Lectures6-10 Flashcards
(247 cards)
1
Q
Asthma is a chronic inflammatory disorder of the airways characterized by:
A
Paroxysmal symptoms of cough, wheezing, dyspnea and chest tightness, usually related to triggers
Airway narrowing that is partially or completely reversible
2
Q
Why does asthma have increasing prevalence?
A
Improved hygiene, increased indoor air pollution, increased incidence of early-onset respiratory viral infections, survival or premature infants, increased awareness & recognition of asthma but pts and clinicians
3
Q
What are some risk factors for asthma?
A
M>F, Low SES, urban dwellers, food allergies, family hx, atopy
4
Q
What is atopy?
A
A genetic disposition to develop an allergic reaction and produce elevated levels of IgE upon exposure to an environmental antigen and especially one inhaled or ingested
5
Q
What are some examples of atopy?
A
Atopic dermatitis, allergic rhinitis, asthma
6
Q
Patho of asthma
A
Smooth muscle constriction around airways, airway wall edema, intra-luminal mucus accumulation, inflammatory cell infiltration of submucosa and basement membrane thickening
7
Q
What immune cells are involved in asthma?
A
Eosinophils, activated helper T cells, mast cells, neutrophils
8
Q
Fatal asthma
A
Severe collagen deposition of basement membrane, desquamation of epithelial lining with loss of ciliated cells, mucosal edema, airway smooth muscle hypertrophy, luminal plugging with inflammatory cells
9
Q
What are the 3 main physiological consequences of asthma?
A
- Chronic airways inflammation
- Reversible or partially reversible bronchoconstriction
- Increased airways hyperresponsiveness to a variety of stimuli
10
Q
What are the “classic’ sign and symptoms of asthma
A
Intermittent dyspnea, persistent cough, sudden onset or persistent wheezing
11
Q
Additional features of asthma
A
Chest tightness, cold that take >10 days to resolve, apparent triggers, symptoms awake pt from sleep, exertional symptoms, seasonal, poor school performance and fatigue
12
Q
The cough of asthma
A
Usually dry hacking, nocturnal, seasonal, response to specific exposures, lasts >3 weeks, frequently the sole complaint
13
Q
What are some common asthma triggers?
A
Pollen, viral URIs, exercise, changes in air temp, perfumes, pets, molds, NSAIDs
14
Q
What can be seen on PE for asthma?
A
Tachypnea, hypoxia if acute flare, cant speak full sentences without stopping to breath*, high-pitched musical wheeze
15
Q
The wheeze of asthma
A
Initially with expiration but in severe cases also with inspiration
16
Q
Critically severe asthma causes what?
A
Decreased breath sounds “silent chest/absent breath sounds”
Medical emergency: “the patient is very tight, not moving air”
17
Q
Extrapulmonary PE findings associated with asthma
A
Pale, swollen nasal turbinates suggestive of allergic rhinitis, nasal polyps, atopic dermatitis
18
Q
What diagnostic studies are used for asthma?
A
PFTs, spirometry with bronchodilator response testing, bronchoprovocation challenge, peak flow, CXR, allergy skin test
19
Q
PFTs
A
Measurement of lung volumes, quantitation of diffusion capacity, measurement fo forced inspiratory and expiratory flow rates
20
Q
What will PFTs show for an airway obstruction?
A
FEV1 decreased, FEV1/FVC ratio <70%
21
Q
Vital capacity
A
Maximum amount of air a person can expel form the lungs after a maximum inhalation
22
Q
What should you do if the baseline spirometry demonstrates an airway obstruction?
A
Administer albuterol 400mcg by MDI -> repeat spirometry 10 mins after
23
Q
What suggests acute bronchodilator responsiveness?
A
Increase in FEV1 of >12%
24
Q
What does the peak flow meter measure?
A
Peak expiratory flow
25
Peak flow meter
Effort dependent, useful for monitoring daily function during treatment of acute flare
26
What is needed to diagnose asthma?
Airflow obstruction symptoms, reversibility or obstruction, symptoms worse at night or early AM, prolonged expiration and wheezes on PE, limitation of airflow on PFT
27
Intermittent asthma severity
<2 days week symptoms and use of rescue inhaler
28
Mild persistent asthma
>2 days/week symptoms and use of rescue inhaler (but not daily)
29
Moderate persistent asthma
Daily symptoms and use of rescue inhaler, some limitation to normal activity
30
Severe persistent asthma
throughout the day symptoms and use of rescue inhaler, extremely limited activity
31
What will the PFTs show for intermittent asthma?
Normal FEV1 between exacerbations, FEV1/FVC >.85
32
What will PFT show for mild persistent asthma?
FEV1 normal, FEV1/FVC >.8
33
What will PFT show for moderate persistent asthma?
FEV1 60-80%
| FEV1/FVC 0.75-0.8
34
What will PFT show for severe persistent asthma?
FEV1 <60%
| FEV1/FVC
35
What are the components of asthma management?
Routine monitoring of symptoms and lung fxn, patient education, controlling environmental triggers, pharmacological therapy
36
What is the treatment for intermittent asthma?
SABA prn
37
What is the treatment for persistent asthma (step 2)
Low dose ICS
38
What is step 3 treatment of asthma
either low dose ICS + LABA or med dose ICS + LABA
39
What is step 4 treatment of asthma
Med dose ICS + LABA
40
What is step 5 treatment of asthma
High dose ICS + LABA
41
What is step 6 for treatment of asthma?
High dose ICS +LABA + short course of oral systemic steroids
42
What is the treatment for acute asthma exacerbation?
02 between 90-96%, Methylprednisolone or prednisone, Albuterol (short acting bronchodilator), Magnesium IV
43
Can COPD and asthma co-exist?
Yes
44
What are some conditions that can exacerbate asthma?
Allergic rhinitis, GERD, cigarette smoking, obesity
45
COPD
A common preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases
46
What are 3 subtypes of COPD
1. Emphysema
2. Chronic bronchitis
3. Chronic obstructive asthma
47
What is Emphysema?
Enlargement of air spaces and destruction of lung tissue
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What is chronic bronchitis?
Obstruction of small airways
49
COPD differences from asthma
Usually from smoking, diagnosed at 50-60YO, obstruction is either irreversible or partially reversible with bronchodilator therapy
50
Asthma differences from COPD
Associated with atopy, diagnosed in childhood usually, reversible with bronchodilator therapy
51
Pathophys of COPD
Inflammation and fibrosis of bronchial wall, hypertrophy of submucosal glands, hypersecretion, loss of elastic fibers and alveolar tissue
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What does COPD result in?
Airways obstruction, decreased surface area for gas exchange and mismatching of ventilation and perfusion
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What does loss of elastic fibers cause in COPD?
Impairs expiratory flow, leads to air trapping, predisposes to alveolar collapse
54
What are common triggers of exacerbations for COPD?
Pulmonary infections
55
What are some risk factors for COPD?
Cigarette smoking*** airway hyperresponsiveness, biomass fuel exposure, 2nd hand smoke, ambient air pollution, genetics- alpha-1-anti-trypsin deficiency for COPD in young pts
56
Chronic bronchitis
Excessive secretion of bronchial mucus, chronic daily cough for 3mos
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What may proceed or follow development of airflow limitation?
Chronic Bronchitis
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What is an abnormal and permanent enlargement of the airspace’s that is accompanied by the destruction of the airspace walls & capillary beds?
Emphysema
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Loss of elasticity
Emphysema
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What are the two types of emphysema?
1. Proximal acinar
| 2. Panacinar
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Proximal acinar emphysema
Initial preservation of alveolar ducts and sacs
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Panacinar emphysema involves what?
Involves both bronchioles and alveoli
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What type of emphysema has an abnormal dilation or destruction of the respiratory bronchiole?
Proximal acinar (centrilobular)
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What is proximal acinar emphysema commonly associated with?
Cigarette smoking
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What can be seen in coal workers pneumoconiosis?
Proximal acinar emphysema
66
Which type of emphysema has enlargement or destruction of all parts of the acinus?
Panacinar emphysema
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Panacinar emphysema is associated with that?
Alpha-1 antitrypsin deficiency
68
What can be seen on CXR for emphysema?
Hyperexpanded lungs, flattening of the diaphragm, volume is much longer looking
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What else can be seen in CXR for emphysema that can lead to pneumothorax?
Blebs
70
What are some symptoms of COPD?
Chronic cough, sputum production, exertional dyspnea, wheezing, chest tightness, weight gain or weight loss
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When do patients typically present with COPD symptoms?
5th or 6th decade of life, symptoms usually present at that point for around 10 years
72
PE findings for COPD
Prolonged expiratory phase, wheezing, barrel chest, enlarged lung volumes, respiratory distress in severe exacerbation, tripod position, pursed lips, cyanosis, weight loss, signs of RHF
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Who are the pink puffers?
Emphysema
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Who are the blue bloaters?
Chronic bronchitis
75
Pink puffer si/sxs
Dyspnea major complaint* scant clear mucus, thin, accessory muscle use, chest is quiet or soft-pitched wheeze
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Blue bloater si/sxs
Chronic cough major complaint* mucopurulent sputum, frequent COPD exacerbations due to infections, mild dyspnea, noisy chest with Rhonchi and wheezing
77
What can be used to diagnose COPD?
Hx of SOB, cough, wheeze, smoking, labs: bicarb, CXR to rule out other causes, PFTs
78
What does serum bicarb identify for COPD pts?
Chronic hypercapnia in chronic disease
79
What else can be drawn for labs to test for COPD?
AAT deficiency, Hgb and BNP to rule out other causes of dyspnea
80
What PFTs should be used to diagnose COPD?
Spirometry, measurement of lung volumes, DLCO, forced inspiratory and expiratory flow rates
81
FEV1 measures what?
Forced expiratory volume in one second
82
FVC measures what?
Forced vital capacity
83
What is the vital capacity?
Maximum amount of air a person can expel from lungs after a max inhalation
84
What is the FRC?
Functional residual capacity, the volume of gas w/in the lungs at end of expiration during normal tidal breathing at rest
85
Conditions that decrease the DLCO
Anemia, emphysema, pulmonary HTN, recurrent PEs, interstitial lung disease
86
DLCO helps distinguish between when for obstructive lung diseases?
Between emphysema and chronic bronchitis or asthma
87
What will the PFTs show for obstructive lung disease?
FEV1 and FEV1/FVC ratio decreased, FVC normal, FEV1 improves with bronchodilators
88
What are the non-pharmacological treatments for COPD?
Stop smoking, reduce risk factors, vaccinations, oxygen therapy, pulm rehab
89
What is the 1st line treatment for newly diagnosed COPD?
Rescue inhaler! SABA: Albuterol or Levalbuterol, short acting anticholinergic: Ipratropium
Combo SABA + Ipratropium: Combivent****
90
What is most commonly prescribed for new diagnosis of COPD?
Combivent*** Combo of SABA + Ipratropium
91
What are the si/sx for an acute exacerbation of COPD
SOB, frequent cough with sputum, wheezing, associated with URI or pulm infection, minimal to no improvement with rescue inhaler
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PE findings for COPD acute exacerbation
Respiratory distress, accessory muscle use, tripod position, pursed lips, hypoxia, tachypnea, wheezing, poor air movement, crackles if pneumonia
93
What is used to treat an acute COPD exacerbation?
O2 between 90-96, Prednisone PO or Methyprednisolone IV, Ipratropium and Albuterol nebulizer, Abx
94
What Abxs can be used for an acute exacerbation of COPD?
Levo and Azithromycin; want to cover atypicals
95
Who should be hospitalized for COPD flare?
Increased dyspnea, inability to eat or sleep, new cyanosis or hypoxia, acute respiratory distress, mental status change, insufficient home support, frequent exacerbations, high risk comorbidities
96
What can be seen when a pt is in acute respiratory distress?
Accessory muscle use, tachypnea, tripod position
97
Hospital admission for COPD
O2, Prednisone daily with a taper, Duoneb, Albuterol nebulizer, Levofloxacin or Azithromycin daily
98
When should you consider adding maintenance meds for COPD?
Frequent chronic symptoms, frequent exacerbations, disease progression
99
Which types of meds are used for maintenance for COPD?
LABA, LABA + ICS, LAMA, chronic steroids, chronic O2
100
What LABA is used for maintenance for COPD?
Salmeterol inhaler
101
What LABA + ICS is used for COPD maintenance?
Salmeterol/Fluticasone (Advair) inhaler
102
What LAMA is used for COPD maintenance?
Triotropium (Spirivia)
103
When are chronic steroids and oxygen used for COPD maintenance?
End stage disease
104
What is 1st line treatment as “rescue inhaler” to manage COPD symptoms?
Short acting bronchodilators
105
What is the most common cause of bronchiectasis?
Cystic fibrosis causes about 50% of cases
106
What else can cause bronchiectasis?
Infections: TB, fungal, lung abscess, localized airway obstructions
107
What is bronchiectasis?
Disorder of the large bronchi where there is permanent, abnormal dilation and destruction of the bronchial walls, localized or diffuse
108
What disease does bronchiectasis share clinical features?
COPD
109
What has a chronic daily cough and viscid sputum production?
Bronchiectasis
110
What other clinical features are seen with bronchiectasis?
Bronchial wall thickening, luminal dilatation, frequent office visits and hospitalizations
111
What is the pathophys belong bronchiectasis?
Infection -> host response -> transmural inflammation, mucosal edema, cratering, ulceration, neovascularization -> impaired drainage, permant dilatation and destruction of bronchi and walls
112
Recurrent infections are common with bronchiectasis, leading to what?
Further damage of airways
113
Which disease involves the abnormal transport of chloride and sodium across epithelium leading to thick, viscous secretions?
Cystic fibrosis
114
What type of infections are most common for cystic fibrosis patients?
Pseudomonas aeruginosa infections
115
How is cystic fibrosis diagnosed?
Sweat chloride test
116
Clinical features of bronchiectasis
Cough, daily production or mucopurulent and tenacious sputum x mos-yrs, repeated respiratory tract infections
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Symptoms of bronchiectasis
Cough w/sputum, dyspnea, rhinosinusitis, hemoptysis, recurrent pleurisy, fatigue, urinary incontinence (stress incontinence)
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PE of bronchiectasis
Chronic pulmonary crackles, wheezing, rarely digital clubbing
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Lab tests utilized for bronchiectasis
CBCD, IgG, IgM, IgA to look for immunodeficiency, antibody tigers after pneumococcal vaccine, sputum gram stain and CX, sweat chloride testing
120
Why are the antibody titers drawn after a pneumococcal vaccination?
To assess the immune response to vaccination
121
What imaging studies are good for bronchiectasis?
CRX, CT
122
What will CXR show for bronchiectasis?
Liner atelectasis, dilated, thickened airways, irregular peripheral opacities (mucopurulent plugs)
123
What will be seen on chest CT for bronchiectasis?
Airway dilatation, bronchial wall thickening, mucopurulent plus, cysts of bronchial wall (destructive bronchiectasis)
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What will PFTs show for bronchiectasis?
Reduced FEV1/FVC, low FVC in advanced disease, 6 min walk test
125
What is the treatment for bronchiectasis?
Treat underlying disease, pneumonia or other infection, HIV, prevent aspirations if possible, immunizations
126
How do you treat an acute exacerbation of bronchiectasis?
Oral Abxs, nebulizer: hypertonic saline to thin secretions, chest physiotherapy, PEP device to loosen secretions, bronchodilators, pulm rehab
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What is the PEP device?
Oscillatory Positive expiratory pressure device used to loosen secretions for bronchiectasis
128
What is virchow’s triad?
1. Alterations in blood flow (stasis)
2. Vascular endothelial injury
3. Alterations in constituents of blood (inherited or acquired hypercoagulable states)
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What are the 3 classifications of pulmonary embolisms?
Acute, subacute, and chronic
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Acute pulmonary embolism
Signs and symptoms develop immediately after obstruction of pulmonary vessels prompting evaluation
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Subacute pulmonary embolisms
Patient present days or weeks following initial event
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Chronic pulmonary embolisms
Slowly develop symptoms of pulmonary HTN over many years
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What can a massive or submassive PE cause?
Hemodynamic instability, hypotension, severe RV failure, death
134
What will a patient who is hemodynamically unstable need?
Fibrinolytic therapy (thrombolytic)
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What are the possible locations of pulmonary embolisms?
Saddle, Segmental, Subsegmental
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Saddle PE
In both right and left bronchi
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Segmental PE
Small branch effected
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Subsegmental PE
Small branch off of a branch is effected
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What are some common risk factors for PE?
Post op, sedentary state, malignancy, hx of VTE, pregnancy, oral contraceptives, obesity, smoking, HTN, hypercoagulable disorders
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What are some examples of inherited thrombophilia?
Factor V Leiden mutations, prothrombin gene mutation, deficiency of proteins C and S, amtithrombin 3 deficiency, anticardiolipin antibodies
141
Venous thrombi dislodge and travel where?
To lungs, arterial system if there is a patent foramen ovals or atrial septal defect, can cause stroke or arterial embolization
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Symptoms of PE
Sudden SOB, pleuritic chest discomfort, heart palpitations
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PE findings for pulmonary embolism
DVT: unilateral swelling, erythema, calf tenderness, tachypnea, hypoxia, tachycardia
144
What is used to determine the likelihood of a PE?
Wells Score
145
What is your change of a PE if the Wells score is <2?
15%
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What is your change of PE if the Wells score is 2-5?
29%
147
What is your chance of PE if your Wells score is >6?
59%
148
Only use D-Dimer when?
For low probability patients when ruling out DVT and low to mod probability when ruling out PE
149
What imaging modalities are used to diagnose PE?
Chest CTA with contrast* CXR, VQ scan, pulm angiography
150
“Hampton’s Hump Sign”
Wedge shaped infarction from PE seen on CXR
151
CTA advantages for diagnosing PE
Readily available, fast, minimally invasive, can detect alternative diagnosis
152
CTA disadvantages
Expensive, radiation exposure, C/I️ in pts with renal failure, contrast allergies and pregnancy
153
Who is a CTA C/I️ in?
Renal failure, contrast allergies and pregnancy
154
Venous ultrasonography relies on what?
The loss of vein compressibility, occasionally the thrombus can be directly visualized
155
EKD features associated with PE
*sinus tachycardia*, S1, Q3, T3, complete or incomplete RBBB, non-specific ST or T wave changes
156
What can an echocardiogram show for a PE?
Evidence of right heart strain, RV enlargement or RV dysfunction
157
Approach to treatment of venous thromboembolism
Primary therapy: clot dissolution with thrombolytic or removal by embolectomy
Secondary: anticoagulation or placement of IVC filter
158
Who are high risk patients for PE?
Hemodynamic instability, RV dysfunction, RV enlargement, elevated troponin
159
What is the anticoagulation treatment for VTE?
Parenteral drug, can bridge to warfarin
160
Which anticoag should cancer patients stay on?
LMWH long term
161
Provoked clot antiocagulation period
3-6 mos
162
Unprovoked clot anticoagulation period?
Indefinite anticoagulation
163
What are the indications for an IVC filter?
Active bleeding, recurrent venous thrombosis despite intensive anticoags, high risk pts who cannot have fibrinolytics
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What are the complications for IVC filters?
Caval thrombosis causing marked bilateral leg swelling, double DVT rate
165
Prevention of VTE
Heparin or LMWH at lower doses for hospitalized pts, warfarin used peri-operatively
166
What are some major adverse outcomes of a PE?
Recurrent thromboembolism, pulmonary HTN, death
167
What is defined as the abnormal elevation in pulmonary artery pressure?
Pulmonary HTN
168
What is the normal PAP (pulmonary artery pressure)
8-20 mmHg measured by R heart catheterization
169
Pulmonary HTN =
MEan pulmonary artery pressure >25mmHg
170
PAH is characterized by what?
Dyspnea, chest pain, syncope
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Pulmonary HTN can be caused by which 3 things?
1. Increased pulmonary vascular resistance
2. Elevated L arterial pressure
3. Increased pulmonary blood flow
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What is the patho behind PAH?
Progressive increase in RV afterload results in RV hypertrophy -> eventually RV dilates resulting in decreased contractility, CO will fall
173
What is the first study to order for PAH?
Transthoracic echocardiogram
174
PH is likely if the PASP is estimated at what?
>50mmHg and tricuspid regurg velocity is >3.4 sec
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PH is unlikely is PASP is estimated what?
<36mmHg and tricuspid regurg is <2.8 sec
176
What is the gold standard and necessary to diagnose PH?
R heart catheterizaiton
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What is R heart catheterization?
Catheter guided to right side and passes into pulmonary artery, measure pressure
178
What does the R heart catheter measure the pressures of?
R atria, R ventricle and pulmonary artery
179
What is the pulmonary capillary wedge pressure? (PCWP)
Indirect measurements of L heart pressures by inflating a balloon in the pulmonary artery
180
What is group 1 pulmonary HTN?
Secondary to diseases that localize to small pulmonary arteries/arterioles
181
What is group 2 PH?
Secondary to L heart disease
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What is group 3 PH?
Secondary to lung disease or hypoxemia
183
What is group 4 PH?
Secondary to thromboembolic disease
184
What is group 5 PH?
Unclear multifactorial mechanisms
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What is WHO?
World Health Organization, functional classification for pulmonary HTN
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What is the WHO 1 classification for pulmonary HTN?
No limitations of physical activity. No fatigue or dyspnea, chest pain, or heart syncope
187
What is the WHO 2 classification for pulmonary HTN?
Slight limitation of physical activity, comfortable at rest. Ordinary physical activity results in undue fatigue or dyspnea, chest pain, or heart syncope
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What is the WHO 3 classification for pulmonary HTN?
Marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes undue fatigue or dyspnea, chest pain, or heart syncope
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What is the WHO 4 classification for pulmonary HTN?
Inability to carry on any physical activity without symptoms, signs of RHF. Dyspnea and/or fatigue may be present even at rest.
190
Group 1 characteristics
Abnormalities in pulmonary endothelial and smooth muscle cells: vasoconstriction, vascular proliferation, thrombosis, inflammation
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What type of dysfunction effects the layers of vascular wall in group 1PH?
Vasoconstriction, vascular proliferation, thrombosis, inflammation
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What criteria must be met for someone to be in PH group 1?
Mean PAP >25 mmHg at rest, mean pulmonary capillary wedge pressure <15mmHg, chronic lung disease is mild to absent, VTE disease is absent, other disorders absent
193
Causes of group 1 PH
Idiopathic, hereditary, drugs or toxins, connective tissue diseases, HIV, portal HTN, congenital heart disease
194
What types of drugs or toxins cause group 1 PH?
Appetite suppressants, cocaine, amphetamines, meds
195
What type of connective tissue diseases cause group 1 PH?
Systemic sclerosis, narrowing arteries/arterioles, interstitial fibrosis
196
Group 1 PH caused by what?
LH disease: L atrial HTN requires increased pulm artery systolic pressure to maintain adequate driving force across pulm vasculature
197
Causes of PH group 3?
COPD, interstitial lung disease, obstructive sleep apnea, other causes of hypoxemia
198
Group 4 PH causes
Chronic thromboembolic disease, multiple small PE, decrease in function or blood vessels
199
Group 5 PH causes
Pulm HTN with unclear mechanisms: hematologist disorders, systemic disorders, metabolic disorders, miscellaneous
200
What type of hematologic disorders can cause PH group 5?
Myeloproliferative disorders
201
Which systemic disorder can cause PH group 5?
Sarcoidosis
202
What metabolic disorder can cases PH group 5?
Glycogen storage disease
203
What miscellaneous disease can cause PH group 5?
Sickle cell disease
204
What is the definition of cor pumonale?
Altered structure and/or impaired function of the RV that results from pulmonary HTN
205
What are some causes of cor pulmonale?
Pulm disease (COPD), vasculature (PAH),, upper airway (OSA), chest wall (kyphoscoliosis)
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What is the patho of cor pulmonale?
RH failure from longstanding pulmonary HTN, RV hypertrophy develops due to high pressure, eventually RV loses contractility
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What is the main cause of death in patients with PAH?
Circulatory collapse (existence in group 1 PAH is bad prognosis)
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Si/sx of pulmonary HTN
DOE, dyspnea at rest in advanced disease, fatigue
209
Si/sx of right heart failure
Angina, exertional syncope, peripheral edema, abdominal discomfort due to hepatic congestion
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Why is angina a sign of right heart failure?
R heart requires more oxygen
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Why does exertional syncope happen with right hear failure?
Inability to increase cardiac output
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What are some PE findings for pulmonary HTN?
Increased intensity of S2 in pulmonic area, RV failure widens S2 split, S3, high pitched sytsolic murmur of tricuspid regurg, elevated JVP, hepatomegaly, peripheral edema, ascites
213
What diagnostic tests are used for pulm HTN?
CXR, EKG, Echo, PFTs, overnight oximetry, polysomnography, V/Q scan
214
What is assessed in the echo for pulmonary HTN?
Assess PASP, R heart size and assess for L to R shunts, can diagnose LV dysfunction
215
What are some echo results that would point to pulmonary HTN?
Enlarged RV, small D-shaped LV, flattened septum
216
Treatment for pulmonary HTN?
Early id and treatment ideal, assess disease severity, primary: directed at underlying cause
Advanced: direct at PH itself
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What is the treatment for group 1 PAH?
No effective primary therapy, advanced therapy often needed
218
PAH treatment
Diuretics, anticoagulation, CCBs, endothelin receptor blockers, PDE-5 inhibitors, prostacyclin, lung transplant
219
What is the primary treatment for group 2 PH?
HF treatment
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What is the primary treatment for group 3 PH?
Treat underlying cause of hypoxemia and correction of hypoxemia with supplemental O2
221
What is the primary treatment for group 4 PH?
Anticoagulation, surgical thromboendarterectomy for selected pts
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What is the primary treatment for group 5 PH?
Target specific underlying cause
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What are some things to consider in all groups for PH?
Diuretics treat fluid retention, O2 can benefit all groups, exercise
224
Which groups of PH can anticoagulation be used for?
IPAH, hereditary PAH, drug-induced PAH or group 4 PH
225
Digoxin improves what?
RV EF of pts with group 3 PH and helps control HR in pts who have SVTs associated with RV dysfunction
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Who is advanced therapy for?
Persistent PH and WHP class 2 3 or 4, should be administered at specialized centers where clinicians are experienced
227
Group 1 PAH advanced therapy
First line
228
Group 2 PH advanced therapy
Possibly harmful, L heart unable to handle increased flow
229
Advanced therapy group 3 PH
Not FDA approved, not recommended, occasionally considered
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Advanced therapy in group 4 PH
Can be considered
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Advanced therapy in group 5 PH
Favorable response in sarcoidosis
232
What is the vasoreactivity test?
Administration of short-acting vasodilator, measure hemodynamic response using RH catheter
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What agents are commonly used for the vasoreactivity test?
Epoprostenol, Adenosine, and inhaled Nitric Oxide
234
What is the vasoreactivity test done for?
Pts who are selected for advanced therapy to determine if they will benefit from CCBs
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What is the treatment if the vasoreactivity test is positive?
Trial of oral CCBs, they are less expensive and fewer side effects than other therapies
236
What is the treatment if the vasoreactivity test is negative?
Prostanoid formulations, endothelin receptor antagonists, PDE-5 inhibitors
237
What are the benefits of using CCBs?
Prolonged survival, sustained functional improvement, Hemodynamic improvement
238
Epoprostenol benefits
Improves hemodynamics, functional capacity, and survival in IPAH
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What is the only therapy that has been shown to prolong survival?
Epoprostenol
240
What are the prostanoid formulations?
Epoprostenol, Treprostinil, Iloprost
241
Endothelin receptor antagonists
Endothelin is a potent vasoconstrictor found in high concentrations in lungs of pts with IPAH and other group 1 PAH
242
What are the endothelin receptor antagonists?
Bosentan, Macitentan, Ambrisentan, and Sitaxsentan
243
What are the benefits for endothelin receptor antagonists?
Improve exercise capacity, dyspnea, and Hemodynamic measures
244
What are the PDE-5 inhibitors?
Sildenafil, Tadalafil
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What are the benefits of the PDE-5 inhibitors?
Prolong vasodilatory effect of nitric oxide, also used to treat ED, improves pulmonary hemodynamics and exercise capacity
246
What is the function of the guanylate cyclase stimulant?
NO receptor stimulators, increase sensitivity of receptor to NO, directly stimulate the receptor to mimic action of NO
247
What is the example of the Guanylate cyclase stimulant?
Riociguat
