CVD Flashcards
(36 cards)
Major causes of CVD
Atherosclerosis
Thrombo-embolism
Vasculitis
Modifiable risk factors for CVD
HTN Tobacco use Elevated blood glucose Physical inactivity Overweight/obesity Cholesterol/lipids (<180 mg/dL is optimal; HDL 40-60; LDL 100-129)
“Paste” “hardening”
Commonly known as “hardening of the arteries”
Dynamic chronic inflammatory condition
Pathogenesis involves lipids, thrombosis, elements of vascular wall, and immune cells
Atherosclerosis
Characteristics of atherosclerosis
Slow, progressive Starts in 2nd or 3rd decade Very long incubation period Often undetectable Initial plaques are sparsely distributed Increased in number and size over time Can affect ANY artery
Common sites for atherosclerosis to form
Femoral branches Popliteus Carotid branches Coronary arteries Common iliac (Whenever you see turbulent flow)
Developmental stage of atherosclerosis: fibrous plaque
Lipoproteins transport LDLs into arterial intima
Fatty streak is covered by collagen and calcium deposits forming a fibrous plaque that appears grayish or whitish
Result= narrowing of the vessel lumen
Developmental stage of atherosclerosis: fatty streaks
Characterized by lipid-filling smooth muscle cells
Potentially reversible
Developmental stage of atherosclerosis: complicated lesion/unstable plaques
Continued inflammation can result in plaque instability, ulceration, and rupture.
Lipid core is exposed to the blood stream, platelets accumulated, and thrombus forms.
Result = narrowing of lumen or thromboembolic event
Complications of atherosclerosis
Calcification of atherosclerotic plaque Rupture or ulceration Hemorrhage into the plaque —> further narrowing Embolization Weakening of vessel wall —> aneurysm
a condition that occur then the vein wall and/or valves in the leg do not work effectively, which impairs the ability for blood to return to the heart from the legs, resulting in venous-stasis
chronic venous insufficiency
3 systems affected by CVI
superficial– lesser and greater saphenous
deep– ant/post tibial, peroneal, popliteal, deep femoral, superficial femoral, and iliac veins
perforating or communicating veins
CVI may result from…
vein wall degeneration, post-thrombotic valvular damage, chronic venous obstruction, or dysfunction of the muscular pumps
clinically apparent increase in the interstitial fluid volume
-develops when starling forces are altered so that there is increased flow of fluid from the vascular system into the interstitium
edema
Edema
due to increase in capillary pressure usually results from an elevation of venous pressure caused by obstruction to venous and/or lymphatic drainage
- imbalance of starling forces
- generalized: HF, hypo-albumenia, nephrotic syndrome, Cirrhosis, sepsis
- localized: musculoskeletal injury, DVT
Grading for pitting edema
1+ barely detectable impression when finger is pressed into skin
2+ slight indentation, 15 seconds to rebound
3+ deeper indentation. 30 sec to rebound
4+ > 30 sec to rebound
PT implications for CVI
Elastic pressure stockings
compression pump
Unna boot
Edema Massage: contraindications–uncompensated CHF, untreated infection or cellulitis, active cancer, renal failure, sever pulmonary problems.
A persistent discontinuity in the integrity of the skin despite sufficient time for healing
ulcer
Venous Ulcer
maleolar location (usually medial)
irregular margins
browning
varicose veins and pitting edema
Arterial ulcer
dorsal or distal location (toes)
sharp margins
painful
pallor, loss of hair, nail dystrophy
Neuropathic ulcer
plantar location
“punched out” margins, correspond to pressure point
insensate, pt often has DM with neuropathy
may have arterial insufficiency sxs
Differences between venous and arterial disorders
VENOUS:
symptoms–aching, burning, heaviness, fatigue while standing
Elevation–lessens symptoms
walking–lessens symptoms
limb size– swollen in chronic disease
Skin temp- Normal
skin color– hyperpigmented
skin appearance–cellulitis, dermatitis
pulses– normal but may be hard to palpate
ulcers–near med malleolus, irregular border, pink base
ARTERIAL:
symptoms–aching, cramping that is predictable with activity and elevation
Elevation–worsens symptoms, dependency improves symptoms
walking–aching begins at specific time/distance, improves with rest
limb size– decreased due to muscle wasting
Skin temp- cool
skin color– cyanotic or pale, dependent rubor
skin appearance–reduced hair, thick/brittle nails, shiny skin
pulses– may be decreased or absent, bruits
ulcers–pale base, discrete borders, high-pressure sites like heal or toes
Wells score for DVT
> 2.0– high
1.0-2.0– moderate
< 2.0– low
+1 – active cancer, calf swelling >3 cm, swollen unilateral superficial veins, unilateral pitting edema, previous DVT, swelling of whole leg, localized tenderness along veins, paralysis, paresis or recent immobilization, recently bedridden or major surgery w/ anesthetic in past 12wks
-2– alternative diagnosis just as likely
Wells score for PE
Clinically suspected DVT-3 Alternative diagnosis is less likely than PE-3 tachycardia-1.5 immobilization in previous 4 wks-1.5 history DVT or PE-1.5 Hemoptysis-1 malignancy or palliative-1 Scoring: > 6.0--high 2.0-6.0--moderate < 2.0-- low > 4--PE likely 4 or less-- PE unlikely
Ischemic syndromes
Angina Pectoris stable angina variant angina unstable angina silent ischemia myocardial infarction
