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CCRN Prep 2019 Pulmonary
This document provides information on various pulmonary conditions and respiratory devices. It defines respiratory failure and describes its causes, signs and symptoms, and treatment. It also discusses ARDS in detail including its pathophysiology, risk factors, signs and symptoms, treatment, and prognosis. Pneumothorax is defined and its causes, signs and symptoms, and treatment are outlined.
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CCRN Prep 2019 Pulmonary
- 1. PULMONARY 2019 Sherry Knowles, RN,CCRN, CMC
- 2. PULMONARY 1 ARDS COPD Air-Leak Syndromes Pneumonia AsthmaPneumothorax Pleural Effusions Pulmonary Embolism Pulmonary Hypertension Failure to Wean Respiratory Failure Thoracic Surgeries
- 3. NON-INVASIVE OXYGEN DEVICES Nasalcannula: • Flow: 2-6L: • FiO2: Up to 41% HFNC: • Flow: 6-15L with standard bubbling humidification • FiO2: Up to 81% Optiflow • Flow: 60L with high humidification • FiO2: Up to 100% • Ideal for patients with Hypoxemic Respiratory Failure or for immediate needs post extubation • Provides positive airway pressure Respiratory Devices
- 4. Simple face mask •FiO2 45% or Up to 6L flow Venti-mask • FiO2 dialed into device NRB • 15L • 100% FiO2 • Best for hypoxemic respiratory failure • Be cautious of High FiO2 in COPD patients Respiratory Devices
- 5. BiPAP • Allows forControl of Positive Pressure on Inspiration (IPAP) and Expiration (EPAP, CPAP or PEEP) • Allows for delivery of a set FiO2 depending on pt needs • Optimal for Hypercapnic Respiratory Failure or to decrease Preload in Pulmonary Edema • Precursor to intubation or bridge immediately after extubation • Can also be used at night for those with sleep apnea CPAP • Provides end-expiratory positive airway pressure • Used for patients with OSA at night • Titrated by pulmonary usually based on results of sleep studies Respiratory Devices
- 6. • Continuous analysisand recording of the carbon dioxide (CO2) concentration in expired respiratory gas • Used for: • Verification of Airway Placement after Intubation • To Determine Effectiveness of Chest Compressions & Detect ROSC • As a Continuous Waveform to Optimize Mechanical Ventilation • Assessment of Pulmonary Circulation, Cardiac Output and Respiratory Status • Normal 30-40mm Hg (about 5mmHg lower than arterial PaCO2) • Available as a module to hardwire monitoring systems End-Tidal capnography (CO2)
- 7. DEFINITION • Failure tomaintain adequate gas exchange • Inadequate blood oxygenation or CO2 removal • PaO2 < 50 mmHg and/or PaCO2 > 50 mmHg and/or pH < 7.35 on Room Air Respiratory Failure
- 8. TYPE I Hypoxemiawithout Hypercapnia TYPE II Hypoxemia with Hypercapnia Respiratory Failure
- 9. CAUSES • V/Q Mismatching •Intrapulmonary Shunting • Alveolar Hypoventilation Respiratory Failure
- 10. V/Q MISMATCHING • COPD •Interstitial Lung Disease • Pulmonary Embolism Respiratory Failure
- 11.
- 12. PULMONARY SHUNTING • AVfistulas/malformations • Alveolar collapse (atelectasis) • Alveolar consolidation (pneumonia) • Excessive mucus accumulation Respiratory Failure
- 13. SIGNS & SYMPTOMS •Restlessness / Agitation • Confusion / LOC • Tachycardia / Dysrhythmias • Tachypnea / Dyspnea • Cool, clammy, pale skin Respiratory Failure
- 14. ARTERIAL BLOOD GASES •pH 7.30 / pO2 45 / pCO2 80 • pH 7.30 / pO2 55 / pCO2 65 • pH 7.32 / pO2 50 / pCO2 50 • pH 7.55 / pO2 65 / pCO2 22 Respiratory Failure
- 15. TREATMENT • Ensure AdequateVentilation • FiO2 • Ineffective with shunting • Prolonged O2 > 40% causes O2 toxicity • Must use caution with CO2 retainers • Too much O2 can depress respirations • Chronic hypercapnia causes CO2 retainers to use hypoxic drive Respiratory Failure
- 16. DEFINITIONS • Severe respiratoryfailure associated with pulmonary infiltrates (similar to infant hyaline membrane disease) • Pulmonary edema in the absence of fluid overload or depressed LV function (Non- cardiogenic pulmonary edema) • Originates from a number of insults involving damage to the alveolar-capillary membrane ARDS
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- 18. PATHOPHYSIOLOGY • Inflammatory mediatorsare released causing extensive structural damage • Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar–capillary membrane • Also causes damage to the surfactant producing type II cells ARDS
- 19. CXR CHARACTERISTICS • Normalsize heart • No pleural effusion • Ground Glass appearance • Often normal early in the disease but may rapidly progress to complete whiteout ARDS
- 20.
- 21. SIGNS & SYMPTOMS •Symptoms develop 24 to 48 hours of injury • Sudden progressive disorder • Pulmonary edema • Severe dyspnea • Hypoxemia refractory to increased O2 • Decreased lung compliance • Diffuse pulmonary infiltrates • Symptoms may be minimal compared to CXR • Rales may be heard ARDS
- 22. Common Risk Factors Other RiskFactors Sepsis Massive Trauma Shock Multiple Transfusions Pneumonia Aspiration Infection Smoke inhalation Inhaled Toxins Burns Near Drowning DKA Pregnancy Eclampsia Amniotic Fluid Embolus Drugs Acute Pancreatitis DIC Head Injury ICP Fat Emboli Blood Products Heart/Lung Bypass Tumor Lysis Pulmonary Contusion Narcotics RISK FACTORS ARDS
- 23. TREATMENT • Respiratory Support •PEEP, CPAP ARDS
- 24. Management • Determine severityof exacerbation • Classified as: Mild – Moderate – Severe – Impending Failure • Based upon symptoms and Peak Expiratory Flow (PEF) • Treat based upon severity • Inhaled Short-acting Beta Blockers • Anti-inflammatory agents • For Status Asthmaticus • Simultaneous Multi-modal therapy • O2 • Fluids • Continuous Nebs and Anti-Inflammatories • If no improvement - may need intubation and mechanical ventilation ARDS
- 25. • The majorpathological feature of asthma is inflammation resulting in hyperresponsiveness of the airways. • Major events in an acute asthma attack are bronchiolar constriction, mucus hypersecretion, and inflammatory swelling. • Exposure to allergens or irritants causes mast cells to release granules and trigger the release of many inflammatory mediators such as histamine, interleukins, immunoglobulins, prostaglandins, leukotrienes and nitric oxide. • Chemotactic factors attract neutrophils, eosinophils and lymphocytes to the area – bronchial infiltration Asthma
- 26. • More intermittentand acute than COPD, even though it can be chronic • Factor that sets it apart from COPD is its reversibility • Occurs at all ages, approx. half of all cases develop during childhood, and another 1/3 develop before age 40 • 5% of Adults and 7-10% of children in U.S. have asthma Asthma
- 27. Definition • “..airway hyperresponsivenessto a variety of stimuli, reversible airflow limitation, and inflammation of the airway submucosa.” (Morton, P. & Fontaine, D. (2013), p. 250) Triggers • Environmental allergens • Infection • Medications • Temperature • Food • Exercise • Stressors Asthma
- 28. • Morbidity andmortality have risen in past 20 years in spite of increased numbers and availability of antiasthma medications. • Runs in families, so evidence genetics plays a role. • Environmental factors interact with inherited factors to increase the risk of asthma and attacks of bronchospasm • Childhood exposure to high levels of allergens, cigarette smoke and/or respiratory viruses increases chances of developing asthma. Asthma
- 29. • Smooth musclespasm in bronchioles due to IgE effect on autonomic neurons • Vascular congestion • Edema formation • Production of thick, tenacious mucus • Impaired mucociliary function • Thickening of airway walls • Increased bronchial responsiveness/hyperreactivity • Untreated, this can lead to airway damage that is irreversible. • Obstruction increases resistance to air flow and decreases flow rates • Impaired expiration causes hyperinflation of alveoli distal to obstruction, and increases the work of breathing Asthma Results
- 30. COPD • Presents withHyper-inflated lung fields • Due to chronic air trapping • May be barrel chested • May lead to Cor Pulmonale • Due to chronic high pulmonary pressures • Often Hypercarbic (high pCO2) • Often dependent upon hypoxic drive Chronic Lung Disease
- 31. COPD TREATMENT • Avoidoveruse of oxygen (when stable) • Bronchodilators • Steroids • Hydration • Education • Pursed Lip Breathing • Leaning Upright Chronic Lung Disease
- 32. Signs and Symptoms •Headache • Drowsiness • Inappropriate sleepiness • Sleep apnea Treat symptomatically • Assist ventilations as needed Pickwickian Syndrome
- 33. Salt Water • Causesbody fluids to shift into lungs • Osmosis: From low to high concentration • Results in hemoconcentration & hypovolemia • Results in acute pulmonary edema Fresh Water • Fluids shift into body tissues • Results in hemodilution & hypervolemia • Can result in gross edema • Damaged alveoli fill with proteinaceous fluid • May lead to pulmonary edema Near Drowning
- 34. Lung infection (bacterial,viral, or fungal) • Most commonly caused by Streptococcus pneumoniae Symptoms include fever, pleuritic chest pain, productive cough, and tachypnea • Often presents bronchial breath sounds over lung area Treatment involves the right antibiotic Pneumonia
- 35. DEFINITION Pneumothorax • Simple Pneumothorax •Results from air or pressure in the pleural space • Spontaneous Pneumothorax • Often due to blebs that rupture • Key risk factors are increased chest length and smoking • Tension Pneumothorax • Involves a buildup of air in the pleural space due to a one-way movement of air • Progressively worsens • Requires immediate intervention
- 36.
- 37.
- 38. CAUSES • Barotrauma • Injury •Blebs Pneumothorax
- 39. SIGNS & SYMPTOMS •Standard Pneumothorax • Sharp "pleuritic" chest pain, worse on breathing • Sudden shortness of breath • Dry, hacking cough (may occur due to irritation of the diaphragm) • May cause mediastinal shift when severe • Tension Pneumothorax • Signs of standard pneumothorax with signs of cardiovascular collapse • Immediately life threatening • May cause mediastinal shift Pneumothorax
- 40. TREATMENT • Spontaneous Pneumothorax •Depends on size & symptoms of pneumothorax • Provide respiratory support • May need chest tube or needle decompression • Some resolve without intervention • Tension Pneumothorax • Requires immediate intervention • May cause cardiovascular collapse • May need chest tube or needle decompression • 2nd intercostal space Pneumothorax
- 41. TREATMENT • Pleurodesis • Chemicalor surgical adhesion of the pleura • Procedure that causes the two layers of the lung lining (the pleura) to stick together • Used for multiple collapsed lungs or persistent collapse Pneumothorax
- 42.
- 43. Pleural Effusions The pleuraconsists of 2 layers • 1 – parietal pleura • 2 – visceral pleura The space between the 2 layers is called the pleural space Normal width of the pleural space is 10-20 mm • Normal volume within the pleural space is10-20 ml
- 44.
- 45. Pleural Fluid Formation Therate of fluid formation is 0.02 ml/kg/hr The rate of fluid clearance is 0.02 ml/kg/hr Many Causes • Fluid build-up • Problem with clearance • capillary pressures • Capillary permeability • Lymphatic obstruction (malignancy)
- 46. Pleural Effusion Symptoms •SOB • Dry Cough • Decreased breath sounds • Dullness to percussion • If pleura irritated = mild or sharp pain • Fluid may be seen on CXR at the bottom of lung
- 47. Pleural Effusion Treatment •May Tap (Thoracentesis) • Therapeutic (relieve symptoms) • Diagnostic (determine underlying diagnosis) • May place Drainage Tube (CT or Pleurx Tube) • May reabsorb on it’s own
- 48. Autoimmune disease • Leadsto inflammation and degeneration of sensory and motor nerve roots (demyelination) Progressive Ascending Paralysis • Progressive tingling and weakness • Moves from extremities then proximally • May lead to respiratory paralysis (25%) Guillian-Barre´ Syndrome
- 49. Self-Limiting • Recovery isspontaneous and complete in 95% of cases • In good outcomes, symptoms clear in 15 to 20 days • Often takes weeks or months Guillian-Barre´ Syndrome
- 50. Treatment based onseverity of symptoms • Control airway • Support ventilation • Oxygen • Intubate in cases of respiratory depression, distress or arrest Guillian-Barre´ Syndrome
- 51. • Autoimmune disease •Attacks the transport mechanism at the NMJ • Episodes of extreme skeletal muscle weakness • Can cause loss of control of airway, respiratory paralysis Myasthenia Gravis
- 52. • Gradual onsetof muscle weakness • Face and throat • Extreme muscle weakness • Respiratory weakness -> paralysis • Inability to process mucus Myasthenia Gravis
- 53. • Treat symptomatically •Watch for aspiration • May require assisted ventilations • Assess for Pulmonary infection Myasthenia Gravis Management
- 54. Definition • Arterial embolus(or other material) that obstructs blood flow to the lung Pulmonary Embolism
- 55. Pathophysiology Virchow’s Triad 1) Venousstasis 2) Hypercoagulability 3) Vessel wall damage Pulmonary Embolism
- 56. Most Common Cause= Blood Clots Vessel Wall Injury Hypercoagulability Venous Stasis Virchow’s Triad Virchow’s Triad
- 57. Other Causes • Air •Amniotic fluid • Fat particles (long bone fracture) • Particulates from substance abuse • Venous catheter Pulmonary Embolism
- 58. Symptoms • Pleuritic pain •Pleural rub • Coughing • Wheezing • Hemoptysis (rare) Pulmonary Embolism
- 59. Signs & Symptoms •Symptoms include sudden dyspnea, cough, chest pain, hemoptysis and sinus tachycardia • Blood gas shows low pO2 & low pCO2 • May present positive Homan’s Sign • May present loud S2 Pulmonary Embolism
- 60. Large PE Symptoms •Preceded by S/S of Small Emboli Plus • Central chest pain • Distended neck veins • Acute right heart failure • Shock • Cardiac arrest Pulmonary Embolism
- 61. Diagnostic Tests • CXR •VQ Scan • Spiral CT • Pulmonary arteriogram/angiogram • Venous ultrasound of the lower extremities • ABG with low pO2 & low pCO2 • D-Dimer Pulmonary Embolism
- 62. TREATMENT • Requires ImmediateIntervention • Provide Respiratory Support • Treat Pain & Comfort • Requires Anticoagulants • Usually includes intravenous Heparin • Reduces risk of secondary thrombus formation while clot is reabsorbed • May Require Embolectomy • May Require Thrombolysis • May Need Umbrella Filter (IVC) • May Need Long Term Anticoagulation Pulmonary Embolism
- 63. Definition • Increased pulmonaryarterial pressure and secondary right ventricular failure. • PH is defined as a mean pulmonary artery pressure greater 25mmHg at rest or 30mmHg with exercise. • Classified into 5 groups according to the mechanistic basis of the disease. Pulmonary Hypertension
- 64. WHO Groups 1) PAH,Idiopathic (some secondary conditions) 2) LVF Causes 3) Pulmonary Causes 4) Embolic/Coagulopathy Causes 5) Grab Bag/Other Causes (Sarcoidosis) Pulmonary Hypertension
- 65. • Chest X-ray-enlargement of the central pulmonary arteries, enlargement of the right ventricle • EKG- signs of right atrial and ventricular hypertrophy, right axis deviation • Echocardiography- used to estimate pulmonary artery systolic pressure, and right ventricle size and thickness, check for shunts, valve function, and pericardial effusions. Pulmonary HTN Diagnostic Tests
- 66. • Pulmonary functiontest- to determine lung disease as a cause. • Overnight oximetry- check for obstructive sleep apnea • V/Q scan- check for thromboembolic disease. • Six minute walk to evaluate which NYHA functional class the patient is in. • Right heart catheterization to confirm diagnosis Pulmonary HTN Diagnostic Tests
- 67. Assessment • CXR; EKG;ECHO; PFTs; V/Q or Spiral CT; (R) Heart Cath Treatment • No cure. • Goal is symptom relief and identify and treat the underlying cause. • O2; Drug Therapy • Lung transplant Complications • Extreme (R) HF; Liver engorgement/cirrhosis Pulmonary Hypertension
- 68. 1) Prostacyclin Agonists • cAMP, Vasodilates 2) Endothelin Receptor Antagonists • Vasodilates 3) PDE5 Inhibitors • cGMP, NO, Vasodilates • Alpha blockers & nitrates contraindicated with PDE5 Inhibitors 4) Guanylate Cyclase Stimulant • Stimulates NO Receptors • Approved for Groups 1 & 4 Pulmonary Hypertension Medications
- 69. 1) Prostacyclin Agonists •Epoprosternal/Flolan/Veletri (IV) • Treprostinil/Remodulin/Tyvaso (IV, SQ, Inhalation) • Ileprost/Ventavis (Inhalation) • Sclexipag//Uptravi) 2) Endothelin Receptor Antagonists • Bosentan/Tracleer (nonselective) • Macitentan/Opsumit (nonselective) • Ambrisentan/Letairis (selective) Pulmonary Hypertension Medications
- 70. 1) PDE5 Inhibitors •Sildenafil/Viagra • Tadelefil/Cialis 2) Guanylate Cyclase Stimulant • Riociguat/Adempas Pulmonary Hypertension Medications
- 71. Arterial Blood GasInterpretation 1) Look at the pH • This always tells you the PRIMARY problem 2) Look at the pCO2 • To confirm or eliminate a respiratory problem 3) Look at the Bicarbonate (HCO3): • To confirm or eliminate a metabolic problem 4) Look at the pO2 5) Look at % O2 Saturation:
- 72. Arterial Blood GasInterpretation • Normal pH • May be a normal ABG • May be a compensated ABG • Abnormal pH • May be an uncompensated ABG • May be a partially compensated ABG • pH Rules • Systems that go with the pH are the problem • Systems that go opposite the pH are compensating
- 73. Weaning is theprocess of withdrawing mechanical ventilatory support and transferring the work of breathing from the ventilator to the patient Ventilator Weaning
- 74. • Before weaning,the patient should have recovered from the acute phase of the disease leading to mechanical ventilation and be able to assume adequate spontaneous breathing • Weaning is gradually started after evaluating the patient’s clinical condition, pulmonary and cardiovascular status • Depending upon these parameters patient may be given spontaneous breathing trials on air and extubated • If SBT unsuccessful patient is taken back on partial ventilatory support or pressure support and gradually the settings reduced and SBT repeated Ventilator Weaning
- 75. • Clinical criteria •Ventilatory criteria • Oxygenation criteria • Pulmonary reserve and measurements 74 Weaning Criteria
- 76. • Adequate Cough& Gag • Adequate Oxygenation • Adequate Spontaneous Tidal Volume • Negative Inspiratory Force (NIF) > -20 • Hemodynamic Stability 75 Weaning Criteria
- 78. References 1. American HeartAssociation. (2010). Guidelines 2010 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Available at: www.americanheart.org. 2. Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):1–14, July 2001. 3. Bridges EJ.(2006) Pulmonary artery pressure monitoring: when, how, and what else to use. AACN Adv Crit Care. 2006;17(3):286–303. 4. Chulay, M., Burns S. M. (2006). AACN Essentials of Critical Care Nursing. McGraw-Hill Companies, Inc., Chapter 23. 5. Finkelmeier, B., Marolda, D. (2004) Aortic Dissection, Journal of Cardiovascular Nursing: 15(4):15–24. 6. Hughes E. (2004). Understanding the care of patients with acute pancreatitis. Nurs Standard: (18) pgs 45-54. 7. Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia: pgs. 35-548.
- 79. References Continued 8. Sole,M. L., Klein, D. G. & Moseley, M. (2008). Introduction to Critical Care Nursing. 5th ed. Philadelphia, Pa: Saunders. 9. Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188. 10. Urden, L., Lough, M. E. & Stacy, K. L. (2009). Thelan's Critical Care Nursing: Diagnosis and Management (6th ed). St. Louis, Mo.: Mosby/Elsevier. 11. Woods, S., Sivarajan Froelicher, E. S., & Motzer, S. U. (2004). Cardiac Nursing. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins. 12. Wynne J, Braunwald E. (2004). The Cardiomyopathies in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine (7th Edition). Philadelphia: W.B. Saunders, vol. 2, pps. 1659–1696, 1751–1803. 13. Zimmerman & Sole. (2001). Critical Care Nursing (3rd Edition). WB Saunders., pgs. 41-80, 176-180, 242-266. 14. Wung, S., Aouizerat, B. E. (Nov/Dec 2004). Aortic Aneurysms. Journal of Cardiovascular Nursing. Lippincott Williams & Wilkins, Inc.:19(6):409-416, 34(2).
Editor's Notes
- #3 CLINICAL JUDGMENT (80%) Pulmonary (17%) Acute Pulmonary Embolus Acute Respiratory Distress Syndrome (ARDS), to include acute lung injury (ALI) and respiratory distress syndrome (RDS) Acute Respiratory Failure Acute Respiratory Infection (e.g., pneumonia) Air-Leak Syndromes Aspiration Chronic Conditions (e.g., COPD, asthma, bronchitis, emphysema) Failure to Wean from Mechanical Ventilation Pulmonary Fibrosis Pulmonary Hypertension Status Asthmaticus Thoracic Surgery Thoracic Trauma (e.g., fractured rib, lung contusion, tracheal perforation)
- #7 Optimizing Mechanical Ventilation Continuous monitoring of the integrity of the ventilator circuit, including the artificial airway (Spahr-Schopfer, Bissonnette, & Hartley, 1993) or bag mask ventilation, in addition to potentially detecting mechanical ventilation malfunctions (Muniz, 2008; Hardman, Mahajan, & Curran, 1999; Kumar et al., 1992) Decreasing the duration of ventilatory support (Cheifetz & Myers, 2007) Adjustment of the trigger sensitivity (Thompson & Jaffe, 2005) Evaluation of the efficiency of mechanical ventilation, by the difference between PaCO2 and the PETCO2 (Kerr et al., 1996) Monitoring of the severity of pulmonary disease (Bedforth & Hardman, 1999; Ghamra & Arroliga, 2005) and evaluating the response to therapy, especially therapies intended to improve the ratio of dead space to tidal volume (VD/VT) and ventilation-perfusion matching (V/Q) (de Abreu et al., 1997; Bolyard et al., 1998; Engoren, 1993; Hardman & Aitkenhead, 1999; Hubble et al., 2000; Jellinek et al., 1993; Kallet et al., 2005; Russell & Graybeal, 1994; Szaflarski & Cohen, 1991; Taskar et al., 1995; McSwain et al., 2010). Monitoring of V/Q during independent lung ventilation (Cinnella et al., 2001; Colman & Krauss, 1999). Monitoring of inspired CO2 when it is being therapeutically administered (Fatigante et al., 1994). Graphic evaluation of the ventilator-patient interface. Evaluation of the capnogram may be useful in detecting rebreathing of CO2, obstructive pulmonary disease, the presence of inspiratory effort during neuromuscular blockade (curare cleft), cardiogenic oscillations, esophageal intubation, and cardiac arrest (Bhavani-Shankar et al., 1992). Measurement of the volume of CO2 elimination to assess metabolic rate and/or alveolar ventilation (Russell & Graybeal, 1994; Brandi et al., "Effects of ventilator resetting," 1999; Brandi et al., "Energy expenditure," 1999; Sullivan, Kissoon, & Goodwin, 2005) There is a relationship between VD/VT and survival in patients with the acute respiratory distress syndrome (Nuckton et al., 2002; Lucangelo et al., 2008; Raurich et al., 2010). Respiratory & Pulmonary Blood Flow Assessment Determining changes in pulmonary circulation and respiratory status sooner than pulse oximetry. In patients without lung disease, substantial hypercarbia may present before pulse oximetry notifies the clinician of a change in ventilation (Poirier et al., 1998; Roberts & Maniscalco, 1995; Hall et al., 1993; Roberts et al., 1995; Shibutani et al., 1994). Monitoring the adequacy of pulmonary, systemic, and coronary blood flow (Shibutani et al., 1994; Levine, Wayne, & Miller, 1997), as well as estimation of the effective (non-shunted) pulmonary capillary blood flow by a partial rebreathing method (de Abreu et al., 2002; de Abreu et al., 1997; vanHeerden et al., 2000). Evaluating the partial pressure of exhaled CO2, especially PETCO2. Screening for pulmonary embolism (Rodger & Wells 2001; Rodger et al., 2001; Bolyard et al., 1998; Rumpf, Krizmaric, & Grmec, 2009).
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- #68 Poor Prognosis
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