Pulmonology 6

have cartilage, smooth muscle, mucus glands

are membranous and held open by tethering forces

23 branched tube structure; Proximal generations have cartilage, smooth muscle, mucus glands; Distal generations are membranous and held open by tethering forces

Inflammation narrows airways (asthma, bronchitis), reducing airflow

More distal involvement can also create alveolar destruction (emphysema)

normal spirogram

Obstruction defined

rough rule below 70%

severity graded by

Restriction defined by

wheezing/SOB; reduced FEV1/FVC and increased RV (during exacerbations or methacholine)

include environment, allergies, GERD, infection, sinuses, stress

Methacholine challenge

(<2/wk, near nl PFT)

(<1/d, near nl PFT)

(daily, mild/mod PFT)

(daily/nocturnal, mod/sev PFT)

mucus gland hypertrophy (cough/sputum); reduced respiratory drive; airway hyper-reactivity

dyspnea - active respiratory drive; reduced DLCO

mucus gland hypertrophy (cough/sputum)

reduced respiratory drive

airway hyper-reactivity

dyspnea - active respiratory drive reduced DLCO

reduced DLCO

middle age/ elderly, cough, phlegm, wheeze, rhonchi, hyperinflation, cor pulmonale, LoPO2/HiPCO2 chronically

blue bloater

middle age/elderly, dyspnea, distant breath sounds, hyperinflation, cor pulmonale late, near normal until late

pink puffer

minute ventilation

MVV

Hyper-reactive airways from: allergies - IgE dust mite, cockroach droppings; induced: occupational exposures - RADS, viruses, environment/inhaled toxins, other (familial) Cellular elements: mast cells, eosinophils, CD4 lymphs

Inhaled toxins: tobacco, others; Anti-protease deficiencies; Airway “remodelling” in persistent asthma

dissipates as immune system “grows up”

waxes/wanes depending on inducing causes; persistent reactivity predisposes to COPD (airway remodelling)

depends on tobacco exposure/sensitivity

Low delivery means must load with more drug; Tidal breathing, long time

Delivery to 40%; Pt coordination required; Spacer for coord, velocity

Delivery to 40%; Easier coordination

Tobacco cessation; Pharmacologic therapy; Oxygen, Rehabilitation; Surgery

Education: [chronic & acute management], Exercise: [deconditioning common; may need bronchodilators/O2]; Psycho-social support

removes overdistended regions to allow more normal regions to re-expand; puts diaphragm at better rest point; being evaluated in large trial (NETT)

Endobronchial valves; Biologically mediated scar formation; New collateral channels for ventilation

LVRS

put needle in & shoot, pop a bubble; & leave a stent

Infections (viral); Acute exposures to allergens; Exercise (cold air); ?Stress; Anaphylactic like reaction (“sudden death”)

Usually infectious trigger; Must rule out: PE, CHF, pneumothorax, other

Bronchodilators, Steroids, Oxygen, Antibiotics, NPPV

increase beta agonist if on inhaled steroid, double dose

increase beta agonist, add/increase oral steroid

increase beta agonist, add/increase oral steroid, proceed to ED

Advanced pigment changes of ________ are characterized by red oozing skin (worse on the left anterior leg) with some scaling on the ankle.

Longstanding edema in this patient with chronic venous insufficiency led to moderately advanced pigment changes on the medial and lateral ankles, which extend onto the dorsum of the foot.

Large venous ulcer on the medial ankle in a patient with chronic venous stasis. The ulcer is shallow and red-based with irregular borders.

Progression of Chronic Venous Insufficiency

Which of the following causes the most deaths in the United States every year? A. Breast cancer; B. Pulmonary embolism, C. Highway fatalities, D. AIDS

Virchow’s Triad:

VTE Risk Stratification: Patient Factors: Clinical

interferes with the function of the calf muscles in pumping blood upstream through the veins.

confers a higher risk than other positions.

Pain, tenderness, swelling, warmth / erythema; Sensation of muscle cramping (“I pulled a muscle”); May be acute or develop over days or longer

Deep venous thrombosis; Postphlebitic syndrome, Cellulitis, Trauma / hematoma, Muscle cramp, Baker’s cyst

Lab Tests: D-dimer

Diagnostic Imaging Tests for Suspected Acute DVT

Diagnostic Imaging Tests for Suspected Acute DVT: most common / practical

Diagnostic Imaging Tests for Suspected Acute DVT: gold standard, rarely done

Diagnostic Imaging Tests for Suspected Acute DVT: also accurate

Diagnostic Imaging Tests for Suspected Acute DVT: very accurate

72 yo. college professor with CHF and acute proximal DVT. How would you treat?

For patients with a high clinical suspicion of DVT or PE, we recommend treatment with

Arterial blood gas; D-dimer; Troponin; BNP

Lab Tests: Pulmonary Embolism: hypoxemia

Lab Tests: Pulmonary Embolism: Sensitive, not specific

Lab Tests: Pulmonary Embolism: + with RV damage

Lab Tests: Pulmonary Embolism: increases with LV or RV dilation

may be present in PE but not diagnostic!

Diagnostic Imaging Tests for Suspected Acute PE: most common test

Diagnostic Imaging Tests for Suspected Acute PE

PIOPED

When the VQ scan is normal, PE is not present; When the VQ scan is high probability, and clinical suspicion is high, PE is considered present; When the VQ scan is nondiagnostic (low prob or intermediate prob), more studies are needed.

CTA sensitivity = 83%, CTA + CTV sensitivity = >90%

an established technique for the diagnosis of PE.

Increased bioavailability compared with UFH; Once or twice daily subcutaneous delivery; Monitoring not generally required; Outpatient therapy facilitated; Lower rate of HIT

for the Initial Treatment of DVT

In patients with acute DVT and severe renal failure, we suggest

In patients with acute DVT treated with LMWH, we recommend against routine monitoring with

For acute nonmassive PE, we recommend initial treatment with

For massive PE, in situations where there is concern about SC absorption, or when thrombolytic therapy is being considered or planned, we suggest

For acute PE treated with LMWH, we recommend against routine monitoring with

In patients with acute PE and severe renal failure, we suggest

for Initial Treatment of PE

In patients with acute PE, if anticoagulant therapy is not possible because of risk of bleeding, we recommend placement of an

For patients with acute PE who have an IVC filter inserted as an alternative to anticoagulation, we recommend that they should subsequently receive a conventional course of

Indication: contraindication to anticoagulation

be used primarily in patients at high risk for bleeding (Grade 1A), or possibly as an adjunct to anticoagulant-based prophylaxis (Grade 2A).

With leg pain / swelling

With sudden onset dyspnea or CP

Look for risk factors if you are considering

Consider starting _______________ before diagnosis is confirmed if your suspicion is high.

For massive PE, consider

With proven DVT or PE, and contraindication to anticoagulation, or with recurrence on therapy

It is indicated in nearly all hospitalized patients.

Mean pulmonary artery pressure of > 25 mmHg at rest; (Right-heart catheterization)

Increased in Pulmonary Arteries of Patients with IPAH

Idiopathic PAH; Familial PAH; Associated with PAH

Connective tissue disease

Congenital systemic-to-pulmonary shunts

Portal hypertension

HIV infection; Drugs and toxins; Other; Associated w/ significant venous /capillary involvement (PVOD, PCH); Persistent PH of the newborn

Left-sided atrial or ventricular heart disease

Left-sided valvular heart disease

COPD & Interstitial lung disease

Sleep-disordered breathing & Alveolar hypoventilation disorders

Chronic exposure to high altitude & Developmental abnormalities

Thromboembolic obstruction of proximal & distal PAs

Non-thrombotic PE (tumor, parasites, foreign material)

dry crackles

due to congenital heart disease or pulm fibrosis or sarcoidosis.

is the most common presenting symptom.

Altered temp, rigors, sweats, cough, sputum, dyspnea, chest pain; Fatigue, myalgias, abdominal pain, anorexia, headache; Lack sensitivity and specificity

the largest epithelial surface in the body (70 m2 alveolar surface)

Epiglottis; Cough reflex; Mucociliary clearance

Humoral (lysozyme, lactoferrin, IgA, collectins, e.g. surfactant proteins A and D); Cellular (alveolar macrophage, pattern recognition receptors)

is the ~8th leading cause of death in the US and the #1 cause of death from infectious disease

Most lethal infection; Outpatient mortality <1%; 12% of those hospitalized die; 40% ICU mortality

patient in the ambulatory setting

patient in extended care, on home infusion therapy, long term hemodialysis within past 30 days, home wound care, exposure to family members with resistant pathogens, or hospitalized more than 2 days within the past 90 days

Pneumonia onset >48 hours after hospital admission

Pneumonia onset >48 hours after initiation of intubation and mechanical ventilation

colonizes 5-10% of healthy adults

most common etiology of CAP, and a likely etiology in much ‘culture negative’ CAP

complications include bacteremia, meningitis, otitis media, sinusitis

higher mortality post-splenectomy

pneumococcal vaccination (23 serotypes)

Serotype b and nontypeable cause most pneumonias

Hib vaccination has decreased carriage rates; More common in smokers; Most empiric regimens cover H. flu adequately

The original ‘atypical’ organism, described in 1944 when atypical meant non-pneumococcal

Occurs in up to 1/3 of CAP in outpatients when serologic testing performed

May have associated non-respiratory syndromes (CNS, immune hemolytic anemia)

Bullous myringitis is classic but uncommon and nonspecific

‘Discovered’ in 1976 during an outbreak of pneumonia; Found in aquatic environments

Urinary antigen is diagnostic, but only detects serogroup 1; DFA is presumptive

50% of 20 year olds have serologic evidence of past infection

TWAR; Diagnosis is difficult so true incidence is unknown; Organism is associated with chronic inflammatory diseases (atherosclerosis)

Uncommon in outpatients, but occurs in ~10% of patients with CAP admitted to hospitals (highest in patients requiring ICU admission)

Patients with medical co-morbidities or recent antibiotic therapy at increased risk (enteric gram negatives, P. aeruginosa)

May cavitate or produce empyema

Uncommon in CAP; Relatively common complication post-influenza; Reports of community acquired MRSA pneumonia have been increasing

May cause necrotizing infiltrates or (in children) pneumatoceles

After inhalation of oropharyngeal or gastric contents and correlates with volume of aspirated material

Risk factors include: neurologic dysphagia, anatomic or functional abnormalities of upper GI tract, nursing home residency, drug overdose, general anesthesia, loss of consciousness

Radiographic changes in dependent lung segments; Both enteric gram negative organisms and anaerobes isolated

May lead to necrotizing pneumonia, empyema, or lung abscess

Lab evaluation of patients with pneumonia

Chest X-ray; Tests for an etiologic agent For outpatients: none considered standard; For hospitalized patients: 2 pretreatment blood cultures and expectorated sputum Gram stain and culture; Serologic tests usually not helpful

deep-cough specimen before antibiotic treatment, transported and processed within a few hours of collection

sputum sample culture contingent on cytologic examination, except for

induced sputum for detection of

urinary antigen tests for serogroup 1 only

Standard methods for pneumococcal diagnosis are