Chapter 9
Acute Respiratory Failure
© 2007 McGraw-Hill Higher Education. All rights reserved.
Topics
• Acute respiratory
failure
• pathophysiology
• Hypoxemia
• Co2 retention
• Diaphragmatic failure
• Types of respiratory
failure
© 2007 McGraw-Hill Higher Education. All rights reserved.
Case Study #9: Ivan
• 45 yr old computer
programmer
• Well until 10 days ago
• Car accident
• Multiple fractures and
lung contusion
• Very SOB, in and out of
consciousness
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Physical exam #9: Ivan
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•
•
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•
2cd day exam
ill, with obvious dyspnea
Temp: 38.5 °C
BP: 125/60
Pulse: 110
Poor breath sounds
No edema
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Investigations
•
•
•
•
•
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Blood counts normal
Grossly abnormal chest radiograph
Whiteout pattern
– Alveolar exudate or edema
Blood gases
– Po2: 51
– Pco2: 45
– pH: 7.35
Diagnosis: Acute respiratory failure (due to trauma)
Treatment
– Intubated and mechanically ventilated (40% O2)
– Swan Ganz catheter inserted in RA (CVP)
– Patient died on 7th day
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Pathophysiology
• Also called ARDS (Adult
respiratory distress
syndrome)
• Respiratory failure
– When lungs fail to
oxygenate the blood or
prevent Co2 retention
– Gas exchange
• Hypoxemia and
hypercapnia
• Fig. 9-3
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Fig. 9-3
Pathophysiology: gas exchange
• Fig. 9-3
– I to A
• Pure hypoventilation
• Increase in Pco2 can be
predicted by alveolar
ventilation eq
• This pattern occurs in
some diseases and
narcotic overdose
– normal to B
• Severe VA/Q mismatch
• Resp failure of COPD
• O2 therapy results in B
to F (there resp drive is
driven by hypoxemia)
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Physiology and Pathophysiology
of gas exchange
• Normal to C
– Severe interstitial lung
disease
– Severe hypoxemia but
no hypercapnia due to
hyperventilation
• Normal to D
– Some ARDS patients
– So they follow D to E
with O2 therapy
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Hypoxemia of Respiratory Failure
• Four mechanisms of
hypoxemia
– Hypoventilation
– Diffusion impairment
– Shunt
– VA/Q mismatch
• Respiratory failure
– All can contribute
– VA/Q mismatch most
important
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Hypoxemia
• Mild hypoxemia
– Few physiologic
problems
– Po2 of ~ 60 mmHg
still about 90%
saturation
– When Po2 falls below
40-50 mmHg
• CNS vulnerable
–Headache,
somnolence,
clouding of
consciousness
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Hypoxemia
• Tachycardia
– SNS activity
increased
• Heart failure
– If heart disease is
present
• Renal function impaired
• Pulm hypertension
– Due to hypoxic VC
• Tissue hypoxia
– Major culprit here
– Increased anaerobic
metabolism causes
fall in pH
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Carbon dioxide Retention
• Two mechanisms
– Hypoventilation
• Pco2 = Vco2/VA
– VA/Q mismatch
• Inefficient gas exchange
• Release of hypoxic VC due
to high O2 therapy
– Some patients depend
on hypoxic ventilatory
drive; despite mild
hypercapnia
– Thus, lower O2
concentration (just
enough to raise PaO2)
• Co2 retention
– Increases cerebral BF
• Headache, elevated CSF
pressure
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Acidosis of resp failure and diaphragm
fatigue
• Acidosis
– Co2 retention
– Metabolic acidosis
• Diaphragm fatigue
– Due to prolonged
elevations in work of
breathing
• Hypoventilation
• Co2 retention
• Sever hypoxemia
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Types of respiratory failure
• Acute overwhelming lung
disease
– Bacterial or viral
pneumonia
– Pulm embolism
– Exposure to toxic gases
(chlorine, nitrogen oxides)
• Neuromuscular disorders
– Causes
• 1) depression of
breathing centers
(drugs)
• 2) diseases of medulla
(encephalitis, trauma,
hemorrhage)
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Fig 9-4
Types of respiratory failure
• 3) Abnormal spinal
conduction pathways
– High cervical
dislocation
• 4) Anterior horn disease
– Polio
• 5) Disease of nerves to
respiratory musculature
– Guillain-Barre
syndrome
• 6) Diseases of
neuromuscular junction
– Myashtenia gravis
and
anticholinesterase
poisoning
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Types of respiratory failure
• 7) Diseases of respiratory
musculature
– Muscular dystrophy
• 8) Thoracic cage
abnormalities
– Crushed chest
• 9) Upper airway
obstruction
– Tracheal compression
• Essential features
– Hypoventilation
– Co2 retention
– Hypoxemia
– Respiratory acidosis
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Acute or Chronic lung disease
• Contains those pts with
– Chronic bronchitis,
emphysema, asthma
and cystic fibrosis
– Those with COPD have
slow downhill slide
• Increasingly severe
hypoxemia and
hypercapnia over
the years
• Infection usu,
pushes these pts
over the edge
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Acute Respiratory Distress Syndrome
• Acute respiratory failure
• Many causes
– Trauma
– Aspiration
– Sepsis
– Shock
• Early
– Interstitial and alveolar
edema
– Hemorrhage, debris in
alveoli, atelectasis
• Later
– Hyperplasia
– Damaged alveolar
epithelium becomes
lined with type II
alveolar cells
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Acute respiratory distress syndrome
• Pathogenesis
– Unclear
– Damage to type I cells
– Accum. Of neutrophils
• Cause release of histamine,
bradykinin and platelet
activating factor
– Oxygen radicals and
cyclooxygenase products
(thromboxane, leukotrienes and
prostaglandins
• Pulm function
– Impaired
– Lungs become stiff
– Severe VA/Q mismatch
– Maybe 50% low VA/Q
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Infant Respiratory Distress Syndrome
• Much in common with
ARDS
– Hemorrhagic edema
– Atelectasis
– Fluid and debris in
alveoli
– Profound hypoxemia
– High degree of VA/Q
inequality
• May also have R to L
shunt (foramen ovale)
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IRDS
• Chief cause
– Lack of surfactant
• Surfactant system
matures late in
fetal life
–Check
lecithin/sphingo
myelin ratio of
amniotic fluid
• Treatment
–Instillation of
surfactant
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Oxygen therapy
• Response depends on cause
of hypoxemia
– Hypoventilation
• Small increases in PiO2
work very well
– PAO2 = PiO2 –[PaCO2/R]
• PaO2 increases about 1
mmHg per mmHg
increase in PiO2
– Diffusion impairment
• O2 also very effective
• Increases driving
pressure
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Oxygen therapy
• VA/Q mismatch
– O2 administration can be
effective
– Cautions
• If regions of the lung
are poorly ventilated
(low VA/Q); takes a
while to wash out the
N2 and raise the PAO2
• Oxygen therapy may
cause poorly
ventilated areas to
become nonventilated (due to
collapse); shunt
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Oxygen therapy
• Shunt
– Does not respond well to
Oxygen therapy
• Blood bypasses ventilated
alveoli and does not benefit
from the additional PAO2
– Thus, 100% is a good
way to detect shunt;
how?
• However, may raise PaO2
enough
– Dissolved Po2 can rise
from 0.3 to 1.8 ml/dl
(PAO2 increase from 100
to 600)
• Note increase in PaO2 for
person with 30% shunt (PaO2
from 55 to 110; increases
SaO2 by about 10%)
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Oxygen delivery: other factors
• Hemoglobin conc.,
position of O2-Hb diss.
Curve, Qc, distribution of
blood flow
– Both [Hb] and Qc
effect O2 delivery
(QO2) in the following
way
• Qo2 = Qc X CaO2
–CaO2 = 1.39 x
[Hb] x SaO2 (%)
+ dissolved
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Position of O2-Hb curve and
blood flow distribution
• Rearrangemnt of the
Fick eq. yields the
following
– CvO2 = CaO2 –[Vo2/Qc]
– Or
–
PcapO2 = PaO2 –[mVo2/Qm]
• Thus, CvO2 and
PcapO2 fall if Cao2
(PaO2) or Qc falls
• CaO2 – Po2
relationship depnds
on position of O2-Hb
curve
– Curve is shifted to
the right by chronic
hypoxemia (2,3
DPG)
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Hazards of O2 therapy
• CO2 retention
– In those with Hypoxic drive
• Give lower O2 conc
– 24-30%
• O2 toxicity
– High O2conc over time can
damage lung
• Swollen cap
endothelium,
replacement of alveolar
type I with type II cells,
edema; long-term:
fibrotic changes
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Atelectasis
• Following airway occlusion
– 100% O2 and mucus
plug
– Note the great diff in total
pressure when 100% O2
is breathed (due to N2
washout)
– This predisposes the
alveoli to collapse as gas
leaves to equalize
pressure
– Will happen in air
breathing and mucus
plug, but process is
slower
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Atelectasis
– Nitrogen is thus
important in keeping
alveoli open
– Closure occurs in
bottom of lung (less
well expanded)
• Secretions tend to
collect at the base
as well
• Instability of units with
low VA/Q
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Atelectasis
• Lung units with
low VA/Q become
unstable when
high O2 is inhaled
– Poorly
ventilated areas
collapse
– Air in much
great than
expired (taken
up by blood)
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Patterns of ventilation
•
PEEP
– Positive end-expiratory
pressure
– Improves PaO2 in Acute
resp diesease
– Why?
• Increases FRC
– Reduces airway
closure
• Reduces shunt
– Minimizes the
VA/Q mismatch
• Increases VD
– Compression of
capillaries
– Increases
conducting zone
volume (as
consequence of
inc. lung vol)
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PEEP
• Note the difference in
the capillary volume
with PEEP
• PEEP also reduces
Qc
– Impedes venous
return
• Can damage
capillaries
– Pulmonary edema
– High lung volume
can cause pulm
cap stress failure
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Other diseases
• Pneumonia
– Inflammation of
lung parenchyma
• Alveoli fill with
exudate
• Can be lobar or
patchy
(bronchopneum
onia)
• Shunting and
hypoxemia
occur
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Other diseases
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•
•
Tuberculosis
– Infection (bacterial)
– Usu. Found in apices due to high
VA/Q and high Po2
• Antibiotics: primary treatment
• Old treatment?
Bronchiectasis
– Dilation of Bronchi with suppuration
• Pus present, due to bacterial
infection (sometimes following
pneumonia)
• Antibiotics
Cystic Fibrosis
– Disease of exocrine glands caused
by abnormal chloride and sodium
transport
– Excessive secretions in lung
(hypertrophied mucus glands)
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Other pneumoconioses
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Coal worker’s lung
– Massive fibrosis
Silicosis
– Inhalation of silica
– Quarrying, mining or snadblasting
– These are toxic particles
– Provoke severe fibrosis
Asbestos-related disease
– Commonly used in insulation, brake linings,
roofing materials (anything that must resist
heat
• Diffuse interstitial pulm fibrosis (Chpt 5)
• Bronchial carcinoma; aggravated by
smoking
• Pleural disease; malignant
mesothelioma (sometimes up to 40 yrs
after exposure)
Byssinosis
– Cotton dust
– Histamine reaction
– Obstructive disease pattern
Occupational asthma
– Allergenic organic dusts
• Flour; wheat weevil
• Gum acacia
• Polyurethane; Toluene diisocyanate
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