Chapter 35: Caring for the Patient with Peripheral ...

 Chapter 35: Caring for the Patient with Peripheral Vascular Disorders Vascular disorders include disorders that affect the arterial, venous, and lymphatic systems. Peripheral arterial disease includes:occlusiveaneurysmal (dilated)vasospastic disordersPeripheral venous disease:predominantly in the legs and due to thrombosis or insufficiency. Lymphatic disease leads to:abnormal fluid collectionedemafibrosis Vascular Disorders HypertensionDefined as an average blood pressure that is higher than the accepted norm over a period of time consisting of two or more consecutive office visits. Regulation of the Blood PressureBlood pressure (BP): the pressure create by circulating blood through the arteries, veins, and the chambers of the heart.Classified into four stages: normal tension, prehypertension, stage 1 hypertension, and stage 2 hypertension. Systolic BP is the pressure in the aorta and major arteries when the left ventricle contracts. Diastolic BP is the minimum pressure in the arteries which occurs prior to the next cycle of ventricular ejection. The difference between the SBP and DBP is called the pulse pressure.Blood Pressure = cardiac output + peripheral resistance (resistance of blood flow and diameter of vessels) .Regulation is done through neural regulation, arterial baroreceptors and chemoreceptors, regulation of fluid volume, and humoral regulation. Neuronal regulation: pons and medullaANS integrated along with vasomotor control center and CV control center. Baroreceptors: located in the walls of blood vessels and respond to changes in the stretch of blood vessels by sending impulses to the CNS. Hormonal regulationRAA systemVasopressinepinephrine and norepinephrine. Etiology Over 74.5 million American adults have hypertension.? of of 18yrs and older have BPs of 140/90 or are already on medications to control their BP. Prevalence is equal in men and women. Increasing BMI contributes to more than 50% of the incidences of hypertension. Hypertension accounts for 18% of CV deaths.Major risk factor for:stroke, heart disease, and heart failurePathophysiologyMultiple body systems interact to cause hypertension:hemodynamic, neural, humoral, and renal mechanisms. SNS controls vascular resistance by releasing vasoconstrictor substances.Kidney increases Na and H20 secretions when BP rises.During hypertension, kidney needs a higher arterial pressure to regulate the release of salt and water. PrehypertensionIndividuals with BP on two or more office visits of 120/80 - 139/89.These individuals are at twice the risk of developing hypertension than normal individuals, Stage of hypertension where need for health education is the primary focus of care. Stage I hypertensionblood pressure of 140/90 - 159/99 measured during multiple office visitsLifestyle changes as well as medications are part of the therapeutic planStage II hypertensionSBP of 160+ and/or DBP of 100+ with multiple office visitsBoth medications and lifestyle changes are part of the therapeutic plan. White Coat phenomenon: elevated blood pressure when patient’s blood pressure assessment is done by a healthcare professional. Often requires physician to ask patient to record their BP at home to determine if they have white coat phenomenon. Two types of hypertension:Essential hypertension: chronic elevation on blood pressure that occurs with evidence of disease. May be systolic and/or diastolic Risk Factors: Age: older population have a higher risk Family History: genetic predisposition Race: African Americans have a higher risk Gender: higher risk for men before 45 y/o; equal for both after 45 y/o Environment Obesity Metabolic syndrome: presence of excess fat accumulated in the torso Sedentary lifestyle High stress levels Alcohol consumption High-sodium/low-potassium diet Secondary hypertension: high blood pressure that results from some other disorder such as kidney disease. Risk Factors: Presence of diseases such as:Kidney disease Other vascular diseases: Renovascular hypertension Coarctation of aorta Vasculitis Drug interactions and exposure to toxinsClinical ManifestationsInitial stages of hypertension are asymptomatic. Hypertension may be present in some people for many years prior to discovers, in which major organs may already be slowly damaged. Signs and Symptoms:headache or dizzinesssleepinessn/virritabilityvisual disturbances More serious complications such as MI, CHF, CVA, and renal failure may occur if hypertension is untreated. Diagnostic Testsnot many tests to perform except for tracking of serial blood plete work-up of the current state of body system organs to establish a baseline. Diagnostic Tests Box (pg 1061)Urinalysis:useful in diagnosis of renal disease.Specific gravity can be low because unable to concentrate urineProteinuria = renal dysfunction Blood Urea NitrogenElevated BUN can indicate prerenal failure, renal failure, or dehydration.BUN/Creatinine Ratiodecrease ratio with acute tubular necrosisincrease ratio with reduced renal perfusionCreatinine (blood) Creatinine is increased in essential hypertension and chronic heart failure. Aldosterone (blood)Increased levels r/t hypertension and hypokalemiaAbnormally high levels can cause kidneys to retain salt and excrete K, causing water retention.Increases volume therefore increased blood pressure. Aldosterone (urine) Increased in hyponatremiaDecreased in hypernatremia Renin (plasma)activates RAA leads to vasoconstriction which releases aldosterone which can lead to hypertension. Increased renin levels can occur in hypovolemia, malignant hypertension, renovascular hypertension, hyperaldosteronism, kidney cancer, acute renal failure, and Addison’s disease. Decreased renin levels in essential hypertension, Cushing’s syndrome, diabetes, hypothyroidism, and high sodium diet. Glucose (blood) Some medications (ex. steroids, thiazide diuretics, and loop diuretics) may cause elevated blood glucose.Sodium (blood)Increased Na levels increase fluid retention which causes increased BP.Medications (ex. thiazide and loop diuretics) can caused increased Na levels which leads to hypertension. Medical Management Factors to consider when forming a plan for a patient:cultural food preferencesagerisk factorsdegree of hypertensioncoexisting diseasescost of medicationsfamily/social supportamount and type of follow-up care neededDietDASH diet (Dietary Approaches to Stop Hypertension) Low: sodium, saturated fat, cholesterol, and total fat. lowering fat consumption doesn’t do anything for hypertension, it does lower cholesterol and risk of CAD. High: fruits, vegetables, nuts, low-fat dairy, potassium and calcium. Believed to be as effective a single-drug therapyPatients with Stage 1 and 2 hypertension should:DASH dietreduced-calorie dietlow cholesterol dietdecreased sat fatslimit alcohol and smokingExerciseRegular exercise assists in promotion of CV fitness, lowers BP, and raises HDL. Essential to have an organized aerobic exercise program on a regular basis for 30-45 minutes. Light weight training is recommended to lower BP, but heavy lifting known to raise BP due to vasovagal response to isometric exercises. Weight ControlHigh BMI puts more at risk of developing hypertensionPresence of excess fat in the torso that is out of proportion to the body (men waist: 40; women waist: 35) are more at risk of developing hypertension. Antihypertensive medication effectiveness is enhanced with weight reduction. During weight loss, BP should should be monitored and medications adjusted. Stress ReductionStress-reduction helps to lower BPalso associated with exerciseAlcohol consumption Regular consumption of three or more drinks puts a patient at risk of hypertension.. Due to unknown reasons, SBP is more affected than DBPPatients may understate how much they drink. Pharmacologic Agents Used to Treat HypertensionReduce the morbidity and mortality r/t hypertension as well as CVA. Drug ClassNursing Responsibility/ InterventionsThiazide Diuretics (initial drug of choice) “-iazide”MOA: reduces blood volume through increased H20 and NA excretion.Reduced blood volume decreases BP Monitor hypokalemia, elevated blood glucose, and elevated uric acid levels. Therefore encourage intake of foods high in potassiumPotassium-sparing diureticsMOA: reduces blood volume through modest dieresis-does not cause hypokalemia-Monitor for hyperkalemia, especially in diabetics.Monitor for dysrhythmias- when given with ACE inhibitors or ARBs, increased risk of hyperkalemia- Loop Diuretics “-ide”MOA: reduces blood volume in diuresis-can cause more significant drop in BP than thiazides-Monitor for hypokalemia, dehydration, and orthostatic hypotension -can cause ototoxicity-ACE inhibitors “-pril”MOA: works on RAA to inhibit vasoconstriction-enhances thiazide effects-Monitor of ACE inhibitor side effects (cough, dizziness, hypotension, hyperkalemia, worsening renal function) Monitor for: orthostatic hypotension, elevated serum (Na, K, and/or creatinine), drug-induced neutropenia-NSAIDS may decrease ACE inhibitor effectiveness- Angiotensin II Receptor Blockers (ARBs) “-ine”MOA: inhibits RAAS, decreases afterload, Na resorption, and increased contractilityMonitor for dizziness, orthostatic hypotension, elevated serum Na, K, and creatinine, and worsening renal insufficiency. Calcium Channel BlockersMOA: relaxes arterial smooth wall muscle to decrease peripheral resistance-supplementary therapy only, especially for elderly and African Americans- Monitor for reflex tachycardia, elevated blood glucose, gingival hyperplasia, palpitations, weight gain, peripheral edema, skin rashes.-avoid grapefruit- Beta-Adrenergic blockers “-olol”MOA: nonselective: beta receptor blocking (doesn’t cause reflex tachycardia or decreased HR)selective: completely blocks beta-1 receptor stimulation in cardiac smooth muscleMonitor fr bradycardia, elevated blood glucose, teach patient to taper off. Alpha adrenergic antagonistsMOA: directly blocks sympathetic receptors in arterooles-used concurrently with other antihypertensives-Monitor for dizziness, light-headedness, syncope, headache, and N/V.May contribute to decreased libido and EDAlpha agonistsMOA: inhibits SNS, lowers peripheral resistance-only when not responding to other antihypertensives--can develop tolerance-Monitor for CNS effects, hepatotoxicity, decreased libido, ED, menstrual cycle irregularities, dry mouth.Drug interactions with: alcohol, lithium, tricyclic antidepressants, and NSAIDS.VasodilatorsMOA: relaxes smooth muscle, decreasing peripheral resistance-treatment of acute hypertension in hospital- Monitor for hypotension, dizziness, lethargy, blurred vision, metabolic acidosis, or ALOC.Prolonged use can lead to thiocyanate toxicityDirect Renin InhibitorMOA: inhibits renin productionMonitor for diarrhea, cough, flu0like symptoms, and rash. Nursing Management The nurse is the coordinator of care and provider of information concerning risk reduction, health promotion, disease prevention, and the nursing care plan. The nurses’ task focuses on educating the patient about lifestyle changes and implementing the therapeutic regimen. The nurse must also consider multiple factors when devising the plan (see medical management) and cultural considerations (pg 1068)Health PromotionHealth care providers starting to put more responsibility in the patient’s hands for healthy lifestyle choices for control of blood pressure.Healthy lifestyle includes:three balanced meals/daymaintaining a healthy weight by exercisinglimiting use of alcohol and smokinggetting adequate sleepreduce stressCollaborative ManagementThe goal for hypertension is to reduce the risks of CV, cerebrovascular, and renal morbidity and mortality by reducing BP to <120/80. < 130/80 in diabetic patientsIt is imperative that the health care team communicates openly including resource professionals such as:Clinical dietitiansFitness/Exercise leaderPharmacistComplications of HypertensionHypertension can cause damage to target organs if uncontrolled.Target organs are: heart, kidney, brain, peripheral vasculature, and retina. Chart 35-1 (pg1068) Target Organ DamageLeft ventricular hypertrophyRetinopathyAngina or prior MIPrior coronary revascularizationHeart failureRenal failureStroke or TIAChronic kidney diseasePADPeripheral ischemiaVision changes leading to blindnessProlonged hypertension can cause blood vessels to become weak and narrow causing blood pressure to increase.The weakened arteries are also more prone to occlusion or rupture causing loss of blood supply to organs and tissues. Small artery damage can cause structural changes in the target organ. An increased DBP can result in injury of the intimal wall of the arteries causing plaque build-up and local inflammation which in turn causes plaque rupture, platelet aggregation, and vessel occlusion. Leads to decreased blood supply to organs leading to loss of function. Ischemic Heart Disease most common site of target organ damage. Coronary arteries unable to deliver blood to myocardiumcauses cardiac muscle to lose contractabiliy causes decreased cardiac outputShearing force of turbulent blood flow along the lumen causes increased buildup of plaquefurther narrowing of the lumen and decreasing blood flow to the myocardium causing ischemic heart disease. Heart failureoccurs because of increased cardiac workload due to the heart having to pump against increased afterload.Afterload is the amount of pressure that the heart must pump against in order to eject blood into the aorta.With hypertension, the pressure in the aorta is increased due to narrowing of the lumen.Eventually left ventricle compensates by hypertrophying left ventricle hypertrophy increases with age and is more prevalent in patients with higher BP. Nephrosclerosis caused by damaged blood vessels not being able to deliver enough blood to kidneys, resulting in decreased renal mon cause of renal insufficiency. hypertension accelerates other types of kidney diseases, particularly diabetes. Diabetespatients with diabetes have high levels of cholesterol and lipids which affects the development of atherosclerosis, arteriosclerosis, and severe coronary heart disease as well as microcirculatory lesions. Atherosclerosis increases the probability of developing hypertension, diabetic retinopathy, cataracts, and chronic renal disease. Metabolic Syndrome? of US has metabolic syndrome. Characteristics: insulin resistance, hypertension, dyslipidemia, high triglyceride levels, diabetes mellitus, low HDL, tendency to form blood clots. Cerebral vascular diseasecaused by arteriosclerotis plaques that occur in the feeder arteries to the brain. when the plaques rupture, it activates the clotting mechanism which can lead to occlusion of the artery. High blood pressure along with an occlusion can cause the vessel to rupture causing the vessel to hemorrhage which compresses local brain tissuewhich also compresses local vessels causing blood vessel blockage. Hypertensive eye diseaseaffects the retinal arterioles, retinal parenchyma, choroids, and optic nerve.hypertension can be detected in the eye by the presence of diffuse arteriolar narrowing, bleeding, cotton wool patches, hard exudates, microaneurysms, zones of nonperfusion, and flame shamed bleeding at or near the retina. Hypertensive EmergenciesHypertensive crisis is a rare and sometimes has a fatal occurrence Characteristics:sudden onset of a DBP of 120-130causes acute vascular damage and structural organ changes.clinical manifestations of target organ vascular damage presence of retinal exudates and hemorrhage.Catecholamines stimulate the RAA system and raises BP even more.S/S:unstable anginapulmonary edemamyocardial infarctioneclampsiastrokelife-threatening arterial bleedingaortic dissectionmorning headacheblurred visiondyspnearenal failurCauses:acute and chronic renal failurexacerbation of chronic hypertensionsudden withdrawal of antihypertensivesvasculitis. Management:hospitalization in the ICUgoal is to bring BP down within 1 hr of crisis without going hypotensive. can cause cerebral and/or myocardial infarctions and renal failure. Medications:labeteol, nicardipine, nitroglycerine, or nitroprussideHypertensive encephalopathy multifocal cerebral ischemia due to severely acute or subacute elevated blood pressure.pathogenesis is the detrimental effect of high blood pressure on the brains’ arterioles. Requires urgent and immediate treatment. Decreased incidence of hypertensive encephalopathy due to effective use of antihypertensives. ................
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