Vascular Disorders
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| Blood Pressure | the tension or pressure exerted by blood against arterial walls.
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| Cardiac Output (CO) | the amount of blood that is pumped by the heart per minute.
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| Mean arterial pressure | (MAP) Average pressure in arterial circulation. Usually a special device inserted in artery or central line.
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| Systolic Blood Pressure | pressure measurement as the heart contracts (90).
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| Diastolic Blood Pressure | minimal pressure during diastole.
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| Arterial baroreceptor Regulation of BP | The atrial cells release peptide in respond to being overfilled, excess blood volume. BP is lowered by vasodilatation.
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| Renin-angiotensin-aldosterone Regulation of BP | Renin is released and converts angiotensin I into angiotension II. Angiotension II is a vasoconstrictor, promoting sodium & water retention directly & related to the release of aldosterone. Aldosterone release causes an > CO (cardiac output), SVR, and BP.
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| Sympathetic nervous system (SNS) Regulation of BP | <BP = epi and norepinephrine. Causes >HR, thus >BP. (Normal way that our body responds). <MAP stimulates SNS, >HR, cardiac output, and constrict arterioles, causing >BP. MAP rises: stimulates SNS to <HR & CO, and arterioles to dilate, causing <BP.
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| Arteriosclerosis | Most common chronic arterial disorder; harder to dilate. Thickening, loss of elasticity, and calcification of arterial walls. Happens naturally with aging.
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| Atherosclerosis | Similar to arteriosclerosis, but fat and fibrin obstruct and harden the arteries. Plaque formation, increasing pressure in blood vessels. Intermittent claudication.
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| Atherosclerosis Manifestations | Rest pain. Paresthesias (numbness, decreased sensation). Diminished or absent peripheral pulses. Pallor with extremity elevation. Thin,shiny, hairless skin. Thickened toenails. Areas of discoloration or skin breakdown.
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| Atherosclerosis Fisk Factors | Obesity, lack of exercise. Smoking. Familial Hyperlipidemia. Diabetes.
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| HDL | high density lipoproteins, good. Like it to be >40.
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| LDL | low density lipoproteins, bad. Should not be >100.
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| High serum levels of homocysteine | can allow cell walls to become vulnerable to plaque buildup. Decreases elasticity, expand and recoil.
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| Hypertension | “Normal” adult systolic BP <120; diastolic <80. SBP ≥ 140 mmHg or DPB ≥ 90 mm Hg in people who do not have diabetes mellitus. Patients with DM 130/90. 1 in 3 US have it, more than 90% have primary hypertension. Need 3 consecutive readings.
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| Hypertension Modifiable Risk Factors | Intake: >sodium, <potassium, calcium, and magnesium. Obesity. Insulin resistance: effects on the SNS, vascular smooth muscle, renal regulation of sodium and water, and changes ion transport across cell membranes. 3 or more alcohol/day. Stress: >BP.
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| Nonmodifiable Hypertension | Age: Older >60 = more risk. Race: More common in blacks, Greater sensitivity to salt. Genetics/Family History: 40% have genetic link.
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| Kinds of HTN | White Coat. Essential/Primary. Secondary. Malignant hypertension or hypertension crisis.
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| White Coat HTN | Some people's blood pressure is high only when they visit the doctor's office. Ask the patient to check and record blood pressure at home with a home monitor.
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| Why is primary HTN called the silent killer? | Asymptomatic, unless BP obtained. Headache in early am that fades during the day. Vague symptoms.
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| Organ damage occurs with all types of HTN | Eyes: narrowed arterioles, hemorrhages, exudates, papilledema (swelling of optic nerve). Kidneys: nephrosclerosis, Renal insuffieiency. Brain: encephalopathy, Altered level of consciousness, seizures. Heart.
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| HTN Interventions: Lifestyle modifications | Nutrition, Smoking cessation, alcohol reduction, tobacco and caffeine avoidance, Decrease stress, relaxation techniques, Aerobic exercise, Reduce weight.
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| HTN Nutrition therapy | <Sodium. Dash diet (Diet Approach to Stop HTN): Grains 7-8/day, Fruit/veggies 4-5/day, Low fat dairy 2-3/day, White meat, poultry, fish 2-3 3 ounce servings/day (Red meat once a week), Nuts/seeds/dried beans 4-5/week, Fats and oils 2-3/day, Sweets 5/week.
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| HTN Drug Therapies | Diuretics. Calcium Channel Blockers. Alpha adrenergic blockers. Beta-Adrenergic Blocking Agents (Beta blockers). Angiotensin converting enzyme (ACE) inhibitors. Angiotensin II Receptor Blockers (ARBs).
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| Thiazide diuretics | Hydrochlorothiazide (HCTZ) (Hydro-DIURIL). Most common initial therapy. Prevents sodium reabsorption, promotes excretion, < BV & BP. Most effective in blacks, obese, older, and cardiac disease. SE: hypokalemia, electrolyte imbalances, hyperglycemia.
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| Loop Diuretics | Act primarily in the Loop of Henle to promote increased urinary excretion of sodium, potassium, and water. More intense than thiazide diuretics. Example: Lasix (Furosemide).
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| Potassium Sparing Diuretics | Often used with Thiazide diuretics to potentiate effects, increase excretion of sodium and water. Example: Aldactone (Spironolactone).
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| Diuretic considerations | Monitor I&O. Know BP before giving. Know what your K level is before giving and identify K imbalances. Daily weights (3lbs/day is significant).
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| Calcium Channel blockers | Relaxes smooth muscle, causes vasodilatation. Decreases ability for things to cross cell membranes. Examples: Amiodipine (Norvasc), Diltiazem (Cardizem), Verapamil (Isoptin), Nifedipine (Procardia).
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| Angiotensin converting enzyme (ACE) inhibitors | Prevent angiotensin I to angiotension II, preventing normal vasoconstriction and sodium/water retention. <effective in black clients and contraindicated in pregnancy. SE: Persistent cough (notify MD), hyperkalemia, swelling of tongue/mouth/glottis.
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| Examples of ACE inhibitors | Benazepril (Lotensin), Capropril (Capoten), Enalapril (Vasotec), Fosinopril (Monopril), Lisinopril (Zestril), Ramipril (Altace).
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| Angiotensin II Receptor Blockers (ARBs) | Block the effect of angiotensin II on receptors –inhibits vasoconstriction. Similar to ACE inhibitors. Same nursing responsibilities and teaching.
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| ARB Examples | Losartan (Cozaar), Valsartan (Diovan), Candesartan (Atacand), Irbersartan (Avapro).
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| Beta-blockers Beta-Adrenergic Blocking Agents (Beta blockers) | Beta 1 is Heart, kidney. Beta 2 is Smooth muscle, lungs, and skeletal muscle. Reduce BP by prevents beta-receptor stimulation in the heart causes decrease in heart rate &decreased BP. Also interferes with renin release by the kidneys.
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| Beta Blocker Examples | Atenolol (Tenormin) (cardio selective) Metoprolol tartate (Lopressor) (cardio selective). Nadolol (Corgard). Propranolol (Inderal). Bisoprolol (Zebeta) (cardio selective).
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| Nursing considerations for Beta blockers | SE: bradycardia, fatigue, impotence, bronchospasms, masks signs of hypoglycemia. Contraindicated for individuals suffering with asthma, chronic lung disease (COPD), bradycardia, heart blocks, severe depression. Post MI, controls heart rate and BP well.
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| Client Teaching about Beta Blockers | Take med as prescribed. Monitor BP/Pulse daily and record. Change positions slowly to avoid falls. Report severe fatigue, lethargy, impotence, SOA, lower extremity edema, and monitor for hypoglycemia. Ask MD before taking OTC meds. Don’t stop abruptly.
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| Alpha adrenergic blockers | Blocks the alpha receptors in smooth muscle causing decreased muscle tone and vasodilatation of arterioles and veins. Prevents vasoconstriction. Reduces LDL. Can result in orthostatic hypotension and reflex tachycardia.
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| Alpha Adrenergic Blocker Meds | Doxazosin (Cardura). Prazosin (Minipress). Terazosin (Hytrin).
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| Alpha Adrenergic Blocker Nursing responsibilities | Administer first dose at bedtime to < risk of “first-dose syncope”. Watch for dizziness and palpitations. Slowly change positions, lightheadedness may occur sit down immediately. Commonly used for Benign Prostatic Hypertrophy (BPH).
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| Nursing diagnosis for all HTN meds | Teach medication compliance, usually for the rest of life. Discuss goals of therapy, potential side effects, and how to identify potential problems. Assist patient to understand therapeutic regimen. Discuss consequence of noncompliance.
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| Secondary Hypertension | elevated BP resulting from an identifiable underlying condition. ^ BP is only 5-10% of the identifiable.
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| Secondary HTN Examples | Kidney: affects angiotensin-aldosterone system. Aorta Narrowing (coarctation): Blood flow stimulates the rennin-angiotensin-aldosterone system and vasoconstricive responses, > BP, un= pressure upper and lower ext, <pulse/capillary refill in lower ext.
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| More Secondary HTN Examples | Endocrine: Cushing’s syndrome and primary aldosteronism. Neurologic: Spine injury. Drugs: Estrogen and oral contraceptive, Sodium/water retention, Stimulants increase systemic vascular resistance and cardiac output. Pregnancy: 10%, unclear.
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| Assessment of patient with secondary HTN | Patient history: May report heads ache, dizzy, fainting, facial flushing. Physical assessment: Identify gruits, tachycardia, pallor, delayed femoral pulse. Psychological assessment: Indentify stressors and ability to cope, Assess past coping skills.
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| Secondary HTN Diagnostic assessment | Renal function and urinalysis: > serum creatinine and BUN, < creatinine clearance, Hematurea, Proteinuria, casts. Blood: Detect abnormalities in endocrine or cardiovascular. IVP (intravenous pyelography) inject dye. Renal ultrasound. CT or MRI.
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| Malignant Hypertension or Hypertensive Crisis | Hypertensive emergency. Immediate treatment is vital to life.
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| Malignant Hypertension or Hypertensive Crisis S/S | Rapid onset hypertension. Plurred vision, papilledema (swelling of optic nerve). Headache. Confusion. Motor and sensory deficits. BP > 180/120.
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| Malignant Hypertension or Hypertensive Crisis Nursing Responsibilities | Treat within 1 hour, come down about 25% every hour. Continuous monitoring (every 5-15 min). Oxygen. Monitor labs. IVP meds, IV gtts. Comfort client and family. Assess cause and teach how to avoid crisis in the future.
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| IV Meds - Hypertensive Emergencies | Vasodiolators: Most common/effective. Sodium Nitroprusside (Nipride) IV (works FAST). Nitroglycerin. Nicardipine (Cardene) IV. Don’t reduce BP to quickly. Observe for neurologic complications. Observe for cardiovascular complications.
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| Arterial Aneurysms | Abnormal dilation of artery usually due to weakness in wall. Cause by atherosclerosis, arteriosclerosis, or trauma. Tend to affect men greater than 65. HTN major contributor.
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| True Aneurysm | slow weakening that effects all wall of vessel
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| False Aneurysm | from trauma
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| Dissecting aneurysm (aortic dissection) | abdomen, thorax, or cerebral
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| Thoracic aortic aneurysm | Asymptomatic, angina. Back pain or angina with compression of the aneurysm on adjacent structures. Shortness of breath, hoarseness, difficulty swallowing. Sudden excruciating back/chest pain = rupture. Edema of the face/neck. Distended neck veins.
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| Abdominal aortic aneurysm | Asymptomatic or steady gnawing pain, unaffected by movement. Abd/flank/back pain. Pulsatile mass. Frequent complication is rupture and is life threatening. >age and smoking most found over 65. After rupture, mortality rate is >50%, even with surgery.
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| Femoral and popliteal aneurysms | Symptoms: None, cramping or pain in the leg muscles by exercise reduced by rest, rest pain, numbness, pulsating mass. Intermittent claudication, exercise induced pain. Surgical treatment.
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| Aortic Dissection | Sudden tear in aortic intima, blood can enter aortic wall (media). Tearing/ripping/stabbing pain. Mild/marked hypertension, Weak/absent P and BP in upper extremities. Dizzy, pass out, Tachycardia. Need surgery. Common with marfans syndrome.
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| Aneurysm Diagnosis | CXR – chest x-ray. Ultrasound. CT or MRI: Allows precise measurements of aneurysm size. Angiography: Contrast solution gives vision to size and location.
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| Nonsurgical Management | Monitor the growth of the aneurysm. Maintain BP at a normal level to decrease the risk of rupture. Depends on size.
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| Abdominal Aortic Aneurysm Repair Preoperative care | Advise of possible need for blood due to loss. Mark pulses for easy access when return from OR. Reduce fear and anxiety by orienting, describing, and explaining as much as possible. Monitor for and implement care to reduce the rick of rupture.
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| Abdominal Aortic Aneurysm Repair Operative procedure | Graft of area that is impaired.
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| Abdominal Aortic Aneurysm Repair Postoperative care | Monitor VS and I/O (30ml/hr). <P (or Doppler only) for 4-12 hrs. Assess for complications: P, VS, neurovascular status of ext., Shock, renal failure, pallor. Assess for signs of graft occlusion/rupture: Change in pulses, severe pain, <CO, abd distention.
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| Peripheral Arterial Disease (PAD) | Disorders that alter the natural flow of blood through peripheral circulation. May here it referred to as peripheral vascular disease (PVD).
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| Peripheral Arterial Disease Risk Factors | Advance age. Arterioclerosis/Atherosclerosis. Hypertension. Men more affected than women. Postmenapausal women. Diabetes. Hypercholesterolemia. HTN. Cigarette smoking. High homocystine levels.
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| Manifestations of PAD | Intermittent claudication (leg/butt cramping /c activity). Rest pain (leg burning, > when elevated)(down red, up white). </0 pulse. Pallor with elevation. Thin/shiny/hairless skin, thick toenails. Discolored areas, skin breakdown. Cold/gray-blue/darkenen.
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| PAD Diagnostic Assessments | Imaging assessment: Arterography (contrast injected). Other diagnostic tests: Segmental pressure measurements (BP on upper and lower ext.), Exercise tolerance testing, Ultrasound, Transcutaneous oximetry (pulse ox), Angiography (contrast injected) or MRI.
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| Nonsurgical Management of PAD | Exercise > arterial flow. Walk, pain, rest, walk more. Positioning, only elevate when swelling, not above heart. Don’t cross legs. No TEDs/SCDs. Promoting vasodilation. Keep legs warm, but don’t apply heat. Foot care, like diabetic. Quit smoking.
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| PAD Meds | Medications to decrease viscosity of blood. Plavix (Clopidogrel). Pletal (Cilostazol). Trental (Pentoxifylline). Aspirin.
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| Revascularization Treatment of PAD | Non-surgical: Angioplasty, Stent, Atherectomy. Surgical: Bypass graft, Endarterectomy.
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| Thromboangiitis obliterans (Buerger’s Disease) | Inflammation and thrombus formation and vasospasms of small and mid sized arteries. Often identified with tobacco smoking.
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| Buerger’s Disease Nursing interventions | smoking cessation specifically. Foot care. Protecting extremities from injury. Exercise. Keep extremities dependant.
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| Raynaud’s Phenomenon | Caused by vasospasm of the arterioles and arteries of the upper and lower extremities.
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| Raynaud’s Drug therapy | Nifedipine (procardia). Diltiazem (Cardizem).
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| Nursing Care of Raynaud’s | Reinforce patient education; restrict cold exposure, or things that cause vasoconstriction. Keep hands warm, wear gloves outside in winter and kitchen gloves when handling cold items. Stop smoking. May stop attack by swinging arms back and forth. <Stress.
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| Acute Arterial Occlusions | Thrombus: clot that adheres to vessel wall due to damage caused by atherosclerosis. Embolus: clot/debris that lodges in vessel and obstructs flow. Can be caused by Inflammation, infection, pooling of blood. Inflammation can cause coagulation.
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| Acute Peripheral Arterial Occlusion | Embolus is the most common cause of occlusions, although local thrombus may be the cause. Assess pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia.
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| Drug therapy for Acute Arterial Occlusions | Heparin (fast) or Coumadin and Lovenox (slower) to prevent more platelets from attaching to the clot. Body will slowly break clot down.
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| What Occurs with Arterial Embolism? | Ischemia. Painful. Pale. Cold or cool skin. Absent pulses distal to blockage. Numbness and tingling. Cyanosis and mottling. Paralysis and spasms.
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| Arterial Embolism is an Emergent Condition | Without prompt treatment, Permanent vessel and limb damage, Tissue necrosis, and Gangrene. Depending on severity of blockage, may need emergency treatment or may have conservative medical management.
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| Treatment of Arterial Embolism | Diagnostic test: Arteriography. Medicine (clot busters): Heparin, Lovenox, Streptokinase or t-Pa, May get Coumadin, but not initial drug. Surgical treatment: Embolectomy, Thromboendarterectomy.
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| Nursing Care of Arterial Embolism | Compare sides. May use Doppler. Assess temp, color, capillary refill, movement, and sensation. Maintain IV fluids. Protect extremity-bed cradle. Avoid flexion of the knee. Assess anxiety, spend time with patient, keep calm atmosphere, clear directions.
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| Venous Thrombosis Pathophysiology | Virchow’s Triad: Stasis of blood, Vessel damage (stimulates clotting cascade), and Increased blood coagulability (Birth control pills, Cancer, Immobility, Dehydration, Venous pooling).
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| Most common Venous Thrombosis sites | Begin in deep veins of calf. Extend into popliteal or femoral veins. Superficial site: greater saphenous vein.
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| Assessment of vein Thrombosis | Calf or groin tenderness or pain. Sudden onset of unilateral swelling of the leg. Localized edema. Dull ache. Palpable cordlike structure (not typical, don’t rub to find it). Venous flow studies. > D/dimer, marks coagulation. - = no DVT. MRI.
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| Nonsurgical Management of Venous Thrombosis | Preventive measures (Move, TEDs, SCDs, don’t cross legs). Do not massage. Warm soaks. Report shortness of breath. Could now be in lungs. Keep legs elevated.
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| Venous Thrombosis Drug therapy | Unfractionated heparin therapy (Normal PTT/APTT 20-40 sec. c/ therapy should bleed 2x greater). Low–molecular weight heparin. Warfarin (coumadin): (Monitor INR (international ratio) 2-3 is goal). Thrombolytic therapy. Lovenox, doesn’t monitor anything.
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| Possible surgery or vena cava filter for Venous Thrombosis | Like umbrella to catch clot.
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| Chronic Venous Insufficiency | Disorder of inadequate venous return over a prolonged period of time. May be caused by DVT, varicose veins, or leg trauma, or may develop without apparent cause.
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| Chronic Venous Insufficiency Pathophysiology | Damage to valve leaflets. Muscle-pumping action cannot propel blood back to heart. Blood collects and stagnates. > Venous pressures. Slows ability to remove wastes from the tissues. Skin atrophies and breaks down. Ulcerations develop.
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| Venous Insufficiency treatment | Manage venous stasis ulcers. Manage edema. Unna boot. Normal pulse/temp. May complain of leg pain. Redish/brown color. Ulcerations common at ankle bone. Manage edema. Elevate extremities. TEDs/SCDs. Do not cross legs. Surgical debrisment.
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| Varicose Veins | Irregular, tortuous veins with incompetent valves, especially the great saphenous vein.
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| Varicose Veins Risk Factors | More common in women >35. Related to pregnancy. Obesity, < exercise. Venous thrombosis. Prolonged standing. Whites are most affected. Sustained pressure on abdominal veins. Distended, protruding veins that appear darkened and tortuous.
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| Varicose Veins Treatment | Elastic stockings. Elevation of extremities. Sclerotherapy. Surgical removal of veins. Radio frequency energy to heat the veins.
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| Disorders of Lymphatic System | Lymphadenopathy: Enlarged lymph nodes, Often palpable in response to minor trauma or localized infection, Generalized may be indicative of malignancy or disease state. Lymphangitis: Red streak along inflamed vessels with pain, heat, swelling.
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| Lymphedema | Edema of extremity due to accumulation of lymph resulting from inflammation, obstruction, or removal of lymphatic vessels. Lymph drainage prevents fluid/protein molecules from returning to circulation. Osmotic pressure draws fluid into tissues.
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| Lymphedema Manifestations | Edema of entire extremity. Initially soft and pitting, then becomes fibrotic with woody texture: brawny edema (like rotten orange pealing). Usually painless, but limb feels heavy.
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| Lymphedema Treatment | Meticulous skin care of foot and leg. Elastic compression stockings or sleeves. Intermittent graduated pneumatic compression devices. Antibiotic therapy as needed to treat infection. Diuretic therapy. Surgery.
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| Lymphedema Nursing Care | No B/P or venipuncture on affected side (in case of mastectomy or other lymph node removal). Educating patients to recognize infection and when to seek medical attention: Red, Warm, Extra swelling, > HR, temp, Fever, chills.
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