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Pulmonary: Clin Med II B > Pulmonary Circulation Disorders > Flashcards

Pulmonary Circulation Disorders Flashcards

1
Q

An obstruction of the pulmonary artery or one of its branches by an embolus
what is this term?

A

Pulmonary Embolism (PE)

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2
Q

3rd leading cause of mortality in hospitalized pts
3rd MC CV cause of death in the US
what condition?

A

Pulmonary embolism

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3
Q

8 types of PE

A
  1. Thrombus - arising from any area of the venous circulation or the heart
    - MC - Deep veins of the lower extremities (LE)
  2. Air - during neurosurgery, central venous catheters
  3. Amniotic fluid - during active labor
  4. Fat - long bone fractures
  5. Foreign bodies - talc in injection drug users, cement emboli (joint replacement)
  6. Parasite eggs - schistosomiasis
  7. Septic emboli - acute infective endocarditis
  8. Tumor cells - renal cell carcinoma
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4
Q

Pathophysiological response from pulmonary vascular obstruction

A
  1. Infarction
    - Most often occurs when small emboli lodge distally where there is little collateral blood flow
  2. Impaired gas exchange = hypoxia
    - Altered ventilation to perfusion ratio
    - Inflammation → Surfactant dysfunction → Atelectasis → Functional intrapulmonary shunting
    - Stimulation of the respiratory drive → hypocapnia and respiratory alkalosis
  3. CV compromise
    - Obstruction of vascular bed → Increased pulmonary vascular resistance → Right heart and intraventricular septal strain
    - Less blood returning to the left ventricle → Reduced CO→ Hypotension
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5
Q

risk factor of PE

A

virchow’s triad

  1. venous stasis
    - Immobility - obesity, stroke, bed rest, post-op
    - Hyperviscosity - polycythemia
    - Increased central venous pressures - low CO states, pregnancy
  2. injury to vessel wall - Prior episodes of thrombosis, orthopedic surgery, or trauma
  3. hypercoagulability
    - Meds - OCs, hormonal replacement
    - Disease - malignancy, surgery
    - Inherited gene defects - Factor V Leiden (MC)
    — Deficiency of dysfunction of protein C, protein S, and antithrombin
    — Prothrombin gene mutation
    — Hyperhomocysteinemia
    — Antiphospholipid antibodies
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6
Q
  1. Sudden onset dyspnea, pleuritic chest pain, cough
  2. Tachypnea
  3. Sx of DVT may precede
    - Lower leg pain / “charley horse”
    - Associated sx: swelling, warmth and/or erythema

this presentation is associated with which dx?

A

PE - “The Great Masquerader”

  • significant pain is associated with small PE’s that result in infarction
  • Tachypnea - most reliable exam finding
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7
Q

how to approach “pre-test” probability with PE dx?

A
  1. Wells Criteria
  2. If Well’s is low = PERC Rules
  • Low risk + no PERC rules criteria → No testing
  • Low risk + at least 1 positive PERC/ Intermediate risk → high-sensitivity plasma D-dimer
    — Normal → no imaging
    — Elevated d-dimer → imaging
  • High risk → Imaging (not D-dimer)
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8
Q

scoring system of Wells Criteria

A
  • > 6 = high risk (78.4%)
  • 2–6 = moderate risk (27.8%)
  • <2 = low risk (3.4%)
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9
Q

what are the PERC rules?

A
  1. low probability (<15% prob. of PE based on gestalt assessment)
  2. <50 y/o
  3. HR <100 bpm during entire stay in ED
  4. pulse ox >94% at near sea level
    - >92% for altitudes near 5000ft above sea level
  5. no hemoptysis
  6. no prior venous thromboembolism hx
  7. no surgery/trauma requiring endotracheal or epidural anesthesia within last 4 wk
  8. no estrogen
  9. no unilateral leg swelling
    - asymmetrical calves on visual inspection w/ pt’s heels raised off bed
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10
Q

diagnostics for PE

A
  1. D-dimer (sensitivity 95–97%; specificity 45%)
  2. CTA (chest/pulmonary artery) - first line imaging
  3. Ventilation–perfusion (V̇/Q̇) scanning
  4. Pulmonary Angiography - gold standard for making dx
    - Safe but invasive requiring interventional radiology and contrast dye
  5. EKG
  6. Chest radiograph - to r/o other etiologies
    - skipped in mod-high probability
  7. additional labs (not necessary to make dx):
    - CBC - 20K
    - ABG - low pO2, rsp alkalosis w/ hypocapnia, more likely to be abnormal in other pulmonary conditions than PE
    - troponin & BNP - related to size of PE causing acute right ventricular myocardial stretch
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11
Q

how to interpret results of D-dimer? what could cause false positives?

A

A protein fragment from a broken down blood clot
(sensitivity 95–97%; specificity 45%)

  1. Normal: < 500 ng/mL
    - Adults >50 w/ low or intermediate probability use age-adjusted threshold (age × 10 ng/mL)
  2. Elevations are not diagnostic
    - false positives: age >50 years, recent surgery or trauma, acute illness, pregnancy or postpartum state, rheumatologic disease, renal dysfunction and sickle cell disease
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12
Q

CTA requires IV contrast, therefore what is needed to do before doing this imaging?

A

pre-tesing BUN/Cr

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13
Q

there is a (+) filling defect in the CTA, what does this indicate?

A

PE

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14
Q

cautions with CTA

A

Pregnancy
Metformin
Allergy to contrast dye

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15
Q

indications for VQ scanning

A
  1. pregnancy
  2. renal insufficiency
  3. severe prior adverse reaction to contrast material
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16
Q

after a VQ scanning, it shows normal perfusion. What does this indicate?

A

r/o PE
PE = reduced perfusion w/ normal ventilation

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17
Q

(+) Intraluminal filling defect is found in a pulmonary angiography, what does this indicate?

A

PE

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18
Q

indication for pulmonary angiography

A

when there is high pre-test probability and inconclusive CTA result

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19
Q

EKG findings of PE

A

1. sinus tach
2. non-specific ST segment and T-wave changes affecting R precordial leads V1-3 +/- V4
3. S1Q3T3 pattern
4. right ventricular strain - R axis deviation
5. new incomplete RBBB

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20
Q

what are the chest radiograph findings of a PE

A
  1. Westermark’s sign (14% sensitivity, 92% specificity)
    - an area of lung oligemia - from complete lobar artery obstruction
  2. Hampton’s hump (22% sensitivity, 82% specificity)
    - dome-shaped dense opacification in the periphery of the lung - indicative of pulmonary infarction
  3. Nonspecific findings are common - cardiomegaly, basilar atelectasis, infiltrate, or pleural effusion
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21
Q

Performed to look for evidence/location of DVT
helps to determine the etiology of the PE and affects disposition

A

Lower Extremity Venous Doppler
70% of patients with PE with have a DVT evident on evaluation

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22
Q

risk stratifications of PE

A
  1. high risk (massive) Hemodynamic instability
    (any of the following)
    - hypotension (SBP < 90 mmHg x >15 min)
    - drop in SBP >40 mmHg below baseline
    - hypotension requiring vasopressors
    - causing a cardiac arrest
  2. Intermediate-risk PE (Submassive)
    - Hemodynamic stability with signs of R sided heart strain/dysfunction via CTA, echo, elevated troponin or BNP.
  3. Low-risk PE (Less severe)
    - Normotension without signs of right ventricular dysfunction
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23
Q

Initial management for all PE patients:

A
  1. supplemental oxygen
  2. ventilatory support
  3. hemodynamic support
    - avoid excessive IV fluids → increased risk of RHF
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24
Q

Three primary forms of PE therapy

A
  1. Anticoagulation - mainstay
  2. Fibrinolysis
  3. Thrombectomy

Anticoagulation will reduce mortality from PE to < 5%

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25
Q

Anticoagulation Management options for PE

A
  1. Unfractionated heparin (UFH)
  2. Low-molecular weight heparin (LMWH)
  3. Direct-acting oral anticoagulants (DOAC’s)
    - Factor Xa Inhibitors - rivaroxaban (Xarelto) and apixaban (Eliquis)
    - Direct thrombin inhibitor - dabigatran (Pradaxa)
  4. fondaparinux
  5. Warfarin
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26
Q

Binds to and accelerates the activity of antithrombin, preventing additional thrombus formation
Reserved for unstable patients, severe renal insufficiency
which anticoag is this

A

UFH

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27
Q

dosing with UFH

A
  1. 80 units/kg/dose IV x 1 (or 5000 U) followed by 18 units/kg/hour (max 2000 u/hr)
    - Monitoring required: obtain aPTT every 6 hours during tx; goal - 60-80 seconds
    - Normal PTT - 25-30 seconds
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28
Q

In high risk patients, which anticoagulation may be give before imaging confirms dx

A

UFH

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29
Q

risks with UFH?
reversal?

A
  • hemorrhage
  • Protamine sulfate - reverses effects of heparin
    — Indicated for life-threatening or intracranial hemorrhage
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30
Q

enoxaparin (Lovenox)

A

LMWH

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31
Q

which anticoag is Preferred over other injectable agents in those who can not take oral anticoagulants
why?

A

enoxaparin (Lovenox)
Greater bioavailability, more predictable dose response, longer half-life compared to UFH

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32
Q

monitoring of enoxaparin (Lovenox) in who?

A

Monitoring only in obese, underweight (<45 kg) or renal impairment

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33
Q

risk with enoxaparin
reversal?

A

Risk of hemorrhage
Protamine sulfate - reverses effects of heparin
Indicated for life-threatening or intracranial hemorrhage

34
Q

rivaroxaban (Xarelto)

A

Factor Xa Inhibitors - DOAC

35
Q

apixaban (Eliquis)

A

Factor Xa inhibitors - DOAC

36
Q

dosing for DOACs

A

Xarelto: initiate BID then QD after 21 days
Eliquis: BID dosing

37
Q

which anticoag is safe in pregnancy

A

enoxaparin (Lovenox) - LMWH

38
Q

which DOAC does not require bridging therapy with LMWH?

A

Factor Xa Inhibitors - rivaroxaban and apixaban
No lab monitoring, few drug-drug or drug-food interactions

39
Q

reversal agent of Factor Xa inhibitors?

A

AndexXa - reversal agent for life-threatening or uncontrolled bleeding

40
Q

dabigatran (Pradaxa)

A

Direct thrombin inhibitor

41
Q

which DOAC requires bridging with UFH/LMWH? for how long?

A

Direct thrombin inhibitor - dabigatran (Pradaxa)
5-10 d of bridging

42
Q

reversal for dabigatran

A

praxbind
reversal agent for life-threatening or uncontrolled bleeding

43
Q

Injectable factor Xa inhibitor
Preferred if hx of heparin-induced thrombocytopenia (HIT)
Less preferred to LMWH
which anticoag?

A

fondaparinux (Arixtra)

44
Q

Vitamin K antagonist prevents activation of coagulation factors II, VII, IX, and X
Many interactions with food and other drugs
which anticoag?

A

warfarin

45
Q

PK of warfarin?

A
  1. Takes 5 days to reach full effects
    - requires bridging with LMWH until INR 2-3
  2. Start dose at 5 mg/d
    - Monitoring required: keep INR 2-3
    - requires variable dosing regimens that changes frequently
46
Q

Alteplase

A

Tissue Plasminogen Activator (tPA) - fibrinolysis

Anticoags started after fibrinolytic

47
Q

indications for alteplase

A

Tissue Plasminogen Activator (tPA)

  • High risk PE patients
  • Intermediate risk PE with elevated troponin or BNP, or persistent hypoxemia with distress
48
Q

CI of alteplase

A
  1. intracranial disease (active tumor or hx of bleed)
  2. uncontrolled HTN (>220 or >110) at presentation
  3. recent major surgery or trauma (<3 wks)
  4. ischemic CVA in last 3 months
  5. metastatic cancer
49
Q

Manual removal of the emboli surgically or with a catheter

what is this PE management called?

A

Embolectomy
Catheter-directed procedure offers the benefit of locally injecting tPA at a lower dose decreasing bleeding risk

50
Q

indications of Embolectomy

A

Hemodynamically unstable patients with a contraindication or failure to respond to tPA

51
Q

prevention of PE

A

IVC filter

  • Indications:
    — active bleeding that prevent anticoagulation
    — recurrent VTE despite intensive anticoagulation
52
Q

indications for inpatient PE tx?

A
  1. Severe illness or presence of comorbidities
  2. Associated DVT
  3. Educational needs (eg, lack of knowledge about PE and its management)
  4. Problematic social situations (eg, prior noncompliance with follow-up care)
53
Q

The presence of any of these factors places patient at high risk and requires admission:
(pulmonary embolism)

A
  • Age > 80
  • Hx of CA
  • Hx of chronic cardiopulmonary dz
  • HR ≥ 110
  • SBP <110
  • O2 Sat <90%
54
Q

management for PE: how long should pts be on anticoagulants? (considerations?)

A
  1. 3-6 months minimum vs indefinite
    - found risk of recurrence in all pts (provoked or unprovoked) was decreased with prolonged anticoagulation therapy
  2. Considerations when determining length of therapy:
    - provoked or unprovoked
    - presence of risk factors (eg, transient or persistent)
    - estimated risk of bleeding and recurrence
    — intensity and duration of the anticoag; concomitant administration of meds, such as aspirin, increased age, previous GI hemorrhage, and coexistent CKD
    - pt preferences and values (eg, occupation, life expectancy, burden of therapy)
55
Q

Hypercoagulation evaluation of these certain disorders if no obvious cause for VTE is identified

A

consult hem:

  1. AT III def
  2. Protein C and protein S def
  3. Lupus anticoagulant
  4. Homocystinuria
  5. Occult neoplasm
  6. CTD
56
Q

physiology of pulmonary circulation

A
  1. Low pressure, low resistance system
  2. Able to accommodate significant increase in blood flow during exercise
57
Q

Mean pulmonary arterial pressure (mPAP) should be between ?

A

10-18 mmHg

58
Q

pathophys of pulm HTN

A

Increase in pulmonary vascular resistance, typically due to vasoconstriction, remodeling, and thrombosis of the small pulmonary arteries and arterioles leading to hyperplasia and hypertrophy of the vessels.

59
Q

value of mPAP to be pulm HTN?

A

(mPAP) >20 mmHg

60
Q

Pulmonary Hypertension: WHO Classifications

A
61
Q

presentation of pulm HTN

A

Non-specific symptoms

  1. Malaise and fatigue - MC
  2. Dyspnea - most common
    - starts with exertion but progresses to resting
  3. Anginal pain
  4. Nonproductive cough
  5. Hemoptysis
    - rare - life threatening - results from rupture of pulmonary artery
    - Exertional syncope
    - more severe cases where CO affected
  6. Often normal early in disease
  7. Late disease - RHF
    - JVD
    - Accentuated P2
    - 3rd heart sound (“Kentucky”)
    results from a dysfunctional right ventricular
    wall
    - Tricuspid regurg murmur
    - Hepatomegaly
    - Lower extremity edema
    - Cyanosis - if an open PFO leading to R→L shunt
62
Q

initial work-up for pulm HTN? findings?

A
  1. CXR/CT
    - may be normal
    - enlargement of the pulmonary arteries may be found incidentally
  2. EKG
    - Signs of RVH may be seen
  3. 2D Transthoracic Echocardiogram with Doppler
    - Signs of PH
    — Elevated estimated pulmonary artery systolic pressure (ePASP)
    — Tricuspid regurgitation, RV enlargement, wall thickness or dysfunction may be seen
    - Normal echo doesn’t r/o PH
63
Q

diagnostics of pulm HTN

A

Right-sided heart catheterization (aka Swan-Ganz catheter) - Gold standard
Labs: to look for less common causes
- CBC; CMP; Coags -pT, apTT; ABG; HIV testing; Hepatitis panel; Urine toxicology

64
Q

what reading in a right-sided heart cath (swan-ganz) is diagnostic for PH?

A

mPAP ≥ 20 mmHg

65
Q

what diagnostic approach assesses left sided heart disease

A

Pulmonary capillary wedge pressure (PCWP)

66
Q

scoring for PCWP

A
  • ≤15 mm Hg = no left sided heart disease
  • Elevated PCWP = L sided heart dz and should be confirmed with a L heart cath
67
Q

Collagen-vascular disease screening has what findings?

A

antinuclear ab (ANA), rheumatoid factor (RF), antineutrophil cytoplasmic ab (ANCA),
Scleroderma: anti-Scl-70, anticentromere, and anti-U1-RNP antibodies

68
Q

general measures in management for PH

A
  1. Exercise and pulmonary rehabilitation
  2. Oxygen therapy
    - resting, exercise-induced, or nocturnal use
  3. Age appropriate vaccinations
  4. Smoking cessation (if applicable)
  5. Maintain healthy body weight
  6. Psychosocial support
  7. Birth control (non-estrogen)
    - PAH is associated with increased maternal and fetal risks, including high risk of death.
69
Q

refer PH to who

A

Pulmonology or specialist in PH management
Cardiology if WHO II

70
Q

how to classify severity of PH?

A

New York Heart Association (NYHA) System

  • NYHA I: No sx, no limitation of activity
  • NYHA II: Slight limitation of activity. sx with ordinary activity
  • NYHA III: Marked limitation of activity. sx with < ordinary activity
  • NYHA IV: Unable to perform any activity without sx. Evidence of right heart failure. Dyspnea and fatigue at rest that worsens on exertion
71
Q

what are the NYHA sx?

A

dyspnea, fatigue, chest pain, or near syncope with exertion.

72
Q

approach management of PH

A

Step1 : Treat any underlying condition

  1. Treat underlying conditions or any condition that may worsen PH
  2. WHO II - treat left sided heart failure
  3. WHO III - treat lung disease and/or hypoxia

Step 2: Is there vasoreactive disease?

  1. Vasoreactive disease
    - CCB used for NYHA class I-III - High dose diltiazem and nifedipine most commonly used
  2. Non-vasoreactive disease
    - Based upon NYHA Classification
    — Only WHO PH 1 and 4 have FDA approved meds for PH
73
Q

pharm management of PH

A
  1. Endothelin receptor antagonists - ambrisentan, bosentan, macitentan,
    - MOA: reduces endothelin release leading to vasodilation
  2. PDE 5 inhibitors (oral) - sildenafil, tadalafil
    - MOA: inhibition of PDE5 leads to vasodilation
    — PDE5 is abundantly expressed in the lungs and causes vasoconstriction
  3. Soluble guanylate cyclase stimulators - riociguat
    - MOA: stimulates the activity of guanylate cyclase
  4. Prostanoid agents - epoprostenol, treprostinil, iloprost
    - MOA: potent pulmonary vasodilation by acting on prostaglandin receptors with an additional benefit of inhibiting platelet aggregation
  5. Prostacyclin receptor agonists - Selexipag
    - MOA: attaches to and activates prostacyclin receptors in the lung resulting in vasodilation
74
Q

what is produced in the cells that line the heart and lungs; when released results in vasoconstriction

A

endothelin

75
Q

what is produced in the lungs as a response to nitric oxide. Cyclic GMP causes the arteries to relax and widen (vasodilation).

A

Guanylate cyclase produces cyclic guanosine monophosphate (cyclic GMP)

76
Q

Selexipag (Uptravi) is more selective for what receptor than the prostanoid agents?

A

prostacyclin receptor than the prostanoid agents

77
Q

which Prostanoid agents are continuous IV pump, inhalation, and has multiple delivery methods?

A
  1. epoprostenol (Flolan) - continuous IV pump
  2. treprostinil - 3 delivery methods - oral, inhalation, continuous IV infusion via pump
  3. iloprost (Ventavis) - inhalation
78
Q

difference between IV and PO Selexipag/prostacyclin receptor agonist

A

IV only for short term if unable to take PO

79
Q

Management: Non-vasoreactive disease

based on (NYHA) System

A
  1. NYHA I - consider monotherapy
  2. NYHA II/III - combo therapy
    - Endothelin antagonists + PDE5 inhibitors
    - Add guanylate cyclase stimulators / oral prostacyclin receptor agonists if uncontrolled
  3. NYHA IV
    - Add on parenteral prostanoid to oral combination therapy
80
Q

additional managements for PH

A
  1. Long-term anticoag - WHO 4 (some WHO 1)
    - warfarin (Coumadin)
    - dabigatran (Pradaxa), rivaroxaban (Xarelto), and apixaban (Eliquis)
  2. Thromboendarterectomy - if no response to meds in WHO 4
  3. Diuretics for symptomatic RHF
    - watch for hypovolemia as pts are preload dependant
  4. Lung transplant reserved for those unresponsive to medical management
    - Double (preferred) or single can be effective

Pulmonary: Clin Med II B (10 decks)

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