Disorders of the Respiratory System

Disorders of the Respiratory
System
1st Respiratory Care Comprehensive Review Course 1

Outlines
• Chronic Obstructive Pulmonary Disease (COPD)
• Asthma
• Bronchiectasis
• Pneumonia
• Tuberculosis
• Pulmonary Edema
• ARDS
• Pneumothorax
• Pleural Effusion
• Atelectasis
• Pulmonary Embolism
• Sleep Apnea

Chronic Obstructive Pulmonary Disease
(COPD)
• COPD - inflammatory disorder
characterized by not fully
reversible, typically
progressive, airflow
obstruction
• Composed of 2 major disease
entities:
1. Emphysema
2. Chronic bronchitis

(COPD)
• Causes
1. Smoking
2. Alpha1 Antitrypsin Deficiency
• Other risk factors:
1. Passive smoking (second hand)
2. Air pollution
3. Occupational exposure
4. AW hyper-responsiveness

(COPD)
Emphysema
• Diminished elastic recoil, which
result in premature AW closure.
• Reduced Exp. flow rates
• Air-trapping leads to increases
FRC
• Lung compliance increased
• Dead space & V/Q mismatch
increased
Chronic Bronchitis
• Mucus glands size increased
• Goblet cells numbers increased
• Inflammation of bronchial walls
• Mucus plugs in peripheral AW
• Loss of cilia
• Emphysematous changes
• Narrowing airways, leading to
airflow limitations
Pathophysiology

(COPD)
Signs & Symptoms
• Common symptoms
• Productive cough
• Wheezing or diminished breath sounds
• Shortness of breath (SOB); particularly on exertion
• Progressive dyspnea; usually manifesting in 6th or 7th decade of life (AAT deficiency ~45
years of age)
• Late signs include
• Barrel chest with flattened diaphragms
• Accessory muscle usage
• Edema from cor pulmonale
• Changes in mental status due to ⇓O2 or ⇑CO2

(COPD), Management
• Establishing diagnosis with airflow obstruction
• Separating COPD from asthma is major challenge
• Features favoring COPD are
• Chronic productive cough, ⇓diffusing capacity
• Diminished vascularity on chest radiograph
• Asthma favored if diminished FEV1 is normalized after use of an inhaled
bronchodilator
• Once COPD established, check for AAT deficiency

(COPD)
Stable COPD
• PRN bronchodilator for all COPD patients
• Sympathomimetic &/or anticholinergic
• Reversibility if post-bronchodilator FEV1 ⇑12%
• No survival benefit, but often improves
symptoms
• Systemic corticosteroid trial (6–29% respond)
• If patient responds (⇑FEV1), use inhaled steroids
• Lung decline continues, but decreases
exacerbations
• May lead to higher rate of pneumonia in COPD
users
• Methylxanthines decrease feeling of dyspnea
• Try to avoid toxicity serum levels of 8–10 µg/mL
Acute Exacerbations
• Inhaled bronchodilators, especially 2-
agonists
• Oral antibiotics if purulent sputum is
present (7–10 days)
• Short course of systemic
corticosteroids
• Supplemental oxygen to keep SaO2
>90%
• With hypercapnia (pH <7.3), NIV is
attractive option
• If NIV fails, then make decision on
intubation & MV
Treatment

Stable COPD

COPD Acute Exacerbations

Asthma
• Definition
• Inflammatory airway disease characterized by reversible airway obstruction
• Incidence
• Increasing prevalence in U.S. since 1980
• Affects people of all ages
• Etiology & pathogenesis
• Genetic susceptibility to allergens, RTI, occupational and environmental
stimuli, etc.
• Whatever trigger, it can produce “asthma”
• Airway inflammation & bronchial hyperreactivity, resulting in airway obstruction
• Once above are present, asthma can be triggered by:
• Exercise, cold dry air, hyperventilation, stress, cigarette smoke, etc….
• Once triggered, asthma causes mast cell degranulation, releasing proinflammatory
substances
• Starts cycle of asthma

Asthma
• Clinical Presentation & Diagnosis
 Diagnosis by clinical & laboratory evaluation
 History plays key role, as patients can be entirely normal between episodes
 Classic symptoms are episodic wheezing, SOB, cough
 If present, send for PFTs to demonstrate reversible airways obstruction
 PFTs may be normal between exacerbations or show some degree of airway obstruction
 ⇓FEV1 & FEV1/FVC ratio
 Airway reversibility in asthma is noted just like in COPD
 Post-bronchodilator FEV1 ⇑12% & 200 ml
 If PFTs are normal, broncho-provocation is undertaken
 Most common agent used: methacholine
 Arterial blood gases taken during an acute attack.
 Most often show hypoxemia with hyperventilation
 Normal PaCO2 level is indicative of severe attack & impending ventilatory failure

Asthma Management
• Goals of asthma management
• Maintain high-quality, asymptomatic life
• No limitations on the job or during exercise
• No medication side effects
• Stepwise approach to long-term management of asthma:
• Medication therapy is based on disease severity
• Control is attained when (there are)
• Minimal to no daily symptoms or limitations
• Infrequent exacerbations, with little or no use of 2-agonists
• PFTs = normal or near normal

Asthma Management (cont.)

Pharmacotherapy in Asthma
• Corticosteroids
• Most effective medication in treatment of asthma
• Reduces symptoms & mortality
• Use of inhaled steroids for long-term treatment preferred
• Use spacer & rinse mouth to eliminate or minimize side effects
• Long-term use of oral steroids should be restricted to patients with asthma
refractory to other treatment
• Short-term oral steroid use during exacerbation reduces severity, duration,
& mortality

• Cromolyn (NSAID)
• Protective against allergens, cold air, exercise
• Administered prophylactically, CANNOT be used during an acute asthma attack
• Of limited use in adults
• Drug of choice for atopic children with asthma
• Nedocromil (NSAID)
• Similar to cromolyn, it is 4–10 times more potent in preventing acute allergic
bronchospasm
• Leukotriene inhibitors
• Leukotrienes mediate inflammation & bronchospasm
• Modestly effective to control mild to moderate asthma
• Inhaled steroids remain anti-inflammatory drug of choice
• Methyxanthines (use is controversial)
• Oral or IV use if admitted for acute asthma attack

• 2-Adrenergic agonists
• Most rapid & effective bronchodilator
• Drug of choice for exercise-induced asthma & emergency relief of bronchospasm
• Should be used PRN
• Improves symptoms not underlying inflammation
• Regular use may worsen asthma control & increase risk of death
• Anticholinergics
• Can be used as adjunct to first-line bronchodilators if there is inadequate response
• Has additive affect to 2-agonists
• Tiotropium when added to corticosteroid enhances asthma control & improve
symptoms
• Anti-IgE therapy:
• IgE plays role in asthma pathogenesis
• Omalizumab (Xolair) blocks IgE biologic effects
• Indicated in patients with allergic asthma, poorly controlled with corticosteroids

Emergency Management of Asthma
• Early & frequent use of aerosolized 2-agonists
• Consider continuous therapy for severe attack
• High-dose parenteral corticosteroids
• Oxygen therapy for hypoxemia
• Antibiotics if evidence of infection
• In severe ventilatory failure, use MV with permissive hypercapnia:
small VT, low rate, PIP <50 cm H2O to avoid air-trapping &
barotrauma

Bronchial Thermoplasty
• Promising new treatment for asthma patients
• Indicated for uncontrolled asthma despite use of corticosteroids &
LABAs
• Uses heat (by ways of radiofrequency waves) to decrease airway
smooth muscle mass
• Reduces ability of airways to constrict
• Long-term side effects have not been studied

Asthma & Environmental Control
• Recognized relationship between asthma & allergy
• 75–85% asthma patients react to inhaled allergens
• Environmental control is aimed at reducing exposure to allergens
• Avoid outdoor allergens by remaining inside, windows closed, AC on
• Indoor allergens are combated by:
• Air purifiers & no pets
• Dust mites: airtight covers on bed & pillow, no carpets in bedroom, chemical agents
to kill mites

Special Considerations in Asthma
Management
• Exercise-induced asthma (EIA)
• Common particularly in cold weather
• Heat loss from airways may precipitate attack
• Prophylactic inhalation of 2-agonists or cromolyn
• Occupational asthma
• Most common form of occupational lung disease
• Early identification & cessation of exposure are key
• Cough-variant asthma
• Cough is sole complaint, amenable to 2-agonists
• Nocturnal asthma
• Present in 2/3rds of poorly controlled asthmatics
• May be due to diurnal decrease in airway tone or gastric reflux
• Treatment should include:
• Steroid treatment targeted to relieve night symptoms
• Sustained release theophylline
• New long-acting 2-agonists
• Antacids for reflux

Special Considerations in Asthma
Management (cont.)
• Aspirin sensitivity
• 5% of adult asthmatics will have severe, life-threatening asthma attacks after taking NSAIDs
• All asthmatics should avoid; suggest Tylenol use
• Asthma during pregnancy
• 1/3rd of asthmatics have worse control at this time
• Much higher fetal risk associated with uncontrolled asthma than that of asthma medications
• Theophyllines, 2-agonists, & steroids can be used without significant risk of fetal abnormalities
• Sinusitis may cause asthma exacerbation
• CT of sinuses will diagnosis problem
• Treatment: 2–3 weeks antibiotics, nasal decongestants, & nasal inhaled steroids
• Surgery
• Asthmatics at higher risk for respiratory complications:
• Arrest during induction
• Hypoxemia with/without hypercarbia
• Impaired cough, atelectasis, pneumonia
• Optimize lung function preoperatively
• Use steroids during procedure.

Bronchiectasis
• Abnormal, irreversible dilation of bronchi caused by chronic airway
inflammation & destruction
• Presents in 3 major anatomical patterns
1. Cylindrical: airway is uniformly dilated
2. Varicose: irregular constrictions & dilations
3. Cystic: progressive distal, sac-like dilations
• Causes
1. Chronic respiratory infections
2. TB lesion
3. Secondary to cystic fibrosis
4. Bronchial obstruction

Bronchiectasis
• Pathophysiology
1. Chronic dilation as a result of the destructive changes in the bronchial walls
cased by inflammation and infection, or possibly a congenital defect of the
airways.
2. Bronchial obstruction may render the mucociliary transport system
ineffective leading to accumulation of thick secretions
3. Atrophy of the mucosal layer as a result of the bronchial wall destruction
4. This disease may be either obstructive or restrictive due to decreased
values in both flows & volumes.

Bronchiectasis
• Clinical presentation & evaluation
• Hallmark: chronic production of copious amounts of purulent sputum resulting in
productive cough
• Dyspnea variable; depends on extent of disease
• Hemoptysis frequent, though rarely severe
• Chest radiograph shows tram lines (airway dilation), segmental atelectasis, flattened
diaphragm
• ABG: Respiratory alkalosis with hypoxemia (early stage); Chronic respiratory acidosis
with hypoxemia (late stage)
• Recurrent Pulmonary Infections
• Digital clubbing and Barrel chest
• Definitive diagnosis made with fine-cut CT
• Reversible airway changes consistent with bronchiectasis may follow pneumonia
• Wait 6–8 weeks following pneumonia resolution

Bronchiectasis
• Management & Treatment
• Antibiotics
• As needed or regularly scheduled
• Sputum cultures should guide therapy
• Bronchopulmonary hygiene
• Postural drainage & cough maneuvers
• Aerosol Therapy
• Mucolytics
• Expectorant
• Bronchodilator therapy
• Massive hemoptysis may embolize artery or surgically repair

RT Role in Chronic Pulmonary Diseases
• Diagnostic role:
• Performing PFTs
• Physical assessment
• Management:
• Medication delivery, bronchial hygiene, oxygen delivery
• Invasive/Non-invasive ventilatory support
• Invasive/Non-invasive blood gas monitoring
•Follow up:
• Smoking cessation
• Pulmonary rehab
• Long-term oxygen therapy
• Invasive/Non-invasive ventilatory support
• Advocacy

Pneumonia
• Classification
 Community-acquired pneumonia (CAP)
 Acute
 Chronic
 Health care–associated pneumonia (HCAP)
 Pneumonia occurring in any patient hospitalized for 2 or more days in past 90 days or:
 Any patient with pneumonia who, in past 30 days, has resided in a long-term care facility
 Hospital-acquired pneumonia (HAP)
 Acute lower respiratory tract infection that occurs in hospitalized patients more than 48 hours
after admission
 Second most common nosocomial infection
 Ventilator-associated pneumonia (VAP)
 Pneumonia that develops more than 48 to 72 hours after intubation

Pneumonia
• Causes
1. A variety of organisms
2. Ineffective airway defense mechanisms
3. Various conditions result in a predisposition to pneumonia
• Pathophysiology
1. Lung reaction to pathogenic microorganism--- increased production of
inflammatory exudates and cells
2. WBCs phagocytize the invading organisms which leads to further inflammation
3. Lungs begin to filling with inflammatory exudates and cells, they become
consolidated
4. If tissue necrosis is not present, the lungs heals and returns to normal function
5. If tissue necrosis occurs, healing is slow and fibrous scar tissue is produced
resulting in pulmonary fibrosis and loss of normal lung function.

Pneumonia

Pneumonia
• Clinical signs & symptoms
 Patients with CAP typically have fever, cough, sputum production, pleuritic
chest pain, dyspnea, tachycardia and inspiratory crackles with bronchial BS on
auscultation
 In elderly, pneumonia may not cause fever or cough; it may simply present as
dyspnea, confusion, worsening of CHF, or failure to thrive
 VAP traditionally presents with new onset of fever, purulent endotracheal
secretions, & new infiltrate
• CXR:
 Consolidation
 Air Bronchogram

Pneumonia
• Diagnostic Studies
 CAP
 Respiratory therapists play key
role in collecting sputum
samples for microbiological
examination
 Satisfactory specimen contains
>25 leukocytes and <10
squamous epithelial cells per
hpf
 Presence of acid-fast bacilli in
stain sputum samples suggests
tuberculosis
 Blood cultures should be
obtained in severe cases of
pneumonia
 Nosocomial Pneumonias: HAP, HCAP,
VAP
 Accurate diagnosis is very
difficult

Pneumonia
• Treatment
 Antibiotics
 Supplemental O2
 Bronchial Hygiene Therapy
 Adequate Hydration
 Adequate Nutrition
 If resulting in Impending or Acute RF, MV support and intubation may be
needed

Tuberculosis (TB)
• TB is acquired by inhalation of airborne droplets containing M. tuberculosis
• Most people exposed to TB do not develop active infection as TB is controlled by
an intact immune system
• People who are positive for TB but asymptomatic are said to have “latent TB”
• If they subsequently become debilitated, it may develop into reactivation TB
• People who acquire infection upon initial exposure have “primary TB”
• Primary TB is most likely to occur in HIV patients
• Primary TB causes fevers in 70% of patients, persisting for 14 to 21 days, in most
cases
• Extrapulmonary TB is defined as spread of organism beyond lung & may involve
any organ
• Most often occurs in CNS, musculoskeletal system, GI tract, & lymph nodes

TB
Pathophysiology

Tuberculosis (TB)
• History is vitally important in diagnosis of patients with TB
• Clinician should ask about symptoms, exposure, travel, prior history of TB, risk
factors, etc…
• Patients diagnosed or suspected of having TB should be placed in
respiratory isolation
• Gold standard for diagnosis of TB is culture isolation of organism
• Culture may take 4 to 6 weeks
• Acid-fast staining of expectorated sputum may be used in diagnosis
• Positive PPD skin test supports diagnosis in appropriate clinical setting
• Negative skin test may occur in patients with HIV who are infected with TB

Tuberculosis (TB)
• Most common symptoms in reactivation TB include fever, cough,
night sweats, & weight loss
• Cough is less common
• Chest x-ray usually shows lymphadenopathy, while an infiltrate is seen
in 25% of cases
• Chest radiograph shows upper lobe infiltrates in 80% to 90% of
reactivation TB cases

Tuberculosis (TB)
• Treatment: Goals of treatment are to cure patient & prevent further
transmission.
1. Placement in respiratory isolation
2. Supplemental O2
3. Antibiotics (2 to 4 months)
- Rifampin
- Isoniazid INH
- Ethambutol
4. Daily observation therapy should be used (bronchial hygiene therapy)
5. Routine treatment should be given for 6 to 9 months

Role of Respiratory Therapist in Pulmonary
Infections
Collection of sputum samples as indicated
Assist with bronchoscopy
Administer chest physical therapy in selected cases
Counsel patients in sputum clearance techniques such as PEP &
autogenic drainage
Model optimal infection control practices

Pulmonary Edema
• Medical emergency!
• Abnormal fluid accumulation within lung parenchyma & alveoli
resulting in hypoxemia
• Causes: LV failure, aortic stenosis, mitral valve stenosis, systemic
hypertension, alveolar capillary membrane leakage, rapid
administration of IVF’s
• May be secondary to CHF or ALI
• Severe ALI is called ARDS or non-cardiogenic pulmonary edema

Pulmonary Edema
• Pathophysiology
• Pulmonary edema
• Fluid first accumulates in interstitial space
• Followed by alveolar flooding
• Impairs gas exchange & reduces lung compliance
• Can be result of hydrostatic pulmonary edema or non-hydrostatic pulmonary edema
• Hydrostatic (Cardiogenic) Pulmonary Edema
• Fluid accumulation in interstitium raises hydrostatic pressure rapidly & alveolar flooding
follows
• Flooding occurs in “all or nothing” manner
• Fluid filling alveoli is identical to interstitial fluid

Pulmonary Edema
• Clinical Manifestations:
• Increasing respiratory distress/ dyspnea, air hunger
• Anxious/agitated/confusion
• Cough/Frothy pink sputum
• Fine Crackles/ Rales
• Tachycardia or other arrhythmias
• Jugular vein distention
• CXR:
• Increased vascular marking
• Interstitial edema
• Enlarged heart shadow
• Air bronchogram
• Kerley B lines

Pulmonary Edema
• Treatment:
• Oxygen Therapy
• CPAP/BiPAP
• Ventilatory support with PEEP (if condition results in ARF)
• Morphine
• Diuretics
• Cardiac glycosides

ARDS
• A group of symptoms causing acute catastrophic respiratory failure,
resulting from pulmonary injury.

ARDS
• Causes:
• Diffused Lung Injury
• Most patient have no previous pulmonary
problems

ARDS
• Pathophysiology
• Fluid accumulates despite normal hydrostatic pressure.
• Vascular endothelial injury alters permeability
• Protein-rich fluid floods interstitial space
• Alveolar flooding occurs as osmotic pressures in capillaries & interstitium equalize
• Alveolar epithelium & pulmonary fluid clearance are impaired
• Common mechanism for development of ARDS appears to be lung
inflammation

ARDS
• Gas Exchange & Lung Mechanics During ARDS
• Restrictive physiology & refractory hypoxemia
• Altered permeability floods lung, resulting in decreased lung compliance (CL)
& consolidation
• Impaired surfactant synthesis & function worsens gas exchange & CL
• Loss of normal vascular response to alveolar hypoxemia
• Unaerated alveoli receive blood flow in excess, which contributes to severe ventilation-
perfusion mismatching & increased shunting

ARDS
• Histopathology & Clinical Correlates of ARDS
• Exudative phase (up to 1 week)
• Proliferative phase (2 to 3rd week)
• Fibrotic phase (beyond 3rd week)

ARDS
• Clinical signs & symptoms of ARDS can vary
in intensity, depending on its cause and
severity, as well as the presence of
underlying heart or lung disease. They
include:
• Severe shortness of breath
• Labored and unusually rapid breathing
• Low blood pressure
• Confusion and extreme tiredness
• CXR findings
• bilateral air space opacification.
• lack of obvious vascular congestion.
Copyright © Jeremy C. Mauldin

ARDS
• Treatment:
• Hemodynamics & fluid management
• Mechanical Ventilation
• Patient Positioning
• Extracorporeal membrane oxygenation
(ECMO) & extracorporeal carbon dioxide
removal (ECCO2R)
• Exogenous surfactant replacement
• Inhaled nitric oxide (INO)
• Inhaled eprostenol (Flolan)
• Corticosteroids
• 2-Agonists

Role of Respiratory Therapists in ARDS
• Close patient monitoring
• arterial puncture
• hemodynamic assessment
• pulse oximetry
• Ventilator –Patient management
• vent initiation
• settings to optimize oxygenation/ventilation while minimizing iatrogenic
hazards/complications
• facilitate weaning from mechanical ventilation

Pneumothorax
• Defined as air in pleural space - can occur through number of mechanisms
• Causes:
• Spontaneous pneumothorax
1. No previous trauma
2. Seen most commonly in tall, thin young males as a result of bleb rupture
3. Seen in patients with COPD as a result of bullous disease and bleb rupture
• Traumatic pneumothorax
1. Blunt trauma (broken ribs)
2. Penetrating chest trauma
3. Chest or neck surgery
4. Insertion of lines for diagnostic procedures
5. High inspiratory pressure (high volumes) in ventilated patients

Pneumothorax
1. Chest pain & dyspnea
2. Decreased or absent BS & hyperresonant to
percussion
3. Asymmetric chest rise
4. Tachypnea, tachycardia & arrhythmias (in severe
cases)
5. Desaturation
• CXR findings
1. Hyperlucency
2. Deviation of trachea, heart, and mediastinum
(tension pneumothorax) (medical emergency)
1st Respiratory Care Comprehensive Review Course55

Pneumothorax
• Treatment:
• Needle aspiration, immediately in tension pneumothorax.
• Placement of chest tube
• Supplemental O2

Pleural Effusion
• Any abnormal accumulation of fluid in pleura is considered pleural effusion
• Fluid enters pleural space from visceral & parietal pleurae, particularly in
light of increased pressure
• Transudative effusions: effusions forming while pleural space is undamaged
will have [protein] <50% of serum level & LDH <60% of serum level
• Exudative effusions: occur due to inflammation of lung or pleura & have
higher protein & inflammatory cell content, account for 70% of all pleural
effusions
• Thoracentesis may be performed to determine type

Pleural Effusion (Causes)
Transudative effusions
• CHF
• Nephrotic syndrome
• Hypoalbuminemia
• Liver disease
• Atelectasis
• Lymphatic obstruction
Exudative effusions
• Viral pleurisy
• Tuberculous pleurisy
• Malignancy
• Postoperative
• Chylothorax
• Hemothorax

Pleural Effusion
1. Chest pain & dyspnea
2. Absent BS & dullness to percussion
• CXR findings
1. Blunting of costophrenic angle
2. Homogeneous density in dependent part of the
hemithorax
• Treatment:
- Thoracentesis
- Chest Tube
- Supplemental O2
1st Respiratory Care Comprehensive Review Course59

Atelectasis
• Partial or complete collapse of alveoli.
• It may involve small localized areas of the lung, a lobe, or the entire
lung.
• Causes:
- Obstructed airways
- Loss of negative pleural pressure
- Right mainstem bronchus intubation
- Deficiency or loss of surfactant
- Hypoventilation
- Decreased pulmonary blood flow

Atelectasis
1. Asymptomatic
2. Hypoxemia & dyspnea
3. Late insp. crackles BS & dullness to percussion
4. Tracheal deviation
• CXR findings
1. Increased density (white)
2. Elevated diaphragm
3. Mediastinal shift
4. Altered bronchial and carinal angles
• Treatment:
- Prevention (IS/IPPB)
- Treatment of the underlying cause
- Humidification (assist in secretion removal)
- Supplemental O2
- CPAP
- PEEP in ventilated patients

Pulmonary Embolism
• Obstruction of the pulmonary artery or one of its branches by a blood
clot
• PEs are most often detached portions of venous thrombi
• Most often (86%), thrombi form in deep veins (DVT) of legs or pelvis
• Conditions that favor thrombus formation (factors known as
Virchow’s triad)
• Venous stasis: i.e., immobilization in hospital
• Hypercoagulable states
• Vessel wall abnormalities
• Massive PE causes death by cardiovascular failure, not respiratory
failure

Pulmonary Embolism
• Pathophysiology
• Emboli obstruct blood flow resulting in
• Alveolar deadspace
• Bronchoconstriction
• Decreased surfactant production
• Hypoxemia
• Pulmonary hypertension
• Shock (saddle embolus)
• No specific signs or symptoms
• Most common symptom is dyspnea

Pulmonary Embolism
• Three tests available for diagnosis
• V/Q scan
• Helical/Spiral CTA
• Pulmonary angiography
• Radiograph is abnormal in 80% of cases
• Enlargement of right pulmonary artery (66%)
• Elevation of diaphragm (61%)
• Cardiomegaly (55%)
• Small pleural effusion (50%)
• Patchy or rounded infiltrates next to pleural surface are less common but
characteristic of PE

Pulmonary Embolism
Prophylaxis of DVT
• High mortality justifies prophylactic
treatment
• Moderate- to high-risk patients
include those
• Undergoing joint replacement
• With acute spinal injury or ischemic
stroke
• With myocardial infarction or heart
failure
• Who are MICU patients (i.e., pneumonia)
• Treatment is anticoagulant therapy
• Heparin or fondaparinux is most
commonly used
Management of DVT
• Heparin is standard therapy
• Immediate action
• Does not lyse existing clots but
prevents clot growth & formation
• Thrombolytic agents
• Streptokinase, urokinase, TPA
• Actually lyse or destroy PE
• Not routinely used
• High risk of limb gangrene
• Risks & benefits not well established

Pulmonary Embolism
• Management of PE
• Similar regimen to DVT
• First-line heparin followed by oral coumarin
• Supportive measures include
• Oxygen therapy
• Analgesia
• Hypotension & shock are treated with vasopressors & fluids
• In persistent hypotension due to massive PE, thrombolytics are indicated

Sleep Apnea
• Sleep apnea is present in patients who have at least 30 episodes of
apnea over 6-hours period of sleep
• The apneic period may last from 20 seconds to more than 90 seconds
• Types
• Obstructive sleep apnea: caused by upper airway anatomic obstruction
• Central sleep apnea: occurs due to failure of the central centers to send
signals to the respiratory muscles

Sleep Apnea
• Symptoms
• Risk factors
• Diagnostic Sleep Studies
• Obstructive sleep apnea: during the apneic period the patient exhibits strong
respiratory effort
• Central sleep apnea: during the apneic period patient will have absent
respiratory effort
• CPAP/BiPAP

• Egan's Fundamentals of Respiratory Care / Robert M. Kacmarek, James K. Stoller, and Al Heuer. – 10th Edition, 2013
• Respiratory Care Principles and Practice / Dean R. Hess, et al – 2nd edition, 2012
• Respiratory Care Exam Review / Gary Persing – 4th edition, 2016

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