Respiratory CIS high yield handout 2 Flashcards
wells criteria 1.0 pts
malignancy
hemoptysis
what does GTPAL for obstetrical history taking stand for
G= gravidity (# of pregnancies)
Term births (term deliveries (full) births (38 wks or more)
Preterm births (preterm deliveries from viability up to 37 wks
Abortions/miscarriages
Living children
potential indications for thrombolytic therapy in venous thromboembolism
presence of hypotension related to PE presence of severe hypoxemia substantial perfusion defect RV dysfunction assocaited with PE extensive DVT
labs to consider checking for inherited thrombophilia
activated protein C/factor V leiden
homocysteine level
antithrombin III/protein C/protein S assay
antiphospholipid antibodies
what is tPA
clot buster
naturally occurring enzyme produced by endothelial cells
binds fibrin, increases its affinity for plasminogen and enhances its activation
are hormones pro thrombotic
yes
HRT and estrogen
S2 splitting during cardiac exam
physiologic splitting of S2 on inspiration can be normal
persistent splitting of S2 during inspiration and expiration can be sensitive and specific for
- heart disease in adults, most likely RBBB
- RV pressure overload situations such as acute massive PE
managment if no personal or family history of VTE but have antithrombin deficiency
propylatic anticoag postop, during pregnacny, and postpartum
types of shock
hypovolemic
cardiogenic
distributive
obstrucive (PE, tension pneumothorax) (pericardial tamponade)
managment of thrombofilia with family history of VTE only (no personal history of it themselves)
if no other risk factor then routine care and education
if other risk factors: prophylactic antigcoag postoperatively, during pregnancy and postpartum
what is virchow’s triad
alteration in blood flow
vascular endothelial injury
alteration in constituents of blood
VTE risk
wells criteria 3.0 pts
clinical symptoms of DVT
other diagnosis less likely than pulmonary embolism
what can be seen on ekg that is indicative of PE
S1 Q3 T3
S in lead 1
Q in III
inverted T in III
management of acute VTE
anticoag for at least 3-6 months
possible indefinite anticoag if:
- unprovoked VTE
- life threat PE
- male
- VTE at odd site
- strong family history of VTE
other risk factors of VTE
homozygous or compound heterozyougs for defect
or FVL or antithrombin defiecnicy
VTE in family member less than 50
wells criteria traditional score
high >6
moderate 2-6
low <2
wells criteria simplified
PE likely over 4
PE unlikely at or under 4
gold standard imaging choice for PE
CT angiogram (CTA) of the chest -consider stability of pt
what is factor V leiden
- mutant form of coag factor V
- mutant is insensitive to actions of activated protein C (anticoag)
- these pts are at increased risk of venous thromboembolism
- common in population and many individulas with mutation will never have ven TE
absolute contraindications of fibrinolytic therapy
prior intracranial hemorrhage
known structural cerebral vascular lesion
known malignant intracranial neoplasm
ischemic stroke within 3 months
suspected aortic dissection
active bleeding or bleeding diathesisis
significant closed head trauma or facial trauma
what can be heard on pulmonary exam of pt with PE, 53% of time
rales
what does total hysterectomy mean
take uterus and ovaires out, usually but not always they take cervix too
what is MAP
mean arterial pressure
diastolic BP + ((systolic - diastolic)/3)
>65 = good perfusion to all organs <65 = hypotension/hypoperfusion
whsat is the most common findings on an EKG pt with a PE
nonspecific ST-T wave abnormalties and sinus tachy
recall CAD risk factors
emotional stress
no exercise
wells criteria 1.5 pts
HR over 100
immobiliztion for 3 or more days or surgery in previous 4 weeks
previous DVT/PE
what is an invasive but hightlly accurate way of measuring BP constantly
good for what pts
arterial line
-excellent in pts with any type of shock
