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
