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CPAP (Continuous Positive Airway Pressure) Cardiogenic Pulmonary Edema Case Study • Call to residence @ 2146 • 76 y/o male, SOB • On arrival: • Pt. seated upright in living room • Conscious, obvious resp. distress, agitated • Pale, diaphoretic, clammy, audibly congested • Assessment/Questions/Initial Tx ? Case Study (cont’d) • Incident Hx; at rest, abrupt onset, now worse • PMHx; MI, CHF/Pulm. Edema, HPT, AAA repair, Renal Tumor, Rx • Presentation; sitting upright, tachypneic, 1-2 word dyspnea, ↓A/E bil. with coarse crackles throughout, now RSCP Case Study (cont’d) • Vitals; P 60, Irr, R 36-40, B/P 200/94, SpO2 76 RA, Skin-Pale/Dia. +++/Cool • Monitor; Sinus with PVC’s, 12-lead neg. • Any other questions/info req’d? • Tx? Case Study (cont’d) • O2 - Device, FiO2? • Position? Why? • Rx – Drug(s) of choice/availability/benefit • Directive • Goals of Tx? Case Study (cont’d) • Current options to improve oxygenation/ventilation? • NRB mask - benefits/limitations • BVM - benefits/limitations • ETT - benefits/limitations • Other options? Definitions • CHF - inability of heart to maintain forward circulation of blood. • Most severe manifestation; pulmonary edema • Pulmonary Edema - extravasation of fluid from pulmonary vasculature to interstitium/alveoli of lungs Pathophysiological Mechanisms • Imbalance of Starling forces • Damage to Alveolar/Capillary barrier • Lymphatic obstruction/dysfunction • Idiopathic Cardiogenic Pulmonary Edema • Normal fluid shift/removal: • Opposing forces of plasma oncotic pressure and pulmonary capillary hydrostatic pressure • Lymphatics remove excess • Abnormal: • Volume in pulmonary veins/left atrial venous • • return exceeds left ventricular output ↑pulmonary venous pressure ↑capillary hydrostatic pressure Pulmonary Edema (cont’d) • Pulmonary capillary pressure exceeds plasma colloidal osmotic pressure • (Norm. PCWP 8-12 mmHg, Normal Colloidal Osmotic Pressure 25-28 mmHg) • Fluid shifts to interstitium • Lymphatic removal does not increase in proportion to fluid accumulation Pulmonary Edema (cont’d) • Stages: • ↑Lt. atrial pressure opens/distends small pulmonary vessels • Fluid/colloids shift to interstitium • Continual filtration overwhelms lymphatics • Fluid accumulates/surround alveoli/bronchioles (compromises small airways first) • Increases space between capillaries/alveoli • Disrupts alveolar membrane-floods alveoli Pulmonary Edema (cont’d) • Effects: – Decreases vital capacity – Causes abnormalities in gas exchange – Decreases respiratory volume – Leads to hypoxemia Pulmonary Edema (cont’d) • Vicious cycle ensues: • ↓CO stimulates sympathetic activity • Renin-Angiotensin-Aldosterone system • Catecholamine production: – – – – – – ↑ PVR ↑ MVO2 exacerbates myocardial ischemia ↓ LV filling/emptying/function Further ↑ pulmonary capillary hydrostatic pressure More fluid shift Pulmonary Edema (cont’d) • Cardiac causes: • CAD • Loss of LV muscle/function • Valvular heart disease • Decreased diastolic ventricular compliance • Congenital heart disease • Myocarditis • Infectious endocarditis • ↑ B/P Pulmonary Edema (cont’d) • Precipitated by: • Ischemia • Dysrhythmia • Cardiac/extra cardiac infection • P.E. • Physical/environmental stress • Non-compliance/changes to Rx • Dietary changes • Iatrogenic volume overload • Pregnancy • Hyperthyroidism Differentials • ARDS • Anaphylaxis • Acute anemia • Bronchitis • COPD • Myopathies • Pneumonia • Pneumo • Shock (septic) • P.E. Treatment • ABC’s • Improve oxygenation/ventilation • O2 to keep SpO2 > 90% • Assist ventilations or provide non-invasive positive pressure ventilation • 3 Goals: • ↓ Preload • ↓ Afterload • Inotropic support Treatment (cont’d) • Preload reduction: • ↓’s pulmonary capillary hydrostatic pressure • ↓’s rate of fluid shift • Afterload reduction: • ↑’s CO • ↑’s Renal perfusion • Inotropic support: • For those that won’t tolerate preload/afterload reduction 2º to hypotension Nitroglycerin • Vasodilator • Used with normotensive/hypertensive patients • Most effective, predictable and rapidacting Rx available for preload reduction • Often occurs within 5 min. • Usually with some afterload reduction as well Nitroglycerine (cont’d) • • • • ↓’s MVO2 by ↓’ng workload ↑’s coronary blood flow ↑’s forward blood flow ↓’s pulmonary hydrostatic pressure/pulmonary congestion • SL spray: • Onset 1-3 min. • Half-life 5 min. Furosemide (Peterborough Region Only) • Long-standing mainstay of therapy • Thought to have two physiological effects: • Immediate venodilation • Diuretic affect • May in fact be more harmful than beneficial • Move away from use in many prehospital services Morphine (Peterborough Region Only) • Third drug in “classic” treatment • Again, thought to have two major benefits: • Preload/Afterload reduction through vasodilation • Anxiolytic/Analgesic effects • No sound evidence supports morphine-mediated • • preload reduction Recent studies show morphine use an independent predictor of mortality Use has declined both in-hospital and prehospital Non-invasive Ventilation • Delivery of ventilatory support without need of invasive artificial airway • Will often eliminate the need for intubation/tracheostomy • Benefits: • Easier to wean off ventilator • Preserves normal cough/swallowing/speech mechanisms NPPV (cont’d) • Two methods: • BiPAP (Bilevel Positive Airway Pressure) • CPAP (Continuous Positive Airway Pressure) CPAP • Delivered by nasal or face mask • Pt. breathes through mask against a continuous positive a/w pressure • Can be delivered by either volume or pressure controlled ventilator • Delivers set pressure with each breath, maintained throughout the respiratory cycle CPAP (cont’d) • Mechanism: • Increases gas exchange 2º to increased alveolar ventilation • Prevents alveolar collapse during exhalation by maintaining a positive intra-alveolar pressure • ↑’s intrathoracic pressure, reducing preload/afterload and improving cardiac output CPAP (cont’d) • Benefits: • Reduces need for intubation • Pt. saves energy otherwise spent trying to reopen collapsed alveoli • ↓’ WOB: improves alveolar ventilation while simultaneously resting respiratory muscles • ↓’s metabolic rate/substrate need to fuel respiratory effort CPAP (cont’d) • Advantages: • Avoidance of intubation-related trauma • Decreased incidence of nosocomial pneumonia • Enhances pt. comfort • Shorter duration of ventilator use/facilitates weaning • Decreased hospital stay • Decreased costs CPAP (cont’d) • Usage: • Currently utilized primarily in-hospital setting and by critical care EMS systems • Also used in-home • Wide-scale EMS use previously limited by cost/complexity of technology • Newer technology and sig. reduced costs lend to increased use pre-hospital • Numerous systems incorporating CPAP as standard for pulmonary edema therapy