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Manual for Pulmonary and Critical Care Medicine E-Book
Judd Landsberg
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- 416 pages
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eBook - ePub
Manual for Pulmonary and Critical Care Medicine E-Book
Judd Landsberg
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Clinical Practice Manual for Pulmonary and Critical Care Medicine, by Judd W. Landsberg, MD, is a unique point-of-care manual that provides essential information on managing inpatients and outpatients with common, serious respiratory and internal medicine presentation and problems. Easy-to-follow diagnostic and therapeutic algorithms are accompanied by case-based illustrations encountered on a daily basis by attendings, fellows, residents, and students. The bulleted format, concise approach, and familiar examples provide a framework for effective teaching, learning, and patient care.
- Identifies common but important misconceptions that are regularly encountered in pulmonary and critical care training.
- Uses a concise, bulleted format throughout, helping you find key information quickly.
- Illustrates cases with primary data such as x-rays, monitor strips, ventilator wave forms, and other familiar documentation.
- Helps you develop your ability to effectively explain your thought process in the clinical setting to other practitioners at the bedside.
- Serves as a 'teachers guide' for clinician educators, organizing topics in an easy to teach fashion, amenable to 'chalk talks' and bedside didactics
- Provides focused discussions of basic physiology and pathophysiology related to pulmonary and critical care medicine.
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Informations
Sujet
MedicineSous-sujet
Pulmonary & Thoracic MedicineSection I
Pulmonary
Chapter 1
Approach to oxygenation, hypoxemia, and hypoxemic respiratory failure
Common misconceptions and mistakes
âą Hypoxemia is a significant cause of dyspnea
âą A cutaneous O2 sat â„92% predicts adequate oxygenation and is the appropriate target for O2 orders
âą 100% O2 suppresses respiratory drive in CO2 retainers
âą O2 supplementation for patients with COPD is given to improve exercise tolerance
âą Confusing failure of oxygen delivery to tissues, hypoxia (the job of the circulatory system) with hypoxemia, and failure to maintain an adequate Pao2 (the job of the respiratory system)
Oxygenation
âą Normal oxygenation (at sea level) predicts:
âą A partial pressure of oxygen (Pao2) of 75â100 mm Hg with 21% Fio2 (room air) and a Pao2 of ~660 mm Hg with 100% Fio2
âą Impaired oxygenation exists on a spectrum from mild (abnormal A-a gradient) to severe (shunt):
âą Pao2<200 mm Hg on Fio2 of 100%=âshunt physiologyâ
âą Without âshunt physiologyâ an Fio2>40% (~>6 L/min via nasal cannula (NC)) should give a Pao2>60 mm Hg, despite pathology causing an abnormally increased A-a gradient
âą Patients demonstrating shunt physiology are at high risk for hypoxemic respiratory failure, necessitating a search for the underlying cause, as well as close observation and aggressive support (e.g. chest imaging, 100% Fi02)
âą What defines adequate oxygenation Pao2, O2 sat, or it depends? Correct answer, Pao2:
âą Tissue oxygenation is a function of the circulatory system (primarily cardiac output (CO) and hemoglobin (Hb))
âą Systemic hypoxia, the result of failed oxygen delivery to tissue (e.g. distributive shock), leads to systemic lactic acidosis
âą Increasing Pao2 does not meaningfully increase oxygen delivery to tissues or decrease lactate
âą The job of the respiratory system is to maintain a Pao2 >60 mm Hg
âą When Pao2 drops acutely to <60 mm Hg (hypoxemia), organ specific symptomatic hypoxia may occur
âą Especially in the brain, heart, and kidney (high metabolic demand)
âą When treating hypoxemia hypoxemia target, a Pao2>60 mm Hg
âą Hypoxemic respiratory failure is practically defined as a Pao2<60 mm Hg
âą An acute drop in Pao2<60 mm Hg (but >54 mm Hg), ie, âmild hypoxemia,â may cause a range of symptoms:
âą Tachypnea (hypoxic hyperventilation reflex)
âą Designed to increase alveolar O2 by decreasing alveolar CO2, thereby increasing work of breathing
âą Tachycardia
âą The right ventricle (RV) attempts to maintain CO in the face of rising pulmonary artery pressure (PAP) (hypoxic vasoconstriction) and decreased stroke volume (SV) by increasing heart rate (HR)
âą Mental status changes (agitation, confusion, and decreased sensorium)
âą Increased left ventricular end-diastolic pressure (LVEDP) (a.k.a. heart failure) from diastolic dysfunction
âą Hypoxia stiffens the left ventricle (LV) and tachycardia shortens diastole, both impairing ventricular filling
âą Decreased glomerular filtration rate (GFR) from increased LVEDP (cardio-renal physiology) or hypoxic renal injury
âą Additionally, asymptomatic patients with an acute drop in Pao2 (<60 mm Hg) are at increased risk for sudden profound/life-threatening desaturations (steep portion of the hemoglobinâoxygen [HbâO2] dissociation curve)
âą When patients in hypoxemic respiratory failure achieve a Pao2>60 mm Hg (without hyperventilation) no further increase in respiratory support aimed at improving oxygenation is required
âą Efforts then focus on resolution of the underlying cause of hypoxemia
âą A low O2 saturation, occurring with a Pao2>60 mm Hg, indicates acidosis (causing Hb desaturation), not hypoxemic respiratory failure
âą Efforts then focus on resolving the acidosis (eg, renal replacement therapy)
âą Symptomatic hypoxemia can be effectively ruled out by demonstrating a Pao2>60 mm Hg
âą And, to a lesser extent, screened for by a cutaneous O2 saturation (with a good wave form) >94%
âą Pulse oximeter readings >92% (but <95%) may mask a Pao2<60 mm Hg because of alkalosis or error (Figs. 1.1 and 1.2)