Exam (elaborations) Adults med-surg 1 cardiac

Adults med-surg 1 cardiac Types of PVD (peripheral vascular disease) - Arterial occlusive disease - Venous Insufficency Arterial Occlusive Disease A common circulation problem; arteries that carry blood to the legs or arms becomenarrow and get clogged Main cause of AOD Atherosclerosis Risk factors of AOD - smoking - diabetes - BMI over 30 - high blood pressure 140/90 - increasing age - family history Effects of AOD It is 6-7 times of a greater risk of a heart attack and stroke Symptoms of AOD - intermittent claudication - painful cramping in hip, thigh or calf muscles after activity - leg numbness or weakness - coldness in your lower leg or foot especially with comparison - hair loss or slower hair growth on your feet/legs - slower growth of toenails - shiny skin on legs - weak or absent pulse in legs or feet - ED in men Treatment of AOD non-surgical, lifestyle changes medications: - Cholesterol lowering agents - BP medication Diagnostic tests: AOD Ankle- Brachial Index Doppler ultrasound Angiography PCD surgical treatments - Angioplasty - Endarterectomy - Stenting - Surgical bypass Venous Insufficency - caused by incompetent or obstructed veins = most common cause of lower extremity swelling Risk factors of VI age obesity trauma history of DVT/phlebitis surgical complications (orthopedic) tight fitting garments prolonged sitting or standing family history How it works:VI A clot will block blood flow through the vein and cause pressure to build up Upgrade to remove ads Only $3.99/month Leg injury of surgery injury or surgery that blocks the flow of blood through a vein can increase pressure Excess weight or weight gain The added weight of pregnancy or obesity can increase pressure in the veins of the legs and damage the veins and valves Standing or sitting for too long Prolonged periods without walking can decrease the movement of blood out of the legs and lead to increased pressure in the veins and pooling of blood -- thats because the muscles in the legs play an important role in circulation of blood, acting like a pump to move blood from the legs back to the heart. Signs and symptoms of VI - less pain than arterial disease - brawy skin discoloration (reddish brown) - edema (improves with elevation) - warm skin - itching/stasis dermatitis -stasis ulcers -veins visible (or not) Diagnostics of VI - venous dopller to rule out DVT - otherwise no tests - clinical diagnosis of exclusion VI treatment - no oral medication has yet been proven useful for the treatment of venous disease - graduated compression - surgery reserved for those with discomfort or ulcers refractory to medical management VI: Chronic disease - dialated (or swollen) veins - swelling (edema in the ankles and lower extremities usually at end of the day can be permanent - may be less prominent in the morning - skin changes (tan-reddish usually at ankle or over shins, iritated itchy dry skin thats oozing fluid and scabbing or crusting) Venous ulcers in chronic disease VI - open non healing sores in the inner or outer ankle - ulcers above the knee are usually secondary to injury - venous ulcers can take a long time (months or years) to heal - healing is a gradual process and the resulting scar is usually shiny pink or red with distinct white marks - venous ulcers can come back even after they heal Nursing measures of AOD - dependent position - progressive exercise - decrease risk factors - foot care - pulse checks Nursing measures of VID - avoid prolonged sitting or standing -elevated position - diuretics of limited value - graded compression stockings -meticulous skin care - analgesics as needed - education about poor circulation Upgrade to remove ads Only $3.99/month Abdominal Aortic Aneurysm - permanent localized dilation of aorta within the abdomen - 90% result from atherosclerosis and worsen from HTN - most common location below the bifurcation of the renal arteries (incidence is 3-4% of population, 15,800 die annually) Treatment of abdominal aortic aneurysm Nonsurgical: - if not leaking will monitor size - Manage BP - smoking cessation Surgical: - Indicated for aneurysm >4.5 cm wide Nursing care for abd - monitor vital signs - S/S infection - urine output - lower extremity circulation - abdmonial distension Venous thromboembolism (VTE) a disease that includes deep vein thrombosis (DVT) and pulmonary embolism - the third most common cardiovascular disease after heart attack and stroke DVT + PE = VTE! If not prevented or caught early a DVT can progress with the blood clot breaking away and traveling to your lungs and becoming a potentially deadly PE, which required immediate medical attention Pathogenesis of VTE - Virchow's triad - hypercoagable state - intimal injury (endothelial injury) - stasis of blood flow venous stasis and vascular wall damage + activation of clotting factors + decrease of clot lysing mechanism --> thrombus Initial site often calf veins (less serious than proximal thrombi) S&S of DVT - unilateral edema - pain and tenderness - palpable cord - erythema, warmth along venous system -proximal veins often asymptomatic -common sites: iliac, common femoral, deep femoral and popliteal pulmonary embolus obstruction of pulmonary artery or branch by blood clot, air, fat, amniotic fluid or septic thrombus "blood clot to lungs" most thrombuses are blood clots from leg veins Presentation of PE can be large or small accounts fro 90% of all acute pulmonary conditions Clinical manifestations of PE - DYSPNEA/pleuretic chest pain - low grade fever - apprehension/restlessness - feeling of impending doom - cough hemoptytsis (coughing blood) Upgrade to remove ads Only $3.99/month Risk factors of PE venous stasis hypercoagablity venous endothelial disease certain disease state: heart disease, trauma, post op/postpartum, DM, COPD Other conditions: pregnancy, obesity, oral contraceptive use, constrictive clothing, previous history of thrombophlebitis PE Obstructed area has diminished or absent blood flow - although area is ventilated, no gas exchange occurs - ventilation perfusion imbalance, right ventricular failure, shock occur - can be fatal 1 hr after symptoms start Diagnosis test of PE Chest CT or pulmonary angiogram PE exam finding - tachypnea - lung crackles -pleural friction rub - tachycardia -diaphoresis -low grade fever - decreased O2 stat PE test: - ABG's - CXR - TEE - V/Q scan - spiral CT - pulmonary angiography Prevention of PE - exercises to avoid venous stasis - early ambulation - anticoagulant therapy - sequential compression devices (SCDs) Treatment of PE - measures to improve resp, CV status - Anticoagulation, thrombolytic therapy PE non surgical treatment - O2 - Telemetry monitor - anticoagulation - heparin PE surgical treatment - embolectomy - vena cava filter placement Anticoagulant drug actions: interferes with cagulation process by interferring with clotting cascade and thrombin formation -- examples: coumadin (warfarin sodium) and heparin Upgrade to remove ads Only $3.99/month Heparin Prevention of thrombus formation: IV HEPARIN: - always administered on an infusion pump - therapeutic effect 45 mins - monitory PTT (goal is 60-80 sec) - reverse with protamine sulfate Lovenox ( low molecular weight heparin) - subcutaneous heparin BID Coumadin - individual dose adjustment - based on INR (test that measures how long it takes for blood to clot) - oral administration - can take up to 3-5 days to see therapeutic effect - vitamin K antidote Novel anticoagulants Direct Xa Inhibiotrs: Rivaroxban (Xarelto), Apixaban (Eliquis) Direct Thrombin Inhibitors Dabigatran (pradaxa) Antiplatelet drugs Alter formation of platelets by decreasing responsiveness of platelets to stimuli that would cause them to stick and aggregate on a vessel wall Example of antiplatelet Asprin: Reduction of risk of recurrent TIA's or strokes -- P2Y12 Inhibitors: Clopiodgrel (Plavix) Thrombolytic Agents - Activate the natural anti clotting system, conversion of plasminogen to plasmin - Activation of this system breaks down fibrin threads and dissolves any formed clot Example: TPA & Streptokinase Afterload systemic vascular resistance Preload volume of blood in ventricle at the end of diastole Cardiac output stroke volume x HR Upgrade to remove ads Only $3.99/month Contractility force of the contracting myocardium Ejection fraction EF % of end diastolic volume that is ejected with each heart beat. Normal ed 55-65% Heart Failure Indicates cardiac disease, in which there is a problem with the contraction of the ventricles or filling of the ventricle -- acute or chronic -- may be reversible, BUT most HF progressive Causes of HF HTN CAD Valve issues Cardiomyopathy - disease of the heart muscles Among other causes Assessment of HF - history and physical exam - chext x ray - cardiac enlargement (cardiomegaly), pulmonary congestion/edema - blood tests - BUN/ Creatine (renal); elevated - Elevated brain natriuretic peptide (BNP) - ECG; LVH, arrhymmias ECHOCARDIOGRAM: E/f calculated, how well the heart is pumping - also assesses heart muscle contractility and valves CARDIAC CATH - check EF check for CAD, and measure pressures in heart chambers *weakened heart less than 40% EF of the blood in :V pumped out with each contraction normal is 55-65) Diagnosis Stage A High risk with no symptoms Diagnosis Stage B ACE inhibitor or RBs in all patients; beta blockers in selected patients Left sided HF LV cannot pump blood effectively out the aorta to the systemic circulation. Pressure backs up from the L side of the heart to pulmonary veins and then capillaries then into the interstitial lung tissue Results in pulmonary edema and impaired gas exchange Left sided heart failure symptoms: - cough - starts dry then can become pink, frothy - dyspnea - paroxysmal nocturnal dyspnea - SOB at night - Orthopnea (difficulty breathing when lying flat) - Decreased activity intolerance Assessments of Left Sided failure - crackles at base or higher (sudden opening of fluid filled alveoli) - Elevated respiratory rate - Decreased oxygen saturation - Elevated HR - S3 - Diffuse apical pulse (>1 intercostal space) Right sided heart failure RV cannot eject sufficient amounts of blood out the pulmonary artery and blood backs up into the systemic venous system Clinical manifestations of Left sided heart failure - SOB/DOE - crackles/rales at bases - tachypnea - diaphoresis - weight gain - fatigue - extra heart sound s - mental status changes - capillary refill > 3 sec Clinical manifestation of Right sided heart failure - hepatomegaly - splenomegaly - ascites - dependant pitting edema - JVD (kussmaul's sign) - Weight gain - Anorexia - Extra heart sounds Medical management of HF 1. eliminate & treat contributory factors 2. relieve symptoms 3. improve functional status and extend survival 4. reduce workload of heart by decreasing systemic vascular resistance (afterload) and preload (volume) Interventions of HF - diet modifications - low Na < 2 gm/ day - helps decrease blood volume -- fluid restriction -- weight reduction regular exercise avoid ETOH/tobacco Mediation for HF - Diuretics - remove excess extracellular fluid and increase rate of urine production - Lasix (loop): inhibits Na and CL reabsorption in kidneys - very potent: can give IV, works withing 5-10 mins - SE: hypokalemi, hypotension, gout, ototoxicity * ACE inhibitors - lisinopril: pivotal with HF promotes vasodilation and diuresis so decrease afterload and preload - decrease workload to the heart - SE: cough, hupotension, hyperkalemia, BUN/creatine elevation - Alterative to ACE inhibitors - is ARB (angiotensin receptor blocker). Ex. diovan, cozaar - beta blockers - coreg toprol xL) decrease SNS stimulation, decrease mortality and morbidity SE - hypotension, bradycardia, asthma Diuretics - Hydrochlorothiazide (HCTZ) - dose: 25 - 100 mg/daily - Inhibits sodium and water absorption in distal tubules Nursing Considerations for Diuretics 1. side effect: hypokalemia 2. potential for orthostatic hypotension (elderly at risk) DIGOXIN Increases force of contraction, slow conduction - Heart rate must be assessed before administering - Used for symptom control as no decrease in morbidity or mortality - Monitory for S&S of toxicity - N/V fatigue, bradycardia, heart block, visual disturbances (yellow/green halos), confusion - Low potassium will enhance digoxin's effects - Monitor digoxin levels NI. 09-2.0 Not used with normal ventricular EF Treatment of CHF Upright position Nitrates Lasix Oxygen ACE inhibitors Digoxins Fluids (decrease) Afterload (decrease) Sodium Restriction Test (digoxin level, ABGs, potassium level) unload fast Respiratory insufficiency due to pulmonary edema - supplemental oxygen (acute) - position to maximize breathing/comfort - sit up high fowlers - anxiety reduction measures Excess fluid volume - Diuretics; low sodium diet; I&Os daily weights - contact provider if 2-3 lbs gain in 1 day or 5 lbs in a week - potential for arrythmias r/t high or low K - Real insufficiency r/t meds, gout, r/t diuretic therapy Activity intolerance and fatigue - plan/pace activity; progress slowly - insomia Medication - side effects, monitor VS, labs - Safety issues -- orthostatic hypotension; dizziness Nursing process of pt with heart failure RN plays key role with patient education, monitoring and discharge planning - interdisciplinary collaboration essential End stage options - implantable cardiac defibrillator (ICD) show the heart out of VF - cardiac resynchronization therapy (CRT): biventricular pacemaker/defibrillator that coordinates ventricular beats to increase cardiac output LVAS: left ventricular assist device - a mechanical pump implanted in the person chest to assist a weeakened heart ventricle pump blood throughout the body -- not mechanical heart just assists - heart transplant