Chapter 9 Acute Respiratory Failure

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Chapter 9Acute Respiratory Failure


Topics

• Acute respiratory failure

• pathophysiology• Hypoxemia

• Co2 retention

• Diaphragmatic failure• Types of respiratory

failure


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


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


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


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


• 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


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


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


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


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


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


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


• 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


• 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



• 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



• 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


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


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


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)


IRDS• Chief cause

– Lack of surfactant• Surfactant system

matures late in fetal life

–Check lecithin/sphingomyelin ratio of amniotic fluid

• Treatment–Instillation of

surfactant


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


• 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


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%)


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


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)


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


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


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


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)


• 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


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


Other diseases• Pneumonia

– Inflammation of lung parenchyma• Alveoli fill with

exudate• Can be lobar or

patchy (bronchopneumonia)

• Shunting and hypoxemia occur


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)


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

Chapter 9 Acute Respiratory Failure

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