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Advanced Diagnostics > Pulmonary Embolism > Flashcards

Pulmonary Embolism Flashcards

1
Q

Pulmonary embolism

A

An obstruction of the pulmonary artery or one of its branches, caused by material (thrombus, tumor, air, or fat) which traveled from another location of the body.

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2
Q

Virchow’s Triad

A
  • Hypercoagulability (cancer, thrombophilia, inflammatory disease).
  • Vessel wall injury (surgery, chemical irritation, inflammation)
  • Stasis of blood
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3
Q

Risk Factors

A
  • pregnancy
  • malignancy
  • central venous catheter
  • surgery
  • trauma
  • heart failure
  • immobilization
  • oral contraceptives
  • hormone therapy
  • congenital heart disease
  • severe liver disease
  • IBD
  • Inherited thrombophilia (factor V, antithrombin deficiency)
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4
Q

Location of embolism

A
  • Saddle (inner)
  • Lobar
  • Segmental
  • subsegmental
  • moving distally
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5
Q

Clinical presentation of PE

A
  • Dyspnea on exertion or at rest
  • pleuritic chest pain
  • calf or thigh pain/swelling
  • orthopnea
  • hemoptysis
  • wheezing
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6
Q

Signs of PE

A
  • Tachypnea(54%)
  • Edema, erythema, tenderness or a palpable cord in the calf or thigh(47%)
  • Tachycardia(24%)
  • Rales(18%)
  • Decreased breath sounds(17%)
  • Accentuated P2(15%)
  • Jugular venous distention(14%)
  • Fever
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7
Q

Lab tests

A
  • CBC: can have leukocytosis
  • ESR: elevated
  • LDH: elevated
  • AST: elevated
  • Metabolic Panel: evaluate renal function to determine ability to give contrast
  • Troponin, BNP or NT-proBNP: used for risk stratification
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8
Q

EKG

A
  • Sinus tachycardia
  • Nonspecific ST segment and T-wave changes
  • Atrial arrhythmias
  • New right bundle branch block
  • S1Q3T3
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9
Q

Chest Xray with PE

A
  • Usually non-specific findings
  • -cardiomegaly
  • -pleural effusion
  • -elevated hemidiaphragm
  • -pulmonary artery enlargement
  • -atelectasis
  • Can also be normal in up to 22% of patients
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10
Q

Chest CT

A
  • Gold standard in diagnosing PE
  • CT angiogram with contrast to visualize pulmonary arteries and assess for filling defect
  • Contrast contraindicated in renal impairment (CrCl <30)
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11
Q

Ventilation perfusion scan

A
  • Need to have “normal” chest Xray, otherwise may have false positive
  • Most are read as “indeterminate”
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12
Q

Assessing RV

A
  • Evaluation of right ventricular (RV) function is an important tool for risk assessment
  • Screening can occur with either echocardiogram or prognostic biomarkers (troponin, BNP,) even if the PESI score is low
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13
Q

Initial treatment

A
  • hemodynamic stability
  • Supple O2
  • IV fluids or vasopressors
  • if diagnostic testing is delayed empiric anticoagulation is often initiated
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14
Q

Is anticoagulation appropriate?

A
  • Determine pts bleeding risk
  • absolute contraindications: hemorrhagic stroke, recent surgery, intracranial/spinal cord tumors, active bleeding
  • Alternative tx: IVC filter or embolectomy
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15
Q

Thrombolytics

A

-TNKase (tenecteplase) and Retavase (reteplase)
=Reserved for hemodynamically unstable patients
-RV strain without hypotension is not an indication for thrombolytics
-“Possible” indications:
Presence of severe hypoxemia, Extensive clot burden, Free floating intracardiac clot

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16
Q

Contraindications for lytics: Absolute/major

A

Intracranial neoplasm or lesion

  • Recent intracranial or spinal surgery/trauma (<2 months)
  • History of hemorrhagic stroke
  • Active bleeding
  • Nonhemorrhagic stroke within last 3 months
  • -Suspected aortic dissection
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17
Q

Relative contraindications for lytics

A

-Uncontrolled hypertension (SBP> 200, DBP >110)
-Nonhemorrhagic stroke >3 months
-Surgery within the past 3 weeks
-Pregnancy
>75 years old
-Current anticoagulation use

18
Q

Alternative tx: These are considered if thrombolytics are contraindicated or has failed

A
  • Catheter directed thrombolysis

- Surgical embolectomy

19
Q

Catheter directed thromboylysis

A
  • Thrombolytics delivered directly to pulmonary arteries
  • Usually reserved for patients who remain unstable after systemic thrombolytics
  • Benefit: utilizes lower dose of lytic which reduces risk of bleeding
20
Q

Initial anticoagulation

A
  • DOAC (apixaban and rivaroxaban can be used on day 1 of treatment, edoxaban and dabigatran requires 5-10 days pf bridging)
  • LMWH
  • UFH
21
Q

Unfractionated Heparin

A
  • Mechanism of Action: Binds to antithrombin, resulting in structural change and increase ability to inactivate factor Xa and thrombin
  • Half life ½- 2 hours
  • Can be used in pregnancy and renal impairment
  • Reversal: Protamine
22
Q

Low Molecular Weight Heparin (Lovenox)

A
  • Same mechanism of action as UFH
  • Contraindicated if creatinine clearance is <30 mL/min
  • Half life approx 12 hours
  • Reversal: Protamine
23
Q

Heparin Induced Thrombocytopenia

A

-Defined as platelet count falling by ≥50%
-4 T’s Criteria (MD Calc)
-Must be confirmed by heparin antibody assay (PF4), if confirmed, list heparin as allergy
-Alternative anticoagulants should be utilized:
Argatroban, bivalrudin, fondaparinux
-If HIT is confirmed, once platelet counts have recovered (typically >50k), can initiate warfarin as there is increased risk of clotting with HIT

24
Q

DOAC

A
  • Rivaroxaban, apixaban, edoxaban, dabigatran
  • Currently no generic in the US
  • All DOACs have overall lower all cause mortality related to bleeding when compared to warfarin
  • Apixaban and low dose edoxaban have lower GI bleeding rates compared to warfarin
25
Q

DOAC MOA

A
  • Oral direct factor Xa inhibitors include apixaban, rivaroxaban, and edoxaban and they work by preventing factor Xa from attaching prothrombin to thrombin.
  • Oral direct thrombin inhibitors (dabigatran) works by preventing thrombin from attaching fibrinogen to fibrin
26
Q

Pros to DOACS

A
  • No dietary restrictions
  • No monitoring
  • Does not require bridging (apixaban and rivaroxaban)
  • Fewer drug-drug interactions
  • Lower rates of bleeding when compared to warfarin
27
Q

Cons to DOACS

A
  • Unclear dosing with obesity
  • Reversal not readily available at smaller institutions
  • Limited research in severe renal impairment
  • Some require twice daily dosing
  • Cost
28
Q

DOAC drug-drug interactions: Increases DOAC blood levels

A

-Clarithromycin/erythromycin
-Verapamil/diltiazem
-Amiodarone
Fluconazole/ketoconazole/itraconazole
-Cyclosporine/tacrolimus

29
Q

DOAC drug-drug interactions: Decreases DOAC blood levels

A
  • Aniepileptics (Phenytoin, Phenobarbital, Carbamazepine)
  • Rifampin
  • St. John’s Wart
30
Q

DOAC reversals: Dabigatran (Pradaxa)

A

-Idarucizumab (Praxbind); initial dose: 5 grams

31
Q

DOAC Reversals: Apixaban (Elliquis), Betrixaban (Bevyxxa), Edoxaban (Lixiana, Savaysa), Rivaroxaban (Xarelto)

A

-Andexanet alfa (AndexXa) if available: initial dose depends on the dose of the factor Xa inhibitors and the interval since the last dose
OR
-4-factor PCC (Kcentra, Octapiex) if andexanet alfa is not available; initial dose 50 units per kg

32
Q

Warfarin

A
  • Mechanism of action: Blocks the conversion of inactive vitamin K to its active form within the liver resulting in non-functioning clotting factors
  • Active clotting factors need to be depleted before fully anticoagulated
  • Full therapeutic affect is usually achieved in 5-7 days
  • Half life 12-72 hours
  • Reversals: Vitamin K, FFP
33
Q

Warfarin Pros

A
  • Inexpensive
  • Several reversal agents, easily accessible
  • Able to monitor for compliance
  • No renal restrictions
  • Once daily dosing
34
Q

Warfarin Cons

A
  • Requires bridging
  • Requires monitoring
  • Dietary restrictions
  • Higher rates of bleeding compared to DOACs
  • Several drug-drug interactions
  • Usually only therapeutic 65% of time
35
Q

Warfarin Bridging

A

-When transitioning to warfarin from LMWH or UFH:
LMWH or UFH should have been used for at least 5 days
-INR should be ≥2.0 for 2 days before discontinuing LMWH or UF
-Does not require hospitalization if patient is stable

36
Q

Duration of therapy

A
  • Provoked VTE should be treated for typically 3 months
  • Malignancy related PE should continue treatment while they have active cancer
  • Unprovoked VTE, after 3 months should be assessed for bleeding risk, but should be considered for prolonged secondary prevention
  • Consider Thrombophilia follow up for guidance on duration of therapy for special circumstances
37
Q

Provoked

A

-Surgery with general anesthesia
-Cesarean section
-Confined to bed for at least 3 days
-Estrogen therapy
-Pregnancy
-Active cancer
-Inflammatory bowel disease
-Reduced mobility >3 days
Inheritable thrombophilia

38
Q

Primary Prevention for VTE

A
  • Heparin (5,000 units subQ every 8 hours)

- Lovenox, typical dose is 40 mg daily

39
Q

IVC Filter

A

Used for patients who anticoagulation is contraindicated, anticoagulation has failed, or complication from anticoagulation has occurred

40
Q

Treatment w/ concurrent malignancy

A

-Prior to 2019, recommendation for treatment of VTE in the setting of malignancy was LMWH, research has shown superior efficacy with apixaban

Advanced Diagnostics (11 decks)

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