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RESPIRATORY DISTRESS. September 8, 2005 Prepared by Christina M. Cabott D.O. RESPIRATORY DISTRESS. DYSPNEA HYPOXIA HYPERCAPNEA WHEEZING COUGH HICCUPS CYANOSIS PLEURAL EFFUSION. DYSPNEA. Common complaint described as “shortness of breath” “breathlessness” “not getting enough air”
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RESPIRATORY DISTRESS September 8, 2005 Prepared by Christina M. Cabott D.O.
RESPIRATORY DISTRESS • DYSPNEA • HYPOXIA • HYPERCAPNEA • WHEEZING • COUGH • HICCUPS • CYANOSIS • PLEURAL EFFUSION
DYSPNEA • Common complaint described as • “shortness of breath” • “breathlessness” • “not getting enough air” • 2/3 of patients presenting to ED with dyspnea have either a cardiac or pulmonary disorder
DYSPNEA • Definitions: • Tachypnea: rapid breathing • Orthopnea: dyspnea in a recumbent position • Most often a result of LV failure • May be associated with diaphragmatic paralysis or COPD
DYSPNEA • Definitions: • Paroxysmal nocturnal dyspnea: orthopnea that awakens the patient from sleep • Trepopnea: dyspnea associated with only one of several recumbent positions • can occur with unilateral diaphragmatic paralysis • ball-valve obstruction • after surgical pneumonectomy
DYSPNEA • Definitions: • Platypnea: dyspnea in the upright position • Result from loss of abdominal wall muscular tone • Rarely, from left-to-right intracardiac shunting (e.g. patent foramen ovale) • Hyperpnea: hyperventilation with a minute ventilation in excess of metabolic demand
DYSPNEA • Pathophysiology • No defined neural pathway, derived from mechanical, chemical, and vascular receptors
DYSPNEA • Processes involved in sensation of dyspnea: 1. Conscious sense of voluntary peripheral skeletal and respiratory muscular efforts with increased work of breathing 2. Stimulation of upper airway mechanical and thermal receptors
DYSPNEA 3. Decreased stimulation of chest all afferents 4. Stimulation of central hypercapneic chemoreceptors in the central medulla 5. Stimulation of peripheral hypoxic chemoreceptors, in carotid body and aortic arch
DYSPNEA 6. Stimulation of intraparenchymal pulmonary stretch receptors, airway irritant receptors, and unmyelinated receptors, responding to interstitial edema or changes in compliance 7. Stimulation of peripheral vascular receptors • right and left atrial mechanoreceptors • pulmonary artery baroreceptor
DYSPNEA • Input from all of these receptors is integrated in the CNS at subcortical and cortical levels
DYSPNEA • Clinical features that may signify impending respiratory failure • Presentation: • shortness of breath or breathlessness • tachypnea • tachycardia • use of accessory respiratory muscles • stridor
DYSPNEA • Clinical features that may signify impending respiratory failure • Presentation: • inability to speak, secondary to breathlessness • agitation or lethargy • paradoxical abdominal wall movement with inspiration (abdominal wall retracts inward)
DYSPNEA • Clinical features • Evaluation • abnormal vital signs • ABCs • Need rapid airway control and intervention • airway obstruction • ineffective respiratory effort • changes in mental status
Most Common Causes Asthma & COPD CHF/ cardiogenic pulmonary edema Ischemic heart dz Unstable angina &MI Pneumonia Psychogenic Most Immediately Life Threatening Foreign body Angioedema Hemorrhage Tension pneumo PE Myasthenia gravis Guillain-Barre Botulism CAUSES OF DYSPNEA
pulse oximetry and ABG CXR EKG peak flows Hgb and Hct BNP (>100 pg/ml) spirometry pulmonary function tests cardiac stress tests echocardiography exercise testing electromyography V/Q scan pulmonary biopsy Ancillary Tests Used for Dyspnea Diagnosis
DYSPNEA • ED treatment • Supplemental O2: PaO2 >60 mm Hg; pulse ox >91 to 93% • CPAP or BiPAP • Bag-valve-mask ventilation • Intubation with mechanical ventilation • Patients with unclear cause of dyspnea and hypoxia require admission for monitoring
HYPOXEMIA • Pathophysiology • Def: inadequate delivery of oxygen to tissues • Amount of oxygen available to the tissues is a function of the arterial oxygen content (CaO2) CaO2 = 0.0031 X PaO2 + 1.38 X Hb X SaO2 • PaO2 < 60 mm Hg
HYPOXEMIA • Relative hypoxemia • Arterial oxygen tension is lower than expected for a given level of inhaled oxygen • Can be calculated by doing A-a gradient
HYPOXEMIA • Simplified formula P(A-a)O2 = 145 - PaCO2 - PaO2 • Normal P(A-a)O2 is under 10 mm Hg in young, healthy patients and increases with age • Predicted A-a gradient with age • P(A-a)O2 = 2.6 + 0.21 (age in years) (+ 11)
HYPOXEMIA • Pathophysiology • 5 distinct mechanisms 1. Hypoventilation 2. Right-to-left shunt 3. Ventilation/perfusion mismatch 4. Diffusion impairment 5. Low inspired oxygen
HYPOXEMIA • Hypoventilation • Rising PaC02 displaces O2 from the aveolus PaO2 O2 diffusion gradient across the pulmonary membrane • Normal A-a O2 gradient
HYPOXEMIA • Right-to-left shunting • Unoxygenated blood enters the systemic circulation • May occur secondarily to under ventilated lung or with congenital heart anomalies • Increase in A-a O2 gradient • Will have failure of arterial oxygen levels to increase in response to supplemental O2
HYPOXEMIA • Ventilation/Perfusion Mismatch • Regional alterations of ventilation or perfusion • Etiologies: PE, pneumonia, asthma, COPD, extrinsic vascular compression • Increased A-a O2 gradient • Hypoxemia improves with supplemental O2
HYPOXEMIA • Diffusion impairment • Impairment of alveolar-blood barrier • Increased A-a O2 gradient • Hypoxemia improves with supplemental O2
HYPOXEMIA • Low inspired oxygen • High altitude hypoxia • Nonobstructive asphyxia • Normal A-a O2 gradient • Hypoxemia improves with supplemental O2
HYPOXEMIA • Acute compensatory mechanisms • 1. Minute ventilation • 2. Pulmonary artery vasoconstriction perfusion to hypoxic alveoli • 3. Sympathetic tone oxygen delivery by HR and cardiac output
HYPOXEMIA • Chronic compensatory mechanisms • 1. Red blood cell mass • 2. Tissue oxygen demand
HYPOXEMIA • Clinical Features • Signs and symptoms are nonspecific • Cardio-pulm: tachycardia and tachypnea • CNS: aggitation, seizures, and coma • At PaO2 < 20 mm Hg, paradoxical depression of respiratory drive • Dyspnea may or may not be present
HYPOXEMIA • Diagnosis and Differential • Pulse ox = screening test • ABG = defines diagnosis • Similar tests used to determine cause of dyspnea may be useful in evaluating hypoxia
HYPOXEMIA • ED treatment • Treatment: support, identify, and aggressively treat underlying cause • Maintain PaO2 >60 mm Hg with supplemental O2 • Arterial line if frequent ABGs Patients with persistent hypoxia require hospitalization
HYPERCAPNEA • Pathophysiology • def: PaO2 >45 mm Hg • Caused by hypoventilation • rapid shallow breathing • small tidal volumes • underventilation of lung reduced respiratory drive • Never due to intrinsic lung disease or increased CO2 production
HYPERCAPNEA • Causes of Hypercapnea • Depressed central respiratory drive • Structural CNS disease: brainstem lesions • Sedating drugs: opiates, sedatives, anesthetics • Exogenous toxins • Endogenous toxins: tetanus
HYPERCAPNEA • Causes of Hypercapnea • Thoracic cage disorders • Kyphoscoliosis • Morbid obesity • Neuromuscular impairment • Neuromuscular disease: myasthenia gravis, Guillain-Barre syndrome • Neuromuscular toxins: organophosphate poisoning, botulism
HYPERCAPNEA • Causes of Hypercapnea • Intrinsic lung disease associated with increased dead space • COPD • Upper airway obstruction
HYPERCAPNEA • Pathophysiology • Alveolar ventilation • Less than minute ventilation • Dependent on the tidal volume less the anatomic dead space and the respiratory rate • Efferent neuronal imput from the medulla’s chemoreceptors control tidal volume and respiratory rate
HYPERCAPNEA • Clinical Features • Signs and symptoms are dependent on rate and degree of elevation • Acute rise in elevation • increase in ICP, confusion, lethargy, asterixis, seizures, and coma • Acute changes to PaCO2 >100 mm Hg may lead to cardiovascular collapse
HYPERCAPNEA • Clinical Features • Acute retention: • For each 10 mm Hg increase of PaCO2, the pH will decrease by 0.1 U • For each 10 mm Hg increase of PaCO2, the HCO3 will increase by 1 mEq/L
HYPERCAPNEA • Clinical Features • Chronic retention: • May be well tolerated • Kidneys retain HCO3 • For every 10 mm Hg of PaCO2 over 40 mm Hg, HCO3 increases by 3.5 meq/L
HYPERCAPNEA • ED treatment • Identify threats to life, evaluate, and aggressively treat deficiencies in the ABCs • e.g. narcotic overdose - tx with naloxone • e.g. neuromuscular disease - tx with assisted or mechanical ventilation
HYPERCAPNEA • ED treatment • Supplemental oxygen should be given to maintain level normal for the patient • Don’t withhold oxygen based on worry of “decreased respiratory drive” • Hypoxia and extreme hypercapnea will kill • Bipap or CPAP - use as a bridge, not definitive care • Mechanical ventilation
WHEEZES • Pathophysiology • Def: musical adventitious lung sounds produced by turbulent flow through the central and distal airways • Obstruction: bronchospasm, smooth muscle hypertrophy, increased secretions, and peribronchial inflammation
WHEEZES • Clinical features • Usually occurs in asthma and other obstructive pulmonary diseases • “Not all that wheezes is asthma.” • Not every obstructive pulmonary disease will cause wheezing • e.g. severe asthma - quiet chest, not moving enough air to produce turbulent flow
WHEEZES • Causes of wheezing • Upper airway (stridor most likely, may have wheezing) • Angioedema: allergic, ACE inhibitor, idiopathic • Foreign body • Infection: croup, epiglottitis, tracheitis
WHEEZES • Causes of wheezing • Lower airway • Asthma • Transient airway hyperreactivity (usually due to infection or irritation) • Bronchiolitis • COPD • Foreign body
WHEEZES • Causes of wheezing • Cardiogenic • Cardiogenic pulmonary edema (“cardiac asthma”) • Noncardiogenic pulmonary edema • Adult respiratory distress syndrome [ARDS] • Pulmonary embolus (rare) • Psychogenic
WHEEZES • Diagnosis • Diagnosis is suspected in the proper clinical situation • Patient improves with relief of airway obstruction • Decreased work of breathing • Improvement of pulse ox • Decreased respiratory rate
WHEEZES • Diagnosis • Definitive diagnosis confirmed by spirometric testing • Cannot be done at the bedside or during an acute exacerbation • Hand held peak-flow meter used as an adjunct to gauge response to treatment • Value >80% predicted = normal • Limitations: effort and usefulness in kids
WHEEZES • Diagnosis • Other ancillary tests • CXR and ABG • May not be needed during an uncomplicated obstructive pulmonary disease
WHEEZES • ED treatment • Initial treatment: directed at identifying threats to life and aggressively treating the underlying condition • Supplemental oxygen: given if hypoxia and degree of obstruction • Monitoring