Explain pneumonia

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Pneumonia

Definition

Pneumonia is an infection of the lung parenchyma that leads to consolidation of the normally air-filled alveoli. It can be caused by bacteria, viruses, mycobacteria, mycoplasma, and fungi. Systemic viral infections (influenza A/B, measles, varicella) can also precipitate secondary bacterial pneumonia.

Textbook of Family Medicine 9e, p. 321

Epidemiology

Pneumonia and influenza account for over 1 million hospital admissions per year in the United States, with an in-hospital mortality rate of 3.3%.
Aggregate hospital charges exceed $35 billion per year.
In children, bacterial pathogens cause only 10-30% of all infectious pneumonias; Streptococcus pneumoniae has historically been the most common bacterial cause, though this is declining with universal vaccination.

Classification

Pneumonia is primarily classified by the setting in which it is acquired:

Type	Definition	Common Pathogens
Community-Acquired (CAP)	Acquired outside a hospital/institution	S. pneumoniae, Mycoplasma, Chlamydia, Legionella, influenza
Hospital-Acquired (HAP)	Develops ≥48 h after hospital admission	Gram-negative rods (Pseudomonas, Klebsiella), Staphylococcus aureus (including MRSA)
Ventilator-Associated (VAP)	Develops ≥48-72 h after endotracheal intubation	Multi-drug-resistant gram-negatives, MRSA
Aspiration Pneumonia	Aspiration of oropharyngeal/gastric contents	Anaerobes (Peptostreptococcus, Bacteroides), gram-negatives
Opportunistic Pneumonia	In immunocompromised hosts	Pneumocystis jirovecii (PCP), Cryptococcus, Aspergillus, CMV

Patients in nursing homes or with prolonged hospitalization are at high risk for colonization with gram-negative organisms and multidrug-resistant (MDR) bacteria.

Pathophysiology

Inoculation: Pathogens reach the lower respiratory tract via inhalation, aspiration of oropharyngeal secretions, or hematogenous spread.
Inflammatory response: The innate immune system responds with cytokine release, neutrophil recruitment, and exudate formation in the alveoli.
Consolidation: Alveoli fill with inflammatory cells, fluid, and debris, replacing air - this is what appears as opacification on chest X-ray and produces the clinical findings of consolidation.
Resolution or complication: In most cases, the lung returns to normal. Complications include parapneumonic effusion, empyema, lung abscess, bacteremia, and ARDS.

Clinical Presentation

The presentation depends on the causative organism:

Typical (Bacterial) Pneumonia

Rapid onset of high fever, rigors, productive cough (purulent or blood-streaked sputum), pleuritic chest pain, dyspnea
Physical exam: decreased breath sounds, dullness to percussion, egophony over the affected lobe
WBC markedly elevated (>15,000 × 10³/mm³) with neutrophilia
Classic example: pneumococcal lobar pneumonia

Atypical Pneumonia

Smoldering onset with low-grade fever, non-productive ("dry") cough, myalgias, headache, fewer constitutional symptoms
Patchy or interstitial infiltrates on CXR ("walking pneumonia")
Caused by Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, and respiratory viruses

In Children

Malaise, cough, chest pain, tachypnea, intercostal retractions
Tachypnea disproportionate to the degree of fever is the earliest clue in children
Viral pneumonia: less toxic appearance, low-grade fever, wheezing
Bacterial pneumonia: high fever, chills, dyspnea, acutely ill appearance
Textbook of Family Medicine 9e, p. 321-322

Diagnosis

Chest X-Ray

The cornerstone of diagnosis. Findings:

Lobar/segmental consolidation - typical bacterial (e.g., pneumococcal)
Patchy bilateral infiltrates - atypical organisms or viral
Interstitial pattern - Mycoplasma, viral, PCP
Pleural effusion if parapneumonic effusion or empyema has developed

Laboratory

CBC: leukocytosis with left shift in bacterial; normal or low in viral/atypical
Blood cultures: positive in 10-15% of hospitalized CAP patients; important for guiding targeted therapy
Sputum Gram stain and culture: most useful when collected before antibiotics
Urine antigens: available for S. pneumoniae and Legionella - results available within the ED timeframe
PCR panels (e.g., BioFire): rapidly identify a wide variety of bacterial and viral pathogens; particularly useful in outbreak settings (e.g., SARS-CoV-2)
Procalcitonin: helps distinguish bacterial from viral etiology
ROSEN's Emergency Medicine, p. 976

Severity Assessment - PSI / CURB-65

The CURB-65 score is widely used to determine the need for hospitalization:

Criterion	Points
Confusion	1
Urea >7 mmol/L (BUN >20 mg/dL)	1
Respiratory rate ≥30/min	1
Blood pressure <90 systolic or ≤60 diastolic	1
Age ≥ 65 years	1

Score 0-1: Outpatient treatment
Score 2: Consider hospital admission
Score 3-5: Hospitalization; score ≥4 consider ICU

Severe CAP Criteria (ATS/IDSA)

Patients with any one major criterion (need for invasive mechanical ventilation, or septic shock requiring vasopressors) or three or more minor criteria are classified as severe CAP and should be admitted to the ICU.

Treatment

Outpatient CAP (Adults)

Clinical Setting	Regimen
Previously healthy, no antibiotics in last 3 months	Amoxicillin 1g PO three times daily x7 days or Doxycycline 100 mg PO twice daily x7 days
Comorbidities (chronic cardiac, lung, liver, or renal disease) or recent antibiotics	Amoxicillin/clavulanate + azithromycin or Respiratory fluoroquinolone (levofloxacin 750 mg daily x5 days)

Note: Macrolide monotherapy is no longer routinely recommended for CAP unless local pneumococcal resistance is <25%. Most areas in the US do not meet this threshold.

Inpatient CAP (Non-Severe)

Beta-lactam (ceftriaxone, ampicillin-sulbactam, or ceftaroline) + macrolide (azithromycin)
OR respiratory fluoroquinolone monotherapy (levofloxacin or moxifloxacin)

Severe CAP / ICU

Beta-lactam + macrolide or beta-lactam + fluoroquinolone
Add vancomycin or linezolid if CA-MRSA is suspected (necrotizing pneumonia, post-influenza, sepsis in a young healthy adult)

Hospital-Acquired / Ventilator-Associated Pneumonia

Broader coverage targeting MDR gram-negatives and MRSA
Piperacillin-tazobactam, cefepime, or carbapenem + vancomycin or linezolid
ROSEN's Emergency Medicine, p. 977-979

Complications

Complication	Notes
Parapneumonic effusion / Empyema	Complicates ~30-40% of streptococcal pneumonia; requires drainage if infected
Lung abscess	Typically due to aspiration or Staphylococcus; cavitating lesion on CXR
Bacteremia	Occurs in 10-15% of cases; worsens prognosis
ARDS	Severe alveolar injury; high mortality
Sepsis/Septic shock	Systemic inflammatory response to infection
Metastatic infection	Meningitis, endocarditis, septic arthritis (especially with bacteremia)

Prevention

Annual influenza vaccine: all persons ≥6 months; especially those >50 years, chronic lung disease, diabetes, immune dysfunction
Pneumococcal vaccine (PCV/PPSV23): recommended for all adults ≥65; revaccinate with PPSV23 after 10 years if first dose was given before age 65
Smoking cessation (smoking is a major risk factor for CAP)
Infection control and hand hygiene in hospitals (HAP/VAP prevention)

Quick Summary Table

Feature	Typical Pneumonia	Atypical Pneumonia
Onset	Abrupt	Gradual
Fever	High, with rigors	Low-grade
Cough	Productive, purulent	Dry, non-productive
WBC	Markedly elevated	Normal/mildly elevated
CXR	Lobar consolidation	Patchy, bilateral, interstitial
Examples	S. pneumoniae, Staph. aureus	Mycoplasma, Legionella, viruses

Sources: Textbook of Family Medicine 9e | ROSEN's Emergency Medicine | Murray & Nadel's Textbook of Respiratory Medicine | Goldman-Cecil Medicine

COPD

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Chronic Obstructive Pulmonary Disease (COPD)

Definition

COPD is a common, preventable, and treatable disease characterized by persistent, progressive airflow limitation that is not fully reversible with bronchodilator therapy. The obstruction reflects an abnormal inflammatory response of the lung to noxious particles or gases, most commonly cigarette smoke. It encompasses two overlapping conditions - emphysema and chronic bronchitis - that typically coexist.

Chronic bronchitis is defined clinically: a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.
Emphysema is defined pathologically: abnormal, permanent enlargement of air spaces distal to the terminal bronchioles, with destruction of alveolar walls.

COPD is the third most common cause of death in the United States and accounts for over $40 billion per year in direct and indirect health care costs.

Etiology and Risk Factors

Risk Factor	Notes
Cigarette smoking	Overwhelmingly the dominant cause; accounts for ~85-90% of cases
Air pollution	Indoor (biomass fuel combustion), outdoor particulates
Occupational exposure	Dust, fumes, chemical vapors (coal mining, construction)
Alpha-1 antitrypsin (AAT) deficiency	Genetic cause; suspect if COPD onset before age 45 or in a non-smoker
Respiratory infections	Recurrent childhood infections reduce lung development
Airway hyperresponsiveness	Even without full asthma phenotype

Any patient developing COPD without significant smoking history or before age 45 should be screened for alpha-1 antitrypsin deficiency.

Pathophysiology

Emphysema

Cigarette smoke activates neutrophils and macrophages in the alveolar walls
These cells release proteases (especially elastase, MMP-12) that destroy the elastic connective tissue of alveolar walls
The resulting loss of elastic recoil leads to:
- Air trapping and static lung hyperinflation
- Collapse of small airways on expiration (dynamic airway collapse)
- Increased lung compliance, barrel chest
Two subtypes:
- Centriacinar (centrilobular): Most common; smoking-related; upper lobe predominance; destruction around respiratory bronchioles
- Panacinar (panlobular): Seen in alpha-1 antitrypsin deficiency; uniform destruction of acinus; lower lobe predominance

Chronic Bronchitis

Toxic inhalants trigger mucus hypersecretion from:
- Hyperplasia of submucosal mucus glands (Reid index >0.4)
- Goblet cell metaplasia in small airways
- Ciliary dysfunction reducing mucociliary clearance
Small airway inflammation and fibrosis causes obstructive bronchiolitis - the main site of airflow limitation
Results in hypoxemia and hypercapnia (V/Q mismatch)
Persistent infection (especially H. influenzae) perpetuates inflammation

Dynamic Hyperinflation

In moderate-to-severe COPD, the increased ventilatory demand of exercise combined with insufficient expiratory time causes air trapping. End-expiratory lung volume (EELV) fails to return to baseline, causing:

Reduced inspiratory reserve volume
Inspiratory muscle weakness and increased work of breathing
Neuromechanical uncoupling (effort >> tidal volume response)
This is the primary driver of dyspnea and exercise intolerance in COPD
Fishman's Pulmonary Diseases and Disorders, p. (block 7)

Gas Exchange Abnormalities

COPD causes V/Q mismatch - perfused alveoli that are poorly ventilated dilute oxygenated blood, reducing arterial PO₂. The classic ABG pattern in a severe COPD patient:

PaO₂: markedly reduced (~60 mmHg)
PaCO₂: may be elevated (type 2 respiratory failure) in bronchitic phenotype, or low if hyperventilating
Compensatory polycythemia over time (chronic hypoxemia stimulates EPO)
Costanzo Physiology 7th Edition

Clinical Presentation

Symptoms

Dyspnea on exertion - the hallmark symptom; slowly progressive over years
Chronic productive cough - especially morning sputum
Wheeze - particularly during exacerbations
Fatigue, exercise intolerance, weight loss in advanced disease

Physical Examination

Sign	Mechanism
Barrel chest (increased AP diameter)	Static lung hyperinflation
Pursed-lip breathing	Creates back-pressure to prevent airway collapse on expiration
Use of accessory muscles	Increased work of breathing
Hyperresonance on percussion	Air trapping
Decreased breath sounds	Loss of lung tissue
Prolonged expiration	Airflow obstruction
Central cyanosis	Hypoxemia
Clubbing	Consider if present - suggests alternative diagnosis (e.g., bronchiectasis, lung cancer)

"Pink Puffer" vs "Blue Bloater" (Classic but Simplified)

Feature	Emphysema ("Pink Puffer")	Chronic Bronchitis ("Blue Bloater")
Body habitus	Thin, cachexic	Obese
Cyanosis	Absent or late	Present (central)
Cough	Minimal	Prominent, productive
PaCO₂	Normal or low	Elevated
PaO₂	Near normal at rest	Reduced
CXR	Hyperinflation, flattened diaphragm	Increased bronchovascular markings
Cor pulmonale	Late	Early

In practice, most patients have a mixed phenotype.

Diagnosis

Spirometry (Gold Standard)

COPD is confirmed by post-bronchodilator spirometry showing:

FEV₁/FVC ratio < 0.70 (obstructive pattern)
FVC may be reduced but FEV₁ is disproportionately reduced
The obstruction is NOT fully reversible (<12% and <200 mL improvement after bronchodilator)

A restrictive pattern (low FVC with normal FEV₁/FVC) points to an alternative diagnosis (fibrosis, CHF, sarcoidosis).

GOLD Severity Classification (Based on Post-Bronchodilator FEV₁)

GOLD Grade	FEV₁ (% predicted)	Severity
GOLD 1	≥80%	Mild
GOLD 2	50-79%	Moderate
GOLD 3	30-49%	Severe
GOLD 4	<30%	Very Severe

The GOLD grading correlates strongly with exacerbation frequency and 3-year mortality (moderate COPD: 11% 3-year mortality; very severe COPD: 24%).

ABCD Assessment (Symptom + Exacerbation Burden)

Combines spirometry grade with:

Symptom burden: CAT score ≥10 or mMRC ≥2 = more symptomatic
Exacerbation history: ≥2 exacerbations/year or ≥1 hospitalization = high risk

This gives groups A, B, E (formerly C/D) to guide therapy escalation.

Additional Investigations

Chest X-ray: Hyperinflation (flattened diaphragms, increased retrosternal space, hyperlucency); useful to exclude other diagnoses
HRCT: Identifies emphysema distribution, bronchiectasis, or ILD
ABG: For patients with FEV₁ <50% or clinical signs of hypoxemia/hypercapnia
Alpha-1 antitrypsin level: Screen when indicated
6-Minute Walk Test: Functional limitation; <149 m indicates severe impairment
ECG/Echocardiogram: Assess for cor pulmonale and right ventricular dysfunction

Differential Diagnosis (GOLD Guidelines)

Condition	Distinguishing Features
Asthma	Early onset, variable symptoms, largely reversible airflow, atopic history
CHF	Fine basilar crackles, dilated heart on CXR, restrictive pattern on PFTs
Bronchiectasis	Large volumes of purulent sputum, coarse crackles, clubbing, CT shows dilation
TB	Infiltrates on CXR, microbiologic confirmation
Obliterative bronchiolitis	Younger, non-smoker, history of RA or fume exposure

Textbook of Family Medicine 9e, p. 314-316

Management

Non-Pharmacological (Most Important)

Smoking cessation - the single most effective intervention to slow FEV₁ decline; all smokers must be offered cessation support
Pulmonary rehabilitation - improves dyspnea, exercise capacity, and quality of life in all symptomatic patients
Long-term oxygen therapy (LTOT) - for patients with resting PaO₂ ≤55 mmHg (or ≤59 mmHg with cor pulmonale/polycythemia); the only therapy proven to improve survival in COPD; use ≥15 hours/day
Vaccination: Annual influenza + pneumococcal vaccine (PPSV23/PCV)
Nutritional support for underweight patients
Exercise training as part of rehabilitation

Pharmacological Treatment - Stepwise Approach

Short-Acting Bronchodilators (Rescue)

SABA (Short-Acting Beta-2 Agonist): Albuterol/salbutamol - for immediate symptom relief
SAMA (Short-Acting Muscarinic Antagonist): Ipratropium bromide - can be used as alternative or combined with SABA

Long-Acting Bronchodilators (Maintenance - First Line)

All symptomatic patients should receive a long-acting bronchodilator:

LAMA (Long-Acting Muscarinic Antagonist): Tiotropium is the prototype; highly M3 receptor-selective, once daily; reduces exacerbations and improves lung function
LABA (Long-Acting Beta-2 Agonist): Salmeterol, formoterol, vilanterol, indacaterol
For patients remaining symptomatic on one, add the other: LAMA + LABA combination

Inhaled Corticosteroids (ICS)

Less central than in asthma due to lower efficacy and increased risk of bacterial pneumonia (especially in elderly COPD patients)
Recommended only for:
- Severe airflow obstruction (GOLD 3-4)
- History of frequent exacerbations (≥2/year)
- Overlap with asthma
- Elevated blood eosinophils (≥300 cells/µL) predict better ICS response
Biomarker-guided ICS use is now recommended in international guidelines

Combination Triple Therapy

ICS + LABA + LAMA - for patients with frequent exacerbations despite dual bronchodilation, particularly if eosinophils are elevated.

Other Agents

Roflumilast (PDE-4 inhibitor): Selective phosphodiesterase-4 inhibitor; reduces exacerbation frequency in severe COPD with chronic bronchitis phenotype; oral once daily
Azithromycin (prophylactic): Daily azithromycin significantly reduces exacerbation frequency in patients with ≥2 exacerbations/year; monitor for QTc prolongation and macrolide resistance
N-acetylcysteine: Mucolytic; modest benefit in reducing exacerbations
Katzung's Basic and Clinical Pharmacology 16e, p. 565-566

Acute Exacerbation of COPD (AECOPD)

Definition

An acute worsening of respiratory symptoms (dyspnea, cough, sputum production or purulence) beyond normal day-to-day variation, requiring a change in medication.

Triggers

Viral respiratory infections (most common - ~50-70%): rhinovirus, influenza, RSV
Bacterial infections: H. influenzae, S. pneumoniae, M. catarrhalis; in severe COPD: Pseudomonas aeruginosa
Air pollution, pulmonary embolism, pneumothorax, cardiac failure

Management of AECOPD

1. Bronchodilators: Intensify short-acting bronchodilators (SABA ± SAMA via nebulizer)

2. Systemic corticosteroids: Prednisolone 40 mg/day for 5 days; reduces treatment failure and speeds recovery

3. Antibiotics: Routinely given because exacerbations frequently involve bacterial infection; active against H. influenzae

Beta-lactams (amoxicillin/amoxicillin-clavulanate), doxycycline, or azithromycin
Fluoroquinolones (levofloxacin/moxifloxacin) for severe or frequent exacerbations

4. Controlled oxygen therapy: Target SpO₂ 88-92% (avoid excessive O₂ - risk of hypercapnic respiratory failure due to blunting of hypoxic drive)

5. Non-invasive ventilation (NIV/BiPAP): First-line for acute hypercapnic respiratory failure (pH <7.35, PaCO₂ >6 kPa); reduces intubation and mortality

6. Invasive mechanical ventilation: If NIV fails or contraindicated

Complications

Complication	Notes
Cor pulmonale	Right heart failure from pulmonary hypertension; signs: edema, raised JVP, RV heave. Oxygen is the only therapy that improves this
Pulmonary hypertension	Prevalence varies; right heart catheterization is gold standard for diagnosis
Respiratory failure	Type 1 (hypoxemic) or Type 2 (hypercapnic + hypoxemic)
Secondary polycythemia	Compensatory response to chronic hypoxemia; increases viscosity and thrombosis risk
COPD-OSA Overlap Syndrome	~16% of COPD patients; more severe nocturnal hypoxemia, hypercapnia, higher mortality; CPAP reduces exacerbations and mortality
Pneumothorax	Ruptured emphysematous bullae
Lung cancer	Shared risk factor (smoking); increased risk independent of smoking history
Depression/anxiety	Highly prevalent; substantially impacts quality of life

Murray & Nadel's Respiratory Medicine

Prognosis

The BODE index (BMI, Obstruction, Dyspnea, Exercise capacity) is a validated predictor of mortality - superior to FEV₁ alone
Each AECOPD accelerates FEV₁ decline and worsens long-term prognosis
FEV₁ decline in COPD is ~50 mL/year (vs. ~25 mL/year normally), though cessation of smoking dramatically slows this
3-year mortality: Moderate COPD (GOLD 2) ~11%; Very Severe (GOLD 4) ~24%

Summary: Key Points


Definition	Irreversible obstructive airflow limitation; FEV₁/FVC <0.70 post-bronchodilator
Cause	Smoking (#1), air pollution, AAT deficiency
Pathology	Emphysema (elastase destruction of alveoli) + Chronic bronchitis (mucus gland hyperplasia)
Hallmark symptom	Progressive dyspnea on exertion
Diagnosis	Spirometry (post-bronchodilator FEV₁/FVC <0.70)
Severity	GOLD 1-4 based on FEV₁ % predicted
First-line therapy	Smoking cessation + long-acting bronchodilator (LAMA or LABA)
Only mortality benefit	Smoking cessation, long-term oxygen therapy (when indicated)
Exacerbation treatment	SABA/SAMA, systemic steroids, antibiotics, controlled O₂, ± NIV

Ambu bag

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Ambu Bag (Bag-Valve-Mask / Manual Resuscitator)

What Is It?

An Ambu bag - formally called a bag-valve-mask (BVM) device or self-inflating manual resuscitator - is a hand-held device used to deliver positive-pressure ventilation to a patient who is not breathing adequately or at all. "Ambu" is an eponym from Ambu A/S, the Danish company that first developed it in 1937 (short for "Artificial Manual Breathing Unit").

It is one of the most essential emergency devices in medicine - found on every crash cart, in every ambulance, in every operating theatre, and used during CPR, pre-hospital emergencies, transport, and as backup whenever a mechanical ventilator fails.

Miller's Anesthesia 10e, p. 2355

Components

The BVM has several distinct parts, each with a specific function:

Component	Function
Self-inflating reservoir bag	Compressible silicone/rubber bag; automatically re-expands after each squeeze, drawing in air or oxygen
Non-rebreathing valve (T-valve)	Directs gas flow: opens to patient during inspiration, closes and vents exhaled gas to atmosphere during expiration - prevents re-breathing of CO₂
Bag inlet valve	One-way valve that allows the bag to refill with oxygen/air between compressions
Face mask	Silicone cushioned mask in various sizes (infant, pediatric, adult); creates a seal over mouth and nose
Oxygen reservoir	A collapsible bag or corrugated tube attached to the back of the bag; stores supplemental O₂ between squeezes, enabling delivery of near 100% FiO₂
Pop-off valve (pressure-relief valve)	Limits peak inspiratory pressure (PIP) to 45 cm H₂O in pediatric/infant devices (ISO standard), preventing barotrauma; has an override
Oxygen inlet port	Connects to an external oxygen supply via tubing

Gas Flow - How It Works

During inspiration (squeezing the bag):

The non-rebreathing valve opens the inspiratory port
Compressed gas from the bag flows into the patient's airway
The expiratory port is simultaneously blocked

During expiration (releasing the bag):

The inspiratory port closes
The expiratory port opens, venting exhaled gas to the atmosphere (NOT back into the bag)
The bag re-inflates by drawing in oxygen from the reservoir or room air

This one-way valve design means the patient never re-breathes exhaled CO₂ - a critical safety feature.

Oxygen Delivery

Configuration	FiO₂ Delivered
No oxygen attached (room air only)	~21%
Oxygen connected, without reservoir bag	~40-60%
Oxygen connected at 10-15 L/min, with reservoir bag	~90-100%

The oxygen reservoir is essential for delivering high-concentration oxygen. Without it, oxygen is diluted by room air drawn in during bag re-inflation.

Sizes

Size	Patient	Bag Volume
Neonatal	Premature/newborn	~240 mL
Infant	<1 year	~450 mL
Pediatric	1-8 years	~500 mL
Adult	>8 years	~1600 mL (deliver only 400-600 mL per squeeze)

Technique

1-Person Technique: The E-C Clamp

Used when only one rescuer is available:

Position the patient: Head tilt-chin lift (or jaw thrust if c-spine injury suspected) to open the airway
Select correct mask size: Should cover nose and mouth without pressure on the eyes
Form the E-C clamp with the non-dominant hand:
- C: Thumb and index finger form a "C" shape, pressing down on the mask
- E: Remaining three fingers (middle, ring, little) form an "E" shape along the mandible, lifting the jaw upward into the mask
Squeeze the bag with the dominant hand - one hand squeeze for adults, two-finger squeeze for neonates
Watch for chest rise - this confirms effective ventilation
Release the bag - allow passive exhalation

2-Person Technique (Preferred)

One person uses both hands to maintain the mask seal (two-handed E-C grip)
Second person squeezes the bag
Produces better seal, more effective ventilation - strongly preferred in clinical settings

Key Ventilation Parameters

Parameter	Recommendation
Tidal volume (adult)	500-600 mL (visible chest rise; avoid over-ventilation)
Rate (adults with pulse)	1 breath every 5-6 seconds (10-12 breaths/min)
Rate (CPR with advanced airway)	1 breath every 6 seconds (10/min); asynchronous with compressions
Rate (CPR without advanced airway)	30:2 compression-to-breath ratio
Rate (infants/children)	12-20 breaths/min
Inspiratory time	~1 second per breath

Clinical Indications

Cardiopulmonary arrest - during CPR when no airway has been placed
Apnea - from any cause (drug overdose, anesthesia, drowning, trauma)
Respiratory failure - as bridge before intubation
Pre-oxygenation before intubation (3-5 minutes of 100% O₂ to maximize apnea tolerance)
Patient transport - when mechanical ventilator unavailable
Back-up device - if anesthesia machine ventilator or O₂ supply fails (required on every anesthesia workstation)
Post-extubation - temporary support if patient fails to maintain adequate ventilation
Neonatal resuscitation - at delivery

Hazards and Complications

Complication	Cause	Prevention
Gastric insufflation	High pressures pushing air into esophagus	Use appropriate tidal volume; avoid excessive force; consider cricoid pressure
Aspiration	Gastric inflation leading to regurgitation	Correct technique; consider nasogastric tube in prolonged use
Barotrauma (pneumothorax)	Dangerously high inspiratory pressures	Use pop-off valve; one-hand squeeze technique; avoid aggressive squeezing
Hypoxia	Inadequate mask seal, poor technique	Two-person technique; check for chest rise
Hyperventilation	Excessive rate or volume	Monitor rate; avoid over-squeezing
Valve failure	Stuck or blocked non-rebreathing valve	Pre-use check; regular equipment inspection
Increased work of breathing	Resistance from non-rebreathing valve	For spontaneously breathing patients, minimise mask time; valve adds inspiratory resistance

Key point from Miller's Anesthesia: "Dangerously high inspiratory pressures may be generated if the operator is untrained, uncareful, or if valve failure occurs. High pressures may lead to barotrauma or gastric insufflation."

Contraindications / Special Considerations

Suspected cervical spine injury: Use jaw thrust instead of head tilt-chin lift; do not hyperextend neck
Facial trauma: May make mask seal impossible; consider alternative airway (LMA, supraglottic airway)
Facial hair: Impairs mask seal; use more gel/pressure or consider alternative
Tracheostomy patients: Use appropriately sized pediatric mask directly over stoma, or use a speaking valve adapter
COVID-19 / airborne infection: BVM creates aerosol; use a viral filter at the mask-patient junction; consider avoiding BVM when intubation is planned

Pre-Use Check (Checklist)

Before every use, verify:

Bag re-inflates after squeezing (valve functioning)
Mask seal is intact (no cracks)
Oxygen reservoir attached and flowing
Pop-off valve present (pediatric devices)
All connections are secure
Correct mask size selected for patient

BVM vs. Other Airway Adjuncts

Device	Advantages	Limitations
BVM	No equipment skill required; immediate; portable	Requires continuous effort; seal may be difficult; gastric insufflation risk
LMA (laryngeal mask)	Hands-free; better seal; less gastric inflation	Training required; not definitive airway
Endotracheal tube	Definitive airway; protects from aspiration	Skill-intensive; can fail; complications with insertion

Sources: Miller's Anesthesia 10e (Self-Inflating Manual Resuscitators, p. 2355-2357) | Medscape BVM Technique

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