vascular problem Flashcards
why do legs swell after DVTs
- occluded deep limb veins
- impaired venous return
- increased hydrostatic pressure
why can a leg get red and hot after DVT
- venous clot = dynamic process
- large clots can produce increase temp
- inflammation ++
- WBC activation
- cytokine release
how do you work out when to treat atrial fibrillation with an anticoagulant
AF + CHADS-VAS score
CHF - 1 hypertension - 1 age >75 - 2 diabetes - 1 stroke - 2 vascular disease - 1 age >65 - 1 sex - female - 1
score >2 (or equal) = warfarin
bleeding risk
H = hypertension A = abnormal blood results (creatinine/LFTs) S = stroke B = bleeding L = labile INR E = elderly (>65) D = drug use (alcohol)
difference between the treatment of AF and DVT/PE
DVT/PE
- urgent
- usually initially as impatient commencing with LMWH
AF
- not so time sensitive
- usually as outpatient
- no LMWH needed
- warfarin vs dabigatran
how do you calculate oxygen consumption
Vo2 = Q * 1.33 * Hb * (SaO2 - SvO2)
Q = cardiac output Hb = haemoglobin conc Vo2 = O2 consumption
therefore if you decrease Hb you have to increase Q to maintain oxygen consumption
effects of reduced oxygen on vessels
increased lactic acid in response to less oxygen (metabolic hypothesis)
causes vasodilation in peripheries so you get increased blood flow to organs
- still have sympathetic activation to heart
equation used to determine turbulence and what its determined by
reynolds number
- turbulence likely if Re > 2400
Re = pVD/u
determined by: p = fluid density V - fluid velocity D - vessel diameter u - fluid viscosity
examination findings for compartment syndrome
- pallor
- paraesthesia
- pain
- pulselessness
- paralysis
why does a patient with compartment syndrome still have a radial pulse when their hands are pale and cold?
systolic pressure is still greater than the pressure inside the cast causing compartment syndrome
what happens to noradrenaline as temperature increases
as you get warmer the affinity of skin alpha receptors to NA decreases so more likely to vasodilate
NA binding to alpha 1
increased IP3 which causes increased cytoplasmic Ca2+ levels
NA binding to alpha 2 post-synaptic
inhibits cAMP and therefore protein kinase A which can causes vasoconstriction in SM cell
NA binding to alpha 2 pre-synaptic
favours vasodilation
describe cardiogenic pulmonary oedema
there’s an increased hydrostatic pressure causing increased fluid filtration into the alveolar
- protein-poor oedema fluid