-
Development of RBC’s /Erythropoiesis
normocytic
microcytic
macrocytic
normochromic
hypochromic
anemia
polycythemia
• Kidneys sense hypoxia & release erythropoietin that stimulates bone marrow to produce RBC’s (takes 5days) - live 110- 120 days before apoptosis
• RBC/erythrocyte = biconcave- • Size RBC: normal = normocytic;small = microcytic; large = macrocytic
- • Color RBC:normal = normochromic; diminished/pale= hypochromic
- • Decrease in RBC’s = anemia
- • Increase in RBC’s = polycythemia - normally found in older men & COPD
-
RED BLOOD CELL COUNT
• Number of erythrocytes (RBC's) - 3.5 - 5.5 mm3
- • Contain hemoglobin Hgb - 12-18 gm/dL
- (O2 carrying protine in blood)
- • Hematocrit (Hct) - volume, expressed as % - 36-50%
- Hct is the packed cell volume -% of RBC's in blood
Hct should be 3x Hgb - and both values should move together with increases and decreases
-
Hemoglobin
- • Transports oxyhemoglobin (O2) to the cells
- • Has an affinity to oxygen
- • Iron is needed for production of hemoglobin
- • RBCs are destroyed about every 120 days
- • After RBC destruction (hemolysis) the hemoglobin turns to bilirubin & is metabolized by the liver -
- Jaundice results if not metabolized by liver
-
A N E M I A
- • Low RBC count or
- • Low Hgb or Hct
- DUE TO:
- • Inadequate production of RBC’s
- • Premature or excessive destruction of RBC’s
- • Blood loss– May be occult
- ETIOLOGY
- • Iron or nutrient deficiency
- • Hereditary
- • Chronic diseases
- • Trauma/bleeding
-
Iron Supplements
Iron in diet not absorbed well
- RNA = 15 - 30 mg/day -body absorbs 1-4 mg
- Actual need about 1 mg/day
*#1 cause of anemia in elderly - low iron in diet
Iron supplemsnts - give 1st thing in moring with OJ - better absorbed with Vic C
(Loose 250 mg Iron in each unit of blood donated)
-
A N E M I A - Signs / Symptoms (for all types of anemia)
- • Weakness
- • Fatigue/malaise
- • Dyspnea on exertion
- • Tachypnea
- • Pallor
- • Tachycardia
- • Palpitations
- • Systolic murmur
- • Night cramps
- • Chest pain/angina due to increased cardiac workload
- • Bone pain due to increased erythropoietin
- • Headache, dizziness or dim vision due to cerebral hypoxia
- • Heart failure with vent. hypertrophy
-
A N E M I A - Classifications
- Nutritional Anemias –
- • Lack of iron
- • Lack of vitamin B12
- • Lack of folic acid
- Hemolytic Anemias -
- • Sickle cell
- • Thalassemia
- • G6PD
- • Acquired/extrinsic
Aplastic Anemia -
- Blood Loss/Secondary Anemia - • Acute bleeding with normal size & shape of RBC’s(normocytic) if sufficient iron present
- -Takes 3 – 4 wks. For RBC’s to return to normal after bleeding episode
-
Iron Deficiency Anemia
• DIAGNOSIS
- • Low serum iron & high total iron-binding capacity
- • Low serum ferritin
- • Low H&H (iron needed for the synthesis of Hgb)
- • RBC’s microcytic, hypochromic & poikilocytosis (malformed RBC's) - small, pale, misshapen
- ETIOLOGY:
- • Inadequate ironintake in diet
- • Malabsorption
- • Chronic blood loss esp. GI bleed & menses
- • Most common type of anemia
-
Iron deficiency anemia - S & S (in addition to general anemia symtpoms)
- • Brittle spoon-shaped nails
- • Cheilosis/cracks around mouth corners
- • Smooth, sore tongue (glossitis)
- • Pica (unusual cravings for starch, clay, ice, cornstarch, etc.)
-
Iron Deficiency Anamia - Treatments
- Diet:
- • Heme & nonheme sources of iron should be 50/50 in diet
- Heme - animal sources - beef, chix, eggs, pork
- *aids in absorption of nonheme iron
- Nonheme - bran flakes, brown rice, whole-grain breads, dried beans, dried fruits, greens, oatmeal
- *absorption enhanced by Vit C and hindered by tea and coffee
- • Iron supplements -– Pills with OJ to enhance iron absorption
- – Liquid – use straw as stains teeth
- – 2 hr before taking Tetracycline
- – Don’t take with milk or antacids
- – N & V side effect/toxicity
- – Constipation – increase fiber & fluids
- – Black or dark green stools
Procrit/ erythropoietin injections available
Blood transfusions of severe
-
B12 Deficiency Anemia
Pernicious Anemia
– B12 is needed to mature RBC's (macrocytic)
- -can be caused by lack of B12 in diet - rare - unually only among vegitarians
- –Animal Sources • Meat/fish (salt water)• Eggs• Dairy (milk & cheese)
- Pernicious Anemia - failure to absorb dietary B12
- – Not absorbed by gastric mucosa due to lack of intrinsic factor or other reasons(malabsorption)
-
Signs/Symptoms of B12Anemia:
Treatments
- • Pallor or slight jaundice
- • Sore, beefy red tongue
- • Diarrhea
- • Paresthesias & decreased proprioception
- • Treatment:
- • Increase diet B12 (muscle meats, fish, eggs,dairy)
- • Oral B12 (Kaybovite) if absorption notproblem
- • B12 injections for rest of life if absorption problem(hydroxycobalamin or cyanocobalamin)
-
Folic Acid Deficiency Anemia Causes
- • Poor consumption/diet-
- – Green leafy veggies
- – Fruits
- – Cereals/yeast products
- – Meat
• Older adults, drug users, and alcoholics- ETOH decreases folate metabolism
- • Increased metabolism-
- – Pregnancy need at least 400 mg /d (neural tubedefects)
- – Rapidly growing teens
• Certain medications (methotrexate, pneumopent,oral contraceptives, dilantin)
-
Folic Acid Deficiency Anemia S & S
Treatments
- • Signs/Symptoms
- • Pallor
- • Weakness/fatigue
- • SOB/dyspnea
- • Palpitations
- • Glossitis
- • Cheilosis
- • Diarrhea
- • No neuro symptoms
- Treatment
- • Correct diet (green leafy veg., organ meats, eggs,milk, cereals)
- • Folic acid supplements(PO or parenteral/IM,SQ, or IV)
-
Hemolytic Anemias:
- • Intrinsic – disorders within RBC
- – Sickle cell anemia
- – Thalassemia anemia - genetic
- – G6PD (glucose-6-phosphate dehydrogenase)anemia - genetic
• Extrinsic – acquired hemolytic anemia (trauma,drugs, bacteria, toxins)
• Hemolytic = destruction/lysis of RBC’s(normocytic & normochromic)
-
SICKLE CELL ANEMIA:
• Genetic defect (HbS gene)
- • Episodes can be triggered by:
- • Infection,
- • High altitudes (hypoxia)
- • Stress/acidosis
- • Surgery/blood loss/anesthesia
- • Excess exercise
- • Pain is caused by ischemia from the sickled cells clumping and decreasing circulation to organs
- • Can affect all organs (esp. spleen & kidney)
-
Sickle cell trait
Sickle cell disease
Sickle cell crisis
Sequestration crises
• Sickle cell trait=inherit gene from 1 parent; 40% HbS hemoglobin; asymptomatic unless severe hypoxia
• Sickle cell disease=inherit gene from both parents so at risk for sickle cell crisis
• Sickle cell crisis= severe episode of fever & intense pain with thrombi & ischemia (4-6 days)
• Sequestration crises= blood pooling in liver & spleen esp. in children with sickle cell
• DX: Sickle cell test & hemoglobin electrophoresis
-
idiopathic
unknown cause or origin
-
Aplastic Anemia
- Malfunctioning bone marrow-no RBC’s, WBC, or Platelets(“Pancytopenia”)
- • Bone marrow replaced by fat
- • Cause: 50% unknown (idiopathic aplastic anemia) Others may be from Chemicals or Radiation (secondary)
• S/S: pallor, fatigue/weakness, dyspnea on exertion, HA,tachycardia, bleeding, infection
- • Tx: remove causative agent, transfusions, bone marrow transplant
- (-allogeneic- from family member
- -autologous -from self)
- corticosteroids,cyclosporine, androgens to stimulate RBC’s
-
Pancytopenia
reduction in RBC, WBC and Platelets
-
ANEMIA NURSING DIAGNOSES
ACTIVITY INTOLERANCE R/T anemia
POTENTIAL DECREASED CARDIAC OUTPUT RT bleeding
ALTERED NUTRITION, LESS THAN BODY REQUIREMENTS RT iron, B12, and/or folic acid deficiencies
INEFFECTIVE MANAGEMENT OF THERAPEUTIC REGIMEN R/T diet & medication
SELF-CARE DEFICITS R/T weakness and fatigue
IMPAIRED ORAL MUCOUS MEMBRANES R/T glossitis & cheilosis
-
POLYCYTHEMIA
- • Increased concentration of RBC’s(erythrocytosis)
- • Red cell count > 6 million/mm3
- • Hgb > 18 g/dl
- Hct > 55%
Primary polycythemia vera – rare; European Jewish men ages 40-70; overproduce RBC’s in absence of erythropoietin
• Secondary polycythemia – most common -response to hypoxia (high altitude, smoker, COPD) with increase in erythropoietin
• Relative polycythemia –due to fluid deficit with normal RBC’s; correct by rehydration
-
POLYCYTHEMIA - Symptoms
- Symptoms caused by Increased blood volume
- • headache
- • dizziness/vertigo
- • blurred vision
- • tinnitus - rining in ears
- • pruritus/itching
- Symptoms caused by Increased blood viscosity
- • hypertension
- • Intermit. claudication - cramping in lower legs due to inadequate blood flow to muscle
- • thrombus formation
- • ruddy complexion(plethora)
- • wt. loss/night sweats
-
Neutropeina
Decreased neutrophil count = < 1,500mm 3
- < 1500 = neutropenia
- < 1000 = risk for infection
- < 500 = high risk for infeciton
- < 200 = agranulocytosis (severe -caused by chemo)
- < 100 = guarnateed to get infeciton
-
Neutropenia S & S
- • S/S: opportunistic infections (bacterial, fungal,protozoa) esp. resp., mouth, GI & vaginal
- – Malaise
- – Fever/chills
- – Extreme weakness/fatigue
- *Temperature is most valid assessment of infection - WBC count will be low anyway
- • TX: GM-CSF, granulocyte macrophage colony stimulating factor to produce WBC’s
- – Antibiotics
- – Reverse/protective isolation - strict handwasing
-
THROMBOCYTOPENIA
Stages
- =DECREASED PLATELETS
- -decreased production of platelets by the bone marrow -increased peripheral destruction of platelets(spleen also sequesters 80%
NORMAL PLATELET COUNT 150,000 - 400,000
- - < 100,000 mm3 thrombocytopenia
- – < 50,000 mm3 symptoms (petechiae, purpura)
- – < 20,000 mm3 spontaneous bleeding
- – < 10,000 mm3 fatal bleeding
-
Thrombocytopenia S & S
- ITP - Immune thrombocytopenia (idiopathic)
- petechiae
- purpura
- nose bleeds/ epistaxis
- hematuria
- bleeding gums
- TTP - Thrombotic Thrombocytopenia (thrombi form)
- Petechiae
- Purpura
- HA
- Seizures
- Altered LOC
-
Thrombocytopenia Nursing Dx:
Intervetions
- Ineffective Protection
- Impaired Oral Mucous Membranes
- Intervetions
- Assess for bleeding (everywhere)
- Hold finger sticks for 5 minutes
- Hold arterial punctures for 20 minutes
- No sharp objects
- no rectal temps or IM injections
- Spone tip swab for oral hygiene
- No Asprin
- No blood thinners
-
Development of WBC’s /Leukocytes (5000 – 10,000 mm3)
KNOW THIS
- • Granulocytes -
- – Neutrophils 60-70% WBC’s, 3000-7000 mm3, phagocytes 1st to arrive at injury, immature bands
- – Eosinophils 1-3% WBC’s, 50-400 mm3, esp. lungs & GI;allergic reactions & parasitic infestations
- – Basophils <1% WBC’s, 25-200 mm3, histamine, heparin & inflammatory mediators in allergic & inflammatory reactions
- • NongranularWBC’s/agranulocytes-
- – Monocytes 3-8% WBC’s, 100-600 mm3
- - -Phagocytes mature into macrophages; bactericidal & proteolytic enzymes
- – Lymphocytes 20-30%, 1000-4000 mm3
- -- Mature in thymus to B & T cells, humoral & cell-mediated immunity
-
Blood Transfusion
- check Dr’s order & pt. consent
- • check labels - 2 Nurses - check crossmatch
- • Pt arm band
- • MAR
- • Label on blood
- • baseline vitals & q 5 min x3 then q 30 min til 1 hr post
- • #18 gauge needle
- • normal saline only
- • set with filter
- • severe reactions first 15minutes• change tubing/filter if giving multiple units
- • return bag to blood bank
- Never add medications to blood products
- Infuse over 2 -4 hours
- Check blood for bubble/ discoloration
Flshing may be normal but stop and check anyway
Diuretics (Lasix) commonly ordered after blood to decrease fluid volume
-
Blood Transfusion Reactions
- - Febrile (1st 15 min.)
- Sensitivity of client’s antibodies to donor’s WBC’s
- • Fever
- Chills
- • Warm flushed skin
- • Headache
- • Anxiety
- • Muscle pain
- Hypersensitive (during or after transfusion)
- • Mild Allergic
- • Sensitivity of client’s antibodies todonor’s plasma proteins (IgA)
- • Itching
- • Flushing
- • Urticaria/wheals
- • Bronchial wheezing
- • Severe Allergic(Anaphylactic)
- • Antibody – Antigen Reaction
- • Dyspnea
- • Chest pain
- • Circulatory collapse
- • Cardiac arrest
- Acute Hemolytic = Discontinue Blood
- ABO incompatibility between client & donor
- • Chills
- • Fever
- • Headache
- • Backache
- • Dyspnea
- • Tachypnea
- • Cyanosis
- • Chest pain
- • Tachycardia
- • Hypotension
- Circulatory Overload
- Blood running too fast for body to accommodate
- • Cough
- • Dyspnea
- • Crackles
- • Distended neck veins (+JVD)
- • Tachycardia
- • Hypertension
- Sepsis
- Contaminated blood was administered
- • High fever
- • Chills
- • Vomiting
- • Diarrhea
- • Hypotension
- 21
- Blood Reactions Acute Hemolytic
- ABO incompatibility between client & donor
- • Chills
- • Fever
- • Headache
- • Backache
- • Dyspnea
- • Tachypnea
- Discontinue Blood
- • Cyanosis
- • Chest pain
- • Tachycardia
- • Hypotension
- Blood Reactions - Circulatory Overload
- Blood running too fast for body to accommodate
- • Cough
- • Dyspnea
- • Crackles
- • Distended neck veins (+JVD)
- • Tachycardia
- • Hypertension
- Blood Reactions - Sepsis
- Contaminated blood was administered
- • High fever
- • Chills
- • Vomiting
- • Diarrhea
- • Hypotension
-
Interventions for Blood Transfusion Reactions
- • Stop the Blood ( tubing & KVO with .9NS IV)
- • Call MD
- • Monitor Vitals, I & O
- • Give Antipyretics, antihistamines as ordered
- • Treat shock if present
- • Recheck crossmatch
- Hemolytic Reactions:
- • blood samples
- • urine sample
- • monitor fluid / lytes
- • evaluate cause of reaction
-
Hypertension Stages
KNOW
- Normal <120/ <80
- - Recheck 2 yrs & cont lifestyle practices
- High Normal (pre-hypertensive)
- 120-139 / 80-89
- -recheck in 1 year - lifestyle changes
- Stage 1 Hypertension
- 140-159 / 90-99
- -confirm in 2 months - lifestyle changes & diuretic
- Stage 2 Hypertension
- >160/ >100
- -evaluate or refer within 1 month - lifestyle changes, diuretic, and anti-HT drigs
-
Hypertension - Definition
- Persistent high blood pressure
- Systolic pressure above 140 mm Hg
- Diastolic pressure above 90 mm Hg
Based on average of 3 readings sep. occasions
- Major cause of:
- Heart failure/CAD
- Stroke/CVA
- Kidney failure
-
Hypertension types
Primary/essential – 90%
Secondary to another problem(renal disease, adrenal tumors,drugs like antihistamines orcorticosteroids, pregnancy) –10%
-
Primary (essential) hypertension
- Onset Age 30-50
- No known cause but Risk Factors are:
- Overactive renin angiotensin,aldosterone with Na & H2O retention
- Diabetes Mellitus
- -Increased fat & plaquein arteries
- - Increased vascular resistance
- Overactive sympathetic
- -causes vaso/ veno constriction
- Obesity (central)
- - Apple vs. Pear
- Insulin Resistance
- - Increases blood clots
- ↑ Alcohol Intake
- - 3 or more drinks/day
- Smoking
- - Nicotine vasoconstricts
- Stress
- - Vascular smooth muscle hypertrophy
-
Secondary Hypertension
- look for secondary if < 20 yr or > 50 yr with sudden onset Causes of Secondary HT:
- Narrowing of Aorta
- Renal Disease
- Spinal Cord Injury
- Pheochromocytoma
- Pregnancy
- Cushing’s Syndrome
- Medications:
- - Cocaine
- - Methampheta.
- - BC Pills/estrogen
- - Pseudophedrine
-
SIGNS & SYMPTOMS
Hypertension vs. Hypertensive Crisis
- Hypertension:
- Asymptomatic except elevated BP
- Headache (back head & neck)
- Nocturia
- Confusion
- Nausea & vomiting
- Visual disturbances
- Retinal hemorrhages
- Papilledema/swelling optic nerve
- Hypertensive Crisis:
- Sudden & severe ↑ in BP (Systolic > 180 mmHg /Diastolic > 120 mmHg)
- S/S: HA, blurred vision, confused, neuro deficits
- Due to:
- under medicated for HTN
- or lack of compliance with regimen
- or from crack, cocaine, PCP, LSD
Causes organ damage: MI, Renal Failure, Pulm.Edema, Aortic Aneurysm, Intracranial Hemorrhage,CVA, or DIC
TX: IV drugs: NTG, Nitroprusside, Hyperstat,Apresoline, Brevibloc, Vasotec, Lasix, Cardene etc.
-
Relationship between diabetes and hypertension
(hypertension) is an important risk factor for the development and worsening of many complications of diabetes, including diabetic eye disease and kidney disease. It affects up to 60% of people with diabetes.
- Having diabetes increases your risk of developing high blood pressure and other cardiovascular problems, because diabetes adversely affects the arteries, predisposing them to atherosclerosis (hardening of the
- arteries)
-
DASH Diet
Dietary Approaches to Stop Hypertension
- Eat fruits and vegetables (up to 10 servings/ day)
- Use low-fat dairy products
- Reduce sodium intake
- Reduce cholesterol, fat and saturated fat intake
- Grains - 7 -8 servings / day
- Meats/ Fish/ Poultry - 2 or less 3 oz servings/day
-
H Y P E R T E N S I O N
Nursing Diagnoses
- H Y P E R T E N S I O N
- Nursing Diagnoses
- Ineffective Health Maintenance RT lack of knowledge of pathology, medications & diet
- Risk for Noncompliance RT medications
- Anxiety RT diagnosis, regimen, & lifestyle changes Sexual Dysfunction RT HTN medications
- Excess Fluid Volume RT renin angiotensin aldosterone system
- Decisional Conflict RT smoking
- Imbalanced Nutrition (More) RT obesity
- Risk for Injury RT Hypertensive Crisis
-
Hypertension Nursing Interventions
- Monitor:
- BP at frequent intervals
- Vision (retinal changes)
- I & O
- Renal Studies
- Weight
- Medication compliance
- Diet-DASH
- Low fat
- Low salt
Stop smoking
- Limit alcohol to
- 1 beer (12oz)
- 5 oz of wine
- 1 oz alcohol
- Physical activity
- Stress reduction
- Exercise
- Biofeedback
- Therapeutic touch
- Yoga
- Meditation
-
hypertension: Medications
D I U R E T I C S
- Decrease Volume
- Inhibit Aldosterone
- Negative Sodium Balance
Thiazide Diuretics- distal tubule 70-80% Na reabsorbed; safe (hypokalemia, skin rashes,gout & hyperglycemia)
- Hygroton, Diuril, Hydrochlorothiazide (HCTZ)
- Loop (of Henle) Diuretics – 10-20% reabsorbed (more potent than thiazides)
- Lasix (hearing loss & hypokalemia), Bumex, Edecrin
Potassium-Sparing Diuretics- inhibit aldosterone Aldactone (gynecomastia over long time)
-
Hypertension Medications
Beta-Adrenergic Blocking Agents
decrease heart rate & cardiac output & interfere with renin release by kidneys
- Atenolol
- Toprol XL
- Lopressor
- Levatol
- Cartrol
- Corgard
- Inderal
Assess for asthma,chronic lung disease, bradycardia Assess BP & apical pulse b/4 giving & hold HR< 50 b/m Report bradycardia,fatigue, dyspnea,altered gluc. levels Chg. positions slowly to prevent dizziness
-
Hypertension Medications
ACE Inhibitors & Angiotensin IIreceptor blockers
- Inhibit conversion of Angiotensin I to Angiotensin II;prevents vasoconstriction & NA & H2O retention or blocks Angiotensin receptor sites
- Captopril
- Lotensin
- Vasotec
- Monopril
- Univasc
- Altace
- Cozaar
- Diovan
- Ck. BP b/4 giving
- Monitor BP for 2 hr post first dose
- Report peripheral edema or cough
- Can cause hyperkalemia & impotence
- Monitor for renal &hematologic changes
- Not if pregnant
-
Hypertension Medications
CALCIUM ANTAGONISTS
- Inhibit calcium influx therefore causing vasodilation & reducing peripheral resistance
- Cardizem
- Procardia
- Cardene
- Norvasc
- Verapamil
- Plendil
- Assess BP, pulse, &liver functions (hold if HR <50 b/m) Report signs of bradycardia or SOB
- Force fluids to prevent constipation
- Watch for reflex tachycardia & CHF
-
Hypertension Medicatons
Peripherally Acting Alpha-ADRENERGIC Blockers
- Decrease vasomotor tone, reduce LDL
- Cardura
- Minipress
- Hytrin
- Give 1st dose at night to prevent “1st dose syncope”
- Assess BP & pulse before each dose for orthostatic hypotension, tachycardia& palpitations
-
Hypertension Medications
Centrally Acting Sympatholytics
- stimulate alpha-2 receptors to suppress sympathetic out flow to heart & vessels, causing vasodilation & ↓ cardiac output
- Catapres
- Tenex
- Aldomet
- Reserpine
- Baseline BP, CBC,Liver Functions
- Give at night(sedates)
- Give gum or fluids for dry mouth
- Severe reflex hypertension if abruptly discontinued
-
Hypertension Medications
VASODILATORS
- Decrease peripheral resistance, peripheral vasodilation, relaxation of smooth muscles
- Apresoline
- Nitroglycerin
- Hyperstat
- Loniten
- Assess BP & Pulse b/4 giving
- Report peripheral edema
- Report muffled heart sounds (Loniten) due to possible cardiac effusion/tamponade
- Report joint pain,fever (signs of SLE)
-
Angina - Pathophysiologly and when to seek medical attention
Angina is chest pain resulting from reduced coronary blood flow, which causes a temporary imbalance between myocardial blood supply and demand (ischemia)
- May be caused by:
- CHD - coronary heart disease
- Atherosclerosis
- vessel constriction that impairs myocardial blood supply
- S & S
- Chest Pain - substernal or precordial - may radiate to neck, arms, shoulders or jaw - tight squeezing, constricting, burning, aching,
- Dispnea
- pallor
- tachycardia
- anxiety
- fear
- Relieved by
- rest,
- position change
- nitro
More than 30 minutes of ischemia causes irreversable damage to myocardial cells
-
CAD
Coronary Artery Disease also called CHD -Coronary heart disease
- caused by impaired blood flow to the myocardium
- Atherosclerotic plaque is the usual cause
-
Risk factors for CAD
- Nonmodifiable
- Age
- - Men >45
- -Women >55
- Gender
- Heredity
- Modifiable
- Smoking
- Obesity
- Physical inactivity
- Atherogenic Diet
- Hyperlipidemai
- Hypertension
- Diabetes
-
Types of Angina
- Stable angina - most common & predicatable - occurs when the work of the heart is increased by physical exertion, exposure to cold, or by stress
- -relieved by rest and nitrates
- Unstalble angina - occurs with increasing frequency, severity, and duration - pain is unpredictable and occurs with decreasing levels of activity and may occur at rest
- -at risk for MI
- Prinzmetal's (variant) angina - atypical -occurs unpredictable (unrelated to activity) and occurs often at night
- -caused by coronary artery spasm with or without atherosclerotic lesion
-
Diagnostic Studies for CAD
- Total serum cholesterol
- C-reactive protein - elevated levels in CAD
- ABI - ankle-brachial blood pressure index
- Exercise ECG testing
- Electron beam computed tomography
- Myocardial perfusion imagin
-
Diagnostic studies for Angina
- Electrocardiography ECG
- Stress ECG
- Radionucline Testing
- ECHOcardiography
- Coronary angiography
-
Drug Therapy for Angina
Goal of treatment is to reduce oxygen demand and increase oxygen supply to myocardium
- Nitrates - Nitroglycerin - fast
- venous and arterial dialation
- Beta Blockers -prophilaxis - first line to treat stable angina
- propranolol
- metoprolol
- nadolol
- atenolol
- block EPI & NOR (cardiac stimulators) -reduce heart rate, contractility, and blood pressure
- Ca Channel Blockers - slow acting - prophilixis
- verapamil
- dittiazem
- nifedipine
- act on cardiac muscle -coronary vasodialtors- lower BP, reduce contractility,
-
Nursing Dx
Angina & CAD
- Ineffective tissue perfusion: Cardiac
- Risk for ineffective therapeutic regimen managment
- Intervetions:
- Keep Nirto on you
- space activity with rest
- smoking cesation
- Modifiable risk factors:
- smoking
- obesity
- physical inactivity
- diabetes
- hypertenion
-
Acute Thrombophlebitis(DVT)
Risk Factors associated with DVT
- Immobility
- Abdominal surgery
- Orthopedic surgery (50% esp. hip & knee)
- Use of hormones (HRT, BC Pills, or ERT)
- Pregnancy
- Certain cancers (pancreas, lung, ovarian,testes, breast, stomach)
- Coagulation disorders/polycythemia
-
THROMBOPHLEBITIS -DVT
SIGNS & SYMPTOMS
- Asymptomatic
- Leg pain, Homan’s sign - leg pain when examiner dorsiflexes foot (knee at 90 degrees)
- Edema
- Inspection compare bilaterally-measure calf
- Tenderness, warmth &red/erythema
-
THROMBOPHLEBITIS -DVT
Nursing Interventions
- PREVENTION:
- Elastic stockings TEDS
- IPC (intermittent pneumatic compression devices)
- Positioning-elevate legs
- Exercise/ROM
- Heparin, Coumadin/INR assess for bleeding
- Intervetions:
- Bedrest – NO Ambulation
- Encourage diversional activities
- Legs elevated 15-20 degrees with knees slightly bent Warm moist packs (Aqua K Pad)
- Check for bleeding on anticoagulant therapy & monitor PT, PTT, INR
- Check pulses in extremities
- Monitor for signs of pulm. emboli
-
Relationship between heparin & coumadin therapies
Heparin & Coumadin - side effects, labs and antidotes
blood thinners - used for DVT
- heparin
- prevents conversion of firbrinogen to firbrin
- started first - IV - test with PTT
- side effects - bleeding
- antidote - protamine sulfate
- warfarin (coumadin) PO started - inhibits synthesis of Vit K dependnet clotting factors
- overlap of 4 to 5 days important
- warfarin full anticoagulant effect is delayed and may actually promote clotting for the first few days of therapy
- -monitired with INR
- -Side effects - bleeding
- antidote - Vitamin K
While on coumadin therapy avaid food high in Vit K - green leafy vegetables (kale, spinach, parsley, etc)
-
PCR - Percutaneous Transluminal Revascularization
also called
PCTA - Percutaneous transluminal coronary angioplasy
used to restore blood flow to the ischemic myocardium in patients with CHD
catheter into arterial circualtion - guide wire used
PCTA - ballon tipped catheter - get to point of athersclerotic plaque & ballon is inflated to force plaque into vessel walls - stint may also be inserted
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Chronic Arterial Diseases/PVD
- ARTERIOSCLEROSIS
- Hardening of the arteries
- Walls become thickened,inelastic & calcified
- ATHEROSCLEROSIS
- Obstruction of arteries(atheromas or plaques)
- Accumulation of lipids,calcium, blood components,carbohydrates and fibrous tissue
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ATHEROSCLEROSIS/PVD
RISK FACTORS
- Age 60-70 yrs.
- Gender/males
- Diet (cholesterol)
- Hypertension
- Diabetes
- Smoking
- High homocystine levels esp. menopause
- Race/Afr. Amer.
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Guidelines for Cholesterol
- Total cholesterol
- < 200= low risk
- 200-239=mod. risk
- 240+ = high risk
- Cholesterol Fractionation
- Triglycerides less than 150
- HDL more than 45 for males
- HDL more than 55 for females
- LDL less than 100 for all people especially those with risk factors
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Signs/Symptoms of PVD
- Pain with exercise/Intermittent Claudication due to lack of circulation(goes away with rest)
- Bruit (audible flow through partially blocked vessel)
- Rest Pain – more of a burning when legs elevated(better when dependent)
- ASSESSMENT
- Pallor with elevation but rubor if dependent
- Paresthesia, decreased sensation
- Peripheral pulses (↓ )
- Nails (cyanosis,clubbing)
- Skin (shiny, thin)
- Hair distribution (↓)
- Cool extremity
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Intermittent claudication
cramping or pain in the leg muscles brought on by exercise and relieved by rest
due to decreased blood flow to the lower extremity
- possible sign of PVD
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Raynaud’s Disease
- Vasospasm of small arteries & arterioles of fingers & toes (bilat.)
- Esp. young women20-40 yrs.
- Due to -
- Exposure to cold or stress
- Genetic predisposition ??
- Signs & Symptoms-
- Blue, White, & Red progression
- Numbness, stiffness,pain
- Brittle nails
- Treatment –
- Ca+ chan. blockers
- NTG transdermal
- Reserpine
- Keep warm (gloves,socks)
- Stop smoking
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BUERGER’S vs. RAYNAUD’S
- BUERGER’S
- * Small & midsize arteries become inflamed & spastic causing clots (unilat)
- * Young men <40 who smoke (stop smoking)
- * Painful ulcers &gangrene may develop
- * Regular exercise
- * Avoid exposure to cold
- * Prevent injury
- * Stress management
- RAYNAUD’S
- * Vasospasms of the fingers and toes(bilat)
- * Young women 20-40
- * Autoimmune condition
- * ?? Genetics
- * Blue, white, & red colors
- * Avoid exposure to cold, heat and trauma
- * Medications may help
- * Stress management
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Pulmonary Embolism
- manifestations similar to MI
- chest pain
- SOB
- anxiety
- sence of impending doom
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