Pulmonary diseases Flashcards

1
Q

COPD - Classifications

A

Two classic types; Chronic Bronchitis and Emphysema.

Chronic B is a clinical diagnosis: chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years(excess mucus narrows airways, inflammation and scarring).

Emphysema is a pathologic diagnosis: permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls.(Excess protease or deficiency of antiprotease -> PMN and macrophages digest human lung)
- The two often coexist.

Most common RF: smoking, a1-antitrypsin-def.

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2
Q

COPD - Symptoms, Dx

A

Sx:
Cough, sputum production, dyspnea.
Signs:
Prolonged expiratory time, end-expiratory wheezes on forced expiration,decr. breath sounds and/or inspiratory crackles. Tachypnea, tachycardia, cyanosis, use of accessory resp. muscles

Dx:
- Pulmonary function testing (spirometry) = Def. diagnostic test.
- Decreased FEV1 and decr. FEV1/FVC ratio - GOLD staging.
- The FEV1/FVC ratio is < 0,70
- Increased TLC, residual volume, FRC (indicating air trapping)
CXR: Hyperinflation, flattened diaphragm, diminished vascular markings
- Measure A1-antitrypsin levels
Arterial blood gas - Chronic PCO2, retention, decr. PO2.

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3
Q

COPD - Tx

A

Smoking cessation - the most important intervention (prolongs the survival rate but does not reduce it to the level of someone who has never smoked)

  1. Inhaled anticholinergic drugs (ipratropium bromide)
  2. Inhaled B2-agonists (e.g albuterol)
    - Those two best in comination
  3. Inhaled corticosteroids (budesonide, fluticasone)
  4. Theyphylline (oral) - role is controversial
  5. Oxygen - shown to improve survival and quality of life
  6. Pulm rehab + Vaccination
  7. AB given in acute exacerbations
  8. CPAP-BiPAP given in acute exacerbations if tx above is not enough
  9. Intubation and mechanical ventilation if needed (if increasing RR, increasing PaCO2and worsening acidosis)
  • Do not use inhaled corticosteroids in acute exacerbations.
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4
Q

COPD - Cx

A
  1. Acute exacerbations (bc infection, noncompliance, cardiac disease)
  2. Secondary polycythemia (Hct >55% in men or >47% in women) - compensatory mechanism to chronic hypoxemia
  3. Pulm HTN and cor pulmonale
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5
Q

Asthma - General

A

Characteristic by the following triad:

a) Airway inflammation
b) Airway hyperresponsiveness
c) Reversible airflow obstruction

Can begin at any age.
Extrinsic asthma - starts early age, often in combination w/atopy.
Intrinsic asthma - not related to anything else

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6
Q

Asthma - Clinical

A

SOB, wheezing, chest tightness and cough. Usually occur within 30min of exposure to triggers. Usually worse at night.
Wheezing (during both inspiration and expiration) is most common finding on physical examination.

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7
Q

Asthma - Diagnosis

A
  1. Pulmonary function tests (PFT) - Decr in expiratory flow rates, decr FEV1 and decr. FEV1/FVC ratio (<0,70)
  2. Spirometry before and after bronchodilators
  3. Peak flow (Peak expiratory flow rate)
  4. Bronchoprovocation test (when PFT are nondiagnostic)
  5. CXR - to rule out other
  6. ABG - Hypocarbia is common. Hypoxemia may be present
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8
Q

Asthma - Tx

A
  1. Inhaled B2-agonists (e.g albuterol in acute, salmeterol in nighttime and excercise-induced)
  2. Inhaled corticosteroids for moderate to severe asthma.
    - preferred over oral steroids due to fewer systemic side effects.
  3. Montelukast - Leukotriene modifiers - useful for prophylaxis
  4. Chromolyn sodium/Nedocromil sodium
  5. Acute severe asthma:
    - Inhaled B2-agonist
    - Corticosteroids
    - IV magnesium
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9
Q

Asthma - Cx

A
  1. Status asthmaticus - does not respond to standard meds.
  2. Acute Respiratory failure (due to resp. muscle fatigue)
  3. Pneumothorax, atelectasis, pneumomediastinum
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10
Q

Bronchiectasis - General, Causes

A

Permanent, abnormal dilation and destruction of bronchial walls with chronic inflammation, airway collapse, and ciliary dysfunction leading to impaired clearance of secretions.
- Less common today bc/o modern AB are used for resp. infections.

Causes:
Cystic fibrosis is most common in western world
Tuberculosis most common in undeveloped countries
Recurrent infections (airway obstruction, immuno.def)
Primary ciliary dyskinesia (e.g Kartagener syndrome)

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11
Q

Bronchiectasis - Clinical, Dx, Tx

A

Chronic cough with large amount of mucopurulent, foul-smelling sputum, dyspnea, hemoptysis, recurrent pneumonia.

Dx: High-resolution CT-scan
PFTs, Bronchoscopy

Tx:

  1. AB for acute exacerbations - superimposed infections are signaled by change in quality/quantity of sputum, fever, chest pain
  2. Bronchial hygiene - hydration, physio, inhaled bronchodilators
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12
Q

Cystic fibrosis

A

Autosomal recessive - primarily affecting Caucasians
Defect in chloride channel protein -> impaired chloride and water transport, which leads to thick, viscous secretions in the resp.tract, exocrine pancreas, sweat glands, intestines, and GU-tract.
- Obstructive lung disease w chronic pulm. infections (often Pseudomonas)

Tx: Pancreativ enzyme replacement, fat-soluble vitamin supplements, chest physical therapy, vaccines, tx of infection with AB, inhaled recombinant human deoxyribonuclease (rhDNase)

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13
Q

Lung cancer - General

A

Two subtypes:

a) Small cell lung cancer (SCLC) - 25% of lung cancers
b) Nonsmall cell lung cancer (NSCLC) -75%, includes squamous cell carcinoma, adenocarcinoma, large cell carcinoma and bronchoalveolar cell carcinoma.

RF: Smoking, second-hand smoke, asbestos, radon, COPD

Staging:
a) SCLC is staged by 1) Limited - confined to chest plus supraclavicular nodes, but not cervical or axillary nodes, 2) Extensive - outside of chest and supraclavicular nodes

b) NSCLC - staged via TNM system

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14
Q

Lung cancer - Clinical

A

Cough, hemopthysis, obstruction, wheezing, dyspnea. Recurrent pneumonia. Anorexia, weight loss, weakness.

If local invasion:
- Superior vena cava syndrome - most commonly occur with SCLC.(-> facial fullness, facial and arm edema, dilated veins over ant. chest, arms and face. JVD)

  • Phrenic nerve pasy
  • Recurrent laryngeal nerve palsy
  • Horner syndrome - due to invasion of cervical sympathetic chain by an apical tumor. (-> unilateral facial anhidrosis, ptosis and miosis
  • Pancoast tumor - an apical tumor involving C8and T1-T2, causing shoulder pain radiating down the arm.
  • Metastatic disease - brain, bone, adrenal glands, liver
  • Paraneoplastic syndromes:
    a) SIADH
    b) Ectopic ACTH secretion
    c) PTH-like hormon secretion
    d) Hypertrophic pulm. osteoarthropathy.
    e) Eaton-Lambert syndrome
    f) Digital clubbing
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15
Q

Lung cancer - Dx and Tx

A

Dx:
CXR: most important in diagnosis
CT w iv contrast: Useful for staging, checking for metastasis
Cytologic examination of sputum - can diagnose central tumors in 80%.
Fiberoptic bronchoscope - not for peripheral lesions
PET scan - for a bigger picture
Transthoracic needle biopsy- for peripheral lesions
Mediastinoscopy

Tx:
NSCLC:
- Surgery is best option. BUT pts. w metastatic disease outside the chest ar not! candidates for surgery. Recurrence may occur even after complete resection.
- Radiation therapy - in adjunct to surgery
- Chemo - if uncertain benefit

SCLC:
Limited disease: chemo+radiation
Extensive: Chemo, then prophylactic radiation.
Surgery has limited role bc tumors are often nonresectable.

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16
Q

Pleural effusion - General

A

Caused by one of the following:

  • Incr. drainage of fluid into pleural space
  • Incr. production of fluid by cells in the pleural space
  • Decr. drainage of fluid from pleural space
  1. Transudative effusions: either:
    - Elevated capillary pressure (e.g CHF)
    - Decr. plasma oncotic pressure (e.g Hypoalbuminemia)
  2. Exudative effusions:
    - Incr. permeability of pleural surfaces or decr. lymphatic flow from pleural surface because of damage to pleural membranes or vasculature. IF suspected exudate: do test of pleural fluid: diff. cell count, protein, LDH, glucose, pH, amylase, TG, microbiology and cytology. Ex.effucion have at least oneof the “Light’s Criteria”: 1) Protein >0,5, LDH>0,6, LDH > two-thirds the upper limit of normal serum LDH.
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17
Q

Pleural effusion - Causes

A
  1. CHF most common
  2. Pneumonia
  3. Malignancies (lung (36%), breast (25%), lymphoma(10%)
  4. Pulm embolism
  5. Viral diseases
  6. Cirrhosis with ascites
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18
Q

Pleural effusion - Clinical

A
Sx: 
Often asymptomatic
Dyspnea on excertion
Peripheral edema
Orthopnea, PND 

Signs:
Dullness to percussion
Decr. breath sounds over the effusion
Decr. tactile fremitus

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19
Q

Pleural effusion - Dx and Tx

A

Dx:
CXR: look for:
- Blunting of costophrenic angle
- About 250ml of pleural fluid must accumulate before an effusion is detected
- Lateral decubitus films: more reliable than PA and lateral CXR for detecting small pleural effusion.

CT: More reliable than CXR for detecting effusions
Thoracocentesis: useful if etiology is not obvious. Also therapeutic - drainage provides relief for large effusions.

Tx:

  1. Transudative effusion:
    - Diuretics and sodium restriction
    - Therapeutic thoracentesis - only if its causing dyspnea
  2. Exudative effusions: treat underlying disease
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20
Q

Empyema - Causes and Clinical

A

Causes:
Exudative pleural effusions, if left untreated, can lead to empyema (pus within the pleural space)
Most cases bc complication of bacterial pneumonia, but other foci of infection can also spread to pleural space.

Clinical:
Those of the underlying disease (pneumonia most common)

Dx: CXR and CT

Tx: Treat with aggressive drainage of the pleura (via thoracentesis) and AB therapy.
- If empyema is severe and persistent, rib resection and open drainage may be necessary.

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21
Q

Pneumothorax - General

A

Air in the normally airless pleural space.
Two major categories: Spontaneous and traumatic pneumothoraces
- Traumatic pneumothoraces are often iatrogenic.
- Spontaneous pneumothorax occurs without trauma.

Spont. pneumothorax:

  1. Primary (simple) pneumothorax
    - Occurs in healthy individuals
    - Bc spontaneously rupture of subpleural blebs at apex of lungs - espace of air from the lung into pleural space causes lung to collapse.
    - More common in tall, lean young men
    - Usually are healthy enough to spare resp.distress
  2. Secondary (complicated) pneumothorax
    - Occurs as a complication of underlying lung disease(e.g COPD, Asthma, Interstitial lung disease, neoplasm, CF, TB)
    - More life-threatening bc lack of pulm.reserve in these pts.
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22
Q

Pneumothorax - Clinical, Dx, Tx

A

Clinical:
- Ipsilateral chest pain, usually sudden in onset
- Dyspnea
- Cough
Physical:
- Decr. breath sounds over affected side
- Hyperresonance over the chest
- Decr. or absent tactile fremitus on affected site
- Mediastinal shift toward the site of pneumothorax

Dx:
CXR . shows the visceral pleural line (Black)

Tx:

  1. Priamary spontaneous pneumothorax
    a) If small and asymptomatic pt.
    - Observation - should resolve spontaneously in ca.10d
    - Small chest tube may benefit some pt.
    b) If larger and/or symptomatic pt.
    - Administration of supplemental O2
    - Needle aspiration or chest tube insertion to allow air to be released and lung to reexpand.
  2. Secondary spontaneous pneumothorax: chest tube drainage.
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23
Q

Tension pneumothorax - General

A

Accumulation of air within the pleural space such that tissue surrounding the opening into the pleural cavity act as valves, allowing air to enter but not to escape.
- The accumulation of air under (positive) pressure in the pleural space collapses the ipsilateral lung and shifts the mediastinum away from the side of the pneumothorax.

24
Q

Tension pneumothorax - Causes

A
  1. Mechanical ventilation w/assoc. barotrauma
  2. CPR
  3. Trauma
25
Q

Tension pneumothorax - Clinical

A
  1. Hypotension - cardiac filling is impaired bc compression of the great veins
  2. Distended neck veins
  3. Shift of trachea away from side of pneumoT. on CXR.
  4. Decr. breath sounds on affected side
  5. Hyperresonance on percussion on side of pneumoT.
26
Q

Tension pneumothorax - Tx

A

Medical emergency!
- Immediately perform chest decompression with a large-bore needle in 2nd or 3rd intercostal space in the midclavicular line, followed by chest tube placement.

27
Q

Interstitial lung disease - General

A

ILD is defined as an inflammatory process involving the alveolar wall tat can lead to irreversible fibrosis, distortion of lung architecture and impaired gas exchange.

28
Q

Interstitial lung disease - Classification

A
  1. Environmental lung disease
    - Coal workers pneumoconiosis
    - Silicosis
    - Asbestosis
    - Berylliosis
  2. ILD assoc. with granulomas
    - Sarcoidosis
    - Histiocytisis
    - Wegener Granulomatosis
    - Churg-Strauss syndrome
  3. Alveolar filling disease
    - Goodpasture syndrome
    - Idiopathic pulm. hemosiderosis
    - Alveolar proteinosis
  4. Hypersensitivity lung disease
    - Hypersensitivity pneumonitis
    - Eosinophilic pneumonitis
  5. Drug-induced
  6. Mischellaneous
29
Q

Interstitial lung disease - Clinical

A

Dyspnea, cough, fatigue + evt connective tissue disorder.

Signs:

  • Rales at bases
  • Digital clubbing
  • Signs of pulm HTN and cyanosis
30
Q

Interstitial lung disease - Dx and Tx

A

Dx:
CXR:
- Usually nonspecific
- Diffuse changes

CT: Shows the extent of fibrosis
PFTs: FEV1/FVC increased. Restrictive pattern
Oxygen desaturation during excercise
Tissue biopsy.
Urinanalysis (for goodpasture and Wegener)

31
Q

Sarcoidosis - General

A

Chromic, systemic granulomatous disease characterized by noncaseating granulomas, often involving multiple orgn systems. Lungs almost always involved. Etiology unknown.

32
Q

Sarcoidosis - Clinical

A

Malaise, fever, anorexia, weight loss.
Vary in severity and can affect multiple organs:
1. Lungs: dry cough, dyspnea
2. Skin: Erythema nodosum, plaques, subcut.nodules, maculopapular eruptions
3. Eyes: Anterior uveitis (75%), post.uveitis, conjuctivits
4. Heart: Arrhytmias, conduction disturbances, death
5. Musculoskeletal: arthralgia, arthritis, bone lesion
6. Nervous system: bells palsy, optiv nerve dysfunction, papilledema, peripheral neuropathy.

33
Q

Sarcoidosis - DX

A

Dx:
CXR:
- Bilateral hilar adenopathy is the hallmark
Skin anergy - typical finding
Angiotensin-converting enzyme is elevated in serum
Hypercalciuria and hypercalcemia
Def.diagnosis requires transbronchial biopsy:
- Must see NONCASEATING GRANULOMAS

Staging:
stage 1: bilateral hilar adenopathy without parnchymal infiltrates
Stage 2: hilar adenopathy with parenchymal infiltrates
Stage 3: Diffuse parenchymal infiltrates without hilar adenopathy
Stage 4: Pulm. fibrosis with honeycombing and fibrocystic parenchymal changes

34
Q

Sarcoidosis - Tx

A

Most cases resolve or significantly improve spontaneously in 2 years and do not require tx.
Systemic corticosteroids are tx of choice. Methotrexate used in pts. with progressive disease refratory to corticosteroids.

35
Q

Wegener granulomatosis

A

Rare, unknown etiology.
Characterized by necrotizing granulomatous vasculitis.
Affects vessel of lungs, kidneys, uper airway espec.
Upper and lower resp.infections, glomerulonephritis, pulm nodules.
Dx: tissue biopsy + c-antineutrophilic cytoplascmic antibodies.

Tx: immunosuppresive agents + steroids

36
Q

Churg-Strauss syndrome

A

Granulomatous vasculitis is seen in pts. with asthma.
Typically presents with pulm.infiltrates, rash and eosinophilia. Systemic vasculitis may result in skin, muscle and nerve lesions.
Assoc. with perinuclear antineutrophilic cytoplasmic antibody.
Tx: Treat with systemic glucocorticosteroids.

37
Q

Alveolar Filling Disease: Goodpastures syndrome

A

Autoimmune disease caused by igG antibodies directed against glomerular and alveolar basement membranes (type II hypersensitivity rxn). Results in hemorrhagic pneumonitis and glomerulonephritis. Ultimately, renal failure is a complication of proliferative glomerulonephritis.
Prognosis is poor, treat with plasmapheresis, cyclophosphamide, and corticosteroids.

38
Q

Acute respiratory failure - General

A

Results when there is inadequate oxygenation of blood or inadequate ventilation(elimination of Co2) or both. The following ar general criteria used to define ARF:

  • Hypoxia (PaO2 < 60mm Hg)
  • Hypercapnia (partial pressure of Co2 (PCO2) > 50 mm Hg.

Can be caused by different systems:
CNS, Neuromuscular disease, Upper airway, Thorax and pleura, Cardiovascular system+blood, Lower airways and alveoli.

Classification:
two main types:
1. Hypoxemic resp. failure:
- Low PaO2 with a PaCO2 that is either low or normal - present when O2 saturation is < 90% despite FiO2 >0,6
- causes: ARDS, Pneumonia, pulm.edema
- V/Q mismatch and intrapulm.shunting are the major pathophysiologic mechanisms.

  1. Hypercapnic (hypercarbic) resp failure -> a failure of alveolar ventilation.
    - Either a decr. in minute ventilation or an incr. in physiologic dead space leads to CO2 retention and eventually results in hypoxemia.
    - May be caused by an underlying lung disease (COPD, Asthma, CF, severe bronchitis, neuromuscular diseases, CNS depression etc).
39
Q

Acute respiratory failure - Clinical

A

Sx:

  • Dyspnea - first symptom
  • Cough may be present

Signs:

  • Inability to speak in complete sentences, use of acc. muscles
  • Tachypnea, tachycardia
  • Cyanosis
  • Impaired mentation (due to fatigue or hypercapnia, or CNS depression)
40
Q

Acute respiratory failure - Diagnosis

A
  1. ABG analysis
    a) Hypoxemia: Mechanisms include V/Q mismatch, intrapulm. shunting or hypoventilation.
    b) Hypercapnia: caused by hypoventilation
    c) Arterial pH: Resp. acidosis occurs whenhypercapnia is present. However, if the resp.failure is chronic, renal compensation occurs and the acidosis is less severe.
    CXR or CT of chest
    CBC and metabolic panel.

Treat symptoms and underlying cause.

41
Q

Acute Respiratory Distress Syndrome - General

A

A diffuse inflammatory process (not necessarily infectious) involving both lungs - neutrophil activation in the systemic or pulmonary circulations is the primary mechanism.
Not a primary disease, but rather a disorder that arises due to other conditions that cause a widespread inflammatory process.

Definition:

a) Acute onset (<1 week)
b) Bilateral infiltrates on chest imaging
c) Pulm edema not explained by fluid overload or CHF
d) Abnormal paO2/FiO2 ratio
- 200-300: mild ARDS
- 100-200: moderate ARDS
- 100: severe ARDS

Pathophysiology: Massive intrapulm. shunting of blood - severe hypoxemia with no significant improvement on 100% O2 (Requires high PEEP to prop open airways).

42
Q

Acute Respiratory Distress Syndrome - Causes

A
  1. Sepsis = most common risk factor
  2. Aspiration of gastric contents
  3. Severe trauma, fractures
  4. Drug overdose, toxic inhalations
  5. Intracranial HTN
  6. Cardiopulmonary bypass
43
Q

Acute Respiratory Distress Syndrome - Clinical and Dx

A

Dyspnea, tachypnea, tachycardia, progressive hypoxemia (not responsive to supplemental o2).

Dx:
CXR: shows diffuse bilateral pulmonary infiltrates
ABG:
- Hypoxemia (PaO2 < 60%)
- Initially, respo alkalosis (PaCO2 < 40) is present, which gives way to resp.acidosis as the work of breathing increases and PaCo2 increases.
- If septic patient -> metabolic acidosis may be present
Pulmonary artery catheter - enables a determination of PCWP - differentiate ARDS from cardiogenic pulm.edema.
Bronchoscopy with bronchoalveolar lavage

44
Q

Acute Respiratory Distress Syndrome - Treatment

A
  1. Oxygen -> keep > 90%
  2. Mechanical ventilation
  3. Fluid management - dont overload the pt.
  4. Treat underlying cause
  5. Adress nutritional needs

Cx:
Permanent lung injury - lung scarring or honeycomb lung
Complications ass. with mechanical ventilation
Renal failure, ileus, stress ulcers.

45
Q

Pulmonary Hypertension - General

A

1.Defined as a mean pulmonary arterial pressure greater than 25 mm Hg at rest
(Les mer s.101-102 om du får tid)

46
Q

Cor Pulmonale - General

A

Defined as right ventricular hypertrophy with eventual RV failure resulting from pulmonary HTN, secondary to pulmonary disease.

47
Q

Cor Pulmonale - Causes

A

Most commonly secondary to COPD

Other causes include recurrent PE, ILD, asthma, CF, sleep apnea, pneumoconioses

48
Q

Cor Pulmonale - Clinical

A
  • Decr. in excercise tolerance
  • Cyanosis and digital clubbing
  • Signs of right ventricular failure: hepatomegaly, edema, JVD
  • Parasternal lift
49
Q

Cor Pulmonale - Diagnosis

A

CXR: enlargement of the RA, RV and pulm. arteries
ECG: right axis deviation, P pulmonale, RV-hypertrophy
Echo: RIght ventricular dilatation, normal LV size and function.

50
Q

Cor Pulmonale - Treatment

A
  1. Treat underlying pulm. disorder
  2. Use diuretic therapy cautiously because pts. may be preload-dependent
  3. Apply continous long-term o2-therapy if pt is hypoxic
  4. Administer digoxin only if there is coexistent LV failure
51
Q

Pulmonary embolism - General

A

Occurs when a thrombus in another region of the body embolized to the pulm. vascular tree via the RV and pulm.artery. Blood flow distal to the embolus is obstructed.
Consider PE and DVT as a continuum of one clinical entity (venous thromboembolism) - diagnosing either PE or DVT is an indication for tx.
- Most commonly arises from a iliofemoral DVT
- Leads to incr. pulm. vascular resistance, pulm.artery pressure, and right ventricular pressure.
- Also hypoxemia and hypercarbia -> tachypnea

52
Q

Pulmonary embolism - Clinical

A
Most often, PE is clinically silent. Recurrences are common. Mortality is 10% in first 60min. 
Sx: 
Dyspnea
Pleuritic chest pain 
Cough
Hemoptysis 
Signs and symptoms of DVT/Hx of DVT
Syncope 

Signs:
Tachypnea
Rales
Tachycardia
S4
Shock with circulatory collapse in massive PE
Low grade fever, decr. breath sounds, dullness on percussion.

53
Q

Pulmonary embolism - Dx

A

Dx:
It is often difficult to definetively diagnose or rule out PE. The following tests provide an adequate basis for treating PE with anticoagulation:
1. Intraluminal filling defects in central, segmental, or lobular pulmonary arteries on CT-Angio
2. DVT diagnosed with USG and clinical suspicion
3. Positive pulmonary angiogram (definitely proves PE)

The following can essentially rule out PE

  1. Low probability V/Q scan (or normal helical scan) + low clinical suspicion
  2. Negative pulmonary angiogram (definite)
  3. Negative D-dimer assay + low clinical suspicion

Also:
Typically, there is a resp. alkalosis (PaO2 and PaCO2 are low and pH is high)
D-dimer: If results are normal, and clinical suspicion is low, PE is very unlikely.
Venous duplex USG is very helpful when positive, but of little value when negative.
CT-angio has been found to have good sensitivity(>90%) - test of choice in most facilities(BUT can not be performed in those with renal failure)
! Pulm angio is the gold standard!

54
Q

Pulmonary embolism - Tx

A
  1. O2 to correct hypoxemia
  2. Acute anticoagulation therapy with either unfractionated or LMWH to prevent another PE. Anticoagulation prevents further clot formation, but does not lyse existing emboli or diminish thrombus size.
    - Do not wait for studies to confirm PE if clinical suspicion is high!
    - Give another bolus, followed by a continous infusion for 5-10d. The goal is an aPTT of 1.5-2.5 times control.
  3. Oral anticoagulation with warfarin or Rivaroxaban for long-term tx.
    - Can start with heparin on day 1
    - Therapeutic INR is 2-3
    - Continue for 3-6months
  4. Thrombolytic therapy (i.e Streptokinase, tPA)
    - Speeds up the lysis of clots
    Situations in which thrombolysis should be considered:
    - Patients with massive PE who are hemodynamically unstable (persistent hypotension), or evidence of heart failure.
  5. Inferior vena cava interruption - If anticoagulation is contraindicated in a patient with PE.
  6. Surgical thrombectomy
    - In pts. with hemodynamic compromize, a large, proximal thrombus, and who are poor candidates for fibrinolytics
55
Q

Pulmonary aspiration - most common site

A

The right lung is most ofteninvolved due to anatomy (right main bronchus follows a more straight path down), particularly the lower segments of the right upper lobe and the upper segments of the right lower lobe.

56
Q

Which tests can you do to distinguish between lung and heart disease?

A
  • CXR
  • Sputum Gram stain and culture
  • PFTs
  • ABGs
  • ECG, echocardiogram
57
Q

Best tests for evaluating hemoptysis

A
  • CXR
  • Fiberoptic bronchoscopy
  • CT scan of the chest