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Clin Med IIB Pulmonology > Pulmonary Circulation Disorders > Flashcards

Pulmonary Circulation Disorders Flashcards

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1
Q

What is the MC PE? What are some other causes?

A

Thrombus that starts in the venous system, gets lodged into the pulmonary system

Air embolus
Amniotic fluid (during delivery, travels through the placenta, into the circulation of the female)
Fat
Foreign bodies (talc in injection from IV users, cemement from surgery)
Parasite eggs (schistosomiasis, not in the US)
Septic emboli (IV drug users w/ infective endocarditis)
Tumor cells (kidney specifically)

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2
Q

How does fat lead to PE?

A

long bone fractures (disruption in vascular supply, and fat inside the fat that gets sucked up into the system)

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3
Q

What is the overview of the pathophys of PE?

A
  1. Infarction (Most often occurs when small emboli lodge distally where there is little collateral blood flow)
  2. Impaired gas exchange
  3. Cardiovascular compromise
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4
Q

What does surfactant do?

A

Dawn dish soap (allows alveoli to open and close easily)

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5
Q

Explain how PE leads to impaired gas exchange

A

Altered ventilation to perfusion ratio
Inflammation → Surfactant dysfunction → Atelectasis → Functional intrapulmonary shunting
Stimulation of the respiratory drive → hypocapnia and respiratory alkalosis

all because of lack of CO2 O2 exchange

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6
Q

Explain the cardiovascular compromise of PE

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

this is what kills them

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7
Q

What is virchow’s triad?

A

Venous stasis
Injury to vessel
hyper-coagulability

risk factors for PE

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8
Q

What are the risk factors for Venous Stasis?

A

Immobility
obesity, stroke, bed rest, post-op
Hyperviscosity (polycythemia, increased in RBC makes it thicker)
Increased central venous pressures
low cardiac output states, pregnancy

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9
Q

What does pregnancy lead to venous stasis?

A

Baby get big and then when you sit flat, it pushes pressure in the IVC and then this coagulates to the lower extremity

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10
Q

What can cause injury to vessel wall?

A

Prior episodes of thrombosis (makes it more likely to clot), orthopedic surgery, or trauma

anything that disrupts normal blood vessel anatomy

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11
Q

What medications can lead to hypercoagubility?

A

Oral contraceptives, estrogen and testosterone

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12
Q

What disease makes someone more likely to have a blood clot?

A

malignancy, surgery

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13
Q

What is the MC gene defect that causes hypercoagubility?

A

Factor V Leiden

can also be other problems

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14
Q

What are the MC symptoms of PE

A

Tachypnea (increased RR) is most reliable exam finding (70%), Pleuritic Chest pain (hurts more when you take a breath), dyspnea, cough

tachpnea, crackles, and tachycardia are most important physical exam finding

often preceded by a DVT

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15
Q

What is the wells criteria for PE and if it does not meet it, what do you use?

A

If greater then 6, straight to D dimer

PERC, if they have ANY then you do a d-dimer

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16
Q

What is a d-dimer and what is normal?

A

a protein fragment from a broken down blood clot

<50 is normal

if >50 years old, then

10 x their age (70 yo x 10 = 700)

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17
Q

what are the false positives of d-dimer?

A

age >50 years (should adjust by calculating 50x10), recent surgery or trauma, acute illness, pregnancy or postpartum state, rheumatologic disease, renal dysfunction and sickle cell disease

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18
Q

What is the first-line imaging modality?

A

CTA

CT angiography which only show pulmonary vessels and you see filling defect (you see it turn from white to grey = grey spot is filling defect)

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19
Q

What are the caution of CTA for PE

A

Pregnancy
Metformin (med is hard on the kidneys and the contrast is also hard on kidneys. Should withhold use for 48 hours).
Allergy to contrast dye (promedicate with methyoprolcin)

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20
Q

What do you see in V/Q scan of PE?

A

Good ventilation and poor profusion
indicated for those who are CI for CTA

Good profusion rules it out

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21
Q

What is the gold standard of PE?

A

Pulmonary angiography, but not first line because it is invasive

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

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22
Q

What do you see in CBC of PE and why?

A

CBC: shows leukocytosis (because the marginal pool WBCs detach thinking they can help)

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23
Q

What does ABG show for PE?

A

Normal or low

respiratory alkalosis with hypocapnia (results from hyperventilation)

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24
Q

What does troponin and BNP show in PE?

A

elevated in up to 25-50% of patients
related to size of PE causing acute right ventricular myocardial stretch

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25
What EKG finding is classic of PE?
S1Q3T3 specifically S wave on lead 1 Q wave and inverted T waves in lead 3 New RBBB
26
What does the CXR show in PE?
Normal typically, but can also see Westermark's sign (an area of lung oligemia - usually from complete lobar artery obstruction) Hampton’s hump (dome-shaped dense opacification in the periphery of the lung - indicative of pulmonary infarction)
27
When do you order a venous doppler of lower extremity for sus PE?
Always even if no DVT s/s
28
What is intermediate risk PE (submassive)?
Hemodynamic stability with signs of R sided heart strain/dysfunction via CTA, echo, elevated troponin or BNP.
29
What is Low risk PE?
Normotension without signs of right ventricular dysfunction
30
What is high risk PE?
Hemodynamic instability (any of the following) hypotension (SBP < 90 mmHg for > 15 minutes) drop in SBP > 40 mmHg below baseline hypotension requiring vasopressors causing a cardiac arrest
31
What is the initial management of PE?
supplemental oxygen ventilatory support hemodynamic support avoid excessive IV fluids → increased risk of right sided heart failure
32
What are the 3 forms of therapy for PE?
Anticoagulation - mainstay Fibrinolysis Thrombectomy
33
Who gets unfractionated heparin?
unstable patients, severe renal insufficiency
34
What is the management of unfractionated heparin?
Binds to and accelerates the activity of antithrombin, preventing additional thrombus formation 80 units/kg/dose IV x 1 (or 5000 U) followed by 18 units/kg/hour (max 2000 u/hr)¹ Monitoring required: obtain aPTT every 6 hours during tx; goal of 60-80 seconds In high risk patients, anticoagulation may be give before imaging confirms dx Reserved for unstable patients, severe renal insufficiency Risk of hemorrhage
35
What is protamine sulfate indiacted?
reverses effects of heparin Indicated for life-threatening or intracranial hemorrhage
36
What is LMWH used for?
Preferred over other injectable agents in those who can not take oral anticoagulants
37
What are DOACs?
rivaroxaban Xarelto Eliquis AndexXa is the reversal
38
What is tissue plasminogen activator (tPA) used for?
High risk PE patients used for fibronlyisis it is used first for high risk PE patients or Intermediate risk PE with elevated troponin or BNP, or persistent hypoxemia with distress
39
What are the CI of fibronlysis?
intracranial disease (active tumor or hx of bleed), uncontrolled HTN (>220/110) at presentation, recent major surgery or trauma (past 3 weeks), ischemic CVA in last 3 months, and metastatic cancer
40
What is an embolectomy and when is it used for PE?
Manual removal of the emboli surgically or with a catheter Indications Hemodynamically unstable patients with a contraindication or failure to respond to tPA Catheter-directed procedure offers the benefit of locally injecting tPA at a lower dose decreasing bleeding risk
41
When is an IVC filter considered?
recurrent VTE despite intensive anticoagulation blood can get through because of the slats (looks like a head scratcher) but nothing large enough like a DVT
42
What are the indications for PE inpatient management?
Age > 80 Hx of CA Hx of chronic cardiopulmonary dz HR ≥ 110 SBP <110 O2 Sat <90% Severe illness or presence of comorbidities Associated DVT Educational needs (eg, lack of knowledge about PE and its management) Problematic social situations (eg, prior noncompliance with follow-up care)
43
How long is a patient on anticoagulants?
At least 3-6 months Einstein choice study - longer you are on AC, the more likely you will not have embolus consider the risk of the patient provoked or unprovoked presence of risk factors (eg, transient or persistent) estimated risk of bleeding and recurrence intensity and duration of the anticoagulation; concomitant administration of medications, such as aspirin, increased age, previous GI hemorrhage, and coexistent CKD patient preferences and values (eg, occupation, life expectancy, burden of therapy)
44
After having a confirmed blood clot
Antithrombin III deficiency Protein C and protein S deficiency Lupus anticoagulant Homocystinuria Occult neoplasm Connective tissue disorders
45
What is the pressure in the pulmonary circulation? What is the advantage of this?
VERY LOW 10-18 is normal - the pressure can go up much higher in the lungs during exercise
46
What is the physiology of pulmonary HTN?
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.
47
What is the definition of pulmonary HTN?
By definition (mPAP) >20 mmHg
48
What is group 1-5 cause of HTN?
1. Idiopathic 2. Left heart disease 3. Lung disease 4. Chronic thromboembolic 5. Catch all
49
What is the clinical presentation of pulmonary HTN and the two MC symptoms?
Malaise/fatigue MC dyspnea MD Anginal pain Nonproductive cough Hemoptysis Exertional syncope
49
What is the physical exam finding of PE?
Normal until progression, then abnormal heart sounds hepatomegaly LE edema Cyanosis if an open PFO leading to R-->L shunt (sending hypoxic blood into the left atria because it is lower pressure)
50
What are the extra heart sounds of pulmonary HTN
Accentuated P2 (louder dub) S3 = compliant ventricle Tricuspid regurg
51
What do you see in CXR of pulmonary HTN?
normal or enlargement of the pulmonary arteries may be found incidentally
52
What is the EKG of pulmonary HTN?
Signs of RVH may be seen
53
What do you see in the TTE with doppler of pulmonary HTN?
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 rule out PH
54
what is the gold standard of diagnosing plmonary HTN?
Right-sided heart catheterization (aka Swan-Ganz catheter)
55
What do we look for in Right-sided heart catheterization (aka Swan-Ganz catheter)?
mPAP ≥ 20 mmHg diagnostic for PH then measure Pulmonary capillary wedge pressure (PCWP) assesses left sided heart disease ≤15 mm Hg = no left sided heart (if elevated then there might be left-sided dysfunction)
56
After getting a Right-sided heart catheterization (aka Swan-Ganz catheter) what do you order?
Order a vasodilator response After injection of a vasodilator, pressures are remeasured Drop of mPAP of 10-40 mmHg indicative of positive acute vasodilator response rare to respond
57
What is the management of pulmonary HTN?
left-sided r/o with 2D echo then COPD (cxr and pft) and OSA (sleep study), ILD cxr,
58
What are the
CBC CMP Coags -pT, apTT ABG HIV testing Hepatitis panel Urine toxicology Collagen-vascular disease screening
59
If you are diagnosed with pulmonary hypertension?
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) because pulmonary HTN is associated with increased maternal and fetal risks, including high risk of death. Pulmonology or specialist in PH management Cardiology if WHO II
60
What is the New York Heart Assocation Sused for and what are the stages?
Severity 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
61
What symptoms does the New York Heart association use?
NYHA Symptoms: dyspnea, fatigue, chest pain, or near syncope with exertion.
62
What are the steps of management for pulmonary HTN?
Step 1 : Treat any underlying condition Step 2: Is there vasoreactive disease?
63
What are the endothelin receptor antagoists?
the entans MOA: reduces endothelin release leading to vasodilation Endothelin is produced in the cells that line the heart and lungs; when released results in vasoconstriction¹
64
What are the phosphodiesterase 5 inhibitors?
the -afil MOA: inhibition of PDE5 leads to vasodilation PDE5 is abundantly expressed in the lungs and causes vasoconstriction they are also used for
65
What is soluble guanylate cyclase stimulators?
riociguat Goal with this therapy is to improve exercise ability and NYHA functional class MOA: stimulates the activity of guanylate cyclase
66
What are the prostanoid agents?
The prosts epoprostenol (Flolan) - continuous IV pump treprostinil - 3 delivery methods iloprost MOA: potent pulmonary vasodilation by acting on prostaglandin receptors with an additional benefit of inhibiting platelet aggregation
67
What are the prostacycin receptor agonists?
Selexipag MOA: attaches to and activates prostacyclin receptors in the lung resulting in vasodilation More selective for the prostacyclin receptor than the prostanoid agents. only PO unless they cannot take oral
68
What nnon-vasoreactive drugs do you use based on your NYHA category?
NYHA I Consider monotherapy NYHA II/III Combination therapy Endothelin antagonists and PDE5 inhibitors is often used initially Add on guanylate cyclase stimulators or oral prostacyclin receptor agonists if uncontrolled NYHA IV Add on parenteral prostanoid to oral combination therapy

Clin Med IIB Pulmonology (12 decks)

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