RESPIRATORY DISTRESS September 8, 2005 Prepared by Christina M. Cabott D.O.
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Transcript of RESPIRATORY DISTRESS September 8, 2005 Prepared by Christina M. Cabott D.O.
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RESPIRATORY DISTRESS
September 8, 2005
Prepared by Christina M. Cabott D.O.
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RESPIRATORY DISTRESS
DYSPNEA HYPOXIA HYPERCAPNEA WHEEZING COUGH HICCUPS CYANOSIS PLEURAL EFFUSION
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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
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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
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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
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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
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DYSPNEA
Pathophysiology– No defined neural pathway, derived from
mechanical, chemical, and vascular receptors
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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
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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
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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
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DYSPNEA
Input from all of these receptors is integrated in the CNS at subcortical and cortical levels
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DYSPNEA
Clinical features that may signify impending respiratory failure– Presentation:
• shortness of breath or breathlessness• tachypnea• tachycardia• use of accessory respiratory muscles• stridor
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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)
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DYSPNEA
Clinical features– Evaluation
• abnormal vital signs• ABCs
– Need rapid airway control and intervention• airway obstruction• ineffective respiratory effort• changes in mental status
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CAUSES OF DYSPNEA
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
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Ancillary Tests Used for Dyspnea Diagnosis
– 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
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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
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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
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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
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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)
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HYPOXEMIA
Pathophysiology– 5 distinct mechanisms
1. Hypoventilation
2. Right-to-left shunt
3. Ventilation/perfusion mismatch
4. Diffusion impairment
5. Low inspired oxygen
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HYPOXEMIA
Hypoventilation– Rising PaC02 displaces O2 from the aveolus
PaO2 O2 diffusion gradient across the pulmonary membrane
– Normal A-a O2 gradient
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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
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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
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HYPOXEMIA
Diffusion impairment– Impairment of alveolar-blood barrier
– Increased A-a O2 gradient
– Hypoxemia improves with supplemental O2
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HYPOXEMIA
Low inspired oxygen– High altitude hypoxia– Nonobstructive asphyxia
– Normal A-a O2 gradient
– Hypoxemia improves with supplemental O2
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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
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HYPOXEMIA
Chronic compensatory mechanisms– 1. Red blood cell mass– 2. Tissue oxygen demand
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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
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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
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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
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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
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HYPERCAPNEA
Causes of Hypercapnea– Depressed central respiratory drive
• Structural CNS disease: brainstem lesions• Sedating drugs: opiates, sedatives, anesthetics• Exogenous toxins• Endogenous toxins: tetanus
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HYPERCAPNEA
Causes of Hypercapnea– Thoracic cage disorders
• Kyphoscoliosis• Morbid obesity
– Neuromuscular impairment• Neuromuscular disease: myasthenia gravis,
Guillain-Barre syndrome• Neuromuscular toxins: organophosphate
poisoning, botulism
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HYPERCAPNEA
Causes of Hypercapnea– Intrinsic lung disease associated with
increased dead space• COPD
– Upper airway obstruction
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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
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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
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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
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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
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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
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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
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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
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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
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WHEEZES
Causes of wheezing– Upper airway (stridor most likely, may have
wheezing)• Angioedema: allergic, ACE inhibitor, idiopathic• Foreign body• Infection: croup, epiglottitis, tracheitis
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WHEEZES
Causes of wheezing– Lower airway
• Asthma• Transient airway hyperreactivity (usually due to
infection or irritation)• Bronchiolitis• COPD• Foreign body
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WHEEZES
Causes of wheezing– Cardiogenic
• Cardiogenic pulmonary edema (“cardiac asthma”)
• Noncardiogenic pulmonary edema – Adult respiratory distress syndrome [ARDS]
• Pulmonary embolus (rare)
– Psychogenic
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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
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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
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WHEEZES
Diagnosis– Other ancillary tests
• CXR and ABG• May not be needed during an uncomplicated
obstructive pulmonary disease
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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
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WHEEZES
ED treatment– Initial treatment of wheezing
• inhaled beta-agonists (e.g. albuterol) and/or anticholinergic agents (e.g. ipratropium bromide)
– Acute setting• steroids to help reduce airway inflammation
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WHEEZES
ED treatment– Admission of patients
• Oxygen requirements• Potential for quick decompensation• Failed treatment• Require mechanical ventilation
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COUGH
Pathophysiology– Protective reflex that acts to clear
secretions and debris from tracheobronchial tree
– Initiated by stimulation of irritant receptors located in larynx, trachea, and major bronchi
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COUGH
Pathophysiology– Receptor signal travel via vagus,
phrenic, and other nerves cough center of the medulla cough pattern
– Cough pattern:• deep inspiration expiration against closed
glottis glottis opens forceful exhalation of air, secretions and foreign debris from tracheobronchial tree
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COUGH
Pathophysiology– Stimulation of receptors
• inhaled irritants (e.g. dust)
• allergens (e.g. ragweed pollen)
• toxic substances (e.g. gastric acid)
• hypo- or hyperosmotic liquids
• inflammation (e.g. asthma)
• cold air
• instrumentation
• excess pulmonary secretions
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COUGH
Categories– Acute– Chronic
• Cough present more than 3 weeks without any periods of resolution
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COUGH
Acute Causes– Upper respiratory infection: rhinitis, sinusitis– Lower respiratory infection: bronchitis, pneumonia– Allergic RXN– Asthma– Environmental irritants– Transient airway hyperresponsiveness– Foreign body
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COUGH
Common Chronic Causes– Smoking and/or chronic bronchitis– Postnasal drainage– Asthma: reactive airway disease - worse at night– Gastroesophageal reflux– Angiotensin-converting enzyme inhibitor - b/c
accumulation of bradykinin and substance P– Angiotensin II receptor blocker
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COUGH
Less Common Chronic Causes– Congestive Heart Failure– Bronchiectasis– Lung cancer or other intrathorcic mass– Emphysema– Occupational and environmental irritants– Recurrent aspiration or chronic foreign body– Cystic fibrosis– Interstitial lung disease
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COUGH
Diagnosis– Most acute cough does not require routine
ancillary tests• CXR: if purulent sputum and/or fever• Spirometry: evaluation of airflow obstruction in
asthmatics
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COUGH
Diagnosis– Chronic cough
• Treatment based on clinical assessment first• Ancillary tests performed only if symptoms
persist– Nasolaryngoscopy - document mucosal inflammation
and excessive mucous drainage– Sinus radiographs or CT - check for sinusitis– Spirometry - check for airflow obstruction
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COUGH
Acute treatment– Cough suppressants
• opioids: dextromethorphan, codeine, and oxycodone
– Demuculants
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COUGH
Chronic treatment
1. Reduce lung irritant exposure
2. Discontinue use of ACE inhibitors, ARBs, and B-blockers
3. Treat post-nasal drainage with oral antihistamine-decongestant and/or nasal steroid
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COUGH
Chronic treatment
4. Evaluate and treat for asthma
5. Obtain CXR and sinus x-ray
6. Evaluate and treat GE reflux
7. Refer patient for bronchoscopy
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HICCUPS
Hiccups a.k.a singultus– Def: an involuntary respiratory reflex with
spastic contraction of the inspiratory muscles against a closed glottis, producing the characteristic sound
– There is no specific protective purpose known for hiccups
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HICCUPS
Pathophysiology– Afferent: phrenic and vagus nerves and thoracic
sympathetic chain– Intensive interconnection among the
hypothalamus, medullary reticular formation, respiratory center, and cranial nerve nuclei
– Efferent: phrenic nerve, recurrent laryngeal branch of the vagus nerve, and the motor nerves to the anterior scalene and intercostal muscles
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HICCUPS
Pathophysiology– 30 to 40 msec after the onset of inspiration,
glottic closure is stimulated– In cases where a specific cause can be
assigned, hiccups appear to result from stimulation, inflammation, or injury to one of the nerves of the reflex arc
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HICCUPS
Causes of Hiccups– Acute: benign, self-limited
• Gastric distention - from food, drinking (especially carbonated drinks), or air
• Alcohol intoxication• Excessive smoking• Abrupt change in environmental temperature• Psychogenic - excitement or stress
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HICCUPS
Causes of Hiccups– Chronic: persistent, intractable
• Central nervous system structural lesions• Vagal or phrenic nerve irritation• Metabolic: uremia, hyperglycemia• General anesthesia• Surgical procedures: thoracic, abdominal,
prostate, urinary tract, craniotomy
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HICCUPS
Diagnosis– Benign hiccups
• Resolves spontaneously or with simple maneuvers
• Do not seek medical attention• Do not require specific diagnosis
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HICCUPS
Diagnosis– Persistent hiccups
• History to determine specific event associated with the onset
• Persistence during sleep– Suggests organic cause
• Resolution during sleep– Suggests psychogenic cause– Most patients with benign hiccups
• Inquiries about general anesthesia, surgical procedures, and metabolic diseases
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HICCUPS
Diagnosis– Persistent hiccups
• Evaluate external auditory canal– hair in canal can press up against the tympanic
membrane and stimulate the auricular branch of the vagus nerve
• CXR– evaluate for intrathoracic pathology
• Fluoroscopy – evaluate unilateral vs bilateral diaphragmatic
movement during hiccups
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HICCUPS
Treatment with physical maneuvers– Stimulating the pharynx will block vagal portion of
reflex arc and abolish hiccups
Treatment with medications– chlorpromazine– metoclopramide– nifedipine– valproic acid– baclofen
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HICCUPS
chlorpromazine – 25 to 50 mg IV, with
repeated dose in 2 to 4 hours, if needed
– If improvement, 25 to 50 mg po tid or qid
– May cause extrapyramidal symptoms
– Usually works within 30 min
metoclopramide – 10 mg IV or IM– If effective, 10 to 20
mg po qid for 10 days– May cause
extrapyramidal symptoms or hypotension
– Usually works within 30 min
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HICCUPS
nifedipine– 10 to 20 mg po tid or qid
valproic acid– 15 mg/kg per day po tid
baclofen– 10 mg po tid
These all work more gradually
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CYANOSIS
Pathophysiology– Indicated by the bluish color of the skin and
mucus membranes– Resulting from an increased amount of
deoxyhemoglobin– Usually 5 g/ 100 mL of deoxyhemoglobin
must be present for cyanosis to occur– Amount of oxyhemoglobin does not matter
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CYANOSIS
Pathophysiology– Various factors affect the presence or
absence of cyanosis• Skin pigmentation• Skin thickness• Subcutaneous microcirculation• Lighting• Ambient temperature
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CYANOSIS
Clinical Features– Presence of cyanosis signals tissue
hypoxia, but not always • Sensitive indicator = tongue• Less sensitive indicators = earlobes,
conjunctiva, and nail beds
– Cause either central or peripheral cyanosis
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CYANOSIS
Clinical Features– Central cyanosis
• Result of unsaturated arterial blood or abnormal hemoglobin (e.g. methemoglobin)
– Peripheral cyanosis• Caused by decreased peripheral circulation and
clinical situations that lead to an increased arterial oxygen extraction
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CYANOSIS
Central cyanosis– Hemoglobinopathies
• Methemoglobin: acquired; hereditary• Sulfhemoglobinemia: acquired
– Decreased arterial oxygen saturation• Pulmonary etiologies: shunt , diffusion, V/Q
mismatch• Hypoventilation• High altitude
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CYANOSIS
Central cyanosis– Anatomic right-to-left shunts
• Cardiac: Ventricular Septal Defect (VSD), Atrial Septal Defect (ASD), and Tetralogy of Fallot (TOF)
• Intrapulmonary• Intrapulmonary shunts
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CYANOSIS
Peripheral cyanosis– Decreased cardiac output– Distributive shock– Cold exposure on extermities– Venous congestion– Arterial thrombosis or embolus
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CYANOSIS
Diagnosis– Presence of cyanosis must be taken in
context with clinical situation– Tests
• ABG: will confirm the diagnosis• Hematocrit: check for polycythemia or anemia• CXR• EKG• Abnormal hemoglobin tests
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PSEUDOCYANOSIS
Blue, gray, or purple cutaneous discoloration that may mimic cyanosis
Causes– Heavy metals: iron (hemochromatosis),
gold, silver, lead, and arsenic– Drugs: phenothiazines, minocycline,
amiodarone, and chloroquine
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PSEUDOCYANOSIS
Chrysiasis– Gray, blue, or purple pigmentation of areas
exposed to light– Rare-dose dependent complication of gold
treatment that causes permanent discoloration of the skin
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PSEUDOCYANOSIS
Argyria– Slate blue to gray coloration of skin– Results of chronic ingestion or local
application of silver salts or colloidal silver,
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CYANOSIS
True cyanosis DOES blanch when direct pressure is applied to skin
Pseudocyanosis DOES NOT blanch when direct pressure is applied to skin
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CYANOSIS
Diagnosis– Methemoglobin, sulfhemoglobin, and
carbon monoxide poisoning must be kept in mind
• Artificially alter peripheral pulse oximetry, secondary to pigment formation in the blood
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CYANOSIS
Diagnosis– Methemoglobin,
• Causes– Drugs: most commonly by benzocaine and nitrates– Hereditary: rare genetic disorder affecting NADH
• Visible cyanosis with as little as 1.5 g/dL• Incapable of binding oxygen• Symptoms related to hypoxia
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CYANOSIS
Diagnosis– Methemoglobin
• Severity of symptoms related to quantity, rapidity of onset, and pts cardiovascular system
• Need to consider if oxygen supplementation does not correct hypoxia
• Venous blood looks chocolate brown• Treatment: methylene blue
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CYANOSIS
Diagnosis– Sulfhemoglobin
• Caused commonly by phenacetin or acetanilid• Inert as an oxygen carrier• Can produce deep cyanosis at level < 0.5 g/dL• Irreversible• Treatment
– symptomatic and supportive care– identification and removal of suspected causes
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CYANOSIS
ED treatment– Central cyanosis
• Supplemental oxygen• supplied in appropriate conditions
– Methemoglobinemia• Methylene blue 1 to 2 mg/kg of body weight IV
over 5 minutes
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PLEURAL EFFUSION
Result from fluid accumulating in potential space between visceral and parietal pleura
Most common causes in developed countries– CHF– Pneumonia– Cancer
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PLEURAL EFFUSION
Pathophysiology– Normally, small amount of fluid is secreted
from parietal pleura into pleural space, where it is absorbed by visceral pleural microcirculation
– Small amount of fluid decreases friction between the pleural layers and allows for smooth lung expansion and contraction during respiration
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PLEURAL EFFUSION
Pathophysiology– Transudates
• Result of imbalance in hydrostatic or oncotic pressure
• Produces an ultrafiltrate across the pleural membrane
• Low protein content
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PLEURAL EFFUSION
Pathophysiology– Exudates
• Result of pleural disease, usually inflammation or neoplasm
• Active fluid secretion or leakage• High protein content
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COMMON CAUSES OF PLEURAL EFFUSION
Transudates– CHF
Transudate or exudate– Diuretic therapy
Exudates– Cancer: primary or
metastatic– Bacterial pneumonia
with parapneumonic effusion
– Pulmonary embolism
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LESS COMMON CAUSES OF PLEURAL EFFUSION
Transudates– Cirrhosis with ascites– Peritoneal dialysis– Nephrotic syndrome
Transudate or exudate– Pulmonary embolism
Exudates– Viral, fungal,
mycobacterial or parasitic infection
– SLE or RA– Uremia– Pancreatitis– Post-cardiac surgery
or radiotherapy– Amiodarone
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PLEURAL EFFUSION
Clinical features– May be clinically silent– Detected by symptoms of underlying
disease– Increase in volume of effusion with
dyspnea– Development of inflammation and
associated pain with respiration
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PLEURAL EFFUSION
Physical exam– Percussion dullness in dependent portions
of the lung– Decreased breath sounds at lung base
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PLEURAL EFFUSION
Diagnosis– Upright CXR: in an adult, 150-200 mL of
pleural fluid in hemithorax required to produce signs
– Supine CXR: haziness in posterior pleural space
– Diagnostic thoracentesis• analyzed to determine cause
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PLEURAL EFFUSION
Detection of exudative pleural effusion– Pleural fluid/serum protein ratio > 0.5– Pleural fluid/serum LDH ratio > 0.6– Pleural fluid LDH > 2/3 of upper limit for
serum LDH
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PLEURAL EFFUSION
Additional tests– Gram stain and culture - detect bacteria– Cell count
Neutrophils- parapneumonic, PE, pancreatitis Lymphocytes- cancer, TB, post-cardiac sz
– Glucose: low in parapneumonic, malignancy, TB, and RA
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PLEURAL EFFUSION
Additional tests– Cytology for malignancy
• Highest yield: adenocarcinoma• Lower yield: squamous cell, lymphoma, or
mesothelioma
– Pleural fluid pH• Normal: around 7.46• Parapneumonic: <7.10, predicted development
of or persistence of empyema
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PLEURAL EFFUSION
Additional tests– Pleural fluid amylase
• Elevated in pancreatitis or esophageal rupture
– Mycobacterial and fungal stains and cultures– Tuberculosis pleural fluid markers:
• PCR for mycobacterial DNA• Pleural fluid adenosine deaminse• Pleural fluid interferon-
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PLEURAL EFFUSION
Treatment– Dyspnea at rest
• Therapeutic thoracentesis with drainage of 1 to 1.5 L of fluid
– Empyema (gross pus or organisms on Gram stain)
• Drainage with large bore thoracostomy tubes
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PLEURAL EFFUSION
Treatment– Parapneumonic effusions
• Thoracostomy tube drainage if + cultures, +Gram stain, or pleural fluid pH < 7.10
– CHF pleural effusions• Diuretic therapy• Usually resolves 75% of effusions within 2 to3
days
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QUESTIONS
1. Causes of central cyanosis
2. Causes of peripheral cyanosis
1. B, D, F. 2. A, C, E, G
A. Decreased cardiac output
B. Methemoglobin
C. Hypothermia
D. Right-to-left shunt
E. Venous congestion
F. High altitude
G. Embolus
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QUESTIONS
3. Causes of upper airway obstruction
4. Causes of lower airway obstruction
3. A, C, D, G. 4. B, C, E, F
A. Angioedema
B. Bronchiolitis
C. Foreign body
D. Croup
E. COPD
F. Asthma
G. Epiglotitis
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QUESTIONS
5. If PaO2 < 20 mm Hg, what happens to the respiratory drive?.
6. In an acute setting, what should the pH be for a patient with a PaCO2 of 60?
5. B 6.C
A. Increases
B. Decreases
C. 7.15
D. 7.25
E. 7. 35
F. 7.55
G. 7.65