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Acute Care I > DVT & PE > Flashcards

DVT & PE Flashcards

1
Q

Prevention
Goals of therapy:

A

Prevent thrombus extension & early & late recurrences of VTE

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2
Q

Clinical Manifestations of DVT include

A

May be asymptomatic, nonspecific
Leg Edema
Tenderness
Discoloration/erythema
Difficulty walking

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3
Q

Clinical Manifestations of DVT include
May depend on size of clot- larger clots tend to?

A

produce more pronounced symptoms

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4
Q

Clinical Manifestations of DVT include
Most clinically significant PEs orginate from?

A

LE DVTs. Can have minor S&S & have extensive clot.

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5
Q

Diagnosing DVT
DVT unlikely what test?
Positive?
Negative?

A

D-DImers
Positive complete venous US
Negative = no DVT

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6
Q

Diagnosing DVT
DVT likely what test?

A

complete venous US

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7
Q

Treatment for Proximal DVT

A

At least 3 mo AC; DOAC in noncancer pts if no contraindications

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8
Q

Reassessment of Proximal DVT occurs when?
may extend for how long? and why?

A

3mo
May extend AC to yearly evaluation d/t risk/benefit, compliance, and patients preference

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9
Q

Treatment of Isolated Distal DVT with High risk recurrence?

A

3 mo AC

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10
Q

Treatment of Isolated Distal DVT with High risk recurrence?

A

Treatment or surveillance 4-6 wk AC (full or lower dose) or venous US surveillance

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11
Q

Modified Wells Criteria: Clinical Assessment for PE
What factors are assessed?

A

Clinical symptoms of DVT (leg swelling, pain with palpation)
Other diagnosis less likely than PE
HR > 100
Immobilization (>/= 3 days) or surgery in the previous four weeks
Previous DVT/PE
Hemoptysis
Malignancy

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12
Q

Prox DVT/PE, no cancer can be treated w/ what?
For how long?

A

Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo

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13
Q

DVT provoked by surgery can be treated w/ what?
For how long?

A

Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo

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14
Q

DVT with no surgery can be treated w/ what?
For how long?

A

Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo

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15
Q

1st unprovoked DVT can be treated with?
for how long?

A

Rivaroxaban - reduced dose
Apixaban - reduced dose
Extended treatment

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16
Q

Active CA & + VTE/PE can be treated with? for how long?

A

Rivaroxaban
Apixaban
Edoxaban
LMWH - may be preferred if luminal GI malignancy

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17
Q

If unprovoked DVT & DCing anticoag use what?

A

ASA

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18
Q

Isolated distal DVT of LE + no symptoms or risks of extension use what?

A

serial dopplers

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19
Q

Drugs that are Factor Xa inhibitors?

A

Rivaroxaban
Apixaban
Edoxaban

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20
Q

Drugs that are Thrombin inhibitors?

A

Dabigatran

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21
Q

Drugs that are Factor Xa/Thrombin Inhibitors?

A

LMWH

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22
Q

Complications of DVT: Post-thrombotic syndrome
Occurs in up to what % of patients with proximal DVT, within how long, despite anticoagulation?
Results from?
Duration?
Symptoms?

A

50%
~ 1-2yrs
valvular incompetence &/or residual obstruction
Chronic & progressive
Pain, edema, sometimes ulcerations

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23
Q

Complications of DVT: Venous Ulceration
From what?
Usually appears where?
Prevent by use of?

A

post-thrombotic syndrome
usually appear perimalleolar area
compression stockings

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24
Q

What type of PE can be life-threatening in normal persons?
What type of PE can be life-threatening in person with impaired physiologic reserves?

A

Massive emboli
Submassive

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25
Q

2/3 of those who die from PE will do so w/n how long?

A

1st hour of presentation

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26
Q

In those with HD instability, mortality increases by how much?

A

7 fold

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27
Q

Heart Failure d/t PE results from?

A

Vascular resistance to RV output increased RV pressure leading to ventricular wall stress increase leading to cardiac ischemia.

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28
Q

In early phase of Heart Failure d/t PE what compensatory mechanisms maintain flow?
Which leads to?

A

Tachycardia & RV dilation
RV output falls d/t wall stress & ischemia leading to decreased LV preload

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29
Q

RV dilation causes interventricular septal shift leading to?

A

decreased LV compliance leading to decreased LV output leading to hypotension

30
Q

Increased pulmonary vascular resistance is d/t?

A

thrombus itself & neural reflexes, humoral factor release from platelets/endothelium, & hypoxia

31
Q

Hypoxia in PE is common d/t

A

V/Q mismatch
intracardiac shunting thru patent foramen ovale in r/t elevated R heart pressures
Intrapulmonary shunting thru areas of atelectasis & decreased CO
all leading to decreased mixed venous O2 sat

32
Q

Increased deadspace in PE occurs d/t

A

ventilated but underperfused areas of lung leading to decreased etCO2 compared to arterial CO2.
Occurs when thrombus occupies >25% of pulmonary vasculature

33
Q

S&S of PE

A

Non-specific/asymptomatic
Dyspnea
Tachypnea
Pleuritic pain
Pre-syncope/sycope
Cough
Orthopnea
Wheezing
Tachycardia/afib
Crackles on lung exam (21%)
Hypoxemia
Hypocapnia

34
Q

Clinical manifestations of Massive PE

A

Acute cardiopulmonary S&S r/t RV failure or ischemia
Sudden cardiopulmonary arrest, often with bradyarrhythmias, PEA
Significant anxiety, impending doom
Substernal CP - sudden, unrelenting, nonradiating
Syncope d/t low CO or bradycardia
Shock
Acute cor pulmonale -
EKGs - nonspecific but may reveal signs of R heart strain (new R axis deviation or new RBBB) or ST
CXR - nonspecific but pt’s w/ PE in PIOPED-I study were more likely to have elevated R diaphragm, pleural based

35
Q

PE may lead to acute cor pulmonale which is shown by?

A

distended neck veins, prominent component of 2nd heard sound

36
Q

PE may cause EKG changes such as?

A

signs of R heart strain (New R axis deviation or new RBBB) or ST

37
Q

PE may cause CXR changes such as?

A

elevated R diaphragm
Pleural based opacities,
Westermark’s sign (dilation of pulm. vessels & sharp cutoff)

38
Q

EKG suspicious for PE will Show S1Q3T3 meaning?

A

S-waves in lead I
Q-waves in lead III
Inverted T-waves in lead III

39
Q

Differential Dx of PE can include?

A

MI
Pericarditis
Heart Failure
Pneumonia
Asthma
COPD
PTX
Rib Fx
Musculoskeletal pain
Intrathoracic CA
Sepsis

40
Q

Diagnosing PE
Need what?
May Utilize objective clinical assessments such as?

A

Clinical suspicion
Wells, Geneva, revised Geneva

41
Q

Diagnosing PE
Why use CXR?
may have nonspecific findings of?

A

utilized in general evaluation of pts w/ possible PE to exclude other causes of clinical presentation
Elevated diaphragm, pleural based infiltrates, focal oligemia (Westermark’s sign), hypovascularity

42
Q

Echocardiography (TTE) may show?

A

greater RV diameter & evidence of RV strain & failure
McConnell’s sign: regional RV dysfunction w/ akinesia of mid free wall but normal motion
May actually identify PE
Echo does not r/o presence of PE

43
Q

Suspected PE in patient w/o hemodynamic instability
Assess clinical probability of PE
Low or intermediate clinical probaility or PE unlikely what test(s)?

A

D-dimer: if negative no treatment
D-dimer: If positive CTPA
CTPA: no PE no treatment
CTPA: PE confirmed treatment

44
Q

Suspected PE in patient w/o hemodynamic instability
Assess clinical probability of PE
High clinical probability or PE likely what test(s)?

A

CTPA: no PE no treatment or investigate further
CTPA: PE confirmed Treatment

45
Q

Suspected PE in a patient w/ hemodynamic instability
Perform what test?
If signs of PE are present, what test(s)?

A

Bedside TTE looking for RV dysfunction
CTPA if immediately available. If not initiate treatment of high-risk PE
CTPA if positive initiate treatment of high-risk PE
CTPA if negative investigate other causes of shock or instability

46
Q

Definition of hemodynamic instability, which delineates acute high-risk PE
Cardiac Arrest
Obstructive shock
Persistent Hypotension

A

Need for CPR
SBP < 90 mmHg or vasopressor required to achieve a BP >/= 90 mmHg despite adequate filling status AND End organ hypoperfusion (AMS, cold, clammy skin, oliguria/anuria; increased serum lactate)
SBP < 90 mmHg or SBP drop >/= 40 mmHg, lasting longer than 15 min and not caused by new-onset arrhythmia, hypovolemia, or sepsis

47
Q

Risk Stratification
Clinical findings?

A

RV failure (TTE, CT)
tachycardia
hypotension
respiratory insufficiency
syncope

48
Q

Risk Stratification
Lab indicators

A

troponin
BNP
Lactate
hyponatremia

49
Q

PE O2 for sats > 90%

A

high flow NC
NIV
Invasive MV

50
Q

Tx of RV failure
Volume optimization
Dose?
Properties and use?
Caveats?

A

Cautious volume loading use NS or LR </= 500 ml over 15-30 min

Consider in patients with low CVP

Volume loading can over-distend the RV worsening ventricular interdependence and reduce CO

51
Q

Tx of RV failure
Vasopressors and inotropes
Norepi
Dose?
Properties and use?
Caveats

A

0.2-1.0 nanogram/kg/min

Increases RV inotropy and systemic BP, promotes positive ventricular interactions, and restores coronary perfusion gradient

Excessive vasoconstriction may worsen tissue perfusion

52
Q

Tx of RV failure
Vasopressors and inotropes
Dobutamine
Dose?
Properties and use?
Caveats?

A

2-20 nanogram/kg/min

Increases RV inotropy, lowers filling pressures

May aggravate arterial hypotension if used alone, w/o a vasopressor; may trigger or aggravate arrhythmias

53
Q

Tx of RV failure
Mechanical circulatory support
Strategy?
Properties and use?
Caveats?

A

Veno-arterial ECMO/extracorporeal life support

Rapid short-term support combined w/ oxygenator

Complications w/ use over longer periods (>5-10 days), including bleeding and infections; no clinical benefit unless combined with surgical embolectomy; requires an experienced team

54
Q

Anticoagulation for high or intermediate probability includes?

A

LMWH, fondaparinux, UFH, NOACs

55
Q

If anticoagulation is initiated parenterally, what is recommended for most patients?

A

LMWH or fondaparinux over UFH

56
Q

When oral anticoagulation is started in patient w/ PE who is eligible for NOAC (which drugs?) a NOAC is recommended in preference to?

A

apixiaban, dabigatran, edoxaban or rivaroxaban

VKA

57
Q

When patients are treated w/ a VKA overlapping w/ what?

Until a INR of what is reached?

A

parenteral anticoagulation

2.5 (range of 2-3)

58
Q

Rescue thrombolytic therapy is recommended for patients with what?

A

hemodynamic deterioration or anticoagulation treatment

59
Q

Systemic Thrombolytic is recommended for?

A

high-risk PE

60
Q

Anticoagulation dosing
Enoxaparin

A

1mg/kg q12 hr
1.5mg/kg once daily

61
Q

Anticoagulation dosing
Tinzaparin

A

175 IU/kg once daily

62
Q

Anticoagulation dosing
Dalteparin

A

100 IU/kg q 12 hr
200 IU /kg once daily

63
Q

Anticoagulation dosing
Nadroparin

A

86 IU/kg q12 hr
171 IU/kg once daily

64
Q

Anticoagulation dosing
Fondaparinux
Body weight < 50kg
Body weight 50-100 kg
Body weight > 100 kg

A

5mg once daily
7.5 mg once daily
10 mg once daily

65
Q

Thrombolytic dosing
rtPA

A

100 mg over 2 hr
0.6 mg/kg over 15 min (max dose of 50 mg)

66
Q

Thrombolytic dosing
Streptokinase

A

250,000 IU as a loading dose over 30 min, followed by 4400IU/kg/hr over 12-24 hr
Accelerated regimen: 1.5 million IU over 2 hr

67
Q

Thrombolytic dosing
Urokinase

A

4400 IU/kg as a loading dose over 10 min, followed by 4400 IU/kg/hr over 12-24 hr
Accelerated regimen: 3 million IU over 2 hr

68
Q

Special circumstances
If IV dye allergy:

A

D-dimer w/ clinical assessment to exclude PE
If mild allergy, pretreat w/ steroids
Venous u/s & VQ scan if severe allergy

69
Q

Special Circumstances
If impaired renal function:

A

D-dimer w/ clinical assessment
venous u/s
VQ scan if u/s (-)

70
Q

Medication tips
LMWH dosing in obesity
VKA monitoring after adjustment
VKA monitoring stable dose
No anti Xa levels in which patients
No monitoring of DOACs when?

A

use actual body weight
</= 4 wks
6-12 wks
obesity or CrCl < 30 ml/min
during bleeding

71
Q

Medication tips
INR w/ VKA 4.5-10 & no bleeding
Elevated INR + life-threatening bleeding
Bleeding on Xa inhibitor
Bleeding on dabigatran
Bleeding on LMWH or UFH
Resume anticoagulation w/n how long of bleed?

A

no intervention
PCC + vit K
+/- PCC or Xa (recombinant), inactivated-zhzo
idarucizumab
protamine
90 days

72
Q

Elderly considerations for anticoagulation

A

no bid differences in timing or dosing
pay attention to renal function

Acute Care I (24 decks)

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