1. Chapter 9 Acute Respiratory Failure

2. Topics Acute respiratory failure pathophysiology Hypoxemia
Co2 retention
Diaphragmatic failure
Types of respiratory failure

3. 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

4. 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

5. 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

6. 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

7. 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)

8. 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

9. 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

10. Hypoxemia Mild hypoxemia Few physiologic problems
Po2 of ~ 60 mmHg still about 90% saturation
When Po2 falls below mmHg
CNS vulnerable
Headache, somnolence, clouding of consciousness

11. 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

12. 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

13. Acidosis of resp failure and diaphragm fatigue
Co2 retention
Metabolic acidosis
Diaphragm fatigue
Due to prolonged elevations in work of breathing
Hypoventilation
Sever hypoxemia

14. 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)
Fig 9-4

15. 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

16. 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

17. 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

18. 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

19. 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

20. 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)

21. IRDS Chief cause Lack of surfactant
Surfactant system matures late in fetal life
Check lecithin/sphingomyelin ratio of amniotic fluid
Treatment
Instillation of surfactant

22. 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

23. 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 non-ventilated (due to collapse); shunt

24. 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%)

25. 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

26. 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)

27. 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

28. 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

29. 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

30. 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)

31. 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)

32. 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

33. Other diseases Pneumonia Inflammation of lung parenchyma
Alveoli fill with exudate
Can be lobar or patchy (bronchopneumonia)
Shunting and hypoxemia occur

34. 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)

35. 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