Pulmonary Circulation Disorders - Exam 2 Flashcards

1
Q

What is the MC source of PEs? What do fat PEs arise from? What do septic emboli arise from?

A

thrombus arising from the deep veins of the lower extremities

long bone fractures

acute infective endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

_______ occurs most often when small emboli lodge distally where there is a little collateral blood flow

A

infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 pathophysiological response from pulmonary vascular obstruction?

A

infarction

impaired gas exchange leading to hypoxia

cardiovascular compromise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does impaired gas exchange leading to hypoxia lead to?

A

altered ventilation to perfusion ratio

Inflammation → Surfactant dysfunction → Atelectasis → Functional intrapulmonary shunting

Stimulation of the respiratory drive → hypocapnia and respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathophys behind cardiovascular compromise?

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

**What is Virchow’s triangle? What does it increase your risk for?

A

venous stasis

injury to the vessel wall

hypercoagulability

increased risk for PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the risk factors for venous stasis?

A

immobility

hyperviscosity

increased central venous pressures (low cardiac output states and pregnancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the risk factors for hypercoagulability?

A

medications

disease: malignancy or surgery

inherited gene defects: factor V leiden, protein C, S and antithrombin deficiency, prothrombin gene mutation, hyperhomocysteinemia, antiphospholipid antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the MC inherited gene defect that leads to hypercoagulability?

A

Factor V leiden

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the MC s/s of PE? What does significant pain indicate? _____ is the most reliable physical exam finding

A

dyspnea, pleuritic chest pain, cough

small PEs that result in infarction

tachypnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are s/s of DVT?

A

Lower leg pain or “charley horse” in the calf
Associated symptoms DVT: swelling, warmth and/or erythema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the scale of Wells criteria for PE tell you? **What are the ranges of the scale?

A

determines the pre-test probability of the s/s being a PE

Determine “pre-test” probability
>6 points = high risk (78.4%)
2–6 points = moderate risk (27.8%)
<2 points = low risk (3.4%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When are the PERC rules used? What are the PERC rules? **What does it stand for?

A

PERC rules are only used if Well’s risk is low risk

PERC Rules (Pulmonary Embolism Rule-Out Criteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do you do if the pt is low risk and no PERC rules criteria are met?

A

no testing is needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do you do if the pt is low risk and there is at least 1 positive PERC rule?

A

move on to plasma D-dimer

Normal → no imaging
Elevated d-dimer → imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do you do if the pt is intermediate risk?

A

D- dimer

Normal → no imaging
Elevated d-dimer → imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do you do if the pt is high risk?

A

Imaging (no D-dimer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does a positive D-dimer indicate? What is normal?

A

A protein fragment from a broken down blood clot

normal is less than 500 ng/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

**What is the equation for age adjusted d-dimer? What age do you need to adjust?

A

Adults over age 50 use an age-adjusted threshold (age × 10 ng/mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T/F: All elevated d-dimer are diagnostic for a PE/DVT

A

False!!! there are lots of false positive aka non-PE reasons why the d-dimer would be elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some reasons why the d-dimer would be elevated?

A

age >50 years, recent surgery or trauma, acute illness, PREGNANCY or postpartum state, rheumatologic disease, renal dysfunction and sickle cell disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the first line imaging modality in PE? Does it require contrast? What will the radiologist report find?

A

CTA

YES! requires IV contrast (need to order BUN/Cr before)

**positive filling defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the cautions for a CTA?

A

pregnancy, metformin and allergy to contrast dye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the preferred imaging of choice for PE when a pt is pregnant? Name some additional indications.

A

V/Q scan

pregnancy, renal insufficiency or adverse reaction to contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

When a PE is present, what will the V/Q results say?

A

PE is likely when there is reduced perfusion with normal ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

** _____ is the gold standard for diagnosing PE. When is it indicate?

A

pulmonary angiography

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

____ and ____ are elevated in up to 25-50% of patients. What are they related to?

A

troponin and BNP

related to size of PE causing acute right ventricular myocardial stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

**What are the MC EKG findings associated with PE?

A

sinus tachycardia

non-specific ST segment and T-wave changes affecting R precordial leads V1-3 +/- V4

S1Q3T3 pattern +/- new incomplete RBBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

**What are 2 rare CXR findings that are associated with PEs?

A

westermark’s sign and hampton’s hump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

**______ is an area of lung oligemia, usually from complete lobar artery obstruction

A

Westermark’s sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

**______ is a dome-shaped dense opacification in the periphery of the lung - indicative of pulmonary infarction

A

Hampton’s hump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Why is a lower extremity venous doppler ordered?

A

to look for evidence of DVT and helps to determine the etiology of the PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What qualifies as a high risk PE?

A

hypotension (SBP < 90 mmHg for > 15 minutes)

drop in SBP > 40 mmHg below baseline

hypotension requiring vasopressors

causing a cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What qualifies as an intermediate risk PE?

A

Hemodynamic stability with signs of R sided heart strain/dysfunction via CTA, echo, elevated troponin or BNP.

aka right heart strain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What qualifies as a low-risk PE?

A

Normotension without signs of right ventricular dysfunction

aka no signs of right heart strain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the initial management of PE in ALL patients? What do you need to avoid?

A

supplemental oxygen
ventilatory support
hemodynamic support

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

37
Q

What are the 3 primary forms of therapy in a PE?

A

Anticoagulation - mainstay
Fibrinolysis
Thrombectomy

38
Q

What is the MOA of unfractionated heparin?

A

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

39
Q

**What is the UFH dosing?

A

80 units/kg/dose IV bolus x 1 (or 5000 U) followed by 18 units/kg/hour (max 2000 u/hr)

40
Q

What is the monitoring requirements for UFH?

A

Monitoring required: obtain aPTT at baseline and every 6 hours during tx with a goal of 60-80 seconds, signs of bleeding, H/H, plt

41
Q

**When is UFH used? Who is it reserved for?

A

in high risk patients! anticoag may be given before imaging confirms dx

Reserved for unstable patients, severe renal insufficiency

42
Q

**What is the reversal agent for UFH? What is a normal aPTT?

A

Protamine sulfate

normal aPTT 25-30 seconds

43
Q

**What is the dosing for LMWH? When is LMWH preferred?

A

enoxaparin (Lovenox) 1 mg/kg SC q12h

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

44
Q

When do you need to monitor LMWH?

A

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

45
Q

**What is the reversal agent for LMWH?

A

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

46
Q

What are the 3 factor Xa inhibitors? What are the dosing for each? Which requires bridging with heparin?

A

rivaroxaban (Xarelto), apixaban (Eliquis), edoxaban (Savaysa)

xarelto starts at BID dosing then decreases to QD

apixaban and edoxaban are BID dosing

savaysa requires bridging therapy with LMWH or UFH

47
Q

What is the reversal agent for factor Xa inhibitors?

A

andexxa

48
Q

_____ is the direct thrombin inhibitor. Does it require UFH/LMWH bridging? What is the reversal agent?

A

dabigaran (pradaxa)- BID dosing

Requires 5-10 days of bridging with UFH/LMWH

Praxbind

49
Q

_____ is the only injectable factor Xa inhibitor. What is the dosing?

A

fondaparinux (Arixtra)

once daily, subq dosing

50
Q

____ is a Vitamin K antagonist prevents activation of coagulation factors II, VII, IX, and X. How long does it take to reach its full effect? What is the ideal INR?

A

Warfarin

5 days to reach full effect

requires bridging with LMWH until INR is 2-3

51
Q

_____ is used in high risk PE patients. How is it given to pts?

A

Tissue Plasminogen Activator (tPA) - Alteplase

100 mg IV infused over 2 hours

52
Q

**What are the CI to tPA?

A

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

metastatic cancer

53
Q

When is embolectomy used in PE management? What is commonly injected during the procedure?

A

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

54
Q

_____ is used to prevent PE recurrence and is indicated in active bleeding that prevents anticoag and/or recurrent VTE despite intensive anticoag

A

IVC filter

55
Q

Where is an IVC filter placed?

A

below the renal arteries in the inferior VC

56
Q

What are the indications for inpt PE treatment?

A

Severe illness or presence risk factors

Associated DVT

Educational needs (eg, lack of knowledge about PE and its management)

Problematic social situations (eg, prior noncompliance with follow-up care)

57
Q

What are the risk factors that indicate admission for PE?

A
58
Q

What is the longterm management for PE? What is the minimum?

A

anticoag therapy for a minimum for 3-6 months but can be indefinite

59
Q

What do you need to do if there is no obvious cause of VTE is identified?

A

consult hematology

60
Q

What is the normal mean pulmonary arterial pressure?

A

10-18mmHg

systolic pressure around 25mmHg

diastolic pressure around 10mmHg

61
Q

What is the pathophys behind pulmonary hypertension? What is the mPap?

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.

Pulmonary hypertension is defined by (mPAP) >20 mmHg

62
Q

according to WHO, what are the 5 classifications of pulmonary hypertension?

A

group 1: idiopathic, hereditary, drug induced, connective tissue disease, congenital heart, HIV

group 2: LEFT sided heart disease

group 3: chronic hypoxia

group 4: chronic PE

group 5: catch all

63
Q

What are the 3 MC symptoms of pulmonary hypertension?

A

malaise, fatigue and dyspnea

64
Q

What does hemoptysis indicate in pulmonary hypertension?

A

rare - life threatening - results from rupture of pulmonary artery

65
Q

What will late disease pulmonary hypertension present like? What additional heart sounds may be heard?

A

right sided heart failure

Accentuated P2¹ (pulmonic valve closure)
3rd heart sound (“Kentucky”)
tricuspid regurg murmur

66
Q

What does cyanosis in pulmonary hypertension indicate?

A

consider open patent foramen ovale

67
Q

What will the EKG of a pt with pulmonary hypertension show? What will TTE with doppler show?

A

signs of RVH

Elevated estimated pulmonary artery systolic pressure (ePASP)
Tricuspid regurgitation, RV enlargement, wall thickness or dysfunction may be seen

68
Q

**What is the gold standard dx test for pulmonary hypertension? What will it show?

A

Right-sided heart catheterization (aka Swan-Ganz catheter)

mPAP ≥ 20 mmHg diagnostic for PH

69
Q

What does a pulmonary capillary wedge pressure assess? What happens if it is increased?

A

LEFT sided heart disease

≤15 mm Hg = no left sided heart disease

Elevated PCWP usually indicates left sided heart disease and should be confirmed with a left heart cath

70
Q

What is the vasodilator response?

A

After injection of a vasodilator, pressures are remeasured

Drop of mPAP of 10-40 mmHg indicative of positive acute vasodilator response

71
Q

What is the diagnostic approach to pulmonary hypertension?

A
72
Q

What are some general management measures for pulmonary hypertension?

A
73
Q

What are the New York Heart Association system for classifying pulmonary hypertension?

A
74
Q

What are the NYHA symptoms for pulmonary hypertension?

A

NYHA Symptoms: dyspnea, fatigue, chest pain, or near syncope with exertion.

75
Q

What is the step wise treatment for pulmonary hypertension?

A
76
Q

When are CCB used in pulmonary hypertension? Which ones specifically?

A

NYHA class I-III

High dose diltiazem and nifedipine most commonly used

77
Q

What is the MOA for endothelin receptor antagonist?

A

reduces endothelin release leading to vasodilation

aka decrease in endothelin leads to decrease in vasorestriction so more dilation

78
Q

ambrisentan (Volibris)
bosentan (Tracleer)
macitentan(Opsumit)

What drug class?

A

Endothelin receptor antagonists

79
Q

What is the MOA for PDE5 inhibitors? What are the 2 medications in this class?

A

inhibition of PDE5 leads to vasodilation

sildenafil (Viagra, Revatio)
tadalafil (Cialis, Adcirca)

80
Q

What is the MOA of Soluble guanylate cyclase stimulators? What is the drug in this class?

A

stimulates the activity of guanylate cyclase which increases CAMP in the lungs as a response to nitric oxide, which causes the arteries to vasodilate

riociguat (Adempas) -> only available PO

81
Q

What is the MOA of prostanoid agents?

A

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

82
Q

epoprostenol (Flolan)
treprostinil
iloprost

What drug class?

A

prostanoid agents

83
Q

What is the MOA of prostacyclin receptor agonists? what form?

A

attaches to and activates prostacyclin receptors in the lung resulting in vasodilation

available IV and PO: IV only for short term if unable to take PO

84
Q

Prostacyclin receptor agonists are more selective for the _____ than the ______

A

prostacyclin receptor

prostanoid agents

85
Q

What is the tx of pulmonary hypertension based on the NYHA categories?

A
86
Q

What is the additional management for pulmonary hypertension?

A
87
Q

**What are the 2 MC EKG abnormalities on the MAJORITIES of PE’s?

A

sinus tachycardia

non-specific ST segment and T wave changes affecting R precordial leads V1-3 +/- V4

88
Q
A