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Clin Med B 2 > pulmonary circulation disorders > Flashcards

pulmonary circulation disorders Flashcards

1
Q

what is a PE

A

An obstruction of the pulmonary artery or one of its branches by an embolus

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2
Q

what is the 3rd leading cause of mortality in hospitalized pts

A

PE

also the 3rd MC CV cause of death

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3
Q

what are types of PEs

A
  • thrombus - arising from any area of venous circulation (MC DVT)
  • air - during neurosurgery, central venous catheters
  • amniotic fluid - during active labor
  • fat - long bone fractures
  • foreign bodies - talc in injection drug users, cement emboli (joint replacement)
  • parasite eggs (schostosomioasis)
  • septic emboli - acute infective endocarditis
  • tumor cells - RCC
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4
Q

what is the pathophysiological response from pulmonary vascularobstruction

A
  • infarction (MC when small emboli lodge distally)
  • impaired gas exchange leading to hypoxia
  • cardiovascular compromise
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5
Q

how does impaired gas exchange lead to hypoxia

A
  • altered ventilation perfusion ratio
  • Inflammation → Surfactant dysfunction → Atelectasis → Functional intrapulmonary shunting
  • Stimulation of the respiratory drive → hypocapnia and respiratory alkalosis
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6
Q

how does cardiovascular compromise occur from pulmonary vascular obstruction

A
  • Obstruction of the vascular bed → Increased pulmonary vascular resistance → Right heart and intraventricular septal strain
  • Less blood returning to the left ventricle → Reduced cardiac output → Hypotension
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7
Q

what is virchows triad

A

MC pulmonary embolism risk factors

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8
Q

what is considered in venous stasis

A
  • immobility (acute loss of ability to walk)
  • hyperviscosity (polycythemia)
  • inceased central venous pressures (low CO states, pregnancy)
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9
Q

what is considered in the risk of injury to vessel walls

A
  • prior thrombosis
  • orthopedic surgery
  • trauma
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10
Q

what are factors that affect hypercoagulability

A
  • medications (OCP, hormonal replacement)
  • Disease (malignancy, surgery)
  • inherited gene defects
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11
Q

what are the inherited gene defects that could lead to hypercoagulability

A
  • Most common is Factor V Leiden ¹
  • Deficiency of dysfunction of protein C, protein S, and antithrombin
  • Prothrombin gene mutation
  • Hyperhomocysteinemia²
  • Antiphospholipid antibodies
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12
Q

what are the MC signs and sympotms of PE

A
  • sudden onset dyspnea
  • pleuritic chest pain
  • cough
  • (sudden onset pain is related to small PEs that cause infarctions)
  • tachypnea!!!!!! Most reliable exam finding
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13
Q

what is meant by “pleuritic” chest pain

A

Chest pain worse with breathing ( i know most people may know this but i didnt lol)

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14
Q

what may precede s/s of PE

A

s/s of DVT such as lower leg pain or “charley horse” in calf. also swelling/warmth/erythema of the lower leg.

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15
Q

why are PEs known as the “great masquerader”

A

because symptoms are often non specific. they can range from asymptomatic to shock and sudden death.

vary based on size of emboliand baseline of cardiopulm status

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16
Q

what is the MC sign and the MC symptom in PE

A

symptom - dyspnea
sign - tachypnea

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17
Q

what are the wells criteria for PE

A

idk if we need this

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18
Q

what is the “pre-test” probabilities determined by wells criteria

A

> 6 points = high risk (78.4%)
2–6 points = moderate risk (27.8%)
<2 points = low risk (3.4%)

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19
Q

when is PERC rules used

A

only when wells is LOW risk!

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20
Q

what are the PERC rules ?

A

yes, we need this

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21
Q

what testing should be done when a patient has low wells risk and no PERC rules criteria

A

none

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22
Q

what testing should be done when a patient has low wells risk and 1 positive PERC rule OR if they just have intermediate wells risk

A

high sensitivity plasma D-dimer
normal -> no imaginge
high –> imaging

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23
Q

what testing should be done in a patient with a high risk wells score

A

imaging (skip D diemr)

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24
Q

how reliable is D-dimer testing

A

high sensitivity (95-97%) and low-moderate specificity (45%)

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25
Q

what is D-dimer

A

a protein fragment from a broken down blood clot

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26
Q

what is normal D-dimer and when is it adjusted

A
  • Normal: < 500 ng/mL
  • Adults over age 50 with a low or intermediate clinical probability of PE use an age-adjusted threshold (age × 10 ng/mL)
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27
Q

what could create a false positive in D-dimer results

A
  • age >50 years
  • recent surgery or trauma
  • acute illness
  • pregnancy or postpartum state
  • rheumatologic disease,
  • renal dysfunction
  • sickle cell disease
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28
Q

are D-dimer elevations diagnostic?

A

no!! must get imaging

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29
Q

what is the first line imaging modality in most PE pateints

A

CTA (requires IV contrast)
+ result is a filling defect

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30
Q

when should you use caution in a CTA

A
  • pregnancy
  • metformin
  • allergy to dye
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31
Q

what are indications for VQ scans in PE patients

A
  • pregnancy
  • renal insufficiency
  • severe prior adverse rxn to contrast
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32
Q

what are the interpretations seen in PE for VQ scan

A
  • normal perfusion rules out PE
  • reduced perfusions with normal ventilation means PE is likely
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33
Q

what is the gold standard for PE diagnosis

A

pulmonary angiography

this is safe but INVASIVE requiring interventional radiology and contrast dye

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34
Q

what is a positive PE results in a pulmonary angiography

A

+ intraluminal filling defect

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35
Q

when is pulmonary angiography indicated

A

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

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36
Q

what are additional labs that may be ordered in PE suspicion and what would they show

A
  • CBC - leukocytosis
  • ABG - low PO2, respiratory alkalosis with hypocapnia.
  • Troponin and BNP - elevated in 25-50%, related to PE size causing RV myocardial stretch)
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37
Q

what are EKG abnormalities that may be seen in PEs

A
  • sinus tachycardia (MC)
  • non-specific ST seg and T-wave changes (MC)
  • S1Q3T3 (poor prognosis)
  • RV strain/R axis dev (poor prognosis)
  • new incomplete RBBB (Poor prognosis)
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38
Q

when is a chest radiograph used to assess PE

A

often ordered to rule out other etiologies in the workup

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39
Q

what nonspecific findings are common in chest radiograph?

A

nonspecific findings common:
- cardiomegaly
- basilar atelectasis
- infiltrate
- pleural effusion

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40
Q

what are the less common (<5%) findings in chest radiographs

A
  • westermarks sign
  • hamptons hump
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41
Q

what is westermarks sign

A

an area of lung oligemia - usually from complete lobar artery obstruction

(14% sensitivity, 92% specificity)

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42
Q

what is hamptoms hump?

A

dome-shaped dense opacification in the periphery of the lung - indicative of pulmonary infarction

(22% sensitivity, 82% specificity)

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43
Q

when are lower extremity venous dopplers used

A

to assess for evidence/location of DVT

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44
Q

what percent of paients with PE have a DVT evident on evaluation

A

70%

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45
Q

what is the risk stratification for high risk PE (massive)

A
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46
Q

what is the risk stratification for intermediate risk PE (sub-massive)

A
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47
Q

what is the risk stratification for low risk PE (less severe)

A
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48
Q

what is the intial management for PE

A
  • supplemental oxygen
  • ventilatory support
  • hemodynamic support

!!!avoid excessive IV fluids → increased risk of right sided heart failure!!!

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49
Q

what are the three primary forms of therapy for PE

A
  • anticoagulation
  • fibrinolysis
  • thrombectomy
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50
Q

how much will anticoagulation reduce mortality for PE

A

will reduce PE mortality rate to <5%

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51
Q

what medications could be used for anticoagulation management of PE

A
  • unfractionated heparin
  • low molecular weight heparin
  • Direct acting oral anticoadulants (DOACs)
  • fondaparinux
  • warfarin
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52
Q

what is the MOA of unfractionated heparin

A

Binds to and accelerates the activity of antithrombin, preventing additional thrombus formation

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53
Q

what monitoring is required when a patient is on unfractionated heparin

A

obtain aPTT every 6 hours during tx (goal of 60-80s)

54
Q

when is anticoagulation given in high risk patients

A

prior to imaging confirming diagnosis

55
Q

who is unfractionated heparin reserved for

A
  • unstable patients
  • severe renal insufficiency
56
Q

what is the dose for unfractionated heparin? (she said we DO need to know this)

A
  • 80 units/kg/dose IV x 1 followed by 18 units/kg/hour (max 2000u/hr)
57
Q

what is the risk associated with unrfactionated heparin and how do we reverse its effects

A
  • risk of hemorrhage
  • protamine sulfate reverses effects (indicated only for life threatening or intracranial bleed)
58
Q

what is the LMWH medication

A

enoxaparin (lovenox)

59
Q

who is LMWH preferred in

A

Preferred over other injectable agents in those who can not take oral anticoagulants

  • greater bioavailability, more predictable dose response, longer half life than UFH
60
Q

who must you monitor when giving LMWH

A

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

61
Q

what is the risk associated with LMWH and how do we reverse its effects

A
  • risk of hemorrhage
  • protamine sulfate reverses effects (indicated only for life threatening or intracranial bleed)
62
Q

what are the DOACs

A

factor Xa inhibitors:
- rivaroxaban(xarelto)
- apixaban (eliquis)

direct thrombin inhibitors:
- dabigatran (pradaxa)

63
Q

what is dosing for rivaroxaban (xarelto) and apixaban(eliquis)

A

Xarelto - BID then QD after 21 days
Eliquis - BID

64
Q

what is the reversal agent for Factor Xa inhibitors

A

AndexXa

used for life-threatening or uncontrolled bleeding

65
Q

what monitoring must be done for factor Xa inhibitors

A

No lab monitoring, few drug-drug or drug-food interactions

66
Q

what is the dosing for dabigatran (pradaxa)

A

BID

67
Q

what bridging is required with factor Xa inhibitors

A

NONE

68
Q

what bridging is required for direct thrombin inhibitors (dabigatran/pradaxa)

A
  • requires 5-10 days of bridging with UFH/LMWH
69
Q

what is the reversal agent for dabigatran (pradaxa)

A

praxbind

70
Q

what is fondaparinux (arixtra)

A

injectable factor Xa inhibitor that is once daily SQ dosing

71
Q

what is preferred anticoag if a patient has a hx of HIT

A

fondaparinux (arixtra)

otherwise its less preffered than LMWH

72
Q

what is warfarin

A

Vitamin K antagonist prevents activation of coagulation factors II, VII, IX, and X

73
Q

how long does it take for warfarin to reach full effects

A

5 days

74
Q

what is the bridging term for warfarin

A

requires bridging with LMWH until INR is 2-3

75
Q

what monitoring is required fro warfarin

A

Monitoring required: adjust to keep INR between 2-3

Often requires variable dosing regimens that changes frequently

76
Q

what is a down side of warafarin

A

interacts with other foods and drugs

77
Q

what medications are given for fibronolysis

A
  • tissue plasminogen activator (tPA) - Alteplase
78
Q

what is the indicaiton for tPA

A
  • high risk PE patients
  • intermediate risk PE with elevated trop or BNP or if they have persisiten hypoxemia with distress
79
Q

what are contraindications for tPA

A
  • intracranial disease
  • uncontrolled HTN >220/110 at presentation
  • recent major surgery or trauma (3 wks)
  • ischemic CVA in last 3 mo
  • metasatic cancer
80
Q

what is embolectomy

A

Manual removal of the emboli surgically or with a catheter

81
Q

what are indications for an embolectomy

A

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

82
Q

what benefit is seen with catheter-directed embolectomy procedures

A

locally injecting tPA at a lower dose decreasing bleeding risk

83
Q

what can be done to prevent PE

A
  • IVC filter with a goal to prevent PE recurrence
84
Q

what is the indication for an IVC filter

A
  • active bleeding that prevents anticoagulation (wWHAT)
  • recurrent VTE despite intensive anticoagulation
85
Q

what are indications for inpatient treatment in PE patients

A
  • severe illness or presence of comorbidities
  • assocaited DVT
  • educational needs (lack of knowledge about PE and management)
  • problematic social situations (prior noncompliance with follow up care)

OR ANYTHING IN THIS PICTURE

86
Q

what is the duration of anticoagulation with PE? what considerations go into this decision?

A

3-6 months minimum vs indefinite anticoagulation

  • provoked or unprovoked PE?
  • presence of risk factors for PE?
  • estimated risk of bleeding and recurrence?
  • patients preferences and values?
87
Q

if no obvious cause for venous thromboembolism is determined, what should be done

A

evaluate for any of the following and consult hematology
- antithrombin III deficiency
- protein C and S deficiency
- lupus anticoagulant
- homocystinuria
- occult neoplasm
- connective tissue disorders

88
Q

what type of system is the pulmonary circulation

A

low pressure, low resistance

(mean pulm arterial pressure shouls be 10-18mmHg)

this means its able to accommodate significant increase in blood flow during exercise

89
Q

seriously billie go watch this

A

https://www.youtube.com/watch?v=WVCOHGHWSG0

90
Q

what is the pathophysiology of pulmonary HTN

A

Pathophysiology: 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.

91
Q

what is pulmonary HTN (like the actual mPAP value)

A

mPAP>20 mmHg

92
Q

what is the WHO classification for group 1 pulm HTN

A
  • idiopathic PAH
  • hereditary PAH
  • drug induced PAH
  • connective tissue disease assocaited PAH
  • congenital heart disease assocaited PAH
  • HIV
93
Q

what is the WHO classification for group 2 pulm HTN

A
  • d/t left sided heart disease
  • risk factors for this type of PH include:
  • CAD
  • HTN
  • DM
    -high cholesterol ect.
94
Q

what is the WHO classification for group 3 pulm HTN

A
  • PH d/t lung disease or hypoxia
  • can be caused by advanced lung disease including:
  • COPD
  • interstitial lung diseases
  • OSA
95
Q

what is the WHO classification for group 4 pulm HTN

A
  • chronic thromboembolic pulmonary HTN is MCC of group 4 PH
96
Q

what is the WHO classification for group 5 pulm HTN

A

this is a miscellaneous group that includes causes of PH that are unclear or have multiple mechanisms such as sarcoidosis

97
Q

what are symptoms of pulmonary HTN

A
  • malaise/fatigue (MC)
  • dyspnea (MC, starts as exertional but then progresses to resting)
  • anginal pain
  • non productive cough
  • hemoptysis (rare, life threatening, results as PA rupture)
  • exertional syncope (severe cases where CO is affected)
98
Q

what are PE findings in Pulmonary HTN

A
  • odten normal in early disease
  • late disease presents w following:
  • JVD
  • accentuated P2
  • 3rd heart sound (kentucky)
  • tricuspid regurgitant murmur
  • hepatomegaly
  • lower extremity edema
  • cyanosis
99
Q

what does the 3rd “kentucky” heart sound result from in pulmonary HTN

A

dysfunctional right ventricular wall

100
Q

what are initial workup studies for PHTN

A
  • CXR/CT
  • EKG
  • 2D transthoracic echo w doppler
101
Q

what is seen on EKG for pulm HTN

A
  • signs of RVH maybe
102
Q

what is seen on a CXR/CT for pulm HTn

A
  • may be normal
  • enlargement of pul arteries
102
Q

what is the gold standard for diagnosing pulm HTN

A

right sided heart catheterization aka swan ganz catheter

102
Q

what mPAP pressure is diagnostic for PH

A

mPAP>20mHg

102
Q

What is seen on 2D transthoracic echocardiograms with doppler in pulm Hypertension

A

signs of PH such as:
- elevated estimated pulm artery systolic pressure
- triscuspid regurgitation
- RV enlargement
- wall thickness
- dysfunction

NORMAL ECHO DOES NOT RULE OUT PH

103
Q

what does pulmonary capillary wedge presure assess

A

left sided heart disease

  • 15 or less = no left sided heart disease
  • elevated PCWP usually indicates left sided heart disease and should be confirmed with a left heart cath
104
Q

what is vasodilator response

A

after injection of a vasodilator pressures are remeasured

drop of mPAP of 10-40 mmHg indicative of positive vasodilator response

105
Q
A
106
Q

what are diagnostics used to look for less common etiologies of pulmonary hypertension

A
  • CBC
  • CMP
  • Coags -pT, apTT
  • ABG
  • HIV testing
  • Hepatitis panel
  • Urine toxicology
107
Q

what are the collagen-vascular disease screening labs done in evaluation of pulmonary hypertension

A
  • antinuclear ab (ANA), rheumatoid factor (RF), antineutrophil cytoplasmic ab (ANCA),
  • Scleroderma: anti-Scl-70, anticentromere, and anti-U1-RNP antibodies
108
Q

what is the management for pulmonary hypertension

A
  • Exercise and pulmonary rehabilitation
  • Oxygen therapy - resting, exercise-induced, or nocturnal use
  • Age appropriate vaccinations
  • Smoking cessation (if applicable)
  • Maintain healthy body weight
  • Psychosocial support
  • Birth control (non-estrogen) - PAH is associated with increased maternal and fetal risks, including high risk of death.
109
Q

who do you refer patients with pulmonary hypertension to?

A
  • Pulmonology or specialist in PH management
  • Cardiology if WHO II
110
Q

how do you classify severity of pulmonary hypertension

A

New York Heart Association System (NYHA)

111
Q

what are the classes of the NYHA system

A
  • NYHA I: No symptoms, no limitation of activity
  • NYHA II: Slight limitation of activity. symptoms with ordinary activity
  • NYHA III: Marked limitation of activity. Symptoms with less than ordinary activity
  • NYHA IV: Unable to perform any activity without symptoms. Evidence of right heart failure. Dyspnea and fatigue at rest that worsens on exertion
  • NYHA Symptoms: dyspnea, fatigue, chest pain, or near syncope with exertion.
112
Q

what are the 2 main steps of management for pulm hypertension

A
  1. treat any underlying condition
    - WHOII - treat left sided HF
    - WHOIII - treat lung disease/hypoxia
  2. is there vasoreactive disease?
    - yes = CCB used for NYHA class I-III (high dose diltiazem and nifedipine MC)
    - no = Based upon NYHA Classification, Only WHO PH classifications 1 and 4 have FDA approved pharmacotherapeutics for PH
113
Q

what are the endothelin receptor antagonists

A
  • oral - “entan’s”
  • ambrisentan, bosentan, macitentan
114
Q

what are the MOA of endothelin receptor antagonists

A
  • MOA: reduces endothelin release leading to vasodilation
  • Endothelin is produced in the cells that line the heart and lungs; when released results in vasoconstriction
115
Q

what are the phosphodiesterase 5 inhibitors

A
  • sidenafil
  • tadalafil
116
Q

what is the MOA of phosphodiesterase 5 inhibitors

A
  • MOA: inhibition of PDE5 leads to vasodilation
  • PDE5 is abundantly expressed in the lungs and causes vasoconstriction
117
Q

what are the soluble guanylate cyclase stimulators

A
  • riociguat (PO)
118
Q

what is the goal of soluble guanylate cyclase stimulator therapy

A

Goal with this therapy is to improve exercise ability and NYHA functional class

119
Q

what is the MOA soluble guanylate cyclase stimulator

A
  • MOA: stimulates the activity of guanylate cyclase
  • Guanylate cyclase produces cyclic guanosine monophosphate (cyclic GMP) in the lungs as a response to nitric oxide. Cyclic GMP causes the arteries to relax and widen (vasodilation).
120
Q

What are the prostanoid agents

A
  • epoprostenol (continuous IV pump)
  • treprostinil (PO, inhaled, IV)
  • iloprost (inahled)
121
Q

what is the MOA of prostanoid agents

A

MOA: potent pulmonary vasodilation by acting on prostaglandin receptors with an additional benefit of inhibiting platelet aggregation

122
Q

what are the prostacyclin receptor agonists

A
  • selexipag (IV and PO, IV only short term)
123
Q

What is the MOA of prostacyclin receptor agonsits

A
  • MOA: attaches to and activates prostacyclin receptors in the lung resulting in vasodilation
  • More selective for the prostacyclin receptor than the prostanoid agents.
124
Q

what is the management for non-vasoreactive NYHA stage I pulmonary HTN

A

consider monotherapy

125
Q

what is the management for non-vasoreactive NYHA stage II/III pulmonary HTN

A
  • Combination therapy
  • Endothelin antagonists and PDE5 inhibitors is often used initially
  • Add on guanylate cyclase stimulators or oral prostacyclin receptor agonists if uncontrolled
126
Q

what is the management for non-vasoreactive NYHA stage IV pulmonary HTN

A

Add on parenteral prostanoid to oral combination therapy

127
Q

what is additional management for pulmonary hypertension

A
  • Long-term anticoagulant therapy indicated for WHO Group 4 (some WHO 1) - warfarin, dabigatran, rivaroxaban, apixaban
  • Thromboendarterectomy is recommended if no response to pharmacologic therapies in WHO Group 4
  • Diuretics for symptomatic right sided heart failure
  • Lung transplant reserved for those unresponsive to medical management (double preferred but single can be effective)
128
Q

Another lecture down! doggo pic flip!

A

Clin Med B 2 (44 decks)

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