Pulmonary Disorders I

Physiology & measurement

• Perfusion, ventilation, diffusion
• Oxygen transport & the dissociation curve
• ABGs, pulse oximetry, capnometry
• PA catheter & hemodynamics
• Fluid resuscitation

Diagnostic currency: numbers — pH, PaO₂, PaCO₂, SvO₂, and the ratios built from them.

Imaging, the ventilator & disease

• The chest X-ray (AP/PA, ABCDEHI)
• Pulmonary function testing
• Mechanical ventilation & weaning
• Respiratory failure — Types 1–4
• COPD, asthma, bronchiectasis
• Pneumonia · TB · ARDS · IPF · sarcoidosis · cardiogenic pulmonary edema

Diagnostic currency: images, spirometry traces, ventilator settings, and FEV₁.

Blood flow through the lung

• Movement of mixed venous blood through the pulmonary capillary bed for gas exchange with alveolar air
• A high-volume, low-resistance system — pulmonary blood flow ≈ 6 L/min, mean pulmonary arterial pressure 15 mmHg
• Lung bases receive a greater percentage of flow than the apices (blood must flow against gravity to the apices when upright)

Air movement into & out of alveoli

• Mechanical movement of air for gas exchange between atmosphere and capillary blood; gas flows from higher atmospheric to lower intrapulmonary pressure on inhalation
• Alveolar ventilation = air that reaches alveoli and participates in gas exchange
• PaCO₂ is the best indicator of alveolar ventilation (normal 35–45 mmHg)

Hydrostatic pressure

Blood must flow against gravity to reach the apices in the upright position — so bases are better perfused than apices.

When it exceeds capillary pressure

• Positive pressure ventilation
• Decreased RV preload — dehydration, hemorrhage
• Air trapping in COPD

Decreased PaO₂

A local reflex that causes vasoconstriction of pulmonary arterioles supplying hypoxic alveoli.

Brain stem & cortex

• Medulla and pons fire automatically — some cells trigger inhalation, others halt it; exhalation is passive
• The cerebral cortex allows voluntary override in response to chemical stimuli and lung inflation changes

What the chemoreceptors sense

• Central chemoreceptors (medulla) respond to ↑ PaCO₂ (hypercapnia) and ↓ pH (acidosis) by increasing depth and rate — hypercapnia is the major stimulus
• Peripheral chemoreceptors (aortic and carotid bodies) respond to ↓ PaO₂ (hypoxemia)

Work of breathing

Effort required to overcome the elastic and resistive properties of the lungs and chest wall.

Distensibility

How easily lungs/thorax stretch. High compliance = easier to expand (COPD). Low compliance = stiff lungs (pneumonia, ARDS).

Airway radius

Determined by airway radius — increased resistance = increased effort and increased WOB.

Dissolved in plasma

PaO₂ — normal 80–100 mmHg. A tiny reserve for times of increased demand.

Bound to hemoglobin

SaO₂ (oxygen saturation) — normal 95%–100%. Assess the hemoglobin level: if Hgb is low yet adequately saturated, the patient is not adequately oxygenated.

Greater affinity

Binds easily in the lung but unloads less to tissue — possible tissue hypoxia from the strong Hgb–O₂ bond.

• Alkalosis
• Hypothermia
• Decreased 2,3-DPG

Decreased affinity

Unloads more O₂ to tissue — delivery improves as long as loading in the lungs is adequate.

• Acidosis
• Increased tissue metabolism, anaerobic metabolism, hyperthermia
• Increased 2,3-DPG

A normal exercise load

Climbing a flight of stairs without stopping suggests adequate oxygenation and ventilation.

Reported or visible distress

Does the patient report distress? Does the patient appear distressed?

Unsaturated hemoglobin

Dusky bluish tint from excess unsaturated Hgb. The more central, the more severe (face/chest > fingertips). No visible cyanosis does not ensure adequate oxygenation.

Three lumina & a thermistor

• Distal lumen opens at the tip (in the PA)
• Proximal lumen opens ~30 cm from the tip (in the right atrium)
• Balloon lumen inflates just proximal to the tip
• ~100–110 cm long, markings every 10 cm; a temperature sensor at the tip permits thermodilution cardiac output

What each port tells you

• CVP (proximal) = RV end-diastolic pressure (preload) → systemic volume status
• PAP (distal, balloon down)
• PCWP (distal, balloon wedged) = LV end-diastolic pressure (preload) → LV function
• SvO₂ — less than 65% indicates systemic delivery is impaired

What signals it

• Hypotension, tachycardia, low CVP, low PCWP
• Flat neck veins in Trendelenburg
• Urine output < 0.5 ml/kg/hr
• History of volume wasting — hemorrhage, emesis/diarrhea, diaphoresis, excess diuresis, sepsis

How you know it worked

• Normalization of BP and heart rate
• Increasing urinary output
• Normalization of CVP, PCWP, CO/CI, SVR
• Resolution of lactic acidosis

Normal saline & LR

0.9% NS is a good routine choice — but of 1 L given, only ~250 mL stays intravascular. High volumes → hyperchloremic acidosis. Lactated Ringer's is common in the OR. Dextrose solutions are not first-line for volume expansion.

Fluid of choice for hemorrhage

Each unit typically raises the hematocrit of a 70 kg person by 3%.

Albumin — intravascular sponges

Oncotic attraction pulls volume intravascularly, but the effect is transient — reserve for specific indications such as refractory hypovolemia. FFP, platelets, and cryoprecipitate are not resuscitation fluids.

Back against the plate

Portable, usually supine. More magnification, less sharpness. Supine limits inspiration and falsely widens the heart up to 15% and the mediastinum — and you can't assess free pleural fluid.

Chest against the plate

X-ray suite, usually upright. Less magnification, sharper, deeper inspiration, dependent pleural fluid more evident, less cardiac distortion, scapulae lifted out.

Left side against film

Best for the posterior mediastinal and retrocardiac spaces and thoracic vertebrae; may reveal free or loculated effusion not seen on supine AP.

Judged by vertebral bodies

• Over-penetration — beam too intense, overly dark, subtle detail lost
• Under-penetration — beam too weak, overly white, detail lost in glare
• Air < fat < soft tissue/water < bone/metal absorb progressively more radiation

Two quick checks

• Beam perpendicular, minimum 6 ft away; clavicles equal length and equidistant from the spinous process
• Expose on deep inspiration — the 7th rib at or above the diaphragm is adequate; poor inspiration falsely widens the heart and crowds the hila

Loss of borders & linear markings

• Silhouette sign — loss of a normal border between densities (e.g., air-filled lung becomes water-dense), localizing the lesion: a density obscuring the right heart border sits in the right middle lung; one obscuring the hemidiaphragm sits in the right lower lung
• Interstitial pattern — distinct linear/nodular markings as the interstitium gains water (IPF, radiation pneumonitis, scleroderma)

Consolidation & air bronchograms

• Alveoli fill/consolidate/collapse — interstitial markings less distinct
• Air bronchogram — air-filled bronchi in contrast against nonaerated lung
• Usually acute; focal, multifocal, or diffuse (pulmonary edema, bronchopneumonia, hemorrhage, atelectasis)

Fleischner-style follow-up

• < 6 mm, low-risk adult — no follow-up imaging
• 6–8 mm — follow-up CT in 6–12 months
• > 8 mm — follow-up CT in 3 months

Who gets yearly low-dose CT

• Aged 55–80 years
• Current smoker or quit within the past 15 years
• 30 pack-years smoking history (packs/day × years)
• Low-dose CT screening decreases mortality by 20%

Can't get air out

• Flow rates reduced compared with predicted
• Lung volumes normal or larger — air trapping and hyperinflation (increased RV and TLC)
• FEV₁/FVC < 70% (adults) = airflow obstruction

Can't get air in

• Flow rates normal or increased
• Lung volumes proportionately reduced — TLC is decreased
• TLC normal or increased in obstructive disease

Depression or failure

• Drugs — opioids, sedatives, NM blockers
• Trauma — spinal cord / phrenic nerve injury
• Disease — Guillain-Barré, ALS, myasthenia gravis, shock
• Exhaustion — status asthmaticus, sustained severe WOB
• Sustained apnea of any cause

Refractory to O₂ & airway care

PaO₂ < 60 mmHg and/or PaCO₂ > 50 mmHg refractory to supplemental O₂ and airway maintenance.

Diffusion · ventilation · perfusion

• Diffusion — aspiration, pulmonary edema, ARDS, COPD, pneumonia
• Ventilation — COPD, Pickwickian, flail chest, pneumothorax, atelectasis
• Perfusion — shock, pulmonary embolus, malignant arrhythmias

Air can't move

Absent or inadequate movement of O₂ in and CO₂ out. Apnea = absence of gas movement; hypopnea = inadequate movement.

Best assessed by PaCO₂ and/or end-tidal CO₂ — a rising PaCO₂ means ventilatory failure.

Types 1–4

Classified by the mechanism that fails — hypoxemia (Type 1), hypercapnia (Type 2), atelectasis from low FRC (Type 3), or hypoperfusion of respiratory muscles (Type 4).

Sedatives, hypnotics, opioids

Medication dose exceeds the body's ability to respond to metabolic and cellular needs. Elderly persons are particularly susceptible. Unintentional (iatrogenic over-sedation, especially in COPD) or intentional.

What impairs gas movement

• Lung infections
• Neuromuscular disease — myasthenic crisis, Guillain-Barré, ALS, head/spinal cord injury
• Pulmonary edema (cardiogenic or noncardiogenic)
• Musculoskeletal derangements — kyphosis
• Conditions limiting thoracic expansion — hiatal hernia, cirrhosis with ascites

Unlabored, sustainable ventilation

Supplemental oxygen via mask or nasal cannula.

Alert, increased WOB

• Humidified high-flow O₂ (Vapotherm, Optiflow)
• CPAP — for hypoxemia alone (e.g., CHF exacerbation)
• BiPAP — for hypoxemia with hypercapnia (e.g., COPD exacerbation)

Intubate

Conventional mechanical ventilation; nonconventional modes (pressure control, APRV, HFOV) or strategies (partial liquid ventilation, ECMO) as needed.

Chronic productive cough

A chronic productive cough for 3 months, lasting into successive years, in the absence of other illness.

Structural change

Abnormal, permanent airspace enlargement distal to the terminal bronchioles with destruction of airspace walls, without overt fibrosis.

Asthma & reactive airway

Chronic inflammation with variable, often reversible airflow obstruction. The asthma/COPD overlap has features of both.

Three cardinal symptoms

• Dyspnea with exertion, chronic cough, sputum production — cough starts in the early morning, then all day
• Sputum usually clear; a change in amount or color matters (management decision)
• Fatigue, chest tightness; weight loss (pulmonary cachexia) = worse prognosis

What you find

• Tripod stance (leaning forward, arms braced) = end-stage; pursed-lip breathing
• Barrel chest (↑ AP diameter; normally axilla-to-axilla ≈ 2× AP)
• Accessory muscles (SCM, intercostals, scalenes); hyperresonance; low-set diaphragm (11th–12th posterior rib)
• Diminished breath sounds; prolonged forced expiratory time (> 3 s); rhonchi; occasional expiratory wheeze
• Clubbing suggests ILD, bronchiectasis, or lung cancer — not COPD

FEV₁/FVC < 70 = obstruction

• FEV₁ 80–100% mild · 50–80% moderate · 30–50% severe · < 30% very severe
• Air trapping = ↑ RV; ↑ TLC/FRC/RV = hyperinflation; FVC may be reduced by trapping

Later & during exacerbations

• Hypoxemia (PaO₂ < 55 mmHg) and hypercarbia (chronic respiratory acidosis) — seen later or in moderate-severe exacerbations
• Oxygenation adequate if SaO₂ > 88% and Hgb > 10 g/dL
• Hct > 55% = secondary polycythemia; serum bicarbonate rises with chronic hypercarbia
• CXR: hyperlucency, flattened diaphragm, ≥ 10 ribs above the diaphragm, blebs/bullae

Slow, mostly fixed

• Smoking-driven, progressive; FEV₁/FVC < 70%, not fully reversible
• Mainstay = anticholinergics (SAMA/LAMA) + LABAs; ICS only when FEV₁ < 60% or frequent exacerbations
• Treatment cannot restore function — it prevents symptoms; the only thing that halts decline is removing toxins
• Exacerbations: most common cause is bronchial infection → steroids + antibiotics ± BiPAP

Variable, often reversible

• Episodic, triggered (exercise, infection, allergens); often childhood onset, family history
• Reversible obstruction demonstrated on spirometry; peak flow monitors but does not diagnose
• Stepwise ICS-based control; SABA PRN at every step; step down after ≥ 3 months of good control
• Inflammatory: bronchial smooth-muscle/mucous-gland hypertrophy, hyperreactivity, bronchospasm + mucus + edema

Copious sputum

• Periodic cough with copious sputum — one or more cups/day, occasionally bloody
• Often postinflammatory — after severe pneumonia, bronchial obstruction by a foreign body, or healed TB
• Exam: inspiratory rhonchi during exacerbations, noisy expiration
• CXR may show fibrosis; CT documents airway dilatation and bronchial wall thickening
• Manage with percussive therapy + postural drainage (flutter valve, percussive nebulizers, The Vest, PEP devices), generous mucolytics, and antibiotics — even prophylactically

Endobronchial tumors & foreign bodies

• Seen on CXR or suspected because of atelectasis; cough, dyspnea, hemoptysis, weight loss
• CT shows a solid mass or irregularly shaped cavity in one lung; CXR shows a mass; fiberoptic bronchoscopy with biopsy; PET to find metastasis
• Treatment follows the pathology — surgery, chemotherapy, radiation, or a combination

What makes the diagnosis

• Cough, exertional dyspnea, fever
• Leukocytosis may be present
• Radiographic infiltrate — required

May be bacterial, viral, fungal, or parasitic.

Who gets into trouble

• Age > 65
• Chronic comorbidities · viral respiratory infection
• Impaired airway protection · smoking
• Recent antibiotic use
• Immunocompromised — HIV, chemotherapy, transplant

What drives mortality

• Congestive heart failure
• Diabetes mellitus
• Chronic liver and renal disease
• COPD

The very young and the very old die disproportionately.

Classic findings

• Fever
• Chills
• Leukocytosis
• Cough, with or without sputum
• Sputum production
• Increased fremitus

Variable presentation

• Fever may be high
• Leukocytosis may be absent — or a left shift with "band" forms
• Cough often dry
• Headache, sore throat, excessive sweating, chest soreness
• More often diffuse; may involve more than one segment or both lungs

Community-acquired

Acquired in the community setting — or within 48 hours of hospital admission.

Most common organism: S. pneumoniae — the most common bacterial cause in adults.

Hospital-acquired

Occurs 48 hours or more after admission, not incubating at admission. Includes VAP and healthcare-associated pneumonia.

Most common: S. aureus, S. pneumoniae, H. influenzae.

Ventilator-acquired

Arises more than 48–72 hours after endotracheal intubation.

Most common organism: Pseudomonas.

Highest sensitivity — rules out when absent

• Fever > 38 °C with chills/shivering
• Pleuritic chest pain
• Cough productive of mucopurulent sputum
• Dyspnea
• Tachypnea — especially over age 65

Highest specificity — rules in when present

• Asymmetric breath sounds
• Pleural rubs
• Egophony
• Increased tactile fremitus

Yearly, for everyone 6 months and older

No preference for vaccine presentation when multiple types are available within an approved age range. Some patients are revaccinated within a season if they:

• Are immunocompromised
• Have severe underlying COPD or heart disease

PCV13 and PPSV23

• PCV13 — conjugate vaccine for infants, children, and adults older than 19 at high risk
• PPSV23 — polysaccharide vaccine for adults older than 65, and those older than 2 at high risk
• If giving both: start with PCV13, give PPSV23 at least 8 weeks later

Guidelines change frequently — check the CDC schedule.

What the patient reports

• Most patients are asymptomatic
• Fever
• Cough — generally productive of purulent sputum that may contain blood
• Weight loss
• Night sweats that may require changing the bed linen

What you find

• Body temperature elevation
• Cachexia
• Rales over affected areas — apical posttussive rales for apical disease

What the workup shows

• Normal CBC
• Low serum cortisol if disseminated disease has destroyed the adrenal cortices
• Acid-fast smears often positive — but treat empirically if findings suggest TB without a positive smear
• Culture usually positive within 6 weeks

X-ray and CT

• Chest X-ray often shows evolving bilateral infiltrates — "whited out"
• CT chest shows the heterogeneous nature of the opacities

What to order

• ABG with PaO₂/FiO₂ ratio
• CBC with differential and platelet count
• Coagulation studies — PT, PTT, fibrinogen, fibrin degradation products
• Renal and liver function · urinalysis
• Blood and urine cultures; sputum culture and Gram stain

Assess and secure

• Assess adequacy of ventilation and the work of spontaneous breathing
• Intubate if ventilation is significantly compromised — especially with altered mentation

Ventilate

• Institute mechanical ventilation if work of breathing is not being met — patient fatigue, elevated PaCO₂
• Or if hypoxemia is not correctable with an FiO₂ of 0.5

Resuscitate

• Vigorous fluid resuscitation if hypotension is present
• Regulated by hemodynamic parameters, especially left ventricular ejection fraction

Idiopathic pulmonary fibrosis

Etiology unknown; strongly linked to cigarette smoking. The most common cause of interstitial lung disease among elderly patients, and more common in men.

Symptoms: progressive dyspnea (slow or rapid) and nonproductive cough.

Noncaseating granulomas

Characterised pathologically by noncaseating granulomas and interstitial lung disease, with systemic manifestations: lymphadenopathy, cardiac involvement, iritis, cutaneous lesions, arthritis, GI involvement.

More common among females, North Americans, African Americans, and northern European Caucasians. Typical onset ages 20–40.

Shared findings

• CXR and high-resolution CT — interstitial infiltrates, nodules, cystic ("honeycombing") changes, especially in the lower lobes
• PFTs — restrictive ventilatory defect; DLCO commonly reduced
• ABG and pulse oximetry — hypoxemia as disease progresses; CO₂ retention indicates severe disease
• Tissue: fiber-optic bronchoscopy with transbronchial biopsy first; bronchoalveolar lavage at the same time; thoracoscopic lung biopsy if more assurance is needed

Don't miss these

• PPD testing should be done in both
• Complement fixation serology for deep fungi — histoplasmosis, coccidioidomycosis, blastomycosis
• Sarcoidosis is associated with hypercalcemia — check calcium
• Sarcoidosis blood panel: CBC, calcium, LFTs, BUN, creatinine; plus EKG, urinalysis, PPD, ophthalmologic exam
• Vaccinate IPF patients against influenza and pneumococcus — these infections are poorly tolerated

IPF — no cure

• No procedure or medication can remove the scarring
• Pirfenidone (Esbriet) and nintedanib (Ofev) slow progression
• Oxygen support to maximise blood oxygen levels
• Lung rehabilitation — helps exercise with less dyspnea
• Noninvasive positive airway pressure by mask may benefit selected patients
• Lung transplant for advanced disease
• Prognosis is often poor; counsel on palliative care and end-of-life issues

Sarcoidosis — individualized

• No cure; treatment based on symptoms and severity of organ involvement
• Refer to specialists for the organs involved
• Alternatives are indicated only when sarcoidosis does not respond to oral corticosteroids, when there is intolerance or contraindication, or when the steroid dose must be reduced
• Options: methotrexate, hydroxychloroquine, azathioprine, cyclophosphamide, infliximab, adalimumab, leflunomide

Ischemia

Coronary artery disease with myocardial ischemia and infarction — aggravated by obesity, limited exercise, dyslipidemia, and cigarette smoking.

Rhythm & pressure

• Arrhythmias — tachycardia especially, and bradycardia
• Hypertension
• Valvular dysfunction

Everything else

• Thyroid dysfunction — hyper- or hypothyroidism
• Diabetes mellitus
• Viral myocarditis
• Idiopathic cardiomyopathy
• Renal failure
• Drug therapy — especially certain chemotherapeutic agents

Signs of fluid retention

• Edema and jugular venous distention
• Rales
• Tachycardia or bradycardia
• Inability to tolerate lying flat — orthopnea
• Tachypnea
• Pleural effusions
• Ascites when CHF is advanced

What to look for

• Vascular redistribution to upper lung fields
• Interstitial edema
• Kerley B lines
• Pleural effusions — usually bilateral or on the right
• Cardiomegaly

Oxygenation vs. ventilation

Oxygenation = getting O₂ into blood (track PaO₂/SaO₂). Ventilation = moving CO₂ out (track PaCO₂). A patient can be well ventilated and still hypoxemic — and vice versa.

Obstructive vs. restrictive

Obstructive = flow ↓ (FEV₁/FVC < 70%), volumes normal/↑. Restrictive = flow normal/↑, volumes ↓ (TLC ↓). One ratio separates them.

ABG interpretation

pH → PaCO₂ → HCO₃ → the 0.08 rule → PaO₂/FiO₂. Every 10 mmHg of PaCO₂ moves pH 0.08 the other way; any leftover is metabolic.

Reading a CXR

Patient → orientation/rotation → penetration → inspiration → ABCDEHI — then compare to priors. Same order, every film, no exceptions.

Type 1 vs. Type 2 failure

Type 1 = PaO₂ < 60 (hypoxemia). Type 2 = PCO₂ > 50 (hypercapnia) in the absence of chronic retention. Type 3 is atelectasis from low FRC; Type 4 is underperfused respiratory muscles.

The barotrauma threshold

Peak pressure > 45 cm H₂O is the barotrauma risk; keep plateau ≤ 30 cm H₂O with tidal volumes of 6–8 mL/kg IBW.

The oximeter lies about content

It reads saturation, not content. Anemia + 100% SpO₂ can still be under-oxygenated — and CO gives a falsely high reading. "100% of half is still half."

Chronic CO₂ retainers

They breathe on their hypoxemic drive. Give O₂ at low flow (1–2 L/min) and watch for apnea — but never withhold needed oxygen.

Weaning gate

FiO₂ ≤ 0.40 and PEEP ≤ 8, SBP ≥ 90 without pressors, no blockade → daily spontaneous breathing trial of 30–120 minutes.