Chapter 33: Alterations Of CV Function Flashcards
Prevalence of CV dz
Leading cause of death in the United States and the world
Total percent of deaths from cardiovascular diseases in the United States: 24.6%
Develop from lifestyle choices: sedentary, smoking, diet
Mechanisms of CV dz
Genetic, neurohumoral, and inflammatory mechanisms:
Underlying tissue and cellular processes ->
Endothelial injury
Remodeling
Stunning -> plaque forms and cannot perfuse
Reperfusion injury
Inflammation
Varicose veins
Vein in which blood has pooled
Usually in the saphenous vein
Distended, tortuous, and palpable veins
Causes of VV
Trauma or gradual venous distention, rendering valves incompetent
Think pressure and weight
RF of VV
genetic predisposition, pregnancy, obesity, prolonged sitting or standing,
Manifestations of VV
Irregular, purplish, bulging veins
Pedal edema
Fatigue
Aching in the legs
Shiny, pigmented, hairless skin on the legs and feet
Skin ulcer formation
Dx of VV
physical examination, Doppler ultrasound, and venogram
tx of VV
rest with affected leg elevated, compression stockings, avoid prolong standing or sitting, exercise, sclerotherapy, and surgical removal
Chronic venous insufficiency
Inadequate venous return over a long period as a result of varicose veins and valvular incompetency
Manifestations of CVI
Lower-Leg swelling, skin color and texture changes -> yellow slough or ruddy skin, venous ulcers (ankles) with irregular borders, dull, achy pain, pulse present, drainage
Deep vein thrombosis
Thrombosis: Clot
Detached thrombus: Thromboembolus; can lead to pulmonary emboli
Clot in a large vein
Obstruction of venous flow leading to increased venous pressure
Virchow triad: DVT
Venous stasis:
Immobile -> sx, long airplane ride, VV, obesity
Venous endothelial damage:
Sx, trauma, VP, atherosclerosis
Hypercoagulable states:
Genetic, malignancy, oral contraception, smoking
Common places of DVT
Typically see in legs, pelvis is hospitalized pt, arms in sedentary person
Prevention of DVT
Mobilization soon after surgery, illness, bed rest, injury
Prophylactic low–molecular-weight heparin, antithrombin agents, warfarin, or pneumatic devices
Inferior vena cava filter -> screen placed in IVC to catch clots
Dx of DVT
D-dimer: test that looks at fibrin degradation products (FDPS) in the blood –increased = blood clot formation
US
Tx of DVT
Low–molecular-weight heparin, unfractionated intravenous heparin, antithrombin agents, or adjusted-dose subcutaneous heparin
Thrombolytic therapy: TPA
Aspirin: Antiplatelet
HTN
Prolonged elevation in blood pressure
Excessive cardiac workload due to increased afterload and vasoconstriction
RF for HTN
advancing age, ethnicity (AA and Hispanic), family history, being overweight or obese, physical inactive, tobacco use, high-sodium diet, excessive alcohol intake, stress, and other chronic conditions
Primary HTN
Most common form
Develops gradually over time
Causes of primary HTN
Essential or idiopathic
Secondary HTN
Tends to be more sudden and severe
Occurs secondary to another cause
Causes of secondary HTN
Causes: renal disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs, pregnancy dt estrogen
Malignant HTN
Intensified form
Does not respond well to treatment
Manifestations of HTN
“Silent killer”
Include: fatigue, headache, malaise, and dizziness