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Nursing Care & Interventions for Clients with Vascular Problems
Keith Rischer RN, MA, CEN
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Today’s Objectives… Review the pathophysiology of arteriosclerosis, including the factors that cause arterial injury Discuss drug therapy for hypertension Evaluate the effectiveness of interdisciplinary interventions to improve hypertension Prioritize nursing care for the patient experiencing vascular disorders Develop a continuing care plan for a client who has hypertension Prioritize postoperative care for clients who have undergone peripheral bypass surgery.
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Serum Lipids:Cholesterol
One of the several types of fats (lipids) Important component of cell membranes, and bile acids Building blocks in certain types of hormones Predominant substance in atherosclerotic plaques Circulates in the blood in combination with triglycerides, encapsulated by special fat-carrying proteins called lipoproteins <200 is desirable for total cholesterol Body produces it in the liver, additional cholesterol is ingested through dietary intake This 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
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Lipoproteins LDL = Low Density Lipoproteins - “bad cholesterol”
<130 is desirable HDL = High Density Lipoproteins - “good cholesterol” >30 is desirable- the higher the HDL, the lower the risk of CAD Triglycerides- combination of glycerol with 3 fatty acids Transportable fuel- energy source Strongly influenced by diet LDL = Low Density Lipoproteins - “bad cholesterol” Main carrier of cholesterol Transport cholesterol to sites throughout the body, where it is used to repair cell membranes or is deposited Increased LDL level- increased incidence of atherosclerosis HDL = 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 CAD The ratio of total cholesterol to HDL is useful in assessing a person’s risk for developing CAD
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Cholesterol Levels LDL Cholesterol Total Cholesterol HDL Cholesterol
<100 Optimal Near optimal/above optimal Borderline High High >190 Very high Total Cholesterol <200 Desirable Borderline High >240 High HDL Cholesterol <40 Low >60 High From National Cholesterol Education Program ATPIII Guidelines
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Hypertension “Vascular Disease” Affects 1 in every 4 adults in the US
Major risk factor for cardiovascular disease (CVD) Stroke, MI, Heart Failure Other Target Organ Damage LV hypertrophy Nephropathy Vascular Disorders PVD Retinopathy Target organ damage… Heart Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart failure Brain Stroke or transient ischemic attack Chronic kidney disease Peripheral arterial disease Retinopathy
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Categories Primary (Essential)- without identified cause
90-95% of all hypertension Pathophysiology: (exact cause unknown) Heredity H2O & Na+ retention Altered renin-angiotensin mechanism Stress and increase sympathetic nervous system activity Insulin resistance and hyperinsulinemia Endothelial cell dysfunction Secondary- results from identifiable cause renal disease, endocrine disorders, neuro disorders, meds, PIH
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Stages of Hypertension
Category SBP(mmHg) DBP(mmHg) Normal <120 <80 Prehypertension Hypertension, Stage 1: Hypertension, Stage 2: Hypertension, Stage 3: >180 >110 Diagnosis is based on the average of 2 or more blood pressure readings at each of 2 or more visits after an initial screening Pre HTN Definition: /80-89 mm Hg Individuals at high risk of developing hypertension in the future Lifestyle modifications (not drug therapy) are necessary at this stage Goal is to normalize BP (<120/80 mm Hg) Associated with 3.5X ↑ risk of MI & 1.7X ↑ risk of CAD Qureshi et al. Stroke, Sep Goal of therapy: Individualize therapy for patient by group stages of HTN with cardiovascular risk factor Goal is to lower BP to less than 140/90 mm Hg Goal is <130/80 mm Hg patients with diabetes or chronic kidney disease
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Clinical Manifestations
Early Elevated BP Asymptomatic (silent killer) Later Symptoms secondary to effects on blood vessels in various organs or tissues Fatigue, reduced activity tolerance, dizziness, palpitations, angina, dyspnea
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Risk Factors for Primary Hypertension
Age Alcohol use Cigarette smoking DM Elevated serum lipids Excess dietary sodium Gender Family history Obesity Ethnicity Sedentary lifestyle Socioeconomic status Stress Patient (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. Ethnicity African Americans, Puerto Ricans, Cubans, and Mexican Americans have a higher incidence of hypertension than Caucasian African Americans have highest incidence of HTN Prevalence increases with age and is higher among women than men
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Knowledge Deficit Encourage healthy lifestyles
Lifestyle modifications for all patients with prehypertension and hypertension Components of lifestyle modifications include: weight reduction, DASH eating plan dietary sodium reduction aerobic physical activity moderation of alcohol consumption Stress reduction DASH Diet Reduced overall amount of fat, saturated fat, and cholesterol Increased amount of fruits, vegetables, and low-fat dairy foods Increased fiber with whole grain products Reduced amount of sodium to preferably 2.4 to 1.5 grams per day Reduced sweets and sugar-containing beverages
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Risk for Ineffective Therapeutic Regimen Management
Interventions: Teach medication compliance, usually for the rest of life. goals of therapy potential side effects Assist client to understand therapeutic regimen. Discuss consequence of noncompliance Most African American clients will need at least 2 medications to achieve blood pressure control ACE inhibitor and calcium channel blocker .
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Diuretics Loop Thiazide-Type Potassium-Sparing Bumetanide (Bumex)
Furosemide (Lasix) Thiazide-Type Chlorothiazide Hydrochlorothiazide (HCTZ) Potassium-Sparing Spironolactone (aldactone)
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Pharmacologic: Diuretics
Mechanism of Action: Thiazides, Loop, Potassium Sparing S/E: fluid and electrolyte imbalances K+, Mg++ CNS effects GI effects Nursing Considerations: Monitor for orthostatic hypotension dehydration Hypokalemia Thiazides, Loop, Potassium Sparing Patho-block Na+ reabsorption in nephron-Na+ follows water and increases water/urine excretion Loop of henle has highest concentration of Na+ in filtrate from glomerulus therefore they are the most potent Recommended for initial drug therapy of uncomplicated HTN (along with beta-blocker Newly diagnosed HTN preferred durg combo for initial treatment = diuretics and beta blockers Thiazides first and most commonly used due to more gentle diuresis
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Adrenergic Inhibitors: Beta Blockers
Cardioselective (β1) Atenolol (Tenormin) Metoprolol (Lopressor) Non-cardioselective (β1, β2) Propranolol (Inderal) Mechanism of Action Blocks beta actions causing: decreased heart rate decreased BP decreased contractility Recommended 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 II For example a patient receiving Rx for minipress (Prazosin HCL) make sure you tell them to take it at bedtime.
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Adrenergic Inhibitors: Beta Blockers
S/E: Orthostatic hypotension Bradycardia Hypotension Fatigue Weakness Nursing considerations Use in caution with heart failure Diabetes who take BB may not have sx of hypoglycemia monitor pulse regularly Diabetes who take BB may not have the usual manifestations of hypoglycemia because the sympathetic nervous system is blocked.
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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 hypotensive Change positions slowly due to orthostatic hypotension Monitor liver and kidney function 17
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Angiotensin Receptor Antagonists (Blockers)
Losartan (Cozaar) Mechanism: Inhibit binding of angiotensin II receptors in blood vessels and other tissues vascular smooth muscle relaxation increased salt and water excretion reduced plasma volume Side Effects: Hypotension Dizziness Cough, Heart failure Angioedema Drug 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
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Calcium Channel Blockers
Amlodipine (Norvasc) Diltiazem (Cardizem) Nifedipine (Procardia) Mechanism of Action Blocks slow channels of Calcium Decreases contractility Vasodilation AV node slows Phase 0- Rapid depolarization: Na+ Phase 1- Peak action potential: Ca++ influx Phase 2- Plateau: Ca Phase 3- Rapid repolarization: K+ outflow Phase 4- Resting state By blocking channels of Ca++-decr contractility and relax smooth muscle lowering peripheral resistence-AFTERLOAD Reduces the force of contraction Slows AV node-decreases HR Vasodilation 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 myocardium ACTIONS: Decrease BP Decrease Angina Decrease Heart Rate/ Dysrhythmias
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Calcium Channel Blockers
S/E: Hypotension Bradycardia AV block Nausea H/A Peripheral edema Monitor I&O closely Nursing considerations: Always obtain BP-HR before giving use with caution in patients with heart failure Orthostatic changes Change position slowly contraindicated in patients with 2nd or 3rd degree heart block Concurrent use w/b-blockers incr risk of CHF
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HTN Case Study 45yr African American male Nursing/medical priorities…
Complaint: new onset severe global HA VS: P-88 R-20 BP-210/142 sats 96% RA Slightly confused to place, time PMH: HTN x10 yrs-unable to afford meds, not taking the last week Labs: K+ 4.2, Na+ 138, creat 2.5, trop neg, 12 lead EKG no acute changes Nursing/medical priorities…
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HTN Case Study MD orders:
Metoprolol 5mg IV push q5” x3 for SBP 5mg/5cc….administer over 2”…how much every seconds??? Nursing priorities/considerations… Admit to ICU VS before transfer: P-68 R-20 BP-192/118
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In ICU… Started on Nipride gtt Started on po: Started at 0.5mcg
BP 180/90….in 2 hours Next am 140/90 Started on po: Lisinopril Diltiazem Metoprolol Concerns to address upon DC???
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Peripheral Arterial Disease
Altered flow of blood through arteries/veins of peripheral circulation Manifestation of systemic atherosclerosis a chronic condition in which partial or total arterial occlusion deprives the lower extremities of oxygen and nutrients 8-10 million have PAD 20% in adults >70 More prevalent w/african americans
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Physical Assessment Intermittent claudication
Pain that occurs even while at rest; numbness and burning Inflow disease affecting the lower back, buttocks, or thighs Distal aorta Outflow disease causing cramping in calves, ankles, and feet Superficial femoral artery (knee and down) Hair loss and dry, scaly, mottled skin and thickened toenails Ulcers arterial ulcers diabetic ulcers venous stasis ulcers Post tib pulses most sensitive distal pulse of PAD because pedal pulse difficult to palpate in many elderly . 25
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Nonsurgical Management
Exercise Positioning avoid extreme raising legs above heart, do elevate for edema Promoting vasodilation warmth and avoid cold temp, stop smoking Drug therapy clopidogrel (Plavix), Pentoxifylline (Trental), ASA Percutaneous transluminal angioplasty Atherectomy Exercise May improve arterial blood flow due to collateral circulation Drug therapy Trental Increases flexibility of RBC…decreases blood viscosity by inhibiting platelet aggregation…incr. blood flow . 26
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Surgical Management Preoperative care Postoperative care
Documentation of distal pulses Postoperative care Assessment for graft occlusion Promotion of graft patency Treatment of graft occlusion Monitoring for compartment syndrome Assessment for infection Graft occlusion most common in first 24 hours .
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Acute Peripheral Arterial Occlusion
Embolus most common cause of occlusions, although local thrombus may be the cause Assessment pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia (coolness) Surgical therapy arteriotomy Nursing care CMS Pain assessment Spasms/swelling Compartment syndrome Nursing care Monitor CMS carefully in distal extremity Pain should diminish..incisional pain OK spasms .
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Anticoagulation Therapy:Heparin
Inhibits (does not dissolve) thrombus and clot formation Given IV/SQ Never given IM D/T risk of hematoma Does not cross placental barrier Antidote Protamine sulfate: Fast acting, short ½ life Note: If sx’s of bleeding stop infusion, be prepared to give antidote Anticoagulants inhibit the synthesis of clotting factors. Heparin: Used in Tx because of its ability to inhibit the synthesis of clotting factors Heparin, cont Heparin prevents clots from getting bigger Low dose heparin used in prevention of DVT after some surgical procedures ASA can ^ heparin’s anticoag effect NTG can diminish heparin effectiveness, may need to ^ dose to achieve anticoag Enoxaprin (Lovenox) introduced in 1993 Fast acting
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Aneurysms of Central Arteries
Patho Middle layer weakened Stretching of intima Fusiform aneurysm Saccular aneurysm Dissecting aneurysm (aortic dissections) Thoracic aortic aneurysms Abdominal aortic aneurysms Patho Atherosclerosis and HTN highest correlation and smoking Aneurysm: a permanent localized dilation of an artery, enlarging the artery to twice its normal diameter Fusiform aneurysm Diffuse dilation affecting entire curcumference Saccular aneurysm Outpouching affecting defined area Dissecting aneurysm (aortic dissections) Intimal tear that allows blood to enter and tear Life threatening emergency Thoracic aortic aneurysms .
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Thoracic & Abdominal Aortic Aneurysm
Back pain shortness of breath hoarseness, and difficulty swallowing Sudden excruciating back or chest pain is symptomatic of thoracic rupture Abdominal Pain steady with a gnawing quality unaffected by movement-may last for hours or days abdomen, flank, or back. Abdominal mass is pulsatile Rupture is the most frequent complication and is life threatening. Thoracic 25% of all Older adults-50% mortality Abdominal 75% of all 4:1 more common in men Most common between renal arteries and bifurcation >6 cm 50% will rupture in 1 year Sx depend on amount of pressure exerted on surrounding structures or rupture Diagnosis and Management X-rays Computed tomography scan to assess size and location of aneurysm Goal of nonsurgical management: monitor growth of the aneurysm and maintain blood pressure at normal level
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Aortic Dissection Patho Pain Emergency care goals include:
Elimination of pain Reduction of blood pressure Immediate OR Surgical treatment Sudden tear in the aortic intima, opening the way for blood to enter the aortic wall Pain described as tearing, ripping, and stabbing
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Abdominal Aortic Aneurysm Repair
Preoperative care Assess peripheral pulses Operative procedure Postoperative care Monitor vital signs Assess for complications Paralytic ileus Assess for graft occlusion or rupture Change in CMS Severe pain Decreased u/o Assess for complications MI Graft occlusion or rupture Hypovolemia-renal failure Resp distress Paralytic ileus .
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Thoracic Aortic Aneurysm Repair
Preoperative care Operative procedure Postoperative care assessments: Vital signs CMS changes Complications Respiratory distress Cardiac dysrhythmias Hemorrhage Paraplegia For surgical repair-will be open heart with bypass and aortic clamping Can also do non surgical repair with femerol artery in groin approach like angiogram .
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Raynaud’s Phenomenon Patho Sx Treatment Education
Blanching >cyanosis Pain Aggravated by cold/stress Treatment Procardia Side effects Education Cold exposure Stop smoking Stress reduction Caused by vasospasm of the arterioles and arteries of the upper and lower extremities Occurs bilaterally Age >30 years More common w/women Cause is unknown-seen more common w/Lupas Drug therapy: Procardia, Cyclospasmol, and Dibenzyline Procardia Side effects…dizziness and hypotension Lumbar sympathectomy Reinforcement of client education; restriction of cold exposure .
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Venous Thromboembolism
Thrombus Virchows Triad Venous blood stasis Endothelial injury hypercoagubility Thrombophlebitis Thrombus w/inflammation Deep vein thrombosis (DVT) Pulmonary embolism Phlebitis Inflammation of superficial veins Assessment: Calf or groin tenderness or pain Sudden onset of unilateral swelling of the leg Localized edema Venous flow studies-US Lab:D-Dimer Thrombus blood clot Phlebitis Management: warm, moist soaks and elastic stocking . 36
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Nonsurgical Management
Treatment Priorities Prevent complications Rest Drug therapy includes: Heparin IV therapy Low–molecular weight heparin-Subq Lovenox q 12 hours Warfarin therapy Thrombolytic therapy TPA
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Venous Insufficiency Patho Sx Edema Stasis dermatitis Stasis ulcers
TEDS Stasis dermatitis Stasis ulcers Occlusive dressings Result of prolonged venous hypertension, stretching veins and damaging valves Stasis dermatitis, stasis ulcers Management of edema Management of venous stasis ulcers Drug therapy Surgical management Varicose veins Distended, protruding veins that appear darkened and tortuous .
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