Presentation on theme: "Nursing Care & Interventions for Clients with Vascular Problems"— Presentation transcript:
1 Nursing Care & Interventions for Clients with Vascular Problems Keith Rischer RN, MA, CEN
2 Today’s Objectives…Review the pathophysiology of arteriosclerosis, including the factors that cause arterial injuryDiscuss drug therapy for hypertensionEvaluate the effectiveness of interdisciplinary interventions to improve hypertensionPrioritize nursing care for the patient experiencing vascular disordersDevelop a continuing care plan for a client who has hypertensionPrioritize postoperative care for clients who have undergone peripheral bypass surgery.
3 Serum Lipids:Cholesterol One of the several types of fats (lipids)Important component of cell membranes, and bile acidsBuilding blocks in certain types of hormonesPredominant substance in atherosclerotic plaquesCirculates in the blood in combination with triglycerides, encapsulated by special fat-carrying proteins called lipoproteins<200 is desirable for total cholesterolBody produces it in the liver, additional cholesterol is ingested through dietary intakeThis is a modifiable risk factor and most significant to assess for a patient with HTN is elevated serum lipids.Building blocks in certain types of hormones, i.e. estrogen, steroidal hormones
4 Lipoproteins LDL = Low Density Lipoproteins - “bad cholesterol” <130 is desirableHDL = High Density Lipoproteins - “good cholesterol”>30 is desirable- the higher the HDL, the lower the risk of CADTriglycerides- combination of glycerol with 3 fatty acidsTransportable fuel- energy sourceStrongly influenced by dietLDL = Low Density Lipoproteins - “bad cholesterol”Main carrier of cholesterolTransport cholesterol to sites throughout the body, where it is used to repair cell membranes or is depositedIncreased LDL level- increased incidence of atherosclerosisHDL = High Density Lipoproteins - “good cholesterol”Carryies cholesterol away from the arteries to the liver where it is altered and removed from the body- i.e. the “clean up crew”>30 is desirable- the higher the HDL, the lower the risk of CADThe ratio of total cholesterol to HDL is useful in assessing a person’s risk for developing CAD
5 Cholesterol Levels LDL Cholesterol Total Cholesterol HDL Cholesterol <100 OptimalNear optimal/above optimalBorderline HighHigh>190 Very highTotal Cholesterol<200 DesirableBorderline High>240 HighHDL Cholesterol<40 Low>60 HighFrom National Cholesterol Education Program ATPIII Guidelines
6 Hypertension “Vascular Disease” Affects 1 in every 4 adults in the US Major risk factor for cardiovascular disease (CVD)Stroke, MI, Heart FailureOther Target Organ DamageLV hypertrophyNephropathyVascular DisordersPVDRetinopathyTarget organ damage…HeartLeft ventricular hypertrophyAngina or prior myocardial infarctionPrior coronary revascularizationHeart failureBrainStroke or transient ischemic attackChronic kidney diseasePeripheral arterial diseaseRetinopathy
7 Categories Primary (Essential)- without identified cause 90-95% of all hypertensionPathophysiology: (exact cause unknown)HeredityH2O & Na+ retentionAltered renin-angiotensin mechanismStress and increase sympathetic nervous system activityInsulin resistance and hyperinsulinemiaEndothelial cell dysfunctionSecondary- results from identifiable causerenal disease, endocrine disorders, neuro disorders, meds, PIH
8 Stages of Hypertension Category SBP(mmHg) DBP(mmHg)Normal <120 <80PrehypertensionHypertension, Stage 1:Hypertension, Stage 2:Hypertension, Stage 3: >180 >110Diagnosis is based on the average of 2 or more blood pressure readings at each of 2 or more visits after an initial screeningPre HTNDefinition: /80-89 mm HgIndividuals at high risk of developing hypertension in the futureLifestyle modifications (not drug therapy) are necessary at this stageGoal is to normalize BP (<120/80 mm Hg)Associated with 3.5X ↑ risk of MI & 1.7X ↑ risk of CAD Qureshi et al. Stroke, SepGoal of therapy: Individualize therapy for patient by group stages of HTN with cardiovascular risk factorGoal is to lower BP to less than 140/90 mm HgGoal is <130/80 mm Hgpatients with diabetes or chronic kidney disease
9 Clinical Manifestations EarlyElevated BPAsymptomatic (silent killer)LaterSymptoms secondary to effects on blood vessels in various organs or tissuesFatigue, reduced activity tolerance, dizziness, palpitations, angina, dyspnea
10 Risk Factors for Primary Hypertension AgeAlcohol useCigarette smokingDMElevated serum lipidsExcess dietary sodiumGenderFamily historyObesityEthnicitySedentary lifestyleSocioeconomic statusStressPatient (50 y.o.) with Stage 1 HTN (with no CV risk factors) general recommendation for management is to begin a 12 month trial of lifestyle changes.EthnicityAfrican Americans, Puerto Ricans, Cubans, and Mexican Americans have a higher incidence of hypertension than CaucasianAfrican Americans have highest incidence of HTNPrevalence increases with age and is higher among women than men
11 Knowledge Deficit Encourage healthy lifestyles Lifestyle modifications for all patients with prehypertension and hypertensionComponents of lifestyle modifications include:weight reduction,DASH eating plandietary sodium reductionaerobic physicalactivitymoderation of alcohol consumptionStress reductionDASH DietReduced overall amount of fat, saturated fat, and cholesterolIncreased amount of fruits, vegetables, and low-fat dairy foodsIncreased fiber with whole grain productsReduced amount of sodium to preferably 2.4 to 1.5 grams per dayReduced sweets and sugar-containing beverages
12 Risk for Ineffective Therapeutic Regimen Management Interventions:Teach medication compliance, usually for the rest of life.goals of therapypotential side effectsAssist client to understand therapeutic regimen.Discuss consequence of noncomplianceMost African American clients will need at least 2 medications to achieve blood pressure controlACE inhibitor and calcium channel blocker.
14 Pharmacologic: Diuretics Mechanism of Action:Thiazides, Loop, Potassium SparingS/E:fluid and electrolyte imbalancesK+, Mg++CNS effectsGI effectsNursing Considerations:Monitor for orthostatic hypotensiondehydrationHypokalemiaThiazides, Loop, Potassium SparingPatho-block Na+ reabsorption in nephron-Na+ follows water and increases water/urine excretionLoop of henle has highest concentration of Na+ in filtrate from glomerulus therefore they are the most potentRecommended for initial drug therapy of uncomplicated HTN (along with beta-blockerNewly diagnosed HTN preferred durg combo for initial treatment = diuretics and beta blockersThiazides first and most commonly used due to more gentle diuresis
15 Adrenergic Inhibitors: Beta Blockers Cardioselective (β1)Atenolol (Tenormin)Metoprolol (Lopressor)Non-cardioselective (β1, β2)Propranolol (Inderal)Mechanism of ActionBlocks beta actions causing:decreased heart ratedecreased BPdecreased contractilityRecommended for initial drug therapy of uncomplicated HTN (along with diuretic)By decr HR and contractility reduce CO and lower SBP…also block/inhibit renin secretion and resultant formation of Angiotensin IIFor example a patient receiving Rx for minipress (Prazosin HCL) make sure you tell them to take it at bedtime.
16 Adrenergic Inhibitors: Beta Blockers S/E:Orthostatic hypotensionBradycardiaHypotensionFatigueWeaknessNursing considerationsUse in caution with heart failureDiabetes who take BB may not have sx of hypoglycemia monitor pulse regularlyDiabetes who take BB may not have the usual manifestations of hypoglycemia because the sympathetic nervous system is blocked.
17 ACE Inhibitors Drug Interactions: NSAIDS (decrease BP control) Diuretics (excessive hypotensive effect)Potassium supplements, potassium-sparing diuretics (increased risk of hyperkalemia)Lithium (increased lithium serum levels)Precautions:“First dose effect “– severe hypotension. Remain in bed for 3 to 4 to prevent falls.Obtain BP before giving - hold if hypotensiveChange positions slowly due to orthostatic hypotensionMonitor liver and kidney function17
18 Angiotensin Receptor Antagonists (Blockers) Losartan (Cozaar)Mechanism:Inhibit binding of angiotensin II receptors in blood vessels and other tissuesvascular smooth muscle relaxationincreased salt and water excretionreduced plasma volumeSide Effects:HypotensionDizzinessCough,Heart failureAngioedemaDrug Interactions:Potassium-sparing diuretics ( serum K+)Mechanism:Inhibit binding of angiotensin II to AT-1 receptors in blood vessels and other tissues causing vascular smooth muscle relaxation, increased salt and water excretion, reduced plasma volume, and decreased cellular hypertrophy.These agents inhibit the renin-angiotensin system more completely and selectively than ACE inhibitors
19 Calcium Channel Blockers Amlodipine (Norvasc)Diltiazem (Cardizem)Nifedipine (Procardia)Mechanism of ActionBlocks slow channels of CalciumDecreases contractilityVasodilationAV node slowsPhase 0- Rapid depolarization: Na+Phase 1- Peak action potential: Ca++ influxPhase 2- Plateau: CaPhase 3- Rapid repolarization: K+ outflowPhase 4- Resting stateBy blocking channels of Ca++-decr contractility and relax smooth muscle lowering peripheral resistence-AFTERLOADReduces the force of contractionSlows AV node-decreases HRVasodilation of smooth muscle in the blood vessels decreased peripheral resistance reduces BP and dec afterload reduced O2 needs.Dilates coronary arteries provide more O2 to myocardiumACTIONS:Decrease BPDecrease AnginaDecrease Heart Rate/ Dysrhythmias
20 Calcium Channel Blockers S/E:HypotensionBradycardiaAV blockNauseaH/APeripheral edemaMonitor I&O closelyNursing considerations:Always obtain BP-HR before givinguse with caution in patients with heart failureOrthostatic changesChange position slowlycontraindicated in patients with 2nd or 3rd degree heart blockConcurrent use w/b-blockers incr risk of CHF
21 HTN Case Study 45yr African American male Nursing/medical priorities… Complaint: new onset severe global HAVS: P-88 R-20 BP-210/142 sats 96% RASlightly confused to place, timePMH: HTN x10 yrs-unable to afford meds, not taking the last weekLabs: K+ 4.2, Na+ 138, creat 2.5, trop neg,12 lead EKG no acute changesNursing/medical priorities…
22 HTN Case Study MD orders: Metoprolol 5mg IV push q5” x3 for SBP5mg/5cc….administer over 2”…how much every seconds???Nursing priorities/considerations…Admit to ICUVS before transfer: P-68 R-20 BP-192/118
23 In ICU… Started on Nipride gtt Started on po: Started at 0.5mcg BP 180/90….in 2 hoursNext am 140/90Started on po:LisinoprilDiltiazemMetoprololConcerns to address upon DC???
24 Peripheral Arterial Disease Altered flow of blood through arteries/veins of peripheral circulationManifestation of systemic atherosclerosisa chronic condition in which partial or total arterial occlusion deprives the lower extremities of oxygen and nutrients8-10 million have PAD20% in adults >70More prevalent w/african americans
25 Physical Assessment Intermittent claudication Pain that occurs even while at rest; numbness and burningInflow disease affecting the lower back, buttocks, or thighsDistal aortaOutflow disease causing cramping in calves, ankles, and feetSuperficial femoral artery (knee and down)Hair loss and dry, scaly, mottled skin and thickened toenailsUlcersarterial ulcersdiabetic ulcersvenous stasis ulcersPost tib pulses most sensitive distal pulse of PAD because pedal pulse difficult to palpate in many elderly.25
26 Nonsurgical Management ExercisePositioningavoid extreme raising legs above heart, do elevate for edemaPromoting vasodilationwarmth and avoid cold temp, stop smokingDrug therapyclopidogrel (Plavix), Pentoxifylline (Trental), ASAPercutaneous transluminal angioplastyAtherectomyExerciseMay improve arterial blood flow due to collateral circulationDrug therapyTrentalIncreases flexibility of RBC…decreases blood viscosity by inhibiting platelet aggregation…incr. blood flow.26
27 Surgical Management Preoperative care Postoperative care Documentation of distal pulsesPostoperative careAssessment for graft occlusionPromotion of graft patencyTreatment of graft occlusionMonitoring for compartment syndromeAssessment for infectionGraft occlusion most common in first 24 hours.
28 Acute Peripheral Arterial Occlusion Embolusmost common cause of occlusions, although local thrombus may be the causeAssessmentpain, pallor, pulselessness, paresthesia, paralysis, poikilothermia (coolness)Surgical therapyarteriotomyNursing careCMSPain assessmentSpasms/swellingCompartment syndromeNursing careMonitor CMS carefully in distal extremityPain should diminish..incisional pain OKspasms.
29 Anticoagulation Therapy:Heparin Inhibits (does not dissolve) thrombus and clot formationGiven IV/SQNever given IM D/T risk of hematomaDoes not cross placental barrierAntidoteProtamine sulfate: Fast acting, short ½ lifeNote: If sx’s of bleeding stop infusion, be prepared to give antidoteAnticoagulants inhibit the synthesis of clotting factors.Heparin: Used in Tx because of its ability to inhibit the synthesis of clotting factorsHeparin, contHeparin prevents clots from getting biggerLow dose heparin used in prevention of DVT after some surgical proceduresASA can ^ heparin’s anticoag effectNTG can diminish heparin effectiveness, may need to ^ dose to achieve anticoagEnoxaprin (Lovenox) introduced in 1993Fast acting
30 Aneurysms of Central Arteries PathoMiddle layer weakenedStretching of intimaFusiform aneurysmSaccular aneurysmDissecting aneurysm (aortic dissections)Thoracic aortic aneurysmsAbdominal aortic aneurysmsPathoAtherosclerosis and HTN highest correlation and smokingAneurysm: a permanent localized dilation of an artery, enlarging the artery to twice its normal diameterFusiform aneurysmDiffuse dilation affecting entire curcumferenceSaccular aneurysmOutpouching affecting defined areaDissecting aneurysm (aortic dissections)Intimal tear that allows blood to enter and tearLife threatening emergencyThoracic aortic aneurysms.
31 Thoracic & Abdominal Aortic Aneurysm Back painshortness of breath hoarseness, and difficulty swallowingSudden excruciating back or chest pain is symptomatic of thoracic ruptureAbdominalPain steady with a gnawing qualityunaffected by movement-may last for hours or daysabdomen, flank, or back.Abdominal mass is pulsatileRupture is the most frequent complication and is life threatening.Thoracic25% of allOlder adults-50% mortalityAbdominal75% of all4:1 more common in menMost common between renal arteries and bifurcation>6 cm 50% will rupture in 1 yearSx depend on amount of pressure exerted on surrounding structures or ruptureDiagnosis and ManagementX-raysComputed tomography scan to assess size and location of aneurysmGoal of nonsurgical management: monitor growth of the aneurysm and maintain blood pressure at normal level
32 Aortic Dissection Patho Pain Emergency care goals include: Elimination of painReduction of blood pressureImmediate ORSurgical treatmentSudden tear in the aortic intima, opening the way for blood to enter the aortic wallPain described as tearing, ripping, and stabbing
33 Abdominal Aortic Aneurysm Repair Preoperative careAssess peripheral pulsesOperative procedurePostoperative careMonitor vital signsAssess for complicationsParalytic ileusAssess for graft occlusion or ruptureChange in CMSSevere painDecreased u/oAssess for complicationsMIGraft occlusion or ruptureHypovolemia-renal failureResp distressParalytic ileus.
34 Thoracic Aortic Aneurysm Repair Preoperative careOperative procedurePostoperative care assessments:Vital signsCMS changesComplicationsRespiratory distressCardiac dysrhythmiasHemorrhageParaplegiaFor surgical repair-will be open heart with bypass and aortic clampingCan also do non surgical repair with femerol artery in groin approach like angiogram.
35 Raynaud’s Phenomenon Patho Sx Treatment Education Blanching >cyanosisPainAggravated by cold/stressTreatmentProcardiaSide effectsEducationCold exposureStop smokingStress reductionCaused by vasospasm of the arterioles and arteries of the upper and lower extremitiesOccurs bilaterallyAge >30 yearsMore common w/womenCause is unknown-seen more common w/LupasDrug therapy: Procardia, Cyclospasmol, and DibenzylineProcardiaSide effects…dizziness and hypotensionLumbar sympathectomyReinforcement of client education; restriction of cold exposure.
36 Venous Thromboembolism ThrombusVirchows TriadVenous blood stasisEndothelial injuryhypercoagubilityThrombophlebitisThrombus w/inflammationDeep vein thrombosis (DVT)Pulmonary embolismPhlebitisInflammation of superficial veinsAssessment:Calf or groin tenderness or painSudden onset of unilateral swelling of the legLocalized edemaVenous flow studies-USLab:D-DimerThrombusblood clotPhlebitisManagement: warm, moist soaks and elastic stocking.36