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Clinical Medicine PA 581: Pulmonary > DVT/PE/PHTN > Flashcards

DVT/PE/PHTN Flashcards

Objectives

1
Q

DVT

A

Thrombus in the deep vein

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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
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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…
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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
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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
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6
Q

Virchow’s triad

A
  • Venous stasis
  • Hypercoagulation state
  • Vessel damage
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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
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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)
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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
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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
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11
Q

PE symptoms

A
  • VARIABLE
    • Classic Triad: (less than 20% pts)
      • Acute pleuritic CP
      • SOB
      • Hypoxia
    • Tachypnea, tachycardia, cracles, fever, shock, hypotension
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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
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13
Q

Chronic thromboembolic Dz

A

multiple chronic clots; need lifetime anticoagulation

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14
Q

Saddle Embolism

A
  • obstruction of both sides of pulmonary artery
  • Can be severely hypoxic and your heart crashes … VASCULAR SURGERY
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15
Q

Prevention of PE

A
  • Anticoagulation w/subq heparin
  • SCDS- suction compression
  • Ted Hoses
  • Early ambulation after surgery
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16
Q

IF your suspicion is HIGH for PE

A

start on anticoagulation ASAP before you start diagnostics

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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”)
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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
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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
  • 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
25
Q

PE long term tx

A
  • 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
Q

PE: Duration of treatment

A
  • 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
Q

Pulmonary HTN

A

**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
Q

Pulmonary Arterial HTN

A

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
Q

Distinguish between the following types of pulmonary hypertension

A
  • 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
Q

pulmonary hypertension: incidence

A
  • 9:1 ratio of female to men
    • MC found in younger women of childbearing age, or in 50s/60s
31
Q

PHTN: risk factors

A
  • heredity, underling lung or heart disease, collagen vascular disease (stiff)
32
Q

PHTN: Prognosis/mortality rate

A
  • NO cure for idiopathic pulmonary arterial HTN
  • Classifications: we have four that range from no limitation to activity to fully limited/unable.
33
Q

PHTN Signs/Symptoms

A
  • dyspnea, sob, doe, fatigue, syncope, heart palpitations…. Vague!
    • Find these with a lot of other dz
34
Q

PHTN DDx

A
  • COPD
  • CAD cardiomyopathy
  • CHF / cor pulmonale
  • ILD/ Pulmonary Fibrosis
  • Mitral stenosis- echos
  • PE- dopplers
  • Scleroderma
  • SLE- rashes
35
Q

PHTN Dx: CXR

A
  • exclude other dz
    • What you can see: cardiomegaly, enlarged RV, mediastinal and hilar fullness/dilated pulm arteries
36
Q

PHTN Dx: EKG

A
  • Large P wave in II, III, aVF suggested a large right atrium
  • R axis deviation, RVH
37
Q

PHTN Dx: Echo

A
  • 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
Q

PHTN Dx: PFT’s

A

underlying lung dz

39
Q

PHTN Dx: VQ scan

A
  • R/O chronic PE (preferred)
40
Q

PHTN Dx: CT scan

A
  • see what it looks like
41
Q

PHTN Dx: rt heart cath

A
  • 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
Q

PHTN Dx: others

A
  • Lung Biopsy
  • ABG
  • Labs- ANA, BNP, HIV, CBC
    • autoimmune
  • 6 min walk- functionality and predicts survival
43
Q

PHTN Tx: edema for R heart failure

A
  • loop diuretics
44
Q

PHTN Tx: poor heart pump

A
  • Anticoagualtion
    • Coumadin if idiopathic of chronic thromboembnolic dz
45
Q

PHTN tx: others

A
  • 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
Q

PHTN: Transplant indications/criteria

A
  • 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

Clinical Medicine PA 581: Pulmonary (9 decks)

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