VTE Flashcards

0
Q

How do you get obstructive shock in PE?

A

Pulmonary artery obstruction by thrombus -> decreased LV filling

If massive PE -> pulm vasoconstriction -> increased RV AFTERLOAD -> RV unable to compensate -> RV dilation which reduced LV CO

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1
Q

What are the sources of PE?

A

90% from DVT, illiofemoral
Renal vein from nephrotic syndrome
Upper extremity if cancer associated

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2
Q

What factors influence the effect of PE?

A

Level of reduction of blood flow
How quickly reduction occurs
Underlying cardiopulmonary reserve

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3
Q

Why does PE cause hypocapnia?

A

V/Q mismatch leads to dead anatomical space leads to HYPERVENTILATION leads to hypocapnia

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4
Q

Risk factors for VTE?

A
Previous DVT
Smoking/OCP/chemo
Surgery 
Travel
Inherited thrombophilias
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5
Q

Signs and symptoms of PE?

A

SOB - sudden, worsening.
DVT - warm, swollen calves. Fever.
If pulm infarction - pleuritic chest pain, HAEMOPTYSIS.

TACHYCARDIA AND TACHYPNOEA

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6
Q

What criteria used to risk stratify PE?

A

Wells criteria used to determine clinical probability which is used in investigation work up.

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7
Q

What LAB Ix?

A
CBE EUC LFT 
COAGS
D-DIMER 
ABG
THROMBOPHILIA SCREEN 
IF THROMBOLYSIS: TROP, BNP
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8
Q

What RADIOLOGICAL Ix?

A

CTPA
VQ scan if contraindicated (renal, allergy to contrast, young)
DOPPLER US
ECHO if critically unwell enough for CT.
ECG
CXR

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9
Q

What ECG findings in PE?

A

Sinus tachy
Right heart strain: tall P, RAD, RBBB
S1 Q3 T3
AF

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10
Q

Short term management of PE?

A

If STABLE: supportive medical care (O2 and analgesia) and anti coagulate

If UNSTABLE: supportive medical care, anti-coagulate and consider thrombolysis.
Anticoagulate with IV UFH? (APTT monitored) for five days until INR > 2
Start warfarin within 48 hours.

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11
Q

What needs to be monitored after anticoagulant therapy?

A

Platelet count for heparin induced thrombocytopenia

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12
Q

How can heparin be reversed?

A

Protamine sulfate.

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13
Q

What anticoagulant used in renal impairment?

A

UFH.

This is because enozaparin and fondaparinaux are renally cleared.

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14
Q

Long term management of VTE?

A

Warfarin for min 3 months if provoked, 6 months if unprovoked.

Can use dabigatran instead of warfarin as no need to monitor and there is a fixed dose.

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15
Q

Management of DVT?

A

Non-pharm: mobilisation, compression stockings
Anticoagulate
- first get COAGS (APTT, PT and platelet count)
- LMWH
- oral warfarin to get INR 2-3

16
Q

UFH mechanism of action? How do you reverse?

A

Indirectly activates thrombin and FXa

Protamine sulfate

17
Q

Advantages of LMWH to UFH?

A

More predictable
Longer half life
Less risk of thrombocytopenia
Negative is significant renal impairment

18
Q

Warfarin MOA? Reversal? Contraindications? How often monitor it with chronic therapy?

A

Inhibits vitamin K dependent synthesis of F2,7,9,10 and protein C and S.

Reversed with vit K and coagulation factors (prothrombin)

Monitor INR monthly if given chronically once stable.

Big contraindications -> pregnancy

19
Q

Approach if INR < 5, 5-9, > 9 and if clinically significant bleeding?

A

< 5 -> lower/omit next dose, resume lower dose once INR stable

5-9 -> cease warfarin, give vit k, measure INR 24 hr

> 9 -> cease warfarin, give vit k, measure INR in 6-12hr and resume once INR lower than < 5

20
Q

What is pulsus paradoxus? Why can it be caused by a PE?

A

Abnormally large decrease in systolic BP on inspiration. Usually > 10.

PE -> increased RV filling
Inspiration -> increased RV filling

Increased RV filling -> dilating -> compression of septum into LV -> reduced CO -> reduced BP systolic