Manual for Pulmonary and Critical Care Medicine E-Book

Judd Landsberg

• Publisher: Elsevier
• Year: 2017
• ISBN:
  9780323480550
• Topic: Medicina
• Subtopic: Medicina polmonare e toracica

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.

Section I

Pulmonary

Chapter 1

Approach to oxygenation, hypoxemia, and hypoxemic respiratory failure

Common misconceptions and mistakes

• Hypoxemia is a significant cause of dyspnea

• A cutaneous O₂ sat ≥92% predicts adequate oxygenation and is the appropriate target for O₂ orders

• 100% O₂ suppresses respiratory drive in CO₂ retainers

• O₂ supplementation for patients with COPD is given to improve exercise tolerance

• 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

• Normal oxygenation (at sea level) predicts:

• A partial pressure of oxygen (Pao₂) of 75–100 mm Hg with 21% Fio₂ (room air) and a Pao₂ of ~660 mm Hg with 100% Fio₂

• Impaired oxygenation exists on a spectrum from mild (abnormal A-a gradient) to severe (shunt):

• Pao₂<200 mm Hg on Fio₂ of 100%=“shunt physiology”

• Without “shunt physiology” 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

• 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)

• What defines adequate oxygenation Pao₂, O₂ sat, or it depends? Correct answer, Pao₂:

• Tissue oxygenation is a function of the circulatory system (primarily cardiac output (CO) and hemoglobin (Hb))

• Systemic hypoxia, the result of failed oxygen delivery to tissue (e.g. distributive shock), leads to systemic lactic acidosis

• Increasing Pao₂ does not meaningfully increase oxygen delivery to tissues or decrease lactate

• The job of the respiratory system is to maintain a Pao₂ >60 mm Hg

• When Pao₂ drops acutely to <60 mm Hg (hypoxemia), organ specific symptomatic hypoxia may occur

• Especially in the brain, heart, and kidney (high metabolic demand)

• When treating hypoxemia hypoxemia target, a Pao₂>60 mm Hg

• Hypoxemic respiratory failure is practically defined as a Pao₂<60 mm Hg

• An acute drop in Pao₂<60 mm Hg (but >54 mm Hg), ie, “mild hypoxemia,” may cause a range of symptoms:

• Tachypnea (hypoxic hyperventilation reflex)

• Designed to increase alveolar O₂ by decreasing alveolar CO₂, thereby increasing work of breathing

• Tachycardia

• 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)

• Mental status changes (agitation, confusion, and decreased sensorium)

• Increased left ventricular end-diastolic pressure (LVEDP) (a.k.a. heart failure) from diastolic dysfunction

• Hypoxia stiffens the left ventricle (LV) and tachycardia shortens diastole, both impairing ventricular filling

• Decreased glomerular filtration rate (GFR) from increased LVEDP (cardio-renal physiology) or hypoxic renal injury

• 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 hemoglobin–oxygen [Hb–O₂] dissociation curve)

• 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

• Efforts then focus on resolution of the underlying cause of hypoxemia

• A low O₂ saturation, occurring with a Pao₂>60 mm Hg, indicates acidosis (causing Hb desaturation), not hypoxemic respiratory failure

• Efforts then focus on resolving the acidosis (eg, renal replacement therapy)

• Symptomatic hypoxemia can be effectively ruled out by demonstrating a Pao₂>60 mm Hg

• And, to a lesser extent, screened for by a cutaneous O₂ saturation (with a good wave form) >94%

• Pulse oximeter readings >92% (but <95%) may mask a Pao₂<60 mm Hg because of alkalosis or error (Figs. 1.1 and 1.2)

Fig. 1.1 Hemoglobin–oxygen dissociation curve. Shown is the Bohr effect (eg, shift in Hb saturation based on pH) where, for any given Pao₂ value, alkalosis promotes increased saturation and acidosis decreases it. The shaded area in red shows individuals whose cutaneous pulse oximet...