6) Pulmonary (Part 2) Flashcards
1
Q
Virchow’s Triad
A
- Stasis
- Endothelial cell injury
- Hypercoagulable states
2
Q
Specific risk factors for venous thromboembolism (VTE)
A
- Malignancy
- Immobilization
- Surgery within last 3 months
- Preexisting respiratory disease
- Prior Hx of VTE
- Chronic heart disease
Stroke - Thrombophilia
- Inflammatory triggers
3
Q
Inflammatory triggers that can pose risk of VTE
A
- Infection
- Tranfusion
- Erythropoiesis stimulating Rx
4
Q
Specific risk factors for VTE in women
A
- Obesity
- Pregnancy
- Hypertension
- Heavy cigarette use
- Oral Contraceptive Pills/Hormone Replacement Therapy (OCP’s/HRT)
5
Q
Most common route of VTE
A
- LE thrombus –> IVC –> R ventricle –> pulmonary arteries
6
Q
Signs and symptoms of VTE
A
- Dyspnea (79%)
- Tachypnea (57%)
- Pleuritic pain (47%)
- Leg edema, erythema, tenderness, palpable cord (47%)
- Cough/hemoptysis (43%)
7
Q
Other possible findings in VTE
A
- Tachycardia
- RV gallop
- Loud P2, & prominent jugular “a” waves suggest RV failure
- Syncope or sudden death with massive PE
8
Q
Typical ABG findings
A
- Hypoxemia (Low PaO2)
- Hypocapnia (Low PaCO2)
- Increased alveolar-arterial oxygen gradient (A-a gradient)
- 15%-20% have normal ABG’s
9
Q
A-a gradient
A
- A measure of how effectively oxygen in your alveoli moves into your pulmonary vasculature
10
Q
A-a gradient calculation
A
- PAO2 – PaO2
- PAO2 is calculated from the alveolar gas equation
- PaO2 is measured in the arterial blood
11
Q
A-a gradient measured from the ABG results
A
- A-a gradient = [ (FiO2) x (Atmospheric Pressure - H2O Pressure) - (PaCO2/0.8) ] - PaO2 from ABG
- A-a gradient = [.21 x (760-47) – (PaC02/0.8) ] - PaO2
12
Q
Normal A-a gradient room air
A
- 10 to 20 mmHg
13
Q
Increased A-a gradient may be a result of
A
- V/Q (ventilation-perfusion) imbalance
- Anatomic shunts
- Impaired diffusion
14
Q
Adjunctive studies in the evaluation of PE
A
- ABG’s
- EKG’s (S1Q3T3)
- CXR’s
- Echocardiograms
- Doppler (to evaluate for DVT)
- Cardiac Enzymes and BNP
15
Q
Primary studies in the evaluation of PE
A
- D-dimer strategy combined with CT angio
- V/Q scan based strategy
- Pulmonary angiography (gold standard, but invasive)
- MRI/MRA
16
Q
CXR findings in PE
A
- That was a “WHALE” of a PE
- W= Westermark Sign
- H =Hampton’s Hump
- A = Atelectasis
- L = Lovely (Meaning perfectly normal)
- E = Effusions
17
Q
Westermark sign
A
- Seen on plain film radiography CRX
- Dilatation of pulmonary vessels proximal to embolism along with collapse of distal vessels (often with a sharp cut off)
18
Q
Hampton’s Hump
A
- Pleural based opacities with convex medial margins on CRX
19
Q
CRX in PE may show
A
- Collapse
- Consolidation
- Small pleural effusion
- Elevated diaphragm
20
Q
Ultrasound
A
- Duplex scanning with compression will aid to detect any thrombus
- Highly sensitive and specific for diagnosing DVT
21
Q
Ultrasound looks for
A
- Loss of flow signal
- Intravascular defects
- Non collapsing vessels in the venous system
22
Q
D-Dimer
A
- Degredation product of crossed linked fibrin
- Detectable above 500 ng/ml in nearly all cases of VTE, but common in many other conditions (sensitive but not specific)
23
Q
V/Q scanning
A
- Radioactive cmpd inhaled (distributes evenly in normal lung)
- Radioactive cmpd injected into vein, travels to tissues in blood vessels (no injected material in a region indicated embolus)
- “Mismatch” of inhaled and injected cmpds on lung scan images = pulmonary embolus
24
Q
Acute treatment for pulmonary embolism
A
- Anticoagulation for most patients
25
Q
Anticoagulation in acute PE Tx
A
- Low molecular weight heparin (IE Lovenox); Fondaparinux (Arixtra); or unfractionated heparin
- There are some new approved Oral anticoagulants for acute treatment (IE Rivaroxaban (Xaletro))