chapter 9 acute respiratory failure
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Chapter 9 Acute Respiratory Failure. Topics. Acute respiratory failure pathophysiology Hypoxemia Co 2 retention Diaphragmatic failure Types of respiratory failure. Case Study #9: Ivan. 45 yr old computer programmer Well until 10 days ago Car accident - PowerPoint PPT PresentationTRANSCRIPT
© 2007 McGraw-Hill Higher Education. All rights reserved.
Chapter 9Acute Respiratory Failure
© 2007 McGraw-Hill Higher Education. All rights reserved.
Topics
• Acute respiratory failure
• pathophysiology• Hypoxemia
• Co2 retention
• Diaphragmatic failure• Types of respiratory
failure
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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
• 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• 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
Fig. 9-3
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• 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)
Pathophysiology: gas exchange
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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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• 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)
Types of respiratory failure
Fig 9-4
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• 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
Types of respiratory failure
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• 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
Types of respiratory failure
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• 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
Acute or Chronic lung disease
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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/sphingomyelin 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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• 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 non-ventilated (due to collapse); shunt
Oxygen therapy
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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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• 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)
Patterns of ventilation
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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 (bronchopneumonia)
• Shunting and hypoxemia occur
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Other diseases• 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• 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