Pulmonary Disorders—9%

BRONCHITIS, PNEUMONIA, LUNG ABSCESS, AND EMPYEMA

Bronchitis

BASICS

Infection of the conducting airways of the lung (bronchial inflammation)

ETIOLOGY

Generally viral (influenza, parainfluenza, respiratory syncytial virus [RSV])

SIGNS AND SYMPTOMS

Cough, fever, sputum production, malaise, congestion

DIAGNOSTICS

Chest x-ray if clinical concern for bacterial pneumonia (PNA)

Clinical criteria:

• Acute cough (2 weeks but up to 2 months)

• No prior lung disease

• Wheezes/rhonchi on lung exam

• Bullous myringitis (may indicate mycoplasma PNA)

TREATMENT

Supportive treatment

Albuterol if wheezing

Antitussive agents (robitussin, codeine, Tessalon Perles)

No antibiotics for healthy individuals (unless pertussis or atypical PNA suspected)

For acute exacerbations of chronic bronchitis, antibiotics are indicated (azithromycin, levofloxacin)

Clinical pearls: up to 20% of patients with cough persisting for 2 to 3 weeks have pertussis

Pneumonia

BASICS

Inflammation of the lung parenchyma characterized by consolidation of the affected area, including terminal airways, alveolar spaces, and interstitium

Sixth leading cause of death in the United States

ETIOLOGY

Four categories:

• Community-acquired

• Hospital-acquired:

Occurs 48 hours after hospital admission

• Health care–associated:

In patients who have been hospitalized within 90 days of the infection

Residing in a skilled nursing facility

• IV antibiotics, chemotherapy, or wound care within 30 days

• Ventilator-associated: occurs 48 hours after intubation

Streptococcus pneumoniae is responsible for up to 90% of all bacterial PNA

E. coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and group A streptococci account for majority of remaining 10%

Legionella and anaerobes (aspiration) are less frequent

Respiratory viruses, Mycoplasma, and Chlamydia are responsible for the majority of atypical PNA (Table 13.1)

Two main routes of infection

• Inhalation of airborne pathogen

• Aspiration of oropharyngeal flora

Less common routes: blood borne (sepsis), direct extension from infection adjacent to the lung

SIGNS AND SYMPTOMS

Typical:

• Sudden onset of fever/chills/rigors, productive cough with purulent sputum, pleuritic chest pain

• Bronchial breath sounds and crackles over affected area

• Egophony, dullness to percussion, increased fremitus

Atypical:

• Gradual onset of headache (HA), myalgias, fatigue, anorexia with a dry cough

• Scattered rhonchi or fine crackles

DIAGNOSTICS

Chest x-ray

Sputum cultures, blood cultures when sepsis suspected or patient requires ICU level of care

TABLE 13.1.

Pathogens and Unique Features

Pathogen	Unique Feature
Pneumococcus	Abrupt; rusty brown sputum
Legionella species	Often involve GI symptoms and AMS Cruise ships; aerosolized water
Mycoplasma	Bullous myringitis
*Chlamydia pneumoniae*	College age, nonproductive cough
*H. influenzae*	More common among smokers and the elderly
Aspiration/anaerobes	Right lower lobe, ETOH or seizure history
*S. aureus*	Follows viral illness particularly measles
*K. pneumoniae*	Currant jelly sputum

GI, gastrointestinal.

TREATMENT

Treatment of patients with high suspicion for PNA should be started empirically

Community-acquired pneumonia (CAP):

• Outpatient: po azithromycin, levofloxacin, doxycycline

• Inpatient: IV fluoroquinolone as monotherapy or ceftriaxone + azithromycin

Health care–associated pneumonia (HCAP)/hospital-acquired pneumonia:

• Antipseudomonal cephalosporin (cefepime/ceftazidime) or

• Antipseudomonal carbapenem (imipenem/meropenem) or

• Piperacillin/tazobactam plus antipseudomonal fluoroquinolone (levofloxacin/ciprofloxacin)

• Consider anti-MRSA agent (vancomycin, linezolid)

• Consider double coverage for Pseudomonas in areas where multidrug-resistant (MDR) Pseudomonas common

Aspiration: consider adding anaerobic coverage, including clindamycin, Augmentin

Admission versus discharge

• HCAP: must be admitted for IV antibiotics

• CAP: admit when there is high suspicion for poor outcomes

• Pneumonia outcome research trial score:

Clinical prediction rule used to calculate the probability of morbidity and mortality among patients with CAP

The presences of any of the following increases the score, thus increasing the likelihood of poor outcomes

Risk class I (outpatient treatment), II to III (case by case basis), IV to V (require admission)

– Age

– Gender: males

– Nursing home resident

– Comorbidity: cerebrovascular, renal, liver disease, congestive heart failure (CHF), cancer

– Physical exam: altered mental status, systolic blood pressure <90, temp <35 or ≥40 respiratory rate ≥30, heart rate (HR) ≥125

– Labs: pH <7.35, PO₂ <60 or Sat <90, Na <130, hematocrit <30, glucose >250, blood urea nitrogen >30, pleural effusion

• Clinical pearl: awareness of airborne pathogens related to bioterrorism is becoming increasingly relevant (Table 13.2)

Pulmonary Abscess and Necrotizing PNA

BASICS

Occurs when necrotic lung tissue is released into adjacent airway structures, causing formation of cavities containing necrotic debris or fluid caused by microbial infection

TABLE 13.2.

Airborne Pathogens

Pathogen	Signs/Symptoms	Treatment
*Bacillus anthracis* (infected spores)	Causes skin lesions and lung infections; 1st flu-like symptoms progress to respiratory failure and coma	Ciprofloxacin or doxycycline
*Yersinia pestis* (etiologic agent of the plague)	48–72 h incubation period; fever, rigors, HA, cough, malaise, cyanosis	Streptomycin or doxycycline
*Francisella tularensis* (etiologic agent of tularemia)	Fever, chills, drenching sweats, severe weakness	Streptomycin

ETIOLOGY

Commonly associated with aspiration PNA, periodontal disease, bacteremia, endocarditis, intravenous drug use (IVDU), and Lemierre syndrome (oropharyngeal infection complicated by septic thrombophlebitis of the internal jugular)

SIGNS AND SYMPTOMS

Fever, chills, cough, sputum production (foul smelling), malaise, anorexia, weight loss

Symptoms may be indolent over weeks or months

DIAGNOSTICS

Complete blood count, sputum culture, acid-fast bacillus stain (if tuberculosis (TB) suspected)

Chest x-ray or chest CT

TREATMENT

Admit, prolonged antibiotic treatment (4 to 6 weeks), physiotherapy with postural drainage

Antibiotics should always include anaerobic coverage

• Clindamycin and Augmentin are both effective

Percutaneous catheter drainage or lobectomy for refractory cases

Empyema

BASICS

Parapneumonic effusion complicated by frank pus in the pleural space

ETIOLOGY

Caused by viral and bacterial PNA, trauma, hematogenous spread, and complications from surgery

Most common bacterial causes include S. aureus, Klebsiella, anaerobes, and mixed flora

SIGNS AND SYMPTOMS

Fever, chills, malaise, cough, chest pain, sputum production, weight loss

DIAGNOSTICS

Chest x-ray: pleural effusion (may appear loculated)

Chest CT: dense collection in the pleural space, often with gas locules

Thoracentesis: pleural fluid with elevated white blood cell, exudative pattern (in terms of lactate dehydrogenase, protein, and glucose)

• Gram stain and culture positive for bacterial organisms

TREATMENT

Hospital admission, antibiotics (CAP/HCAP coverage), and chest tube placement (at least 28 Fr )

Thoracic surgery consultation for thoracoscopy/video-assisted thoracoscopic surgery

CHRONIC OBSTRUCTIVE PULMONARY DISEASE, ASTHMA, BROCHIOLITIS

Chronic Obstructive Pulmonary Disease

BASICS

Characterized by chronic dyspnea and expiratory airflow obstruction

Fourth leading cause of death in the United States

Men more than women, predominantly over 40 years old

Characterized by airway inflammation, fibrosis, and mucous hypersecretion

Forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC): standard measure, FEV1 and its ratio to FVC

ETIOLOGY

Smoking (most common), cystic fibrosis, α-1 antitrypsin deficiency, bronchiectasis and bullous lung diseases (rare), occupational exposures

Two main types

• Chronic bronchitis

Damage to endothelium → excessive mucous → airway obstruction → decreased ventilation and increased cardiac output → rapid circulation in a poorly ventilated lung → hypoxemia and polycythemia → hypercapnia and respiratory acidosis → pulmonary artery vasoconstriction and cor pulmonale

“Blue bloaters”: obesity, cyanosis, peripheral edema, wheezes/rhonchi

• Emphysema

Destruction distal to the terminal bronchiole → gradual destruction of alveolar septa and of the capillary bed → decreased oxygenation → decreased cardiac output and hyperventilation → limited blood flow through a fairly well oxygenated lung → tissue hypoxia and pulmonary cachexia → muscle wasting and weight loss

“Pink puffers”: pink, thin, cachectic, pursed lip breathing, diminished breath sounds

SIGNS AND SYMPTOMS

Chronic obstructive pulmonary disease (COPD) exacerbation: an acute increase in symptoms beyond normal day-to-day variation, usually from respiratory infection or environmental factors

• Cough increases in frequency and severity

• Sputum production increases in volume and/or changes character

• Dyspnea on exertion, increased O₂ requirement

DIAGNOSTICS

Oxygen saturation

Arterial blood gas (ABG) in severe exacerbations

Chest x-ray to assess for signs of PNA, pulmonary edema, pneumothorax (PTX)

EKG

TREATMENT

Continuous monitoring of oxygen saturation, cardiac monitoring

Pharmacotherapy

• Oxygen:

Goal saturation of 90% to 94% and PaO₂ of 60 to 70 mm Hg

• Inhaled β-agonist:

Albuterol 2.5 mg diluted to 3 mL via nebulizer

• Inhaled anticholinergic agent:

Ipratropium (often combined with albuterol—Duoneb)

• Systemic corticosteroid:

Oral glucocorticoids, appear equally efficacious to IV

IV glucocorticoids used with severe exacerbations, those who respond poorly to oral glucocorticoids, or unable to take oral medications

Optimal dosing is unknown (e.g., methylprednisolone 60 to 125 mg IV or prednisone 30 to 60 mg po)

Five-day course often effective, although a taper may be necessary

• Antibiotics:

Optimal regimen undetermined

Target likely pathogens (levofloxacin 750 mg IV/po or alternative)

Consider risks of Pseudomonas or local patterns of antibiotic resistance

Noninvasive positive pressure ventilation (NPPV)

• Moderate to severe exacerbations

• Use only if tracheal intubation not immediately necessary and no other contraindications

• Contraindications:

Impaired consciousness

Inability to clear secretions or protect airway

Facial deformity

High aspiration risk

• Initial settings for bi-level NPPV: 8 cm H₂O inspiratory pressure (may increase up to 15 cm H₂O) and 3 cm H₂O expiratory pressure

Endotracheal intubation

Criteria for hospitalization

• Inadequate improvement of symptoms with initial therapies

• Worsening hypoxemia or hypercapnia

• Mental status changes

• Inadequate response to outpatient management

• Acute respiratory acidosis

Asthma (Acute Exacerbation)

BASICS

Obstructive lung disease characterized by airway narrowing, hyperreactivity, and airway inflammation

ETIOLOGY

May occur at any age, but generally diagnosed in childhood

May be precipitated by viral illness, environmental exposure, or exercise

Has been associated with maternal cigarette smoking

SIGNS AND SYMPTOMS

Wheezing, shortness of breath, cough, chest tightness

DIAGNOSTICS

Clinical exam findings

• Use of accessory muscles, diaphoresis, and inability to lie supine

Pulse oximetry

Peak flow

• Normal values based on height, age, and gender

• Peak flow <200 L per minute indicates severe obstruction

• While useful, peak flow has not yet been shown to improve outcomes, predict need for admissions, or limit morbidity/mortality when used in the emergency department (ED)

ABG: elevated or even normal PaCO₂ indicates severe airway narrowing

Chest x-ray: obtain if at high risk for comorbidities or if suspect underlying bacterial infection

TREATMENTS

Goal: rapid reversal of airflow obstruction and correction of hypoxemia and hypercapnia

Inhaled β-agonists

• Albuterol, levalbuterol

• Standard regimens:

Nebulized: albuterol 2.5 to 5 mg every 20 minutes for three doses, then 2.5 to 10 mg every 1 to 4 hours as needed

Metered-dose inhaler joint with spacer: albuterol 4 puffs every 10 minutes, or 8 puffs every 20 minutes, for up to 4 hours, then every 1 to 4 hours as needed

Inhaled anticholinergics

• Ipratropium for severe airflow obstruction in those who fail to improve despite inhaled β-agonists, as well as patients with concomitant COPD

• Standard regimens:

Nebulized: ipratropium 500 mcg every 20 minutes for three doses, then as needed

Metered-dose inhaler joint with spacer: ipratropium 8 puffs every 20 minutes, then as needed for up to 3 hours

Systemic glucocorticoids

• Moderate (peak expiratory flow <70% baseline) or severe exacerbation (peak expiratory flow <40% of baseline) or without significant improvement in peak flow with inhaled β-agonists

• Peak serum levels achieved ~1 hour after administration; clinical benefit may not be apparent for up to 6 hours

• Optimal dosing regimen unknown and based on expert opinion

• Standard regimens:

PO and IV forms have identical efficacy and bioavailability

Impending or actual respiratory failure: methylprednisolone 60 to 125 mg IV initially

Prednisone 40 to 60 mg po per day in a single or divided dose

Pediatric asthma: prednisolone 1 to 2 mg per kg daily or divided dose

Duration:

• Based on resolution of symptoms and return of peak expiratory flow measurements to >70% of baseline

• Generally 3 to 7 days, although taper should be considered in certain cases

Magnesium sulfate

• Exacerbation is life-threatening or remains severe (peak expiratory flow <40% of baseline) after 1 hour of intensive conventional therapy

• Magnesium sulfate 2 g IV infused over 20 minutes

• Contraindicated in renal insufficiency

Admission or observation

• Peak expiratory flow <40% predicted at time of disposition

• For new onset asthma patients with peak expiratory flow 40% to 70% predicted

• Multiple prior hospitalizations or ED visits for asthma, prior intubation

• Failure of outpatient treatment with oral glucocorticoids

Bronchiolitis

BASICS

Upper respiratory symptoms followed by lower respiratory infection with inflammation that results in wheezing and/or rales

Clinical syndrome that occurs in children <2 years old (peak 2 to 6 months)

Most common cause of respiratory distress/wheezing in infants

More common in the fall and winter

Clinical diagnosis, usually self-limited

ETIOLOGY

Viruses → terminal bronchiolar epithelial cells → damage and inflammation in the small bronchi and bronchioles → edema, excessive mucus, and sloughed epithelium → obstruction of small airways and atelectasis

Most common: RSV, rhinovirus, parainfluenza

• Two or more viruses are detected in approximately one-third of children hospitalized

• Adenovirus tends to cause more severe cases (bronchiolitis obliterans)

Risk factors for severe disease

• Prematurity (gestational age <37 weeks)

• Age <12 weeks

• Chronic pulmonary disease, congenital and anatomic defects of the airways, congenital heart disease, and immunodeficiency

• Environmental risk factors: passive smoke inhalation, crowded household, daycare, concurrent birth siblings, older siblings, and high altitude

SIGNS AND SYMPTOMS

Usually presents 3 to 6 days after symptom onset

Preceded by 1 to 3 days of rhinorrhea and mild cough

Fever (usually <38.4°C), cough, and mild respiratory distress

Tachypnea, intercostal/subcostal retractions, and expiratory wheezing, prolonged expiratory phase and coarse/fine rales

Mild hypoxemia

Severe: respiratory distress, cyanosis with poor peripheral perfusion

Wheezing may not be audible if airways are narrowed and when increased work of breathing results in exhaustion

Complications: dehydration, apnea, respiratory failure, and hypercapnia

DIAGNOSTICS

Clinical exam findings

Radiographs: not routinely indicted, chest x-ray abnormalities are variable and nonspecific

Laboratory studies: not necessary to make the diagnosis; however, may be necessary to assess the severity of illness

Virology studies: not routinely performed

TREATMENT

Supportive care: nasal/oral suctioning, supplemental O₂, IV fluids

Bronchodilators and saline nebulizers are widely used, but data is mixed on their effectiveness

When to admit

• Persistent resting O₂ sat below 92% on room air

• Persistent tachypnea, respiratory distress

• Age younger than 3 months, prematurity, or significant comorbidities (congenital heart disease)

• Inability to feed or maintain oral hydration

INTERSTITIAL LUNG DISEASE

BASICS

The term interstitial can be misleading since many disorders characterized as interstitial lung disease (ILD) involve pathology of the lung parenchyma as well as perivascular and lymphatic tissue

ETIOLOGY

Occupational and environmental exposures

• Asbestosis, silicosis, berylliosis, Coal worker’s pneumoconiosis, (Farmer’s lung)

Drug-induced pulmonary toxicity (amiodarone, bleomycin, methotrexate)

Radiation-induced lung injury

Connective tissue disease related

• Systemic lupus erythematosus, scleroderma, rheumatoid arthritis

Idiopathic

• Sarcoidosis, cryptogenic organizing PNA

• Idiopathic pulmonary fibrosis

Complete medical history can help identify the cause of suspected ILD

High mortality

SIGNS AND SYMPTOMS

Dyspnea, cough, pleuritic chest pain

Lung exam: wheezes, rales, rhonchi, or may be normal

Cardiac exam: usually normal or may suggest pulmonary hypertension (HTN) and cor pulmonale in advanced disease

Extrapulmonary: clubbing, systemic arterial HTN, skin and eye changes, lymphadenopathy, pericarditis, hepatosplenomegaly, and muscle weakness

ILD presenting with respiratory failure

• Infection may unmask an underlying, previously undiagnosed ILD

• Consider investigation into etiology of acute decompensation

Chest x-ray: infiltrates in the lower lung zones, ground-glass opacities, honeycombing in later stages

Consider chest CT, transthoracic echocardiogram, pulmonary artery catheterization, bronchoalveolar lavage, transbronchial biopsy, open lung biopsy

• Acute ILD

Consider after other causes are excluded

– Acute interstitial PNA

– Acute exacerbation of interstitial pulmonary fibrosis

– Cryptogenic organizing PNA

TREATMENT

Antibiotics if underlying infection present

Supplemental O₂

Discontinue exposure to pulmonary irritants

High-dose corticosteroids with or without immunosuppressive therapy

PNEUMOTHORAX

BASICS

Introduction of air into the pleural space

Types

• Primary PTX:

Absence of underlying lung disease

Risk factors: smoking, tall, thin stature, family history, Marfan syndrome

Usually in early 20s to 30s

• Secondary PTX

Occurs with an underlying lung disease

Risk factors: COPD, cystic fibrosis, CA, necrotizing PNA

• Traumatic PTX:

May occur with a hemothorax

Requires a 36 Fr chest tube

• Tension PTX:

Hypotension, tracheal deviation, elevated jugular venous pressure

Requires emergent needle decompression followed by 24 to 36 Fr chest tube

Needle decompression with 14G angiocath into the second intercostal space at the midclavicular line

SIGNS AND SYMPTOMS

Shortness of breath, tachypnea, tachycardia, hypoxia, decreased breath sounds, subcutaneous emphysema

Tracheal deviation is a late finding

Hemodynamic instability may indicate a tension PTX

DIAGNOSTICS

Clinical exam findings

Chest x-ray

Ultrasound will show absence of lung sliding

Chest CT scan

TREATMENT

Small (<15% volume):

• Observation, high-flow O₂ with non-rebreather facemask

• Repeat chest x-ray

• May resolve spontaneously

Large (2 cm on upright posteroanterior chest x-ray equals a 50% PTX)

• Chest tube insertion

• Pigtail catheter placement

Video-assisted thoracoscopic surgery pleurodesis:

• Reserved for recurrent pneumothoraces and failure of lung to reexpand after chest tube placement

PULMONARY EMBOLISM

BASICS

Thrombi originating in the venous circulation of the right side of the heart

ETIOLOGY

Virchow triad:

• Venous stasis

• Hypercoagulability

• Vessel intimal injury

General risk factors

• Age

• Immobilization longer than 3 days

• Pregnancy and postpartum period

• Major surgery in previous 4 weeks

• Long plane or car trips (>4 hours) in previous 4 weeks

Medical

• Cancer, previous deep venous thrombosis (DVT), stroke, acute myocardial infarction, CHF, sepsis, nephrotic syndrome, ulcerative colitis, systemic lupus erythematosus, lupus anticoagulant

Trauma

Hematologic

• Inherited disorders of coagulation/fibrinolysis

• Antithrombin III deficiency, factor V Leiden, protein C and S deficiency

Drugs/medications

• IVDU

• Oral contraceptives

• Estrogens

Pulmonary embolism (PE) develops in 50% to 60% of patient with lower extremity DVT: 50% of events are asymptomatic

Hypoxemia results from vascular obstruction, leading to dead space ventilation, right to left shunting, and decreased cardiac output

SIGNS AND SYMPTOMS

Dyspnea, pleuritic chest pain, cough, hemoptysis, palpitations, leg pain/swelling

Tachypnea, tachycardia, rales, fourth heart sound

DIAGNOSTICS

EKG: most common finding is sinus tachycardia

S1Q3T3 on EKG is pathognomonic, but not common

Chest x-ray:

• Atelectasis, infiltrates, pleural effusions

• Westermark sign: focal oligemia with prominent central pulmonary artery

• Hampton hump: wedge-shaped opacity against the pleural surface from intraparenchymal hemorrhage/infarct

Labs including: complete blood count, basic metabolic panel, prothrombin time/partial thromboplastin time, cardiac enzymes, B-type natriuretic peptide

• D-dimer may be used to exclude PE in low to moderate risk groups

Ventilation-to-perfusion (V/Q) scan

Helical CT arteriography is gold standard

Venous thrombosis studies (ultrasound)

Pulmonary angiography

Bedside echocardiogram: may see evidence of right ventricular (RV) strain

PE rule-out criteria (PERC) rule

• If age <50

• HR <100

• O₂ sat >94%

• Without history of DVT

• Recent trauma/surgery

• Exogenous estrogen

• Leg swelling

• Hemoptysis

The Wells score:

• Clinically suspected DVT—3.0 points

• Alternative diagnosis is less likely than PE—3.0 points

• Tachycardia (heart rate >100)—1.5 points

• Immobilization (≥3 days)/surgery in previous 4 weeks—1.5 points

• History of DVT or PE—1.5 points

• Hemoptysis—1.0 points

• Malignancy (treatment within 6 months) or palliative—1.0 points

• Traditional interpretation

Score >6.0—high

Score 2.0 to 6.0—moderate

Score <2.0—low

• Alternative interpretation

Score >4—PE likely, consider diagnostic imaging

Score 4 or less—PE unlikely, consider D-dimer to rule out PE

Massive PE: acute PE with sustained hypotension, pulselessness, or persistent bradycardia with signs of shock

Submassive PE: acute PE without systemic hypotension but with either RV dysfunction or myocardial necrosis

TREATMENT

Admit for anticoagulation and monitoring

Classic anticoagulation regimen of unfractionated heparin (UFH) followed by warfarin to maintain the INR 2.0 to 3.0

Factor Xa inhibitors or fondaparinux

Thrombolytic therapy: indicated for massive PE and may be considered for submassive PE with significant RV dysfunction/myocardial injury

Inferior vena caval filter

Pulmonary embolectomy: reserved for patients with refractory shock who have an absolute contraindication to thrombolytic therapy

RESPIRATORY FAILURE

BASICS

Hypoxemic (type I):

• Arterial oxygen tension (PaO₂) <60 mm Hg with a normal or low arterial carbon dioxide tension (PaCO₂)

• Most common form of respiratory failure

• Common causes: COPD, PNA, pulmonary edema, pulmonary fibrosis, asthma, PTX, PE, pulmonary arterial HTN, cyanotic congenital heart disease, bronchiectasis, acute respiratory distress syndrome (ARDS), fat embolism, kyphoscoliosis, obesity

Hypercapnic (type II):

• PaCO₂ >50 mm Hg

• Etiologies such as drug toxicities, neuromuscular disease, chest wall abnormalities, and severe airway disorders

• COPD, severe asthma, drug toxicity, myasthenia gravis, polyneuropathy, poliomyelitis, porphyria, head and cervical spine injury, obesity, hypoventilation syndrome, pulmonary edema, ARDS, myxedema, tetanus

Acute versus chronic hypoxemic failure

• Cannot easily be determined through blood gas analysis

• Look for clinical signs of chronic hypoxemia such as polycythemia or cor pulmonale

Acute hypercapnic respiratory failure

• Develops over minutes to hours

• pH <7.3

Chronic hypercapnic respiratory failure

• Develops over days or more, giving time for renal compensation through an increase in bicarbonate

• pH only slightly decreased

ETIOLOGY

Result of a malfunction in:

• Transfer of oxygen across the alveolus

• Transport of oxygen to the tissues

• Removal of carbon dioxide from blood into the alveolus and then into the environment

Hypoxemic respiratory failure

• Mechanisms

V/Q mismatch

– Most common cause of hypoxemia

– Hypoxemia can be corrected by administration of 100% O₂

– Minute ventilation rate is increased

– PaCO₂ generally not affected

Shunt

– Deoxygenated blood bypasses ventilated alveoli and mixes with oxygenated blood

– Persistent hypoxemia despite 100% O₂ inhalation

Hypercapnic respiratory failure

• Mechanism

Alveolar ventilation decreases due to a reduction in minute ventilation rate or an increase in the proportion of dead space ventilation

As ventilation decreases below 4 to 6 L per minute, PaCO₂ rises

SIGNS AND SYMPTOMS

Dyspnea, altered mental status (AMS), diaphoresis, somnolence

Tachypnea, tachycardia, accessory muscle use, wheezes/rales

DIAGNOSTICS

ABG

Chest x-ray

EKG

Consider echocardiogram, pulmonary function test, and/or right heart catheterization

TREATMENT

ABCs, IV, monitor

Stabilize patient’s respiratory and hemodynamic status

Correct patient’s hypoxemia with high-flow O₂, 100% non-rebreather, NPPV, endotracheal intubation when indicated

Identify and correct underlying pathophysiologic process

• Broad-spectrum antibiotics if underlying infection suspected

• β-Agonists for asthma/COPD

• Nitrates/diuretics for CHF

SLEEP APNEA

BASICS

Pauses in breathing (apnea) during sleep, due to sleep-related changes in ventilatory control

Breathing often resumes with choking or snorting sound

ETIOLOGY

Risk factors

• Obesity

• Enlarged airway tissues/adenoids/tonsils

• Men > women

• Increased risk with age

If untreated, associated with major health problems

• HTN, myocardial infarction, costovertebral angle, diabetes mellitus, obesity, heart failure, arrhythmia

• Work-related or car accidents

• Increased mortality

• Increased surgical complications

SIGNS AND SYMPTOMS

Loud snoring, daytime sleepiness, morning HAs

Poor memory and concentration, depression, sore throat on waking

DIAGNOSTICS

History from patient, family, partner

Exam for obesity, enlarged tonsils/uvula

Sleep study

TREATMENT

Weight loss, side sleeping, smoking cessation

Avoid alcohol and sedating medication

Continuous positive airway pressure

Surgery (tonsillectomy, uvuloplasty)

Obstructive sleep apnea has little bearing on emergency medicine

TUBERCULOSIS

BASICS

Airborne infection caused by a bacterium called Mycobacterium tuberculosis

Usually involves the lungs, but can also have manifestations of the kidney, spine, and brain

Transmission occurs via infectious droplets

Most common cause of death from infectious disease (other than complications of HIV/AIDS)

Risk factors include homelessness, HIV+, foreign-born, residents of shelters/prisons, IVDU

Primary TB

• Most frequently presents with new positive Mantoux test (purified protein derivative [PPD])

• When symptomatic, most often presents with active pneumonitis or extrapulmonary symptoms

Ghon complex: calcified focus of infection with an associated lymph node

Reactivation TB

• Symptoms

Fever, night sweats, productive cough, hemoptysis, pleuritic chest pain, dyspnea

May present subacutely with cough, weight loss, fatigue, night sweats

• Exam findings: rales, rhonchi, cervical lymphadenitis (scrofula)

• Extrapulmonary symptoms develop in 15% of the cases of reactivation TB and include

Lymphadenitis (most common)

Pleural effusion

Pericarditis

Peritonitis

Meningitis

Miliary TB

• Multisystem involvement caused by massive hematogenous dissemination

Primarily affects children and the immunocompromised

Signs and symptoms include fever, cough, weight loss, lymphadenopathy, hypercalcemia

The HIV patient and TB

• Highly susceptible to TB and have atypical presentations (extrapulmonary TB is common)

• Always consider TB in the HIV patient with respiratory complaints even if chest x-ray is normal

• Likely to develop MDR-TB

MDR-TB

• Foreign-born persons accounted for 72% of MDR-TB in 2,000

• Increase suspicion in patients with suboptimal medical care, homeless, HIV, and drug users

DIAGNOSTICS

Chest x-ray: most useful diagnostic tool for active TB in the ED

• Active primary TB: parenchymal infiltrates in any lung field, hilar and/or medial adenopathy can be seen with or without infiltrate

• Reactivation TB: lesion in the upper lobes or superior segments of the lower lobes, cavitary lesions, scarring, atelectasis, and effusion may also be seen

• Miliary TB: diffuse small nodular infiltrates (1 to 3 mm) in size

Clinical pearl: cavitary lesion on chest x-ray is associated with higher rates of infectivity