DVT/PE/PHTN Flashcards
Objectives
1
Q
DVT
A
Thrombus in the deep vein
2
Q
DVT location
A
- Underlying source of 90% of PE (little clots are ok, big clots will kill you)
- 95% DVT are deep veins in LE: popliteal, common iliac, tibial veins, superficial femoral, external iliac
- UE: brachial, axillary, subclavian, IJ, brachiocephalic – Most likely due to pic line placement in UE
3
Q
How you get DVT?
A
- Normally due to a disruption in the flow that starts to allow a clot to form….The clot grows and builds…
4
Q
how can DVT become a pulmondary embolism (PE)
A
- A part of this loose, soft clot breaks away and travels upward to the lungs and gets trapped in pulmonary artery
5
Q
risk of getting DVT
A
- Virchow’s triad
- Risk factors: > 75 yo, immobilization/sedentary lifestyle/obesity, surgery, travel, anatomic variation, pregnancy, SMOKING****, OCP, iatrogenic causes, sickle cell anemia
- Obesity: due to increased pressure/weight on body that can decrease BF
- Sickle Cell anemia: pain crises from RBC getting stuck together
6
Q
Virchow’s triad
A
- Venous stasis
- Hypercoagulation state
- Vessel damage
7
Q
DVT symptoms
A
- VARIABLE ; you MUST perform diagnostics due to the lack of classic symptoms with almost 50% of patients with DVT
- Most specific symptoms is edema of extremity
- Calf pain, erythema, superficial thrombophlebitis
- Homan’s Sign: dorsiflex the foot and have pain behind the knee
8
Q
PE
A
**a blood clot breaks free and circulates through the veins, thorugh right heart and lodges in pulmonary arteries
- Very rapid and sudden; pts can die within hours
- MC from deep venous system of LE (iliac, femoral, popliteal)
9
Q
what happens to lungs in PE
A
- Lung will be ventilated (gets airs) but not perfused (no blood flow)
- This causes dead space ventilation and is a V/Q mismatch
- A PE that is big enough and left untreated can cause necrosis of tissue from vascular obstruction
- Pulmonary Infarction
- On CXR/CT: this will show as a wedge shaped infiltrate
- Sx: hemoptysis, palpiations, dizzy, syncope, hypotension
10
Q
what happends to heart in PE
A
- Due to the dec in pulmonary vascular bed size, there is an increase in pulmonary vascular resistance. This can inc RV afterload…. RVHF can occur.
- With the body can inc constriction of the pulmonary artery.
- The Right heart strain will show as bulging on the echo due to overcompensation
11
Q
PE symptoms
A
- VARIABLE
-
Classic Triad: (less than 20% pts)
- Acute pleuritic CP
- SOB
- Hypoxia
- Tachypnea, tachycardia, cracles, fever, shock, hypotension
-
Classic Triad: (less than 20% pts)
12
Q
Massive acute PE
A
- hemodynamically unstable
- This can be suggested by presence of right ventricular heart failure
- Hypotension
- On diagnostic testing: rv strain and increased BNP, inc Troponin, inc JVP bc backing up from right side
- This can be suggested by presence of right ventricular heart failure
13
Q
Chronic thromboembolic Dz
A
multiple chronic clots; need lifetime anticoagulation
14
Q
Saddle Embolism
A
- obstruction of both sides of pulmonary artery
- Can be severely hypoxic and your heart crashes … VASCULAR SURGERY
15
Q
Prevention of PE
A
- Anticoagulation w/subq heparin
- SCDS- suction compression
- Ted Hoses
- Early ambulation after surgery
16
Q
IF your suspicion is HIGH for PE
A
start on anticoagulation ASAP before you start diagnostics
17
Q
PE diagnostics: CXR
A
- usually cant tell
- Hampton’s Hump (wedge of opacity in peripheral) and Westermark’s Sign (collapse of distal vaculature with appearance of sharp cut off aka “Tree is pruned”)
18
Q
PE diagnostics: d-dimer
A
- degradation product of fibrin; just tells you when a clot is being formed and broken down
- When you coagulate and de-coagulate is when your d-dimer is broken down
-
Can be elevated in a number of circumstances
- Lipemia, bilirubin, rheumatoid factor or hemolysis can falsely elevated D-dimer
19
Q
PE diagnostics: VQ scan
A
-
nuclear medicine study: looking for a mismatch
- Indicated for pts with low CrCl or too obese to fit in CT scan
- If negative, you can r/u PE.
- If read as indeterminate, need more tests.
- If read as high +, tx with anticoagulation —- perfusion scan will be positive
20
Q
PE diagnostics: EKG
A
- Right heart strain and Acute cor pulmonale (rare)
- Deep S1, deep Q3, peaked T3
21
Q
PE diagnostics: doppler ultrasound
A
- Get one of lower extremity to check for DVT/cause
- If it’s a new clot, it will be soft and depressible on US
22
Q
PE diagnostics: spiral CT
A
-
CT-PE protocol = gold standard / MC used
- Always get a BMP first bc it needs contrast!
-
CONTRA:
- Morbid obesity
- Renal insufficiency
- IV dye allergy
23
Q
PE diagnostics: pulmonary angiogram
A
- not normally a diagnostic tool for PE
- invasive
- You inject contrast and look for the vessels to be seen and find where its not
24
Q
PE Treatment
A
- Admit to telemetry or ICU
- Give oxygen!!
- IF it’s a massive pe/saddle emboli:
- Can they get thrombolytics?
- Contra: recent stroke/hemorrhage or recent surgery
- Can they get thrombolytics?
- Meds: INITIAL MANAGEMENT
- Acute non-massive PE: use LMWH not a heparin drip (UFH)
-
LMWH is 1st line for stable pts
- Expensive, subcutaneous, no routine draw, fast acting
- Types:
- Fondaparinus – dvt/pe prophylaxis
- Enoxaparin (Lovenox)- dvt/pe prophylaxis MC used
- Dalteparin (Fragmin)
-
Contra: obesity, renal insufficiency, massive pe/saddle emboli
- Pregnancy
- Malignancy- not with cancer pts
-
UFH: recurrent DVT/PE — CHECK CBC Q 2-3 DAYS
- Inhibits thrombin/ this is reversible with protamine sulfate
- Prevents distal propagation
- Indicated: massive PE or saddle embolisms
- Given IV only- fast acting
- CHECK PTT &&MONITOR PLATELETS- can cause thrombocytopenia and HIT
- HIT: heparin induced thrombocytopenia
-
LMWH is 1st line for stable pts
- Acute non-massive PE: use LMWH not a heparin drip (UFH)
25
PE long term tx
* Warfarin: Vitamin K antagonists – slower acting
* **You must anticoagulated your pt before starting on warfarin**
* Reverse with vit K injections/new plasma
* You want INR to be 2-3 for therapeutic
* Major drug interactions
* Can effect clotting factors II, VII, IX, X
* Factor Xa inhibitors: Xarelto
* Inhibits platelet activation – will take for 6 months
* Not reversible
* Direct thrombin inhibitor
* Dabigatran: not reversible
* Start on heparin and then change to warfarin once stable
**For a massive PE/submassive PE:**
* Need 5 days of both UFH and Coumadin and need to get INR at therapeutic levels for 2 days before discharging pt!
* Use UFH
* Don’t use LMWH
\*\*Heparin: will stop you from forming further clots
\*\*Fibrinolytic tx: this will break up the clots (TPA)
26
PE: Duration of treatment
* DVT: 3-6 months
* Acute PE: 3-6 months if reversible risk factor (Sx/trauma)
* Idiopathic PE
* Lifelong anticoagulation and workups
* **Lifelong coumadin** and hematology visits:
* Hypercoaguable states
* Malignancy (use LMWH for 3-6 months)
* Recurrent dvt/pe
* Irreversible factors
* You need to evaluate if pt is good for long term outpatient coumadin use:
* Not good: Risk of fall, dementia, Gi bleeds, surgery, HTN will inc risk of ICH
* CONTRA: \> 75 due to inc fall risk and GI bleeds
* **IVC Filter: 2nd line for lifetime treatment**
* Indicated if: not good Coumadin pt, failed Coumadin, before surgery, compliance problems
* Greenfield IVC filter MC and its removal - it will sit in the renal vein
\*\*Last choice treatment for acute PE: not common bc meds work
* Thoracotomy- take out clot
* Suction catheter or balloon catheter
27
Pulmonary HTN
\*\*elevated pressure in pulmonary vascular bed \> 25 mmHG at rest or \> 30 mmHG w/exercise
* Pulm HTN is more common than PAH
* **\*\* lung disease and hypoxemia are associated with this!!!**
* Etiologies:
* Lung dx, hypoxemia (COPD/ILD/Sleep disorders, altitudes)
* Left heart disease
* Sarcoidosis, hisotcytosis X, chronic thromboembolic dz
28
Pulmonary Arterial HTN
elevated pressure in pulmonary vasculature that is **limited to arteries/arterioles**
* Etiologies:
* **Idiopathic and chronic PE MC**
* **Idiopathic has NO CURE!!!**
* Familial, genetic
* Drugs and toxins
* HIV, collagen vascular dz, congential cardiac shunts (L to R), pulm HTN of newborn
* **MCC of death in PAH is cor pulmonale**
* To diagnose: requires right heart cath and assessment using pulmonary capillary wedge pressure
29
Distinguish between the following types of pulmonary hypertension
* pre-capillary hypertension: primary/idiopathic pulm arterial HTN
* Vascular destruction
* no apparent cause
* Could be caused by:
* Familial, l to r shunt, pe, cvd, chronic thromboembolic dz
* passive hypertension
* reactive hypertension: increased BP due to a stimulus
30
pulmonary hypertension: incidence
* 9:1 ratio of female to men
* **MC found in younger women of childbearing age, or in 50s/60s**
31
PHTN: risk factors
* heredity, underling lung or heart disease, collagen vascular disease (stiff)
32
PHTN: Prognosis/mortality rate
* **NO cure for idiopathic pulmonary arterial HTN**
* **Classifications:** we have four that range from no limitation to activity to fully limited/unable.
33
PHTN Signs/Symptoms
* dyspnea, sob, doe, fatigue, syncope, heart palpitations…. Vague!
* Find these with a lot of other dz
34
PHTN DDx
* COPD
* CAD cardiomyopathy
* CHF / cor pulmonale
* ILD/ Pulmonary Fibrosis
* Mitral stenosis- echos
* PE- dopplers
* Scleroderma
* SLE- rashes
35
PHTN Dx: CXR
* exclude other dz
* What you can see: cardiomegaly, enlarged RV, mediastinal and hilar fullness/dilated pulm arteries
36
PHTN Dx: EKG
* Large P wave in II, III, aVF suggested a large right atrium
* R axis deviation, RVH
37
PHTN Dx: Echo
* **heart funct/pressures- all pts get**
* This is very important
* Idiopathic PAH: enlarged RV and RA with normal or reduced LV side
* IF pressure of RVSP is \> 55 then its severe…. The pressures could be equalizing which is bad befcause it functions on a pressure gradient
38
PHTN Dx: PFT's
underlying lung dz
39
PHTN Dx: VQ scan
* R/O chronic PE (preferred)
40
PHTN Dx: CT scan
* see what it looks like
41
PHTN Dx: rt heart cath
* **measure pressures in varying areas**
* **This is essential for diagnosis and treatment!**
* Vasodilator challenge study using adenosine to see effectiveness of adenosine vs using other drugs for treatment (CCB) determined by pressure drop of 10-40 mmHg
42
PHTN Dx: others
* Lung Biopsy
* ABG
* Labs- ANA, BNP, HIV, CBC
* autoimmune
* 6 min walk- functionality and predicts survival
43
PHTN Tx: edema for R heart failure
* loop diuretics
44
PHTN Tx: poor heart pump
* Anticoagualtion
* Coumadin if idiopathic of chronic thromboembnolic dz
45
PHTN tx: others
* Oxygen up to 90%
* CCB: only use when responsive to vasodilator study \< 10%
* Doc: diltiazem or nifedipine
* Response will drop over time to CCB
* Endothelin Receptor antagonists- vasoconstriction $$$$
* Teratogenic, dec sperm count, inc LFTs
* Drugs: Bosentan – adjust with Coumadin
* Ambrisentan- don’t have to adjust with Coumadin
* Better for LFTs
* PDE-5
* Sildenafil (20 mg)
* Prostacyclins to lower PA pressures
46
PHTN: Transplant indications/criteria
* Indications
* Not responding to therapy
* Heart transplant only needed if RV dysfunction present
* Long term survival still poor- rejection
* Criteria for Transplant
* Varies on center
* Patients with PAH related to disease are limited
* Double lung transplant: \<60 yo
* Heart/Lung Transplant: \< 50 yo
