2.2 Cardiovascular Vascular Flashcards
anemia
↓ RBCs &/or ↓ hemoglobin
anemia defined
Results in reduced oxygen-carrying capacity of blood
Incidence increases with aging, not always a clear cause
anemia S/S
S/S depend on degree & if onset is gradual or acute and are RT tissue hypoxia
S/S: ↑HR, ↑R, angina, fatigue, SOB, pallor, HA, dizziness
anemia causes?
Causes:
Decreased RBC production or impaired HgB synthesis
-Altered Hgb synthesis: iron deficiency, chronic inflammation
-Altered DNA synthesis: B12 or folic acid deficiency
-Bone marrow failure
Increased RBC loss/destruction
- Acute or chronic blood loss (loss of volume, cells, & components)
- Increased hemolysis
Nutritional anemias
IRON DEFICIENCY
IRON DEFICIENCY: most common, Fe supply inadequate
↓# RBCs, microcytic (small), hypochromic (pale), malformed RBCs
Can be due to chronic blood loss, inadequate intake/absorption, or increased needs
Nutritional anemias
IRON DEFICIENCY S/S
S/S: spoon-shaped nails, cheilosis (corners of the mouth become inflamed, which can lead to cracking and pain at the corners of the mouth), smooth, sore tongue, pica (craving) + common anemia S/S
Nutritional anemias VITAMIN B12
VITAMIN B12 DEFICIENCY: B12 animal sources
- PERNICIOUS ANEMIA (B12 deficiency): unable to absorb due to lack of intrinsic factor secreted by gastric mucosa
- Other absorption problems (gastric bypass, ETOH, chronic gastritis)
- Dietary deficiency in vegans
RBCs large (macrocytic), misshapen, thin membranes, short-lived & fragile
Nutritional anemias VITAMIN B12 S/S
S/S: pallor, slight jaundice, weakness, diarrhea, sore beefy red tongue, also neuro symptoms with deficiency
Nutritional anemias FOLIC ACID
FOLIC ACID DEFICIENCY: green, leafy vegs, fruits, cereals and meats, intestinal absorption,
RBCS: megaloblastic cells (lg, immature)
Inadequate intake: in chronically undernourished, elderly
Impaired metabolism: ETOH suppresses folate metabolism, some meds (chemo drugs)
Impaired absorption: celiac, med-related
Increased needs: pregnancy, dialysis, hemolytic anemias
Nutritional anemias FOLIC ACID S/S
S/S: gradual onset of pallor, weakness, glossitis (looks like B12 deficiency, but NO NEURO symptoms)
Assessment (megaloblastic anemia):
Tissue hypoxia causes the symptoms
Clinical S/S: (depend on severity of anemia)
- Beefy red tongue, sore
- Anorexia, nausea, vomiting
- Abd pain
- Weakness
- Tachycardia
- Ataxia
- Muscle weakness
- B12 only: Neuro: paresthesias; (hands/feet) gait ataxia; impaired thought
- Impaired thought processes (confusion to dementia).
Assessment (megaloblastic anemia):
Labs
Treatment
Labs:
Cobalamin, folate levels, Hgb/Hct, MCV, test for IF antibodies,
Treatment:
Supplements (cobalamin can’t be oral if IF deficiency – give IM)
Polycythemia
Increased production of RBCs.
Impaired circulation due to increased blood viscosity.
Polycythemia 2 Type
2 Types:
Polycythemia Vera: Chronic chromosomal mutation with ↑RBCs, WBCs and platelets uncommon (HCT >55%)
Secondary Polycythemia:
Hypoxia driven - ↑ oxygen demand (high altitudes, smoking, COPD) = ↑EPO (erythropoietin) most common
Hypoxia independent- malignant or benign tumors
Assessment of polycythemia
HTN: HA, dizziness, vision & hearing changes
Venous stasis: plethora (ruddy color), itching of fingers/toes
Retinal engorgement
Hypermetabolism: weight loss, night sweats
Altered mental status: drowsiness, delirium
Splenomegaly (primary only)
GI bleeding
Intermittent claudication
thrombosis
Teaching management of polycythemia
Primary Polycythemia
Primary Polycythemia Vera (not preventable). Perform phlebotomy (500ml) Monitor I & O -hydration Prevent stasis & DVT exercise, ASA Meds (leukemia risk)
Teaching management of polycythemia
Secondary polycythemia
Secondary polycythemia Controlling chronic pulmonary disease Smoking cessation Avoid high altitudes. Monitor I & O, hydration Prevent stasis & DVT
Peripheral Arterial Disease Pathophysiology
Pathophysiology
Progressive thickening of walls, narrowing lumen, and ↓elasticity of the arteries of the neck, abdomen, and extremities.
Atherosclerosis is major cause
4 to 5 times the risk of dying from MI/stroke.
Strongly RT other CVD
Peripheral Arterial Disease PAD Risk Factors
PAD Risk Factors 4 most significant factors: Cigarette smoking Hyperlipidemia Hypertension Diabetes Other risks: Obesity Hypertriglyceridemia Hyperuricemia Family history Sedentary lifestyle Stress
Intermittent claudication
Ischemic muscle ache or pain precipitated by exercise which resolves within 10 minutes or less with rest and is reproducible.(lactic acid)
Progresses slowly causing atrophy of the skin and underlying muscles.
Delayed healing of wounds of lower extremities
Amputation of extremity with gangrene.
Management PAD Diagnostic testing
Diagnostic testing
Doppler Ultrasound
Angiography to detect the location and extent of the disease process.
MRA is alternative to angiography(no dye)
Management PAD
Treatment
Treatment Smoking cessation Medications: Antiplatelet agents: Aspirin, Plavix, Ticlid Ace inhibitors Trental, Pletal
Management PAD Risk factor
Risk factor modification:
control DM, HTN, wt
Exercise therapy
Surgical therapy
Nursing Implications for PAD
Assess pulses, pain, color, temperature & capillary refill. (R) Establishes baseline assessment data.
Position extremities dependent- (R) promotes arterial flow, increases perfusion, decreases pain.
Teach exercise benefits: (R) promotes collateral circulation to ischemic tissues & slows atherosclerosis. Teach rest when claudication begins with extremity dependent & resume when pain subsides.
Keep extremities warm- socks, slippers, light blankets NO heating pads. – (R) promotes circulation & prevents vasoconstriction.
Encourage position changes & ROM exercises- (R) ↓ pressure, ↑ circulation, ↓ tissue ischemia. ROM prevents muscle atrophy
Nonatherosclerotic PAD
Buerger’s Disease
Buerger’s Disease: (Thromboangitis Obliterans)
- Thrombosis & fibrosis occur inside the vessel →ischemia.
- Nonatherosclerotic, autoimmune?
- Segmental: isolated UE, LE, single leg, foot, or hand
- Inflammatory cells invade artery wall, thrombus formation & vasospasm = impaired flow, intermittent with remissions
- Progressive disease leads to scarring & collateral involvement
Nonatherosclerotic PAD
Buerger’s Disease
S/S
Treatment
S/S: pain, skin changes over time, ↓ distal pulses, ulcers
Incidence: smokers, men< 40
TX: Smoking cessation, foot care, prevent vasoconstriction, exercise, meds for symptomatic relief, surgery (sympathectomy, bypass grafts, amputation)
Nonatherosclerotic PAD
Raynaud’s
Raynaud’s :
Episodic vasospastic disorder of small cutaneous arteries of fingers and toes .
“disease”- no identifiable cause
“phenomenon”- secondary to disease or exposure
Can be RT trauma and pressure to fingertips in typists, pianists, and those using in handheld vibrating equipment.
Common in young women 15-45 years.
Nursing assessment Raynaud’s
Fingers, toes, ears, and nose change colors (blue, white, red)
Patient describes coldness, numbness, followed by throbbing, aching, tingling and swelling.
Episodes lasts minutes to hours.
Precipitated by cold, emotional upsets, caffeine, and tobacco use
Skin becomes thickened and nails brittle over time
Raynaud’s management
Diagnosis : persistent symptoms, HX
Treatment PREVENTION: -Keep warm, wear gloves -Avoid injury -Increase perfusion –swinging hands -Smoking cessation -Stress management
MEDICATION
- Calcium channel blockers (nifedipine(Procardia)
- Vasodilators
- Alpha blockers
Chronic Venous Insufficiency:
One-way valves in the veins are damaged = retrograde flow, pooling, and swelling
Chronic Venous Insufficiency: Causes
Causes: incompetent valves in the legs, pressure in the vein ↑and forces fluid & RBCs into the tissue → edema and hemosiderosis (brownish discoloration)
Ulcerations RT complex inflammatory & circulatory factors
Chronic Venous Insufficiency: S/S
S/S: Brawny, brownish, leathery fragile skin Cyanosis if dependent Persistent edema in LEs Stasis dermatitis-itching with standing Ulcers above medial malleolus Pain ↑ if dependent Recurrent ulcerations & cellulitis
Care of venous vascular disease
COMPRESSION: essential
Ace wraps, ,custom-fitted compression stockings, SCD, Unna boot
Moist environment wound dressings
Nutritional evaluation & education
Education: avoid trauma, skin care, compression stockings
Activity: avoid prolonged standing/sitting or crossing legs, elevate to reduce edema, avoid constrictive clothing, avoid trauma, ambulation if indicated
Comparison of arterial and venous ulcers: (table 32-6 pg 1004 Lemone)
Arterial vs. Venous PVD
Arterial disease
Arterial disease pulses: dim or absent Cap refill: > 3 sec Ulcers: toes, foot, lateral malleolus Round, smooth margins Minimal drainage Eschar, pale pink granulation Pain: intermittent claudication, rest pain Skin: rubor, pale elevated Thin, shiny, taunt, hairless Cooler gradient down leg Thick toenails
Arterial vs. Venous PVD
Venous disease
Venous disease
pulses: +
Cap refill <3 sec
Ulcers:
Near medial malleolus
Irregular shape
Mod to copious drainage
Yellow slough, dark red granulation
Pain: dull ache, heaviness
Skin: brown discoloration
Thick, hardened, indurated
Warm
Itchy
