Vascular Disorders PDF

Tuesday, October 1, 2024 Vascular Disorders Objectives De nition: Thickening of artery walls which results in progressively narrowed arteries in the upper and lower extremities Prevalence increases with age....

Tuesday, October 1, 2024 Vascular Disorders Objectives De nition: Thickening of artery walls which results in progressively narrowed arteries in the upper and lower extremities Prevalence increases with age. Patients are typically symptomatic between 50-70 People w/ Diabetes show symptoms earlier Strong correlation to other types of Cardiovascular Dz. Higher risk for general mortality PAD remains underdiagnosed and undertreated Apply the nursing process for a client with vascular alterations. Assessment, Diagnosis, Planning, Implementation, and Evaluation Discuss the priority diagnostics associated to vascular alterations and review and their related nursing implications. Discuss commonly used therapies with a focus on pharmacology used in the treatment of clients experiencing vascular alterations Apply the nursing process to potential complications associated with vascular alterations to allow for e ective communication and collaboration among the healthcare team Analyze best practices with an emphasis on nursing implications related to vascular alterations Identify teaching needs for priority health promotion and disease prevention for clients with vascular alterations PERIPHERAL ARTERY DISEASE - Causes Involves progressive narrowing and degeneration of arteries of upper and lower extremities Atherosclerosis gradual thickening of the innermost layer of the arterial wall #1 cause in most cases is TOBACCO!!!! Tobacco Abuse Hypercholesterolemia Chronic Kidney Disease Hypertension Diabetes Mellitus Age - Stages Asymptomatic Rest = pain Claudication Necrosis/Gangrene - Signs and Symptoms Classic symptoms | intermittent claudication Clinical symptoms occur when vessels are 60% to 75% blocked. The ischemic pain is a result of the buildup of lactic acid resulting from anaerobic metabolism. Once the patient stops exercising, the lactic acid is cleared and the pain subsides. Ischemic muscle pain that is caused by a constant level of exercise Resolves within 10 minutes or less with rest Reproducible Paresthesia - results from nerve tissue ischemia > Neuropathy proceeds severe shooting or during pain in the extremity > Numbness or tingling in the toes or feet > Produces loss of pressure and deep pain sensations 1 fi ff  > Injuries often go unnoticed by patient Thin, shiny, and taut skin Loss of hair on the lower legs and thickened toenails Diminished or absent pedal, popliteal, or femoral pulses Pallor of foot with leg elevation >Reactive hyperemia (redness) of foot with dependent position: dependent rubor - Rest Pain PROGRESSION: involves multiple arterial segments and continuous pain develops at rest. Rest Pain most often in foot/toes Blood ow does not meet basic metabolic needs of the distal tissues Occurs most often at night when patient is trying to sleep r/t cardiac output dropping during sleep and the limbs are at heart level Patients use gravity to relieve pain by dangling legs over bedside or sleeping in a chair Leads to Critical Limb Ischemia (CLI) wh/ is characterized by rest pain lasting >2 weeks, non-healing arterial leg ulcers or gangrene - Complications Atrophy of skin and underlying muscles Wound infection Delayed healing Tissue necrosis Arterial ulcers > Most often occur over bony prominences of the toes, feet, and lower legs Gangrene > Critical Limb Ischemia > Chronic ischemic rest pain lasting more than 2 weeks > Arterial leg ulcers or gangrene > Optimal therapy for the patient with critical limb ischemia is revascularization Amputation > May be required if tissue necrosis is extensive, gangrene or osteomyelitis develops, or all major arteries in the limb are blocked, precluding the possibility of successful surgery. - Diagnostic Studies Health history and Doppler Ultrasound Segmental Blood physical Studies Pressures ABI > Done using a hand-held Doppler > The ankle-brachial index (ABI) is a non-invasive tool for the assessment of vascular status. It is the ratio between the systolic blood pressure of the lower extremity, speci cally the ankle, and the upper extremity. > A palpable pulse and a Doppler pulse are not equivalent, and the terms are not interchangeable. > The ABI is calculated by dividing the ankle systolic BPs by the higher of the left and right brachial systolic BP. > A normal ABI is 0.91 to 1.30 and indicates adequate BP in the extremities. An ABI less than 0.90 indicates PAD > Angiography and magnetic resonance angiography delineate the location and extent of PAD. > CTA with run-o s Duplex Imaging Magnetic Resonance Imaging (MRI) Angiography - Conservative Treatment Tobacco cessation Nutrition Therapy Exercise: walking Weight Loss: Goal BMI > distended neck veins and edema of face and arms Abdominal aortic aneurysms (AAA) Often asymptomatic May cause back pain, ank pain, epigastric discomfort, altered bowel elimination, intermittent claudication Pulsation Mass in the periumbilical area slightly to the left of the midline may be present Bruits may be osculated over the aneurysm Complications Cardiac tamponade Occlusion of arterial supply to vital organs Spinal cord ischemia A temporary lumbar drain may be inserted for cerebrospinal uid removal to reduce spinal cord edema and help prevent paralysis Renal ischemia Abdominal (mesenteric) ischemia Rupture—serious complication Severe back pain Tachycardia, hypotension, pale clammy skin, decreased urine output, altered level of consciousness, and abdominal tenderness May/may not have back/ ank ecchymosis (Grey Turner’s sign) Most do not survive long enough to get to the hospital Surgical therapy If ruptured, emergent surgical intervention required 90% mortality with ruptured AAAs Causes of death also include MI, sepsis, and stroke. - Diagnostic Studies CT scan with contrast: Most accurate test Gives length and diameter Presence of thrombus Ultrasonography Useful in screening for aneurysms Monitors aneurysm size TEE -> for Dissections An electrocardiogram (ECG) may rule out MI, since thoracic aneurysm or dissection symptoms can mimic angina. - Treatment Goal – prevent aneurysm from dissecting/rupturing 5 fl fl fl  Early detection/treatment imperative Initial goal HR and BP control Titrated to a target heart rate of 60 beats per minute or less or to a systolic BP between 100-110 mm Hg. BP and myocardial contractility to diminish pulsatile forces within aorta: IV Esmolol Conservative therapy: If no symptoms Pain relief, HR, and BP control: Morphine, Beta Blockers, ACE inhibitors or ARBs, and statins CV Dz. risk factor modi cation: tobacco cessation, decreasing BP, optimizing lipid pro le Close surveillance with CT or Ultrasound every 6 to 12 months 5.5 cm is threshold for repair Intervention may occur earlier in Patients with a genetic disorder Symptomatic patients Rapidly expanding aneurysm High rupture risk - Surgical Repair Open aneurysm repair (OAR) Incising diseased segment of aorta Removing intraluminal thrombus or plaque Inserting synthetic graft (Dacron) Suturing native aortic wall around graft Acts as protective cover Considerations Require cross-clamping of aorta proximal and distal to aneurysm Multiple blood transfusions Risk of postop renal complications ↑ signi cantly when repair is above renal arteries - Endovascular Repair Endovascular abdominal aortic aneurysm repair (EVAR) Involves placement of suture-less aortic graft into abdominal aorta inside aneurysm Minimally invasive: Done through femoral artery cutdown The insertion of a woven polyester tube (graft) covered by a tubular metal web (stent). The stent graft is inserted through a large blood vessel (e.g., femoral artery) using a delivery catheter. The catheter is positioned below the renal arteries in the area of the aneurysm. The stent graft is slowly released (deployed) into the blood vessel. When the stent comes in contact with the blood vessel, it expands to a preset size. A second stent graft can be inserted in the contralateral (opposite) vessel if necessary. Fully deployed bifurcated stent graft Potential complications Endoleak Aneurysm growth/rupture/dissection Bleeding Stent migration resulting in renal artery occlusion Graft thrombosis - emergency Site infection Graft dysfunction may require traditional surgical repair - Nursing Assessment: Pre-op Establish baseline data to compare postoperatively Note quality and character of peripheral pulses and neurologic status Mark/document pedal pulse sites and any skin lesions on lower extremities before surgery and after surgery Do not palpate large masses 6 fi fi fi  Insert two large-bore IV catheters 0.9% sodium chloride and medication Indwelling catheter Pre-op antibiotics per orders - Nursing Assessment: Post-op Monitor for infection Monitor for bowel Foley, ECG, Pulse Ox Assess pulses ischemia Pain Medications Assess Neuro status Arterial Lines Avoid severe NPO/NG Beta Blockers hypertension Peripheral perfusion status Pulse assessment Temperature, color, capillary re ll time, sensation, and movement of extremities Neurologic status Level of consciousness Ability to move upper extremities Pupil size and response to light Quality of hand grasps Facial symmetry Renal Perfusion Speech UOP and Creatinine - Post-op discharge teaching Avoid lifting heavy objects HTN control Wound care F/U appts as scheduled S/S of Rupture/Dissection Stair climbing restriction Activity level instructions-no pulling, pushing or straining until M.D. f/u OTHER ARTERIAL HEALTH PROBLEMS - Buerger Disease Associated with smoking- claudication in feet and lower extremities which is worse at night causes ischemia and brosis of vessels, sensitivity to cold, gangrene ulcers tx, vasodilating drugs, chronic pain mgmt., and ulcer mgmt. nsg, priorities: avoid cold, tob cessation, med. s/e - Raynaud Phenomenon/Disease Possibly autoimmune trigger- causes painful vasospasms , red and white skin color changes with cold or stress, more common in women tx. Same as for Buerger Dz nsg priorities: same as for Buerger Dz. - Subclavian Steal Syndrome Caused by a subclavian artery occlusion causing ischemia and pain in the arm, paresthesia and numbness as well as di ering B/P in the arms. tx. Surgical intervention for unrelenting symptoms nsg. priorities: monitor pt. closely post op, check pulses, watch for ischemic changes, skin color as well as severe pain - Thoracic Outlet Syndrome Caused by compression of subclavian artery by a rib/muscle tx. Physical therapy, avoid aggravating positions, surgery as a last resort for severe pain nsg. priorities: Health teaching, avoiding aggravating positions, neurovasc. assess., monitoring for new s/s PERIPHERAL ARTERIAL DISEASE VS PERIPHERAL VASCULAR DISEASE - Peripheral Venous Disease (PVD) Venous Thromboembolism (VTE) Venous Insu ciency: Venous leg ulcers Varicose Veins Stage 1: Spider Veins Stage 2: Reticular Varicose Veins 7 ffi fi fi ff  Stage 3: Venous Nodes Stage 5: Trophic Ulcers or Varicose Stage 4: Chronic Venous Insu ciency Eczema VENOUS THROMBOSIS Phlebothrombus= a clot without in ammation Thrombophlebitis=clot with in ammation wh/ most commonly occurs in the deep veins of the lower extremities Super cial: super cial vein (rarely need anticoagulation) Deep: Deep vein =need for antigoagulation Venous thromboembolism (VTE) Comprised of DVT’s and PE’s - S/S Unilateral edema, pain, erythema - Diagnosis: Venous Duplex US ( rst-line) Lab: D-Dimer testing Venography CT Scan vs MRI - Complication Venous Thromboembolism leading to a Pulmonary embolism - Prevention Early and frequent ambulation Compression stockings Pneumatic compression devices Drug therapy prevention: SQ Heparin SQ low dose Lovenox - Risk Factors Virchow’s Triad Venous stasis: inactive or damaged venous valves Pregnant, obese, long trips, spinal cord injury, fractured hip Damage of endothelium stimulates platelet activation Surgery, trauma, burns, chemotherapy, DM, sepsis Hypercoagulability of blood Sepsis, Malignancies, polycythemia, (protein C or S de ciency) Factor V de ciency, estrogen replacement, smoking - Treatment SQ Lovenox at full dose (treatment) Longer half-life, no lab monitoring necessary Reversal agent: protamine Adverse e ect: Avoid in renal insu ciency IV Heparin (treatment) Monitor therapeutic level via labs: aPTT or aXa Reversal Agent: Protamine Adverse e ect: Heparin induced thrombocytopenia (HIT) PO Warfarin with IV heparin for 5 days, then warfarin PO by itself Monitor therapeutic levels via labs: PT/INR. INR goal 2-3 Reversal agent: Vitamin K, avoid green leafy vegetables NOACs: PO dabigatran (Pradaxa) rivaroxaban (Xarelto) or apixaban (Eliquis) No lab monitoring, renally dose Reversal agent -> FDA approved only for dabigatran (Pradaxa) ALL: Treat for 3mths or longer and monitor for bleeding 8 fi ff ff fi fi ffi fl ffi fl fi fi  IVC Filter -> repeat DVTs or unable to tolerate NOAC HIT: immune reaction to heparin results in decrease in platelets and increase risk of developing clots: measure heparin antibodies circulating Lovenox: less likely to cause HIT Multiple co morbidities or LARGE VTE: inpt treatment necessary NOACs: Novel oral anticoagulation VENOUS INSUFFICIENCY Result of prolonged venous hypertension that stretches veins and damages valves Leg edema, stasis dermatitis, stasis ulcers Nonsurgical management unless complicated by stasis ulcer - S/S Brownish, thick skin (leathery), Itching, Eczema, Painful Chronic - Complication: Rare: Osteomyelitis which may lead to amputation - Treatment ALWAYS compression and elevation Moist dressings, diet high in protein and calories, control DM, - If s/s of infection are con rmed by wound culture: Treat with wound debridement and Oral antibiotics – do not use topical Anbx. VARICOSE VEINS Dilated tortuous veins - Risk Factors Female VTE hx Tobaccos abuse Occupations that require long hours of Age standing Obesity - S/S Achy pain relieved with elevation or walking - Complication Super cial venous thrombosis - Diagnostics Physical exam Duplex US - Conservative treatment: Three E’s Elevation Elastic compression Exercises stockings - Advanced treatment: Sclerotherapy: a direct IV injection that chemically destroys the veins. - Teaching for PVD Wearing compression stockings Proper foot care New stockings every 6 mths Encourage walking Daily moisturizing Avoid standing/sitting long periods - Nursing Interventions for DVT/VTE Patient education Do not massage area of DVT Leg exercises Slow gradual ambulation is preferred Early ambulation Post op over bedrest Adequate hydration Make sure compression devices are Compression stocking/ compression on devices (SCD’s) Venous foot pump Elevate extremities while up in chair Anticoagulant therapy Monitor patient for s/s of PE( ie… sob,chest pain, acute confusion) 9 fi fi