Transcript Respiratory Distress

RESPIRATORY DISTRESS
September 8, 2005
Prepared by Christina M. Cabott D.O.
RESPIRATORY DISTRESS
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DYSPNEA
HYPOXIA
HYPERCAPNEA
WHEEZING
COUGH
HICCUPS
CYANOSIS
PLEURAL EFFUSION
DYSPNEA
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Common complaint described as
– “shortness of breath”
– “breathlessness”
– “not getting enough air”
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2/3 of patients presenting to ED with
dyspnea have either a cardiac or
pulmonary disorder
DYSPNEA
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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
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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
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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
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Pathophysiology
– No defined neural pathway, derived from
mechanical, chemical, and vascular
receptors
DYSPNEA
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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
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Input from all of these receptors is
integrated in the CNS at subcortical and
cortical levels
DYSPNEA
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Clinical features that may signify
impending respiratory failure
– Presentation:
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shortness of breath or breathlessness
tachypnea
tachycardia
use of accessory respiratory muscles
stridor
DYSPNEA
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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
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Clinical features
– Evaluation
• abnormal vital signs
• ABCs
– Need rapid airway control and intervention
• airway obstruction
• ineffective respiratory effort
• changes in mental status
CAUSES OF DYSPNEA
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Most Common
Causes
– Asthma & COPD
– CHF/ cardiogenic
pulmonary edema
– Ischemic heart dz
• Unstable angina &MI
– Pneumonia
– Psychogenic
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Most Immediately
Life Threatening
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Foreign body
Angioedema
Hemorrhage
Tension pneumo
PE
Myasthenia gravis
Guillain-Barre
Botulism
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
DYSPNEA
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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
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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
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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
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Pathophysiology
– 5 distinct mechanisms
1. Hypoventilation
2. Right-to-left shunt
3. Ventilation/perfusion mismatch
4. Diffusion impairment
5. Low inspired oxygen
HYPOXEMIA
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Hypoventilation
– Rising PaC02 displaces O2 from the aveolus
 PaO2   O2 diffusion gradient across
the pulmonary membrane
– Normal A-a O2 gradient
HYPOXEMIA
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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
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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
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Diffusion impairment
– Impairment of alveolar-blood barrier
– Increased A-a O2 gradient
– Hypoxemia improves with supplemental O2
HYPOXEMIA
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Low inspired oxygen
– High altitude hypoxia
– Nonobstructive asphyxia
– Normal A-a O2 gradient
– Hypoxemia improves with supplemental O2
HYPOXEMIA
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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
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Chronic compensatory mechanisms
– 1.  Red blood cell mass
– 2.  Tissue oxygen demand
HYPOXEMIA
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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
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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
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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
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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
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Causes of Hypercapnea
– Depressed central respiratory drive
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Structural CNS disease: brainstem lesions
Sedating drugs: opiates, sedatives, anesthetics
Exogenous toxins
Endogenous toxins: tetanus
HYPERCAPNEA
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Causes of Hypercapnea
– Thoracic cage disorders
• Kyphoscoliosis
• Morbid obesity
– Neuromuscular impairment
• Neuromuscular disease: myasthenia gravis,
Guillain-Barre syndrome
• Neuromuscular toxins: organophosphate
poisoning, botulism
HYPERCAPNEA
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Causes of Hypercapnea
– Intrinsic lung disease associated with
increased dead space
• COPD
– Upper airway obstruction
HYPERCAPNEA
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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
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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
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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
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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
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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
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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
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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
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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
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Causes of wheezing
– Upper airway (stridor most likely, may have
wheezing)
• Angioedema: allergic, ACE inhibitor, idiopathic
• Foreign body
• Infection: croup, epiglottitis, tracheitis
WHEEZES
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Causes of wheezing
– Lower airway
• Asthma
• Transient airway hyperreactivity (usually due to
infection or irritation)
• Bronchiolitis
• COPD
• Foreign body
WHEEZES
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Causes of wheezing
– Cardiogenic
• Cardiogenic pulmonary edema (“cardiac
asthma”)
• Noncardiogenic pulmonary edema
– Adult respiratory distress syndrome [ARDS]
• Pulmonary embolus (rare)
– Psychogenic
WHEEZES
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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
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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
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Diagnosis
– Other ancillary tests
• CXR and ABG
• May not be needed during an uncomplicated
obstructive pulmonary disease
WHEEZES
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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
WHEEZES
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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
WHEEZES
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ED treatment
– Admission of patients
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Oxygen requirements
Potential for quick decompensation
Failed treatment
Require mechanical ventilation
COUGH
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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
COUGH
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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
COUGH
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Pathophysiology
– Stimulation of receptors
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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
COUGH
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Categories
– Acute
– Chronic
• Cough present more than 3 weeks without any
periods of resolution
COUGH
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Acute Causes
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Upper respiratory infection: rhinitis, sinusitis
Lower respiratory infection: bronchitis, pneumonia
Allergic RXN
Asthma
Environmental irritants
Transient airway hyperresponsiveness
Foreign body
COUGH
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Common Chronic Causes
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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
COUGH
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Less Common Chronic Causes
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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
COUGH
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Diagnosis
– Most acute cough does not require routine
ancillary tests
• CXR: if purulent sputum and/or fever
• Spirometry: evaluation of airflow obstruction in
asthmatics
COUGH
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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
COUGH
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Acute treatment
– Cough suppressants
• opioids: dextromethorphan, codeine, and
oxycodone
– Demuculants
COUGH
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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
COUGH
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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
HICCUPS
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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
HICCUPS
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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
HICCUPS
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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
HICCUPS
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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
HICCUPS
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Causes of Hiccups
– Chronic: persistent, intractable
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Central nervous system structural lesions
Vagal or phrenic nerve irritation
Metabolic: uremia, hyperglycemia
General anesthesia
Surgical procedures: thoracic, abdominal,
prostate, urinary tract, craniotomy
HICCUPS
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Diagnosis
– Benign hiccups
• Resolves spontaneously or with simple
maneuvers
• Do not seek medical attention
• Do not require specific diagnosis
HICCUPS
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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
HICCUPS
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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
HICCUPS
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Treatment with physical maneuvers
– Stimulating the pharynx will block vagal portion of
reflex arc and abolish hiccups
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Treatment with medications
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chlorpromazine
metoclopramide
nifedipine
valproic acid
baclofen
HICCUPS
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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
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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
HICCUPS
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nifedipine
– 10 to 20 mg po tid or qid
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valproic acid
– 15 mg/kg per day po tid
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baclofen
– 10 mg po tid
These all work more gradually
CYANOSIS
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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
CYANOSIS
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Pathophysiology
– Various factors affect the presence or
absence of cyanosis
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Skin pigmentation
Skin thickness
Subcutaneous microcirculation
Lighting
Ambient temperature
CYANOSIS
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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
CYANOSIS
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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
CYANOSIS
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Central cyanosis
– Hemoglobinopathies
• Methemoglobin: acquired; hereditary
• Sulfhemoglobinemia: acquired
– Decreased arterial oxygen saturation
• Pulmonary etiologies: shunt , diffusion, V/Q
mismatch
• Hypoventilation
• High altitude
CYANOSIS
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Central cyanosis
– Anatomic right-to-left shunts
• Cardiac: Ventricular Septal Defect (VSD), Atrial
Septal Defect (ASD), and Tetralogy of Fallot
(TOF)
• Intrapulmonary
• Intrapulmonary shunts
CYANOSIS
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Peripheral cyanosis
– Decreased cardiac output
– Distributive shock
– Cold exposure on extermities
– Venous congestion
– Arterial thrombosis or embolus
CYANOSIS
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Diagnosis
– Presence of cyanosis must be taken in
context with clinical situation
– Tests
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ABG: will confirm the diagnosis
Hematocrit: check for polycythemia or anemia
CXR
EKG
Abnormal hemoglobin tests
PSEUDOCYANOSIS
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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
PSEUDOCYANOSIS
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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
PSEUDOCYANOSIS

Argyria
– Slate blue to gray coloration of skin
– Results of chronic ingestion or local
application of silver salts or colloidal silver,
CYANOSIS

True cyanosis DOES blanch when
direct pressure is applied to skin
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Pseudocyanosis DOES NOT blanch
when direct pressure is applied to skin
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
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
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
CYANOSIS
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Diagnosis
– Sulfhemoglobin
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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
CYANOSIS
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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
PLEURAL EFFUSION
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
Result from fluid accumulating in
potential space between visceral and
parietal pleura
Most common causes in developed
countries
– CHF
– Pneumonia
– Cancer
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
PLEURAL EFFUSION

Pathophysiology
– Transudates
• Result of imbalance in hydrostatic or oncotic
pressure
• Produces an ultrafiltrate across the pleural
membrane
• Low protein content
PLEURAL EFFUSION

Pathophysiology
– Exudates
• Result of pleural disease, usually inflammation
or neoplasm
• Active fluid secretion or leakage
• High protein content
COMMON CAUSES OF
PLEURAL EFFUSION
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Transudates
– CHF
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Transudate or
exudate
– Diuretic therapy
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Exudates
– Cancer: primary or
metastatic
– Bacterial pneumonia
with parapneumonic
effusion
– Pulmonary embolism
LESS COMMON CAUSES
OF PLEURAL EFFUSION
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Transudates
– Cirrhosis with ascites
– Peritoneal dialysis
– Nephrotic syndrome
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Transudate or
exudate
– Pulmonary embolism
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Exudates
– Viral, fungal,
mycobacterial or
parasitic infection
– SLE or RA
– Uremia
– Pancreatitis
– Post-cardiac surgery
or radiotherapy
– Amiodarone
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
PLEURAL EFFUSION

Physical exam
– Percussion dullness in dependent portions
of the lung
– Decreased breath sounds at lung base
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
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
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
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
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-
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
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
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
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
QUESTIONS
5. If PaO2 < 20 mm Hg,
what happens to the
respiratory drive?.
A. Increases
B. Decreases
6. In an acute setting,
what should the pH
be for a patient with
a PaCO2 of 60?
C. 7.15
D. 7.25
E. 7. 35
F. 7.55
G. 7.65
5. B 6.C