Respiratory— Failure

,Click to edit Master title style,*,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,Respiratory Failure,Dr. Sat Sharma,Univ of Manitoba,RESPIRATORY FAILURE,“inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue oxygenation and/or failure of CO2 homeostasis.,RESPIRATORY FAILURE,Definition Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O,2,from atmosphere to blood and remove CO,2,from blood.,Clinically Respiratory failure is defined as PaO,2,50 mmHg.,Respiratory system includes:,CNS (medulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature,Potential causes of Respiratory Failure,HYPOXEMIC RESPIRATORY FAILURE(TYPE 1),PaO,2,50 mmHg,Hypoxemia is always present,pH depends on level of HCO,3,HCO,3,depends on duration of hypercapnia,Renal response occurs over days to weeks,Acute Hypercapnic Respiratory Failure (Type II),Acute,Arterial pH is low,Causes,- sedative drug over dose,- acute muscle weakness such as myasthenia gravis,- severe lung disease: alveolar ventilation can not be maintained (i.e. Asthma or,pneumonia),Acute on chronic:,This occurs in patients with chronic CO,2,retention who worsen and have rising CO,2,and low pH.,Mechanism: respiratory muscle fatigue,Causes of Hypercapnic Respiratory failure,Respiratory centre (medulla) dysfunction,Drug over dose, CVA, tumor, hypothyroidism,central hypoventilation,Neuromuscular disease Guillain-Barre, Myasthenia Gravis, polio, spinal injuries,Chest wall/Pleural diseases kyphoscoliosis, pneumothorax, massive pleural effusion,Upper airways obstruction tumor, foreign body, laryngeal edema,Peripheral airway disorder,asthma, COPD,Clinical and Laboratory Manifestation,(non-specific and unreliable),Cyanosis - bluish color of mucous membranes/skin indicate,hypoxemia,- unoxygenated hemoglobin 50 mg/L - not a sensitive indicator,Dyspnea - secondary to hypercapnia and hypoxemia,Paradoxical breathing,Confusion, somnolence and coma,Convulsions,ASSESSMENT OF PATIENT,Careful history,Physical Examination,ABG analysis -classify RF and help with cause,1) PaCO,2,=,VCO,2,x 0.863,VA,2) P(A-a)0,2,= (PiO,2,-,PaCO,2,) PaO,2,R,Lung function OVP vs RVP vs NVP,Chest Radiograph,EKG,Clinical & Laboratory Manifestations,Circulatory changes,- tachycardia, hypertension, hypotension,Polycythemia - chronic hypoxemia - erythropoietin synthesis,Pulmonary hypertension,Cor-pulmonale or right ventricular failure,Management of Respiratory Failure Principles,Hypoxemia may cause death in RF,Primary objective is to reverse and prevent hypoxemia,Secondary objective is to control PaCO,2,and respiratory acidosis,Treatment of underlying disease,Patients CNS and CVS must be monitored and treated,Oxygen Therapy,Supplemental O,2,therapy essential,titration based on SaO,2, PaO,2,levels and PaCO,2,Goal is to prevent tissue hypoxia,Tissue hypoxia occurs (normal Hb & C.O.) - venous PaO,2, 20 mmHg or SaO,2, 40% - arterial PaO,2, 38 mmHg or SaO,2, 60 mmHg(SaO,2, 90%) or venous SaO,2, 60%,O,2,dose either flow rate (L/min) or FiO,2,(%),Risks of Oxygen Therapy,O,2,toxicity,: - very high levels(1000 mmHg) CNS toxicity and seizures - lower levels (FiO,2, 60%) and longer exposure: -capillary damage, leak and pulmonary fibrosis - PaO,2,150 can cause retrolental fibroplasia - FiO,2,35 to 40% can be safely tolerated indefinitely,CO,2,narcosis:,- PaCO,2,may increase severely to cause respiratory acidosis, somnolence and coma,- PaCO,2,increase secondary to combination of a) abolition of hypoxic drive to breathe b) increase in dead space,MECHANICAL VENTILATION,Non invasive with a mask,Invasive with an endobronchial tube,MV can be volume or pressure cycled For hypercapnia: - MV increases alveolar ventilation and lowers,PaCO,2, corrects pH,- rests fatigues respiratory muscles,For hypoxemia: - O,2,therapy alone does not correct hypoxemia caused by shunt,- Most common cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema),POSITIVE END EXPIRATORY PRESSURE (PEEP),PEEP increases the end expiratory lung volume (FRC),PEEP recruits collapsed alveoli and prevents recollapse,FRC increases, therefore lung becomes more compliant,Reversal of atelectasis diminishes intrapulmonary shunt,Excessive PEEP has adverse effects - decreased cardiac output - barotrauma (pneumothorax, pneumomediastinum) - increased physiologic dead space - increased work of breathing,PULMONARY EDEMA,Pulmonary edema is an increase in extravascular lung water,Interstitial edema does not impair function,Alveolar edema cause several gas exchange abnormalities,Movement of fluid is governed by Starlings equation,QF = KF (P,IV,- P,IS,) +,(,IS,-,IV,),QF = rate of fluid movement KF = membrane permeability P,IV,& P,IS,are intra vascular and interstitial hydrostatic pressures,IS,and,IV,are interstitial and intravascular oncotic pressures,reflection coefficient,Lung edema is cleared by lymphatics,Adult Respiratory distress Syndrome (ARDS),Variety of unrelated massive insults injure gas exchanging surface of Lungs,First described as clinical syndrome in 1967 by Ashbaugh & Petty,Clinical terms synonymous with ARDS Acute respiratory failure Capillary leak syndrome Da Nang Lung Shock Lung Traumatic wet Lung Adult hyaline membrane disease,Risk Factors in ARDS,Sepsis 3.8% Cardiopulmonary bypass 1.7% Transfusion 5.0% Severe pneumonia 12.0% Burn 2.3% Aspiration 35.6% Fracture 5.3% Intravascular coagulopathy 12.5% Two or more of the above 24.6%,PATHOPHYSIOLOGY AND PATHOGENESIS,Diffuse damage to gas-exchanging surface either alveolar or capillary side of membrane,Increased vascular permeability causes pulmonary edema,Pathology: fluid and RBC in interstitial space, hyaline membranes,Loss of surfactant: alveolar collapse,CRITERIA FOR DIAGNOSIS OF ARDS,Clinical history of catastrophic event Pulmonary or Non pulmonary (shock, multi system trauma),Exclude chronic pulmonary diseases left ventricular failure,Must have respiratory distress tachypnea 20 breath/minute Labored breathing central cyanosis CXR- diffuse infiltrates PaO,2,O.6 Compliance 50 ml/cm H,2,O increased shunt and dead space,ARDS,MANAGEMENT OF ARDS,Mechanical ventilation corrects hypoxemia/respiratory acidosis,Fluid management correction of anemia and hypovolemia,Pharmacological intervention Dopamine to augment C.O. Diuretics Antibiotics Corticosteroids - no demonstrated benefit early disease, helpful 1 week later,Mortality continues to be 50 to 60%,