinand02Transport
? 280 million
hemoglobin/RBC.
? Each hemoglobin has 4
polypeptide chains and
Insert fig. 16.32
4 hemes.
? In the center of each
heme group is 1 atom
of iron that can
combine with 1
molecule 02.
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Hemoglobin
? Oxyhemoglobin:
? Normal heme contains iron in the reduced form (Fe2+).
? Fe2+ shares electrons and bonds with oxygen.
? Deoxyhemoglobin:
? When oxyhemoglobin dissociates to release oxygen,
the heme iron is still in the reduced form.
? Hemoglobin does not lose an electron when it
combines with 02.
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Hemoglobin(continued)
? Methemoglobin:
? Has iron in the oxidized form (Fe3+).
? Lacks electrons and cannot bind with 02.
? Blood normally contains a small amount.
? Carboxyhemoglobin:
? The reduced heme is combined with carbon
monoxide.
? The bond with carbon monoxide is 210 times
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stronger than the bond with oxygen.
? Transport of 02 to tissues is impaired.
Hemoglobin(continued)
? Oxygen-carrying capacity of blood determined by its
[hemoglobin].
? Anemia:
? [Hemoglobin] below normal.
? Polycythemia:
? [Hemoglobin] above normal.
? Hemoglobin production controlled by erythropoietin.
? Production stimulated by PC0 delivery to kidneys.
2
? Loading/unloading depends:
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? P0 of environment.
2
? Affinity between hemoglobin and 02.
OxyhemoglobinDissociationCurve
Insert fig.16.34
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EffectsofpHandTemperature
? The loading and
unloading of O2
influenced by the
affinity of
Insert fig. 16.35
hemoglobin for 02.
? Affinity is decreased
when pH is
decreased.
? Increased
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temperature and
2,3-DPG:
? Shift the curve to the
right.
Effectof2,3DPGon02Transport
? Anemia:
? RBCs total blood [hemoglobin] falls, each RBC
produces greater amount of 2,3 DPG.
? Since RBCs lack both nuclei and
mitochondria, produce ATP through
anaerobic metabolism.
? Fetal hemoglobin (hemoglobin f):
? Has 2 g-chains in place of the b-chains.
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? Hemoglobin f cannot bind to 2,3 DPG.
? Has a higher affinity for 02.
C02Transport
? C02 transported in the blood:
? HC0 -3 (70%).
? Dissolved C02 (10%).
? Carbaminohemoglobin (20%).
ca
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H20 + C02 H2C03
High PC02
ChlorideShiftatSystemicCapillaries
? H
-
20 + C02 H2C03 H+ + HC03
? At the tissues, C02 diffuses into the RBC; shifts the
reaction to the right.
? Increased [HC0 -3] produced in RBC:
? HC0 -
3 diffuses into the blood.
? RBC becomes more +.
? Cl- attracted in (Cl- shift).
? H+ released buffered by combining with
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deoxyhemoglobin.
? HbC02 formed.
? Unloading of 02.
CarbonDioxideTransportandChloride
Shift
Insert fig. 16.38
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AtPulmonaryCapillaries
? H
-
20 + C02 H2C03 H+ + HC03
? At the alveoli, C02 diffuses into the alveoli;
reaction shifts to the left.
? Decreased [HC0 -
-
3 ] in RBC, HC03 diffuses into the
RBC.
? RBC becomes more -.
? Cl- diffuses out (reverse Cl- shift).
? Deoxyhemoglobin converted to oxyhemoglobin.
? Has weak affinity for H+.
? Gives off HbC02.
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ReverseChlorideShiftinLungs
Insert fig. 16.39
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RespiratoryAcidosis
? Hypoventilation.
? Accumulation of CO2 in the tissues.
? PCO2 increases.
? pH decreases.
? Plasma HCO -3 increases.
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RespiratoryAlkalosis
? Hyperventilation.
? Excessive loss of CO2.
? PCO2 decreases.
? pH increases.
? Plasma HCO -3 decreases.
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VentilationDuringExercise
? During exercise, breathing
becomes deeper and more rapid.
? Produce > total minute volume.
? Neurogenic mechanism:
Insert fig. 16.41
? Sensory nerve activity from
exercising muscles stimulates
the respiratory muscles.
? Cerebral cortex input may
stimulate brain stem centers.
? Humoral mechanism:
? PC0 and pH may be different at
2
chemoreceptors.
? Cyclic variations in the values
that cannot be detected by
blood samples.
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AcuteRespiratoryFailure
? Results from inadequate gas exchange
? Insufficient O2 transferred to the blood
? Hypoxemia
? Inadequate CO2 removal
? Hypercapnia
ClassificationofRF
? Type 1
? Type 2
? Hypoxemic RF
? Hypercapnic RF
? PaO2 < 60 mmHg with ? PaCO2 > 50 mmHg
normal or PaCO2
? Hypoxemia is common
qAssociated with acute ? Drug overdose,
diseases of the lung
neuromuscular disease,
qPulmonary edema
chest wall deformity,
(Cardiogenic,
COPD, and Bronchial
noncardiogenic (ARDS), asthma
pneumonia, pulmonary
hemorrhage, and collapse
PathophysiologiccausesofAcuteRF
Hypoventilation
V/P mismatch
Shunt
Diffusion
abnormality
ClassificationofRespiratoryFailure
Fig. 68-2
Mechanismsofhypoxemia
? Alveolar hypoventilation
? V/Q mismatch
? Shunt
? Diffusion limitation
AlveolarHypoventilation
Restrictive lung disease
CNS disease
Chest wall dysfunction
Neuromuscular disease
Perfusionwithoutventilation
(shunting)
Intra-pulmonary
? Small airways occluded ( e.g asthma, chronic bronchitis)
? Alveoli are filled with fluid ( e.g pulm edema, pneumonia)
? Alveolar collapse ( e.g atelectasis)
Deadspaceventilation
? DSV increase:
? Alveolar-capillary interface destroyed e.g
emphysema
? Blood flow is reduced e.g CHF, PE
? Overdistended alveoli e.g positive-
pressure ventilation
Diffusionlimitation
?Severe emphysema
?Recurrent pulmonary emboli
?Pulmonary fibrosis
?Hypoxemia present during exercise
DiffusionLimitation
Fig. 68-5
Hypercarbia
? Hypercarbia is always a reflection of inadequate
ventilation
? PaCO2 is
? directly related to CO2 production
? Inversely related to alveolar ventilation
PaCO2 = k x VCO2
VA
Hypercarbia
? When CO2 production increases, ventilation
increases rapidly to maintain normal PaCO2
? Alveolar ventilation is only a fraction of total
ventilation
VA = VE ? VD
? Increased deadspace or low V/Q areas may
adversely effect CO2 removal
? Normal response is to increase total ventilation
to maintain appropriate alveolar ventilation
HypercapnicRespiratoryFailure
? Imbalance between ventilatory supply
and demand
EtiologyandPathophysiology
? Airways and alveoli
? Asthma
? Emphysema
? Chronic bronchitis
? Cystic fibrosisS
EtiologyandPathophysiology
? Central nervous system
? Drug overdose
? Brainstem infarction
? Spinal chord injuries
EtiologyandPathophysiology
? Chest wall
? Flail chest
? Fractures
? Mechanical restriction
? Muscle spasm
EtiologyandPathophysiology
? Neuromuscular conditions
? Muscular dystrophy
? Multiple sclerosis
DiagnosisofRF
1?Clinical(symptoms,signs)
? Hypoxemia
? Hypercapnia
? Dyspnea, Cyanosis
? Cerebral blood flow,
? Confusion, somnolence, fits and CSF Pressure
? Tachycardia, arrhythmia
? Headache
? Tachypnea (good sign)
? Asterixis
? Use of accessory ms
? Papilloedema
? Nasal flaring
? Warm extremities,
collapsing pulse
? Recession of intercostal ms ? Acidosis (respiratory, and
? Polycythemia
metabolic)
? Pulmonary HTN,
? pH, lactic acid
Corpulmonale, Rt. HF
RespiratoryFailure
Symptoms
? CNS:
? Headache
? Visual Disturbances
? Anxiety
? Confusion
? Memory Loss
? Weakness
? Decreased Functional Performance
RespiratoryFailure
Symptoms
Cardiac:
Orthopnea
Peripheral edema
Chest pain
Other:
Fever, Abdominal pain, Anemia, Bleeding
Clinical
? Respiratory compensation
? Sympathetic stimulation
? Tissue hypoxia
? Haemoglobin desaturation
Clinical
? Respiratory compensation
? Tachypnoea RR > 35 Breath /min
? Accessory muscles
? Recesssion
? Nasal flaring
? Sympathetic stimulation
? Tissue hypoxia
? Haemoglobin desaturation
Clinical
? Respiratory compensation
? Sympathetic stimulation
? HR
? BP
? Sweating
Tissue hypoxia
? Altered mental state
? HR and BP (late)
? Haemoglobin desaturation cyanosis
RespiratoryFailure
LaboratoryTesting
Arterial blood gas
PaO2
PaCO2
PH
Chest imaging
Chest x-ray
CT sacn
Ultrasound
Ventilation?perfusion scan
ManagementofARF
? ICU admission
? 1 -Airway management
? Endotracheal intubation:
? Indications
? Severe Hypoxemia
? Altered mental status
? Importance
? precise O2 delivery to the lungs
? remove secretion
? ensures adequate ventilation
ManagementofARF
? Correction of hypoxemia
? O2 administration via nasal
prongs, face mask,
intubation and Mechanical
ventilation
? Goal: Adequate O2
delivery to tissues
? PaO2 = > 60 mmHg
? Arterial O2 saturation
>90%
Indicationsforintubationand
mechanicalventilation
? Innability to protect the airway
? Respiratory acidosis (pH<7.2)
? Refractory hypoxemia
? Fatigue/increased metabolic demands
? impending respiratory arrest
? Pulmonary toilet
ManagementofARF
? Mechanical ventilation
? Increase PaO2
? Lower PaCO2
? Rest respiratory ms
(respiratory ms fatigue)
? Ventilator
? Assists or controls the
patient breathing
? The lowest FIO2 that
produces SaO2 >90% and
PO2 >60 mmHg should be
given to avoid O2 toxicity
ManagementofARF
? PEEP (positive End-
Expiratory pressure
? Used with mechanical ventilation
? Increase intrathoracic pressure
? Keeps the alveoli open
? Decrease shunting
? Improve gas exchange
? Hypoxemic RF (type 1)
? ARDS
? Pneumonias
ManagementofARF
? Noninvasive
Ventilatory support
(IPPV)
? Mild to moderate RF
? Patient should have
? Intact airway,
? Alert, normal airway
protective reflexes
? Nasal or full face mask
? Improve oxygenation,
? Reduce work of breathing
? Increase cardiac output
? AECOPD, asthma, CHF
ManagementofARF
? Treatment of the
underlying causes
? After correction of hypoxemia,
hemodynamic stability
? Antibiotics
? Pneumonia
? Infection
? Bronchodilators (COPD, BA)
? Salbutamol
? reduce bronchospasm
? airway resistance
ManagementofARF
? Treatment of the
underlying causes
? Physiotherapy
? Chest percussion to loosen
secretion
? Suction of airways
? Help to drain secretion
? Maintain alveolar inflation
? Prevent atelectasis, help
lung expansion
ManagementofARF
? Weaning from mechanical ventilation
? Stable underlying respiratory status
? Adequate oxygenation
? Intact respiratory drive
? Stable cardiovascular status
? Patient is a wake, has good nutrition, able to cough and
breath deeply
This post was last modified on 07 April 2022