Acute Respiratory Failure Respiratory System • Consists of two parts: • Gas exchange organ (lung): responsible for OXYGENATION • Pump (respiratory muscles and respiratory control mechanism): responsible for VENTILATION NB: Alteration in function of gas exchange unit (oxygenation) OR of the pump mechanism (ventilation) can result in respiratory failure Normal Lung Lung Anatomy Normal Alveoli Gas Exchange Unit Fig. 66-1 Normal ABGs • pH = 7.35-7.45 • CO2 = 35-45 • HCO3= 23-27 Respiratory and Metabolic Acidosis and Alkalosis • CO2 is an acid and is controlled by the Respiratory (Lung) system • HCO3 is an alkali and is controlled by the Metabolic (Renal) system • Respiratory response is immediate; Metabolic response can take up to 72 hours to respond (except in patients with COPD who are in a constant state of Compensation!) ABG Interpretation Step 1: Check the pH: Is it acidotic or alkalotic or normal? pH below 7.35 is acidotic; pH above 7.45 is alkalotic If pH is normal, then the ABG is compensated; if pH not normal, then the ABG is uncompensated ABG Interpretation (cont’d) Step 2. Check the CO2 and HCO3: If the CO2 (acid) is above 45, the pt is acidotic; if the CO2 is below 35, the pt is alkalotic If the HCO3 is above 27, the patient is alkalotic; if the HCO3 is below 23, the patient is acidotic ABG Interpretation (cont’d) Step 3 If the CO2 is high (above 45), then the patient is in Respiratory Acidosis; if the CO2 is low (below 35), then the patients is in Respiratory Alkalosis. If the HCO3 is high (above 27), then the patient is in Metabolic Alkalosis; if the HCO3 is low (below 23), then the patient is in Metabolic Acidosis. ABG Example #1 • pH = 7.36 • CO2 = 41 • HCO3 = 27 Diagnosis: ? ABG Example #2 • pH = 7.49 • CO2 = 37 • HCO3 = 32 Diagnosis: ? ABG Example #3 • pH = 7.29 • CO2 = 50 • HCO3 = 26 Diagnosis: ? ABG Example #4 • pH = 7.40 • CO2 = 32 • HCO3 = 30 Diagnosis: ? Acute Respiratory Failure • Results from inadequate gas exchange Insufficient O2 transferred to the blood • Hypoxemia Inadequate CO2 removal • Hypercapnia Acute Respiratory Failure with Diffuse Bilateral Infiltrates Acute Respiratory Failure • Not a disease but a condition • Result of one or more diseases involving the lungs or other body systems • NB: Acute Respiratory Failure: when oxygenation and/or ventilation is inadequate to meet the body’s needs Acute Respiratory Failure • Classification: – Hypoxemic respiratory failure (Failure of oxygenation) – Hypercapnic respiratory failure (Failure of ventilation) Classification of Respiratory Failure Fig. 66-2 Acute Respiratory Failure • Hypoxemic Respiratory Failure – PaO2 of 60 mm Hg or less (Normal = 80 - 100 mm Hg) – Inspired O2 concentration of 60% or greater Acute Respiratory Failure • Hypercapnic Respiratory Failure – PaCO2 above normal (>45 mm Hg) – Acidemia (pH <7.35) Hypoxemic Respiratory Failure Etiology and Pathophysiology • Causes: – Ventilation-perfusion (V/Q) mismatch – Shunt – Diffusion limitation – Alveolar hypoventilation V-Q Mismatching I) V/Q mismatch • Normal ventilation of alveoli is comparable to amount of perfusion • Normal V/Q ratio is 0.8 (more perfusion than ventilation) • Mismatch d/t: Inadequate ventilation Poor perfusion Range of V/Q Relationships Fig. 66-4 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes V/Q mismatch – COPD – Pneumonia – Asthma – Atelectasis – Pulmonary embolus Hypoxemic Respiratory Failure Etiology and Pathophysiology II) Shunt – An extreme V/Q mismatch – Blood passes through parts of respiratory system that receives no ventilation • d/t obstruction OR fluid accumulation • Not Correctable with 100% O2 Diffusion Limitations III) Diffusion Limitations • Distance between alveoli and pulmonary capillary is one- two cells thick • With diffusion abnormalities: there is an increased distance between alveoli (may be d/t fluid) • Correctable with 100% O2 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes Diffusion limitations – Severe emphysema – Recurrent pulmonary emboli – Pulmonary fibrosis – Hypoxemia present during exercise Diffusion Limitation Fig. 66-5 Alveolar Hypoventilation IV) Alveolar Hypoventilation • Is a generalized decrease in ventilation of lungs and resultant buildup of CO2 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes Alveolar hypoventilation – Restrictive lung disease – CNS disease – Chest wall dysfunction – Neuromuscular disease Hypoxemic Respiratory Failure Etiology and Pathophysiology • Interrelationship of mechanisms – Hypoxemic respiratory failure is frequently caused by a combination of two or more of these four mechanisms • Effects of hypoxemia – – – – Build up of lactic acid → metabolic acidosis → cell death CNS depression Heart tries to compensate → ↑ HR and CO If no compensation: ↓ O2, ↑ acid, heart fails, shock, multisystem organ failure Hypercapnic Respiratory Failure Etiology and Pathophysiology • Imbalance between ventilatory supply and demand • Occurs when CO2 is increased Causes Hypercapnic Respiratory Failure I) Alveolar Hypoventilation and VQ Mismatch: – Ventilation not adequate to eliminate CO2 – Leads to respiratory acidosis – Eg. Narcotic OD; Guillian-Barre, ALS, COPD, asthma Causes Hypercapnic Respiratory Failure II) VQ Mismatch: - Leads to increased work of breathing - Insufficient energy to overcome resistance; ventilation falls; ↑PCO2; respiratory acidosis Hypercapnic Respiratory Failure Categories of Causative Conditions • I) Airways and alveoli – Asthma – Emphysema – Chronic bronchitis – Cystic fibrosis Hypercapnic Respiratory Failure Categories of Causative Conditions • II) Central nervous system – Drug overdose – Brainstem infarction – Spinal cord injuries Hypercapnic Respiratory Failure Categories of Causative Conditions • III) Chest wall – Flail chest – Fractures – Mechanical restriction – Muscle spasm Hypercapnic Respiratory Failure Categories of Causative Conditions • IV) Neuromuscular conditions – Muscular dystrophy – Multiple sclerosis Respiratory Failure Tissue Oxygen Needs • Major threat is the inability of the lungs to meet the oxygen demands of the tissues Respiratory Failure Clinical Manifestations • Sudden or gradual onset • A sudden in PaO2 or rapid in PaCO2 is a serious condition Respiratory Failure Clinical Manifestations • When compensatory mechanisms fail, respiratory failure occurs • Signs may be specific or nonspecific Respiratory Failure Clinical Manifestations • Severe morning headache • Cyanosis – Late sign • Tachycardia and mild hypertension – Early signs Respiratory Failure Clinical Manifestations • Consequences of hypoxemia and hypoxia – Metabolic acidosis and cell death – Cardiac output – Impaired renal function Respiratory Failure Clinical Manifestations • Specific clinical manifestations – Rapid, shallow breathing pattern – Sitting upright – Dyspnea Respiratory Failure Clinical Manifestations • Specific clinical manifestations – Pursed-lip breathing – Retractions – Change in Inspiratory:Expiratory ratio Respiratory Failure Diagnostic Studies • • • • • Physical assessment ABG analysis Chest x-ray CBC ECG Respiratory Failure Diagnostic Studies • • • • Serum electrolytes Urinalysis V/Q lung scan Pulmonary artery catheter (severe cases) Acute Respiratory Failure Nursing and Collaborative Management • Nursing Assessment – Past health history – Medications – Surgery – Tachycardia Acute Respiratory Failure Nursing and Collaborative Management • Nursing Assessment – Fatigue – Sleep pattern changes – Headache – Restlessness Acute Respiratory Failure Nursing and Collaborative Management • Nursing Diagnoses – Ineffective airway clearance – Ineffective breathing pattern – Risk for imbalanced fluid volume – Anxiety Acute Respiratory Failure Nursing and Collaborative Management • Nursing Diagnoses – Impaired gas exchange – Imbalanced nutrition: less than body requirements Acute Respiratory Failure Nursing and Collaborative Management • Planning – Overall goals: • ABGs and breath sounds within baseline • No dyspnea • Effective cough Acute Respiratory Failure Nursing and Collaborative Management • Prevention – Thorough physical assessment – History Acute Respiratory Failure Nursing and Collaborative Management • Respiratory Therapy – Oxygen therapy – Mobilization of secretions • Effective coughing and positioning Acute Respiratory Failure Nursing and Collaborative Management • Respiratory Therapy – Mobilization of secretions • Hydration and humidification • Chest physical therapy • Airway suctioning Acute Respiratory Failure Nursing and Collaborative Management • Respiratory Therapy – Positive pressure ventilation (PPV) Acute Respiratory Failure Nursing and Collaborative Management • Drug Therapy – Relief of bronchospasm • Bronchodilators Acute Respiratory Failure Nursing and Collaborative Management • Drug Therapy – Reduction of airway inflammation • Corticosteroids Acute Respiratory Failure Nursing and Collaborative Management • Drug Therapy – Reduction of pulmonary congestion • IV diuretics Acute Respiratory Failure Nursing and Collaborative Management • Drug Therapy – Treatment of pulmonary infections • IV antibiotics Acute Respiratory Failure Nursing and Collaborative Management • Drug Therapy – Reduction of severe anxiety, pain, and agitation • Benzodiazepines • Narcotics Acute Respiratory Failure Nursing and Collaborative Management • Medical Supportive Therapy – Treat the underlying cause – Maintain adequate cardiac output and hemoglobin concentration – Monitor BP, O2 saturation, urine output Acute Respiratory Failure Nursing and Collaborative Management • Nutritional Therapy – Maintain protein and energy stores – Enteral or parenteral nutrition – Supplements