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113 Cards in this Set

  • Front
  • Back
what % of PE pts dies w/in the 1st hr
8-10%
what is a PE
abrupt blocking of a pulmonary artery or one of its branches by a thrombus or foreign material
large thrombi lodge where and cause what?
lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise
where are smaller thrombi found
continue traveling distally, occluding a smaller vessel in the lung periphery
what is more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura
PE: smaller thrombi
what is the pattern of most PE
they are multiple, and the lower lobes are involved more commonly than the upper lobes
how should beta 3 agonist be used in asthma pts?
never as sole agents only as supplemental agents
when follwing an astham pt. what should be monitored to gauge how well the asthma is being treated
eosinophil count/ how pt. tells you he/she is doing
what are some other types of emboli
amniotic fluid/fat emboli
is PE a dz?
no it is a complication of DVT
what is the natural Hx. of venous thrombosis
Virchow triad of factors that lead to the pathogenesis of venous thrombosis:
1. Venous stasis,
2. Injury to the intima,
3. Changes in the coagulation properties of the blood.
what is virchow's triad
factors that lead to the pathogenesis of venous thrombosis:
1. Venous stasis,
2. Injury to the intima,
3. Changes in the coagulation properties of the blood.
thrombosis usually originates as what
as a platelet nidus (point/focus/loci) in the region of venous valves located in the veins of the lower extremities
what is a nidus
point/focus/loci
how does a PE develop
originates as a platelet nidus (point/focus/loci) in the region of venous valves located in the veins of the lower extremities. Further growth occurs by accretion of platelets and fibrin and progression to red fibrin thrombus, which may either break off and embolize or result in total occlusion of the vein
what are the common causes of PE
venous stasis, Polycythemia, dehydration, immobility, compression of a vein by a tumor, Hypercoagulable states, Immobilization
Surgery and trauma
Pregnancy, malignancy
what is polycythemia and what are the most common causes
increased RBC; smoking and hypoxemia
what is the frequency of PE
60-80% of patients with DVT, even though more than half the patients are asymptomatic.
300,000-650,000 a yr is US
what is the pattern of PE among sexes
women increased risk
who is at increased risk for PE
pregnant women, women, during post partum period, older pts.,
when is PE commonly missed
in hospitalized elderly pts.
what is the pattern found in symptoms of PE
they are nonspecific and high index of suspicion is required
what is the Tx of a pt. who has overdosed on warfarin
if a small amount vitamin K; otherwise fresh frozen plasma
what is the most frequent symptom of a PE
dyspnea
what are the symptoms of PE
dyspnea, chest pain, hemoptysis, cough, sweats, anxiety/hypertension
what type of chest pain is seen in a pt. with PE
pleuritic
what is the most frequent sign of a PE
tachycardia
If pt has had B clot and later has hair loss (alopecia) check them for what
lupus
what are the signs of PE
tachycardia, wheezing/reduced breathing sounds, neck vein distention, crackles, loud pulmonic second sound, pulm. outflow murmors (not common), pleuritic friction rub w/ peripheral pulm. infarct, DVT
what is a surrogate marker in the presence of signs and symptoms of pulmonary embolus
DVT
what are the D dx of PE
Myocardial infarction
Pericarditis
Pneumonia
Pneumothorax
Chest wall pain
Congestive heart failure
Pleuritis
what are the labs done for a PE
ABG, D-dimer
what is seen on the ABG of a PE pt
hypoxemia, hypocapnia, and respiratory alkalosis
what is seen on the d dimer of a PE pt
elevated (>500ng/mL) in 97% of patients
what imaging studies should be done for PE pts
Chest radiograph
Spiral CT scanning (helical CT scan), Ventilation-perfusion (V/Q) scanning of the lungs, Doppler ultrasonography, Pulmonary angiography
what test for PE is most frequently used in the past few years
spiral CT scan (helical CT)
a normal lung scan (VQ) rules out what
PE
what is the best form of heparin
low molecular weight heparin
what is the criterion standard for the diagnosis of PE
pulmonary angiography
what should you check when giving heparin
PTT- make sure you don't over coagulate
what is the cut off sign
Darker area of Reduced Perfusion  (Westermark's sign)- PE
if the pulmonary angiograms show lobulated defects in the dye column filling the pulmonary arteries what has been proven
PE
Diagnostic difficulty of PE is a reason for what
immediate referral to specialist
what is considered to be the gold standard diagnostic test for PE
pulmonary angiography
what is used to determine whether pulmonary angiography is necessary
integrated diagnostic approach (combining clinical symptoms with noninvasive testing)
what is the immediate Tx of a pt. suspected to have a DVT or PE
Immediate full anticoagulation
initial anticoagulation in a PE/DVT pt is done with what
IV heparin
never start warfarin until when
after the pt has been on heparin for a few hours
after the pt. (PE) has been started on heparin what else should be done
should be started simultaneously on oral anticoagulation with Coumadin (warfarin)
when should the heparin Tx of a PE pt. be discontinued
After a therapeutic dose of warfarin is established, heparin is discontinued and warfarin therapy is maintained
what has the highest level of vit. K in a vegetable
guacamole (avacodo)
what rapidly dissolves the obstructing pulmonary thrombus and the source of the thrombus in the pelvic or deep leg veins
thrombolytic therapy
what is the mainstay of therapy and 1st drug of choice for PE
heparin
what prevents conversion of fibrinogen to fibrin
heparin
what does heparin prevent
conversion of fibrinogen to fibrin
will heparin dissolve an existing clot
no, but it does prevent clot propagation and embolization
how is heparin given
IV or infussion intermittent IV
what will grapefruit juice do with a drug
increase activity of what ever drug it is given with (binds with it)/prolongs action of drug
The efficacy of heparin depends on what
achieving therapeutic levels of the drug within the first 48h of therapy. The aPTT should be 1.5–2.5X control
how many times can striptokinase be given
once b/c of anaphylatic reactions
what are the side effects of heparin
Hemorrhage, thrombocytopenia, new thrombus formation (white-clot syndrome)
what are the Coumadin (warfarin) vitamin K–(antagonist) dependent factors
factors II, IIV, IX, X
what is the drug of choice for chronic Tx of PE
coumadin
what does the full effect of coumadin
requires up to 5 days of treatment
what might coumadin initially cause
hypercoagulable state, necessitating concurrent therapy with heparin during initiation of therapy
what is the oral dose of coumadin
5mg daily for 2-4 days, then adjust dose. Usual maintenance dose is 2-10mg/day
INR (international normalized ratio) is maintained how in treating with coumadin
therapuetic range: 2-3
what are the side effects of coumadin
first few days of warfarin therapy produce a hypercoagulable state
Numerous drug Interactions
what has effects similar to those of heparin
Enoxaparin sodium (Lovenox) and dalteparin sodium low molecular weight heparins (LMWHs)
Enoxaparin sodium (Lovenox) and dalteparin sodium low molecular weight heparins (LMWHs) are different from heparin how
they have improved bioavailability, have
longer half-life, and may be associated with
fewer bleeding complications. They also require less monitoring than is required with conventional heparin
true or false: LMWHs are as effective as heparin in preventing venous thromboembolism
true
what is the dose of LMWH's
Subcutaneously: twice daily (BID)
what Is a recommended therapy for the acute treatment of deep vein thrombosis (DVT)
LMWH's
what are Streptokinase and urokinase
thrombolytic agents that rapidly dissolve the obstructing pulmonary thrombus and the source of the thrombus in the pelvic or deep leg veins
what drugs rapidly dissolve the obstructing pulmonary thrombus and the source of the thrombus in the pelvic or deep leg veins.They also decrease the likelihood of recurrence
streptokinase and urokinase
true or false: Thrombolytic therapy is not generally recommended for the routine treatment of pulmonary embolism because it is contraindicated in many patients
true
what are tissue plasminogen activators
Alteplase and reteplase
true or false: There is some evidence that tissue plasminogen activators have a better safety profile and efficacy than other thrombolytics.
true
Pulmonary embolectomy is indicated in patients with what
massive pulmonary emboli, but it is only performed when thrombolysis is contraindicated and in patients with refractory shock and hypotension
what is the chronic Tx plan for PE
6 mo of anticoagulation (reduces rate of recurrence to half of the recurrence rate observed when only 6 wk of anticoagulation is given).
when is long term anticoagulation indicated
for patients with an irreversible underlying risk factor and recurrent DVT or recurrent PE
what is one of the most common risk factors for PE
Hx of immobilization
when is prophylaxis for DVT indicated
in bedridden pts
women at risk for thromboebolism taking oral contraceptives should be advised what
to consider other forms of contraception
what contributes to coexisting complication dzs for PE
tobacco use
when is routine thromboprophylaxis used in prevention therapy
in high risk pts scheduled for surgical procedures (particularly major orthopedic surgery)- PE
what is increase in blood pressure in the pulmonary artery, pulmonary y vein, or pulmonary capillaries. i.e. the pulmonary vasculature
pulmonary hypertension
what is pulmonary hypertension
increase in blood pressure in the pulmonary artery, pulmonary y vein, or pulmonary capillaries. i.e. the pulmonary vasculature
what leads to Shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion
pulmonary hypertension
what does pulmonary hypertension lead to
Shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion
what are the 5 types of pulm. hypertension
Arterial,
Venous,
Hypoxic,
Thromboembolic or
Miscellaneous / idiopathic
Arterial,
Venous,
Hypoxic,
Thromboembolic or
Miscellaneous / idiopathic
are 5 types of what
pulm. hypertension
Whatever the initial cause, pulmonary arterial hypertension (WHO Group I) involves what
vasoconstriction
vasoconstriction results in what
obstruction to flow through pulm. vasculature
what happens as a result of obstruction to flow through the vasculature
vascular fibrosis that leads to further flow restriction
increased workload of the hear leads to what
hypertrophy of the right ventricle eventually leading to right heart failure
what is cor pulmonale
right heart failure
what happens during right heart failure
1. decreased pulm. flow= left heart received less B
2. decreased LH oxygen
3. decreased systemic oxygenation=increased demand on heart, HR, contractility
WHO I refers to what
arterial hypertension
WHO II refers to what
pulmonary venous hypertension
who III refers to what
hypoxic pulm. hypertension
compare PAH and PVH
PVH: no obstructive B flow in the lungs, due to left heart failure PAH: obstructive B flow to lungs, causes right heart failure
the result of PVH is what
pulmonary edema and pleural effusion caused by obstruction/back pressure on venous flow through the heart
PVH is due to what
left heart failure resulting in obstruction and back pressure on venous flow through the heart
what causes hypoxic pulm. hypertension
low levels of oxygen cause vasoconstriction of pulm. arteries leading to HPH
what is the result of HPH
similar patho as pulm. artery hypertension
what does the WHO IV group refer to
chronic thromboembolic pulm. hypertension
what caused thromboembolic pulm. hypertension
B vessels are blocked/narrowed w/ B clots= thromboembolic pulm. hypertension
what does thromboembolic pulm. hypertension cause
similar patho to pulm. arterial hypertension
what is in the WHO 1973 classification
1.Primary PH
A. Arterial plexiform,
B. Veno-occlusive and
C. Thromboembolic forms

2. Secondary PH
what addressed the causes of secondary pH
WHO 1998
WHO 1998 addressed what
causes of secondary pH
what modified the WHO classification based on new understandings of dz: risk factor descriptions, the classification of congenital systemic to shunts were revised
3rd world symposium on pulmonary arterial hypertension 2003 (venice)