W3 Dyspnea (Review By EOD Friday 28th) Flashcards
Dyspnea — acute and chronic causes
ACUTE
Pleural — pneumothorax
Parenchyma — pneumonia
Vascular — PE
Upper Airway — Asthma
Lower AIrway — Aspiration, anaphylaxis, COPD
CHRONIC
Airway Obstruction
—asthma
—COPD
—neoplasm
Parenchyma:
1. Alveolar : pneumonia, ARDS, COPD, neoplasm
2. Vessels : PE, pulmonary hypertension
—Pleural: masses, effusion
—Chest Wall: neuromuscular, kyphoscoliosis, abdominal distention
Pulmonary HTN
—characterised by?
—WHO 5 classes
—which class are meds directed at
—which is the most common
—Normal pulmonary circulation has a pressure of 25/8 mmHg (mean 12 mmHg) and low resistance (200-250 dynes/sec/cm-5).
—Pulmonary hypertension = the artery pressure rises to an inappropriate level for a given cardiac output.
—not a diagnosis, ⭐️a hemodynamic state characterized by a mean pulmonary artery pressure of > 25 mmHg ⭐️
⭐️WHO 5 classes ⭐️
1. Primary Pulmonary/Artery Hypertension (PAH):
—idiopathic is most common cause
—meds directed at this class
2.PH secondary to left heart disease
—most common cause of PH
—aortic stenosis, mitral stenosis, low EF etc
3.PH secondary to lung diseases and chronic hypoxia:
—COPD, interstitial lung disease, OSA
4.PH secondary to PE
—chronic thromboembolic pulmonary hypertension (CTEPH)
5.PH secondary to unclear or multifactorial causes
WHO Class 1: Idiopathic PAH
Patho
Presentation
Signs/ PE
Brief patho for:
Group 2: left heart disease
Group 3: PH secondary to lung diseases and chronic hypoxia
Group 4: Chronic Thromboembolic (CTEPH)
—rare
—pathology results from increased vascular resistance and blood vessel narrowing as a result of genetic/molecular causes (BMPR2)
—hypertrophy of smooth muscle
—fibrosis occurs : irreversible
—RV has increased filling/stroke volume which further increases PAH
—RVH develops followed by right sided heart failure (cause of death)
Presentation
—Dyspnea
—Fatigue
—Decreased functional capacity
—angina
—presyncope/syncope
Signs/Physical Exam
—abnormal pulse oximetry
—usually are related to RV failure
—elevated JVD
—hepatomegaly/ascites
—peripheral edema
—Tricuspid regurgitation murmur and increased pulmonic component of S2
—if left sided heart failure, can auscultate murmurs such as mitral/aortic stenosis/regurgitation
Group 2: left heart disease
—primarily a pulmonary venous process and results from passive pulmonary venous congestion with vasoconstriction and venous remodeling
Group 3: PH secondary to lung diseases and chronic hypoxia
—result from destruction of the alveolar capillary bed or chronic hypoxic vasoconstriction
Group 4: Chronic Thromboembolic (CTEPH)
—develops from thrombotic macrovascular obstruction with subsequent vasoconstriction and remodeling of the pulmonary arterial arterial bed
WHO Class 1: Idiopathic PAH
Diagnostics
EKG findings?
Echo findings?
EKG:
—Can show signs of left heart disease (LVH) in group 2
—RAD as well as upright R waves in V1-2 indicating RVH
—RV strain (ST depression or t wave inversion in V1-2)
—RBBB
—Chronic lung disease can have frequent PACs or MAT
—PE can have a S1Q3T2 pattern. Most common is tachycardia in clinical practice
inverted Q and T in lead III. Bigger S wave than R wave in I
Echo:
—Measured pulmonary artery systolic pressure > 40 mmHg or mean PAP of > 25 mmHg
—Examines left sided heart disease
—RV enlargement
Right Heart Catheterization:
—confirmatory
—Right jugular vein
—Measurement of pulmonary arterial pressure (PAP) mean as well as PCWP
—can assess for a shunt
—needs to be obtained prior to vasodilators therapy in PAH.
—reserved for WHO type 1 (idiopathic) or significant/severe
Other studies that are useful guide diagnosis of underlying condition
—PFTs
—Sleep study
—V/Q scan or CTA chest (PE)
—LFTs, HIV, drug screen, collagen-vascular serology
WHO Class 1: Idiopathic PAH
Symptom classification Class I-IV
Which test to diagnose/classify SYMPTOMS??
Treatment Group 1
Medications, which one is for about 5% of cases and how do you determine that for them?
Patients w/ chronic thromboembolism should be referred for:
Groups 2-5
SYMPTOM CLASSIFICATIONS
CLASS I: symptom free when resting or exercising/physically active
CLASS II: No symptoms at rest but normal activities (grocery shopping) cause shortness of breath and fatigue
CLASS III: Moderate dyspnea with activities of daily living but no symptoms at rest
CLASS IV: Inability to perform minimal activities AND dyspnea at rest. Signs of right sided heart failure.
Can use a 6 minute walk test to determine symptoms
Group 1/ idiopathic:
—stepwise progression on initiation and addition of medications
—frequent monitoring of response every 3-6 months
Medication: can try any, except last one is reserved, it’s IV
—Calcium channel blockers: only if the RHC proved vaso-reactivity to CCB i.e amlodipine
—Endothelin Receptor Antagonists
bind to endothelin and inhibit vasoconstriction (oral: ambrisentan, bosentan, macitentan)
—Phosphodiesterase 5 (PDE-5) Inhibitors
result in pulmonary/systemic vasodilation (sildenafil)
—Guanylate Cyclase Stimulators
increase NO and vasodilation indicated for PAH and CTEPH
—Prostaglandin Analogs
activate the prostacyclin receptor leading to vasodilation (Epoprostenol = continuous IV infusion or Treprostinil = IV, sq, inhalation)
Patients with chronic thromboembolism should be referred for:
—a pulmonary ENDARTERECTOMY (clear clot and scar tissue CTEPH) and should receive lifelong ANTICOAGULATION in absence of contraindications
—Optimize comorbid conditions (class II-V) including use of LOOP DIURETICS for left and right sided heart failure and controlling hypertension
—O2 supplementation and CPAP if qualify
—Influenza and age appropriate pneumococcal vaccinations
—Lung Transplant
Groups 2-5 (Left HD, lung disease, PE, uncertain) should focus on treatment of the underlying disease and there is no established role for specific PAH medications for these diseases
PAH — algorithm
Lung cancer
5 main histological categories
Which is the most common?
—Cigarette smoking accounts for 85-90% of lung cancer.
—Other exposures include: radon, asbestos, diesel exhaust, ionizing radiation, arsenic, nickel, and industrial carcinogens
—Median age of diagnosis is 70
—Combined 5 year survival rate for all stages of lung cancer is 21%
Five main histological categories of bronchogenic carcinoma:
1. Squamous Cell Carcinoma (23 - 28% of all cases)
—arise from the bronchial epithelium and present as intramural masses.
—Centrally located and typically patients have hemoptysis
2. Adenocarcinomas (50%)
—arise from mucus glands or from any epithelial cell within or distal to the terminal bronchioles.
—Present as PERIPHERAL nodules or masses.
3. Adenocarcinomas in situ or Bronchoalveolar Cell Carcinoma (2%)
—typically arise CENTRALLY but occasionally peripherally and can spread along alveolar structures without evidence of invasion
4. Large Cell Carcinomas (5-10%)
—heterogenous group of undifferentiated tumors that share large cells and do not fit into the other categories.
—Typically aggressive course with rapid doubling time.
—Present as mostly CENTRAL and occasionally peripheral masses.
5. Small Cell Carcinomas (15%)
—tumors of bronchial origin that begin CENTRALLY and infiltrate submucosally to cause narrowing of the bronchus without a discrete luminal mass.
—AGGRESSIVE cancers that often have regional or distant metastasis on presentation.
Lung cancer
Division / staging
Presentation
Divided into:
—SCLC (small cell lung cancer)
—NSCLC (non-small cell lung cancer)
1.SCLC
—prone to hematogenous spread; rarely amenable to surgical resection; very aggressive with median survival (if untreated) of 6-18 weeks
—poor prognosis
2.NSCLC
—groups the other 4 cancers; spread more slowly; may be cured in the early stages following resection
Presentation
—Dyspnea: obstruction in the lumen, wheezing, external and compress
—Low grade fever
—Anorexia/weight loss
—New cough or change in chronic cough
—Hemoptysis
—Pain : nonspecific chest pain or bone pain (metastasis to vertebrae, ribs, pelvis)
—Dysphagia: tumor can compress the esophagus
—Local spread can cause endobronchial obstruction with atelectasis and postobstructive pneumonia
—Pleural effusion
—Rarely a pneumothorax from erosion of pleura and air entering between the visceral/parietal layers, or rupture of bullae
—Change in voice, hoarseness (compromise of recurrent laryngeal nerve)
—SVC Syndrome : compressed SVC leads to swelling of the face or trunk, chest pain, cough, and SOB. Results in supraventricular engorgement from collateral circulation
—Horner Syndrome : ipsilateral ptosis, miosis, and anhidrosis from involvement of the inferior cervical ganglion and paravertebral sympathetic chain
—Distant metastasis to the LIVER, BRAIN (10% in NSCLC, 20-30% in SCLC)
Lung Cancer
What are paraneoplastic syndromes? 4
What are the presentations of hypercalcemia?
Where does lung cancer metastasise to?
Patterns of organ dysfunction related to immune mediated or secretory effects of neoplasms;
NOT directly related to the tumor mass (occur in 10-20% of lung cancer patients)
1.Hypercalcemia:
—mental status changes, GI constipation, kidney stones
2.Syndrome of Inappropriate Antidiuretic Hormone (SIADH):
—euvolemic patient with hyponatremia; SCLC usually responsible
—two things that can cause this, pneumonia or cancer
3.Lambert-Eaton Myasthenic Syndrome:
—proximal muscle weakness, decreased deep tendon reflexes, and autonomic dysfunction. Also seen in SCLC
4.Hematologic:
—erythrocytosis, granulocytosis, thrombocytosis, and thromboembolic complications
Metastasis
“BLAB”
—Brain
—Liver
—Adrenals
—Bone
Lung Cancer
Diagnosis
What does a diagnosis rest on?
What would you use to evaluate for metastasis?
Screen with imaging:
—Chest X-Ray (can also see a pleural effusion or pneumothorax in addition to a nodule/mass)
—CT Scan (better resolution)
PET SCAN
—requires glucose, uptake
—If suspicious for malignancy, PAN CT (evaluate for metastasis) or PET SCAN
TISSUE OR CYTOLOGY SPECIMEN to DIAGNOSE
Sputum cytology :
—yield highest if central airways involved
Thoracentesis
—if have malignant pleural effusion
CT Guided Biopsy
—of peripheral nodules (80-90% yield at expense of 15-30% pneumothorax)
Fine Needle Aspiration (FNA)
—of palpable supraclavicular or cervical lymph nodes
Bronchoscopy
—acquire cytology brushing of visible lesions or lavage of lung segments
—biopsy of endobronchial abnormalities; biopsy of mediastinal lymph nodes with EBUS and needle aspiration
VATS
—video assisted thoracoscopy, minimally invasive surgery
Lung cancer
What is a solitary pulmonary nodule
What are the characteristics?
What is the probability for different population groups?
What should you assess? Associated with?
Which diagnostician to evaluate further?
—Referred to as a “coin lesion” is a < 3 cm isolated, round opacity on a chest x-ray that is NOT associated with an infiltrate, atelectasis, or adenopathy. Probably not malignant
—Most are asymptomatic and represent an unexplained finding (Granuloma, TB or fungal infection, cocci/histo).
—However, it does carry a risk of malignancy dependent on the patient.
—Increased probability : age > 30-50 years, smoker (+), prior malignancy
—Review old films to assess doubling time.
—Rapid doubling (< 30 days) is associated with infection; long term stability (> 450 days) is typically benign
—Malignancy risks increases with size of the lesion, ill defined border, cavitary lesions
—High resolution CT is recommended for further evaluation
Lung Cancer staging
Non small cell lung cancer (NSCLC)
Crucial for prognosis and treatment
NSCLC uses the TNM INTERNATIONAL STAGING SYSTEM and describes the neoplasm (small cell is too aggressive for this staging)
—T describes the size and location of the primary tumor
—N describes the presence and location of nodal metastases
—M refers to presence or absence of distant metastases
The TNM stages (I-IV) guide therapy
—Stages I and II are cured with surgery
—Stages IIIB and IV do not benefit from surgery
—Stage IIIA may benefit from surgery
Lung Cancer staging
SCLC
Does not use the TNM staging because micrometastases are assumed to be present on diagnosis
LIMITED DISEASE (30%):
—tumor limited ot the unilateral hemithorax
EXTENSIVE DISEASE (70%)
—tumor extends beyond the hemothorax
—Need to determine the degree of metastases with a PET/PAN CT.
—The sensitivity and specificity of identifying metastases to the mediastinal lymph nodes or distant sites is improved by combining CT and PET imaging.
Screening with CT scans has not been shown to improve mortality rates for lung cancer. Current recommendation is an annual chest CT for smokers aged 50-80 years who have at least a 20 pack year history (active smoker or quit in last 15 years)
Lung cancer
Treatment — NSCLC
Surgical resection offers best cure
—possible and if so, will patient survive the surgery.
—Recurrence rates are higher in limited resection versus lobectomy. VATS (video assisted thoracoscopic surgery) is being utilized more to standard thoracotomy.
Radiation therapy for non-surgical candidates with stage I disease.
—Also can improve survival in those with locally advanced stage IIIA and IIIB who are not surgical candidates
NEOADJUVANT CHEMOTHERAPY:
—giving antineoplastic drugs in advance of surgery or radiation.
—Possible survival benefit in those with stage IIIA and IIIB disease.
ADJUVANT CHEMOTHERAPY:
—administer antineoplastic drugs following radiation or surgical therapy
Lung cancer
Treatment — SCLC
—Response rates to chemotherapy are excellent (> 80%) in limited stage disease and ~60-80% in extensive disease.
—However, remissions are short lived with a duration of only about 6-8 months.
—Once the disease has recurred, survival is only 3-4 months.
Thoracic radiation improves survival in those with SCLC but not those with extensive disease
PALLIATIVE THERAPY
—(pain/symptom control, radiation on tumors with endobronchial obstruction or SVC syndrome)
PROGNOSIS: overall 5 year survival is 20%
Newer options with TARGETED THERAPY of mutations and IMMUNE CHECKPOINT INHIBITORS
—Molecular characterize tumor cells from tissue biopsy to aid in adjuvant treatment, metastatic disease, and those who relapse from primary therapy
1.Targeted Therapy
—analyze tumor cell DNA for mutations (molecular targets) that are causing the cells to replicate. Use medications to target these mutations and prevent the cancer cell from functioning. Only patients with targeted mutations are candidates. Less side effects.
2. IMMUNOTHERAPY: IMMUNE CHECKPOINT INHIBITORS
—the immune system uses checkpoints (proteins found on certain immune cells) to identify which cells are normal and which should be attacked. Sometimes cancer cells “trick” these checkpoints by appearing normal. Immunotherapy blocks their ability to appear normal, so the immune system knows to attack the cancer cells.
Pleural effusion
Normal fluid
What is pleural effusion
Know the 5 pathological processes that occur
Understand transudative and exudate
(See Bill’s sketches in PowerPoint)
—Normally the pleural space has 5-15 cc of fluid and is in constant movement from the parietal pleural capillaries into the pleural space followed by absorption into the parietal pleural lymphatics
Pleural effusion is an abnormal accumulation of fluid in the pleural space
⚠️ Always ask, is this exudative or transudative! ⚠️
Five pathophysiologic processes occur. Top 3 are most common:
1. Increased production of fluid in the setting of normal capillaries from INCREASED HYDROSTATIC (out of capillary) or DECREASED ONCOTIC (into capillary) pressures (TRANSUDATIVE)
2. Increased production of fluid due to abnormal capillary permeability (EXUDATE)
3. Decreased lymph clearance of fluid in the pleural space: think malignancy (EXUDATE)
4. Infection in the pleural space (EMPYEMA)
5. Bleeding into the pleural space (HEMOTHORAX). Interruption of diaphragmatic integrity allows fluid to enter the pleural space
transudative: excess volume states
—CHF, cirrhosis, nephrotic syndrome
—PE
exudative: malignancy
—inflammation and increased capillary permeability
—pneumonia, cancer, TB, viral infection, PE, autoimmune
**DIagnostic thoracentesis should be performed whenever there is a new pleural effusion and no clinically apparent cause OR failure of an effusion to resolve. Observation is appropriate if there is a known clinical cause and improvement.
Pleural effusion
Presentation
Exam
Diagnostics, CXR, what do you see?
Thoracentesis — when is small volume aspirated?
What is large volume aspirated? 2
Which presentation does NOT warrant a Thoracentesis?
Ph <7.3 could mean?
Glucose < 60 could mean?
Presentation:
—Can be asymptomatic
—Dyspnea
—Cough
—Chest Pain (inflammation of parietal pleura)
Exam:
—Dullness to percussion
—Decreased breath sounds
Diagnostics:
—Chest X-Ray shows blunting of the costophrenic angle 200 cc on the posteroanterior view OR 50 cc on the lateral view.
—Lateral decubitus view can determine if it is free flowing (transudative) or loculated (infected)
—ULTRASOUND (can guide a thoracentesis)
—CT Scan can detect smaller amounts of fluid
Neither is able to detect if the fluid is transudative or exudative therefore a thoracentesis should be performed for both diagnostic and therapeutic benefits
—Diagnostic small volume aspiration of pleural fluid (50-60 cc) is indicated when the underlying cause of effusion is unknown
—Large volume aspiration is reserved for treatment of dyspnea or in a PARAPNEUMONIC EFFUSION or EMPYEMA (infected fluid) as they are unresponsive to treatment
—Emergent thoracentesis with possible chest tube placement is necessary in patients with a pleural effusion and significant respiratory or cardiac decompensation
Patients with suspected BILATERAL TRANSUDATIVE pleural effusions should NOT undergo thoracentesis unless they have atypical features such as fever, pleuritic chest pain, or effusions of disparate size
THORACENTESIS FLUID ANALYSIS:
Gross appearance:
—color, opacity, and for particles
—transudative looks like beer, light yellow, amber
—exudative: bloody, dark
—cloudy: infection
LIGHT’S CRITERIA: ⭐️
—protein and lactate dehydrogenase levels to determine if TRANSUDATE OR EXUDATIVE. Pleural:serum protein ratio and pleural:LDH ratio. So draw blood as well. See next slide with the table
Cell Count⭐️
—neutrophil more an acute process; lymphocyte might be long standing
Culture with Gram Stain and AFB stain
—causative pathogen
Cytology
—malignancy
pH
—< 7.3 usually seen with empyema, TB, malignancy, collagen vascular disease
Amylase
—elevated might be related to a pancreatic disease
N-terminal pro-BNP
Glucose
—less < 60 mg/dL likely TB, malignancy, RA, or parapneumonic effusion
[SKILLS OSCE]
What is this?
Pleural effusion
⭐️ Lights Criteria — pleural effusion ⭐️
Transudate vs exudate
Serum protein
Serum LDH
Pleural fluid
Causes
Pleural effusion
Treatment for:
Transudative
Malignant — keeps coming back?
Paraneumonic pleural effusion
1.Transudative:
—usually occur in the absence of pleural disease and treatment is directed at the underlying condition.
—loop diuretic to treat their HF etc
2.Malignant Pleural Effusion:
—can be systemic and related to the underlying malignancy (cancer) or local to address the effusion. Sometimes you drain, they have cancer, and they keep coming back with pleural effusions
—Can perform a thoracentesis and if reaccumulation occurs, place a chest tube.
PLEURODESIS:
—placement of an irritant (talc, doxycycline) in the pleural space following drainage to form fibrous adhesions between the visceral and parietal pleura resulting in an obliteration of the pleural space. —To prevent recurrent pleural effusions
3. Hemothorax: trauma usually:
—Observation or if large, can place a chest tube.
—Might require a thoracotomy to control hemorrhage, remove clot, and treat complications like a bronchopleural fistula formation.
4. Parapneumonic Pleural Effusions:
—Parapneumonic = pleural effusion that followed a pneumonia
—Small might not require drainage and only antibiotic therapy.
—More complicated effusions require drainage.
Chest wall diseases
3
Defined as
—Bony deformities of the chest wall can cause restrictive disease
Scoliosis
—lateral curvature of the spine (more serious; backwards protuberance of the ribs)
Kyphosis
—posterior curvature of the spine
—The patient will complain of dyspnea and have rapid/shallow breaths.
—This will later lead to hypoxemia, CO2 retention, and cor pulmonale (from pulmonary vascular resistance : PH from chronic hypoxia).
—Parts of the lung will be compressed and cause atelectasis (ventilation-perfusion mismatch).
—If the patient smokes, higher risk of getting bronchiectasis.
PFTs
—reduction in all lung volumes
Ankylosing Spondylitis
—Disease of unknown etiology which results in a gradual loss of immobility of the vertebral joints and fixation of the ribs
—Results in decreased movement of the chest wall and decreased compliance
—Reduction of FVC but the FEV1/FVC ratio and airway resistance are norma
—Overall though, the parenchyma is preserved and respiratory failure DOES NOT occur
Chest wall diseases
NEUROMUSCULAR DISORDERS — 6
What do they cause?
Affect the muscles of respiration or their nerve supply including:
a.Poliomyelitis
b.Guillain-Barre syndrome
c.Amyotrophic Lateral Sclerosis
d.Myasthenia Gravis
e.Botulism
f.Muscular Dystrophy
All can cause DYSPNEA and RESPIRATORY FAILURE
—The patient is unable to take a deep breath > causes reduced FVC, inspiratory capacity, and FEV1
—Eventually will affect the DIAPHRAGM, the most important muscle of respiration
—By then the ventilatory reserve is compromised, affecting maximal inspiratory and expiratory pressures, and ultimately lead to the need for assisted ventilation
These are all extrinsic factors leading to restrictive lung disease
Lung cancer — carcinoid tumour
Just be aware
Neuroendocrine Tumor (1-2% of lung cancers) although these tumors more likely develop elsewhere like the GI tract. Usually CENTRAL but occasionally peripherally
—Can secrete hormones like endocrine glands
—Can secrete neurotransmitters like nerve cells
Not related to smoking or pollutants. Unknown cause but possibly genetic with higher incidence in those with MEN1 (multiple endocrine neoplasia type 1)
CARCINOID SYNDROME relates to increased serotonin production
WHEEZE/Asthma from smooth muscle constriction in bronchioles
GI smooth muscle contraction causes DIARRHEA
FACIAL FLUSHING from increased capillary blood flow to skin
