Respiratory Failure 2

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Respiratory Disorders Associated With Acute Respiratory Failure

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Definition: The term Acute Respiratory Failure (A.R.F ) is used clinically to indicate a disease or disorder of the respiratory system , recent in onset, which has resulted in a level or pattern of external gas exchange that is inadequate for the metabolic needs of the body .

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This deficiency is reflected in arterial hypoxemia, hypercapnia and respiratory acidosis. If the initiating mechanism is not arrested, corrected & reversed the abnormalities in the blood gases are apt to progress to intolerable levels. There is no precise level of arterial Po 2 or Pco 2 that defines [ARF]. However, an arterial P a o 2 < 50-60 mmHg can be life threatening because further impairment of gas exchange can cause a drop in P a o 2 to levels that would compromise Oxygen Delivery [Do 2 ] to vital organs.

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Acute rise of PaCo 2 to >50 mmHg i.e. Acute Hypercapnia with Respiratory Acidosis result in mental confusion, depressed sensorium that end in coma and death. The effects of acute hypoxemia and acute hypercapnia may overlap, resulting in severe C. N. S depression .

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The respiratory apparatus consists of two components : 1- Pump system: includes the entire ventilatory apparatus [Respiratory Center, Thoracic Cage, Air ways]. 2- Gas Exchange system : pulmonary parenchyma [alveoli with alveolar air & alveolo-capillary membrane.

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Respiratory Failure can therefore be divided into : Pump Failure or hypercapnic respiratory failure with Co 2 retention. Lung Failure or gas exchange failure with arterial hypoxemia i.e. hypoxemic respiratory failure.

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Lung Failure (Hypoxemic Respiratory Failure): Adult respiratory distress syndrome ARDS. Cardiogenic pulmonary edema. End stage pulmonary fibrosis, resulting from different fibrotic lung diseases. Massive Pulmonary Embolism. Severe Pneumonia.

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Pump Failure ( Hypercapnic Respiratory Failure ): Neuromuscular disease, atrophic or pseudo hypertrophic myopathies. Guillain Barre syndrome. Myasthenia gravis. Amyotrophic lateral sclerosis. Cervical quadriplegia. Botulism.

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Respiratory Poliomyelitis. Bilateral diaphragmatic paralysis. Hereditary myopathies. Multiple sclerosis. Collagen vascular disease e.g. vanishing lung syndrome in SLE. Central nervous disorders “C.V.S”. Drug over dose. Head trauma.

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Hypothyroidism e.g. myxedema coma. Brain stem infarction& brain neoplasm. Disorders of the chest bellows. Kyphoscoliosis & Chest wall deformities. Chest trauma and Flail Chest. Tension pneumothorax. Massive pleural effusion. Airway obstruction.

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Acute severe asthma. COPD "Chronic Obstructive Pulmonary Disease" Anaphylaxis Cystic fibrosis Upper airway obstruction e.g. Epiglottitis & F.B inhalation.

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Hypercapnia due to hypercapnic respiratory failure can arise in one of two ways: Alveolar hypoventilation secondary to a subnormal low minute ventilation . Ventilation-Perfusion (V /Q ) mismatch .

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Pathophysiologic mechanisms in Acute Respiratory Failure: Mechanism Type of failure Feature Global alveolar hypoventilation Pump Hypercapnia Ventilation –perfusion mismatch Pump and /or lung Hpercapnia and /or hypoxemia Shunt Lung Hpoxemia Diffusion abnormality Lung Hpoxemia

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BASIC PRINCIPLES OF OXYGEN TRANSPORT ■ Gas exchange in the lungs concerns ventilation, perfusion and diffusion. ■ Arterial hypoxemia may occur because of: A decrease in PIO 2 . Alveolar hypoventilation. Ventilation/perfusion disturbance. Impaired diffusion at the alveolar capillary barrier.

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Oxygen Delivery and Utilization DO 2 = CO x CaO 2 x 10 DO 2 = O 2 delivery, ml/min. CO = Cardiac output L/min. CaO 2 = O 2 content of arterial blood ml/dl. CaO 2 = ([Hb] x 1.34 x Sa O 2 %) + (PaO 2 x 0.003) Hb = Hemoglobin conc. gm/dl. 1.34 = O 2 carrying capacity of Hb at 37  C ml/gm. Sat. O 2 % = Percentage saturation of Hb with O 2 . 0.003 = Solubility coefficient for O 2 .

Advantages and disadvantages of oxygen sources : 

Advantages and disadvantages of oxygen sources

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Oxygen Therapy in Acute exacerbation of COPD: Rationale: low flow O 2 by nasal cannula or ventura mask is given during acute vent. failure to achieve PaO 2 of 60 Hg and SaO 2 of 92%. Intubation is indicated on the basis of objective undersirable effects of respiratory acidosis (PH< 7.20) ,consciousness level deterioration or development of arrhythmias. O2 induced hypercapnia is related to an increase in (VD/VT) or (V/Q) mismatch. NPPV significantly decreased the rate of intubation.

Domiciliary O2 & Long Term Oxygen Therapy: 

Domiciliary O 2 & Long Term Oxygen Therapy Indications of LTOT: Chronic airflow obstruction specially if PaCO 2 > 45 mmHg. Advanced interstitial pulmonary disease. Advanced pulmonary malignancy. Advanced cystic fibrosis. Severe congestive heart failure. Cong. cyanotic heart disease. (Breslin et al., 1991).

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Patients who need oxygen Cardio pulmonary Resuscitation [CPR] in Respiratory or Cardio pulmonary arrest. Fluid in the alveoli . Pulmonary edema . Pneumonia . Near drowning . Chest trauma .

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Collapsed alveoli (alveolar atelectasis ) as in cases of : Airway obstruction : Any unconscious patient. Choking & FB inhalation. Failure to take deep breaths : Severe pain as in rib fracture & severe pleurisy ) . Paralysis of the respiratory muscles .

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Depression of the respiratory center (head injury ,drug overdose ) Collapse of an entire lung (pneumothorax or massive pleural effusion ) Other gases in the alveoli : Smoke inhalation . Toxic inhalations . Carbon monoxide poisoning .

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Any patient complaining of shortness of breath . Any patient in shock . any patient with signs of respiratory insufficiency . Any patient breathing fewer than 10 times / minute i.e. bradypnea. Any patient in cardiac arrest.

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Any patient complaining of chest pain . Any patient suspected to be suffering a stroke . ( Caroline , 1995 )

Adverse Effects of O2 Therapy: 

Adverse Effects of O 2 Therapy These may be related to the device used e.g. nasal irritation, epistaxis, conjunctivitis inspissated secretions or barotrauma and volutrauma associated with mech. ventilation. O 2 induced hypercopnia in COPD is due to V/Q mismatch. Hyperoxia produces pulmonary toxicity through production of O 2 free radicals (O 2 -, OH-, O1, H 2 O 2 ) at a rate that overwhelmes the antioxidant defences. O 2 free radicals damage cell membranes, enzymes and nucleic acids leading eventually to cell death.