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RESPIRATORY DISTRESS

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Title: RESPIRATORY DISTRESS


1
RESPIRATORY DISTRESS
  • September 8, 2005
  • Prepared by Christina M. Cabott D.O.

2
RESPIRATORY DISTRESS
  • DYSPNEA
  • HYPOXIA
  • HYPERCAPNEA
  • WHEEZING
  • COUGH
  • HICCUPS
  • CYANOSIS
  • PLEURAL EFFUSION

3
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

4
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

5
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

6
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

7
DYSPNEA
  • Pathophysiology
  • No defined neural pathway, derived from
    mechanical, chemical, and vascular receptors

8
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

9
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

10
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

11
DYSPNEA
  • Input from all of these receptors is integrated
    in the CNS at subcortical and cortical levels

12
DYSPNEA
  • Clinical features that may signify impending
    respiratory failure
  • Presentation
  • shortness of breath or breathlessness
  • tachypnea
  • tachycardia
  • use of accessory respiratory muscles
  • stridor

13
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)

14
DYSPNEA
  • Clinical features
  • Evaluation
  • abnormal vital signs
  • ABCs
  • Need rapid airway control and intervention
  • airway obstruction
  • ineffective respiratory effort
  • changes in mental status

15
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

16
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

17
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

18
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

19
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

20
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)

21
HYPOXEMIA
  • Pathophysiology
  • 5 distinct mechanisms
  • 1. Hypoventilation
  • 2. Right-to-left shunt
  • 3. Ventilation/perfusion mismatch
  • 4. Diffusion impairment
  • 5. Low inspired oxygen

22
HYPOXEMIA
  • Hypoventilation
  • Rising PaC02 displaces O2 from the aveolus ??
    PaO2 ? ? O2 diffusion gradient across the
    pulmonary membrane
  • Normal A-a O2 gradient

23
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

24
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

25
HYPOXEMIA
  • Diffusion impairment
  • Impairment of alveolar-blood barrier
  • Increased A-a O2 gradient
  • Hypoxemia improves with supplemental O2

26
HYPOXEMIA
  • Low inspired oxygen
  • High altitude hypoxia
  • Nonobstructive asphyxia
  • Normal A-a O2 gradient
  • Hypoxemia improves with supplemental O2

27
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

28
HYPOXEMIA
  • Chronic compensatory mechanisms
  • 1. ? Red blood cell mass
  • 2. ? Tissue oxygen demand

29
HYPOXEMIA
  • Clinical Features
  • Signs and symptoms are nonspecific
  • Cardio-pulm tachycardia and tachypnea
  • CNS aggitation, seizures, and coma
  • At PaO2 respiratory drive
  • Dyspnea may or may not be present

30
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

31
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

32
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

33
HYPERCAPNEA
  • Causes of Hypercapnea
  • Depressed central respiratory drive
  • Structural CNS disease brainstem lesions
  • Sedating drugs opiates, sedatives, anesthetics
  • Exogenous toxins
  • Endogenous toxins tetanus

34
HYPERCAPNEA
  • Causes of Hypercapnea
  • Thoracic cage disorders
  • Kyphoscoliosis
  • Morbid obesity
  • Neuromuscular impairment
  • Neuromuscular disease myasthenia gravis,
    Guillain-Barre syndrome
  • Neuromuscular toxins organophosphate poisoning,
    botulism

35
HYPERCAPNEA
  • Causes of Hypercapnea
  • Intrinsic lung disease associated with increased
    dead space
  • COPD
  • Upper airway obstruction

36
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 medullas
    chemoreceptors control tidal volume and
    respiratory rate

37
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

38
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

39
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

40
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

41
HYPERCAPNEA
  • ED treatment
  • Supplemental oxygen should be given to maintain
    level normal for the patient
  • Dont 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

42
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

43
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

44
WHEEZES
  • Causes of wheezing
  • Upper airway (stridor most likely, may have
    wheezing)
  • Angioedema allergic, ACE inhibitor, idiopathic
  • Foreign body
  • Infection croup, epiglottitis, tracheitis

45
WHEEZES
  • Causes of wheezing
  • Lower airway
  • Asthma
  • Transient airway hyperreactivity (usually due to
    infection or irritation)
  • Bronchiolitis
  • COPD
  • Foreign body

46
WHEEZES
  • Causes of wheezing
  • Cardiogenic
  • Cardiogenic pulmonary edema (cardiac asthma)
  • Noncardiogenic pulmonary edema
  • Adult respiratory distress syndrome ARDS
  • Pulmonary embolus (rare)
  • Psychogenic

47
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

48
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

49
WHEEZES
  • Diagnosis
  • Other ancillary tests
  • CXR and ABG
  • May not be needed during an uncomplicated
    obstructive pulmonary disease

50
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

51
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

52
WHEEZES
  • ED treatment
  • Admission of patients
  • Oxygen requirements
  • Potential for quick decompensation
  • Failed treatment
  • Require mechanical ventilation

53
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

54
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

55
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

56
COUGH
  • Categories
  • Acute
  • Chronic
  • Cough present more than 3 weeks without any
    periods of resolution

57
COUGH
  • Acute Causes
  • Upper respiratory infection rhinitis, sinusitis
  • Lower respiratory infection bronchitis,
    pneumonia
  • Allergic RXN
  • Asthma
  • Environmental irritants
  • Transient airway hyperresponsiveness
  • Foreign body

58
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

59
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

60
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

61
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

62
COUGH
  • Acute treatment
  • Cough suppressants
  • opioids dextromethorphan, codeine, and oxycodone
  • Demuculants

63
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

64
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

65
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

66
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

67
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

68
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

69
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

70
HICCUPS
  • Diagnosis
  • Benign hiccups
  • Resolves spontaneously or with simple maneuvers
  • Do not seek medical attention
  • Do not require specific diagnosis

71
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

72
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

73
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

74
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

75
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

76
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

77
CYANOSIS
  • Pathophysiology
  • Various factors affect the presence or absence of
    cyanosis
  • Skin pigmentation
  • Skin thickness
  • Subcutaneous microcirculation
  • Lighting
  • Ambient temperature

78
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

79
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

80
CYANOSIS
  • Central cyanosis
  • Hemoglobinopathies
  • Methemoglobin acquired hereditary
  • Sulfhemoglobinemia acquired
  • Decreased arterial oxygen saturation
  • Pulmonary etiologies shunt , diffusion, V/Q
    mismatch
  • Hypoventilation
  • High altitude

81
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

82
CYANOSIS
  • Peripheral cyanosis
  • Decreased cardiac output
  • Distributive shock
  • Cold exposure on extermities
  • Venous congestion
  • Arterial thrombosis or embolus

83
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

84
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

85
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

86
PSEUDOCYANOSIS
  • Argyria
  • Slate blue to gray coloration of skin
  • Results of chronic ingestion or local application
    of silver salts or colloidal silver,

87
CYANOSIS
  • True cyanosis DOES blanch when direct pressure is
    applied to skin
  • Pseudocyanosis DOES NOT blanch when direct
    pressure is applied to skin

88
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

89
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

90
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

91
CYANOSIS
  • Diagnosis
  • Sulfhemoglobin
  • Caused commonly by phenacetin or acetanilid
  • Inert as an oxygen carrier
  • Can produce deep cyanosis at level
  • Irreversible
  • Treatment
  • symptomatic and supportive care
  • identification and removal of suspected causes

92
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

93
PLEURAL EFFUSION
  • Result from fluid accumulating in potential space
    between visceral and parietal pleura
  • Most common causes in developed countries
  • CHF
  • Pneumonia
  • Cancer

94
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

95
PLEURAL EFFUSION
  • Pathophysiology
  • Transudates
  • Result of imbalance in hydrostatic or oncotic
    pressure
  • Produces an ultrafiltrate across the pleural
    membrane
  • Low protein content

96
PLEURAL EFFUSION
  • Pathophysiology
  • Exudates
  • Result of pleural disease, usually inflammation
    or neoplasm
  • Active fluid secretion or leakage
  • High protein content

97
COMMON CAUSES OF PLEURAL EFFUSION
  • Transudates
  • CHF
  • Transudate or exudate
  • Diuretic therapy
  • Exudates
  • Cancer primary or metastatic
  • Bacterial pneumonia with parapneumonic effusion
  • Pulmonary embolism

98
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

99
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

100
PLEURAL EFFUSION
  • Physical exam
  • Percussion dullness in dependent portions of the
    lung
  • Decreased breath sounds at lung base

101
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

102
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

103
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

104
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 persistence of empyema

105
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-?

106
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

107
PLEURAL EFFUSION
  • Treatment
  • Parapneumonic effusions
  • Thoracostomy tube drainage if cultures, Gram
    stain, or pleural fluid pH
  • CHF pleural effusions
  • Diuretic therapy
  • Usually resolves 75 of effusions within 2 to3
    days

108
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

109
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

110
QUESTIONS
  • 5. If PaO2 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
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