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Module 1 study guide

Medications: Beta adrenergic blocker- (Inderal)(Lopressor) for angina or CHF, slows HR, decreases BP, lowers myocardial contractility, decreases O2 needs to heart. Watch for bradycardia, caution pt not to stop abruptly (can develop a MI) must titrate down! Calcium Channel blockers-(Norvasc, verapamil, cardiazime, procardia) blocks the influx of calcium, relaxes blood vessels, increases cardiac perfusion, decreases BP. Need to watch for hypotension Coumadin- oral anticoagulant given at home. Test with PT/INR. PT compare with control 11-12.5 seconds. INR standard- 2.0-3.0 High dose- 3.0-4.5 Antidote- vitamin K Heparin- prevents formation of new clots. Test with PTT. Compare with control 25-35 seconds. Antidote- protamine sulfate *Start Coumadin before stopping IV heparin because Coumadin can take up to 3 days for a therapeutic level in the blood. Cardiac glycosides-(Digoxin, Digitalis) Slows the HR and strengthens contractility to improve cardiac output. Starlings Law- the greater the stretch of fibers in the heart the greater the force. *Diuretics and hypokalemia increase dig effectiveness, increases the risk for dig toxicity *Dig has a diuretic effect by increasing cardiac output which increases urinary output. *Dig toxicity- bradycardia, visual disturbances, anorexia, n/v, decreased HR, decreased BP, heart blocks. Isuprel- antiarythmic, used for v-tach, heart blocks, and cardiac arrest. SE- flushing, sweating, tachycardia Atropine- antiarrythmic, treats severe bradycardia. SE- tachycardia Thrombolytic agents- to dissolve and lyse clots SE- Bleeding t-PA- used within 6 hours of onset with chest pain. Pt cannot have any bleeding. Streptokinase-Not used if pt has had strep in the last 12 months AntistreplaseCardiac Disorders: CHF- term used when referring to left sided or right sided heart failure. Complication of MI. Impairment of contractility of heart which causes a decrease in cardiac output. Pt can have edema because it cannot perfuse the kidneys.

Left sided failure: s/s- tachycardia with s3 heart sound, pulmonary congestion, crackles, ronchi, wetness, SOB, decreased energy level, fatigue, frothy sputum, cough that is productive or non productive, nocturnal dyspnea, edema. Right sided failure: Cannot propel blood into the lungs. s/s- peripheral edema, dependent edema. Principles of treatment- balance between blood supply and demand, remove and prevent accumulation of excess fluid, promote rest to reduce workload on heart, increase force of heart contraction. *must weigh pt daily, 1 L of fluid equals 2.2 lbs of weight Lab test- BNP tests for CHF, diagnoses CHF and determines its treatment by severity. Vasoactive drugs: vasodialation to complete ventricular emptying, decrease pulmonary congestion Sodium nitroprusside (Nipride) - decreases afterload, potent rapid acting vasodilator, given IV by pump, dose is titrated. Inocor- improves myocardial contractility, causes vasodilatation, can be used in short term management in CHF if other drugs are not effective. Tridil (NTG) - to control BP, antianginal, decreases myocardial O2 consumption Diuretics- give in morning if not on bed rest. IV lasix works in 5 minutes Pt teaching for CHF- Know meds, know s/s of K+ depletion, teach how to check BP and pulse. Fluid and sodium restriction, stool softeners, diuretics, small meals, daily weights, skin assessment because at increased risk for skin breakdown. Pulmonary Edema: from left side heart failure Precipitating factors: MI, stroke, to rapid infusion of blood and IV infusions S/S- SOB, dyspnea, breathlessness, sense of suffocation, restlessness, frothy sputum, loud, moist rails. Treatment: O2- priority, on mask or mechanical vent Morphine- IV increments to decrease anxiety and SOB, monitor for Resp depression Diuretics- Lasix or Bumex. Lasix IV- onset is 5 min, duration is 2 hours Lasix PO- onset is 1 hour, duration is 6-8 hours Digitalis- to improve contractility, decrease HR and increase strength, promotes dieresis by increasing cardiac output. Aminophylline- reduces bronchospasms Positioning- head up and legs down when pt is in circulatory overload. It takes the fluid away from the lungs and promotes venous return Circulatory overload s/s- neck vein distention, rapid weak pulse, skin warm and moist. Pulmonary embolism: Blood clot in the lungs, symptoms depend on size of thrombus S/S- dyspnea, SOB, crushing chest pain, tachycardia, diaphoretic, restlessness, sense of doom, anxious Diagnosis- EKG, blood enzyme(troponin, CKMB), ABGs, lung scan, pulmonary angiogram

Prevention- anticoagulation therapy, leg compression devices, passive and active devices, exercise. Interventions- anticoagulation (heparin, Coumadin), thrombolytic (TPA), surgical (embolectomy). Hemodynamic Monitoring: CVP- central venous pressure- pressure in vena cava or right atrium, checks right ventricular function and venous blood return to the right side of the heart. *check CVP to monitor for CHF or hypovolemia CVP most valuable in monitoring-fluid and blood volume -adequacy of central venous return to right side of heart -right ventricular function (filling pressure) -differentiates between right and left side of heart, determines left failure or right failure *if over hydrated or dehydrated look a CVP to see how much diuretic or fluid to give. Pulmonary artery pressure monitoring- reflects the left side of the heart, pulmonary circulation, and left ventricular function (Cardiac output) *monitors cardiac output and pulmonary Swans-Ganz catheter: measures both right and left side at the same time. It is a balloon tip cath that is inserted into a large vein to the superior vena cava, into the right atrium, into the right ventricle, then into the pulmonary artery where it is advanced into the smaller veins until it is wedged and cannot advance anymore, the balloon is then deflated and the catheter is stitched into place. Indications for insertion: -differentiate between cardiac and pulmonary conditions -provides central venous access for drugs or fluids -monitors effects of fluid replacement -provides port for blood draws Parameters that can be measured: -Pulmonary artery pressure, wedge pressure, O2 sat ??(there was 3 more but I missed them) Potential complications: -Infection, dysrythmias, pulmonary artery rupture by inserting, inadvertently wedging of cath tip, pulmonary thromboembolism, pulmonary infarction, catheter kinking, air embolism, system disconnection. Cardiogenic Shock: decreased cardiac output leading to inadequate tissue profusion. Heart fails to pump effectively. If in shock long enough, heart will wear out and not function properly. S/S- classic signs r/t decreased cardiac output. SOB, fatigue, hypotension, decreased urine output, increased respirations, crackles, increased pulse, cold clammy skin, oliguria, cerebral hypoxia, dysrythmias. -Early- restlessness, confused, tachycardia, decreased urine output

-later- cold, clammy skin, metabolic acidosis -Late- organ damage Nursing/Medical management: Improve tissue profusion, decrease work load of the heart -Fluid replacement- especially if hypovolemic, dieresis if hypervolemic, monitor I&O -Vasopressors to increase BP and vasodilators to decrease blood pressure -Cardiac support- antiarrythmias, digoxin, NTG IABP- intraaortic balloon pump, catheter with a sausage shaped balloon. It is a mechanical support system. -Resp support -Renal support IABP- sausage shaped cath that is placed in the femoral artery, positioned in descending thoracic aorta, synchronized with EKG by connecting to a machine. Improves cardiac output. It is a mechanical support for left ventricular dysfunction. It decreases the work load to the left side of the heart. It increases circulation without increasing the workload. Balloon inflation occurs during diastole (relaxation of the ventricles) Balloon deflation occurs during systole HTN: Primary- high BP, dont know the cause, majority of people Secondary- caused by a factor -Kidney- chronic glomerular nephritis causes HTN -s/s- proteinuria, polyuria, HTN -tx- renal bypass graft, nephrectomy -Coarctation of the Aorta- Aorta pressing together (congenital defect) -s/s- greater pressure before the coarctation and lesser pressure after. Increased BP in the upper ext . as compared to lower ext. -tx- repair the aorta -Endocrine disturbances- adrenal medulla tumor ( Pheochromocytoma) -tx- remove the tumor Hypertensive crisis- HTN emergency. Increased BP that if sustained long enough can cause organ damage Tx- decrease BP immediately. Nipride is the drug of choice, Tridil, vasotec. Give IV for immediate action. Monitor BP every 5 minutes. Short duration. Nursing management of HTN- lifestyle changes, diet, exercise, weight control, decrease salt intake, teach about meds, they must take meds consistently and cannot stop abruptly. Angina: chest pain d/t lack of O2 to heart Assessment- pain can radiate, occur during rest, anxiety, extreme temp changes, exercise

Implementation- relieve by rest, NTG During acute stage- stop activity, bed rest to decrease O2 demands to the heart, implement O2 2-4L, monitor O2 sat, monitor VS, give NTG During sub acute stage- to prevent from reoccurring. Increase activity to toleration, small, meals, stool softeners, ASA, watch for bleeding tendencies in stool. Teaching- weight, diet, activity. NTG teaching- Lasts 6 months, keep in dark container. Percutaneous transluminal coronary angioplasty- less invasive. Opening up coronary arteries. Need to watch for bleeding (cold ext, no pulses, pale, cyanotic) Call MD MI: Assessment- chest pain cannot be relieved by NTG and rest, increases in severity, persistent, skin pale and diaphoretic, N/V, SOB, c/o dizziness. PlanningAcute phase- morphine IV in 1-2mg increments given for pain, anxiety, and vasodilatation which will increase cardiac output; NTG IV given for vasodilatation; increase HOB, support arms on pillows to decrease chest discomfort, monitor I&Os Morphine- doesnt falsely raise enzymes, decreases preload, decreases coronary artery spasms, decreases pain perception in cerebral cortex, relaxes bronchioles to improve circulation. SE- decreased respirations, confusion, hypotension Sub acute phase- (when acute phase is over) increase activity as tolerated, cardiac rehab Pt teaching and discharge planning- explain meds, planning activities, know what signs to look for, plan rest periods, disease process and adherence to treatment, avoid heavy lifting, dont sit more than 2 hours, avoid emotional stress, avoid constipation(valsalva maneuver), take meds as directed. Cardiac Rehab: Rehabilitation is in 3 stages. 1. Pt education when acute phase is over, low level activities 2. Have them walk down hallway or walk a mile, get them back to state prior to illness 3. Long term conditioning, in a maintenance program CABG: Candidate- person with angina not controlled by therapy or meds, positive cardiac stress, left coronary artery occluded more than 60%, unsuccessful angioplasty or stent. Post op care- neuro checks, I&O, heart sounds, chest tube management, pain (incisional, sternum) type, duration, monitor for dysrythmias, monitor for reaction to analgesics.

Observe for complications- Hemorrhage, taponade, CHF, MI, renal failure (assess BUN, Albumin, Creatinine, electrolytes), hypotension, embolism, CVA(from decreased CO), psychosis Tamponade- bleeding into pericardial sac, will impair filling of ventricles, CVP reading will increase, BP will decrease, cardiac output will decrease. Will notice sudden stop of chest tube drainage and muffled heart sounds. *Need to be able to know the difference of chest pain from CABG or chest pain from MI, if the pt is c/o chest pain after surgery. -CABG chest pain- pain meds will relieve -MI- T wave changes in EKG, pain meds will not relieve. Pericarditis: inflammation of the pericardium, primary infection or secondary to strep, staph, MI, cardiac surgery, renal disorders, rheumatic fever, or lupus s/s- pericardial friction rub, chest pain aggravated by inspiration, pain when coughing or rotation of trunk and radiates to shoulder, neck, and arm. Dx- by s/s and echocardiogram tx- to help to relieve pain have pt sit up or lean forward, morphine, ASA and steroids for inflammation, antibiotics if has strep or infection. Chronic constrictive pericarditis- membrane becomes fibrotic, decrease cardiac output s/s- associated with decreased cardiac output and CHF, dyspnea on exertion is the most prominent symptom. Tx- Digoxin, surgical excision of damaged pericardium is tx of choice, pericardectomy Myocarditis: Inflammation of the muscle of the heart, caused by viral or bacterial s/s- fatigue, dyspnea, SOB, chest pain, palpitations tx- bed rest, if bacteria give steroids and antibiotics, if having dysrythmias- treat the dysrythmias. Infective Endocarditis: infection of valves and inner lining of the heart, caused by bacteria, virus, preexisting injury or disease. Predisposed with coarctation of the aorta s/s-fever,weightloss, back and joint pain, Jane Way lesions (small painless rash found on palms of hands and soles of feet, red/blue in color) tx- bed rest, antibiotics, serial blood cultures to monitor therapy Rheumatic Endocarditis: Acute or chronic, infection of the cardiac valves and endothelial surface of the heart, caused by strep. Found in mitral valve causing mitral valve regurgitation, can cause permanent damage. s/s- depends on defect, fatigue, SOB, wheezing, symptoms will progress Dx- ASO titer tx-antibiotics, steroids, ASA, prevention (ASO titer)

S/S of streptococcal pharyngitis- sore throat, fever, enlarged lymph nodes, chills, otitis media, diffuse redness of throat with exudates on the pharynx, acute sinitus *Prevent heart problem by getting tested for strep* Cardiomyopathy: enlarged heart s/s- SOB especially on exertion, JVD, dependent pitting edema, tachycardia Dx- CXR, echocardiogram tx- treat heart failure, to cure need transplant Mitral Stenosis- stenosed MV, blood leaks backward s/s- SOB on exertion, fatigue tx- bed rest to decrease myocardial O2 demand, if infection- needs antibiotics, if s/s of heart failure- tx heart failure, replace valve. Aortic Valve Stenosis: Narrowing of orifice of left ventricle and aorta s/s- exertional SOB, dizziness, fainting d/t decreased blood to brain, chest pain tx- replace valve Aortic insufficiency (regurgitation): backflow of aorta into left ventricle s/s- exertional SOB, fatigue, awareness of increased heartbeat tx- replace valve Peripheral ischemia: Assessment of lower ext- peripheral pulses, calf tenderness, pain, temp, color, cap refill, humans sign, varicose veins, intermittent claudication, gangrene, ulceration Intermittent claudication (leg pain when walking or exercise and goes away when at rest) caused by inadequate blood flow to tissues, Arterial problem. Buergers Disease- reoccurring inflammation of the small arteries and veins. Primarily in lower ext. results in thrombus formation and occlusion of vessels -Unknown cause, can be linked to autoimmune disorder, smoking and chewing is a contributing factor because is causes vasoconstriction s/s- intermittent claudication, pain, cramps in feet and legs, decreased or absent pulses, numbness, tingling, edema, cold aggravates symptoms, reddish-blue discoloration, intense rubor. Pt teaching- avoid products that cause vasoconstriction (nicotine), lifestyle changes (weight, diet,activity, skin care), avoid injury by protecting extremity (hot water, clipping toenails). *vasodilator not good because it affects all the vessels, not just the lower ext, it can divert blood flow away from lower extremities. Raynauds Disease- intermittent arterial vasoconstriction s/s- classic symptoms: first pale then changes to blue, then changes to red, this is usually seen in

bilateral hands. Constriction-paleness then changes to blue Vasodialation- changes color to red tx- avoid cold, avoid tobacco, wear protective clothing (gloves) calcium channel blockers treat vasospasm (nifedipine, procardia, resperine) sympathectomy- interrupting the sympathetic nerves by removing the sympathetic ganglia or dividing the branches. Vein Disorders: Thrombophlebitis- inflammation of vein and clot formation, can immobilize and go to lungs or brain s/s- swollen limb, pale, cold, vein is red and warm, pain tx-bed rest, elevate affected ext, compression stockings, warm moist packs, IV heparin or Coumadin. Varicose veins- abnormally dilated, tortuous, superficial veins caused by incompetent valves in veins. Predisposing factor- prolonged standing, heart disease, hereditary, pregnancy s/s- dull aches, muscle cramps, muscle fatigue in lower ext, ankle edema, heavy feeling in legs, leg cramping at night dx- assessment when standing, duplex scan of vessels tx- prevention(decrease standing time with rest periods), no constricting garments, ligation and stripping of veins. Pt teaching- avoid standing and sitting for long periods of time. Lab values and rationales: PTT- measure for heparin, 1.5 to 2.5 times the control, 25-35 seconds. Antidote- protomine sulfate PT- measure for Coumadin, 1.5-2.5 times the control, 11-12.5 seconds. Antidote- vitamin K INR- ratio to evaluate Coumadin, standard dose-2.0-3.0 high dose-3.0-4.5 Antistreptolysin titer (ASO) - measures antibodies against strep, increase can indicate recent strep infection, <100 Sedimentation rate (ESR)- identifies and inflammatory process, Measures the rate at which RBCs settle out of unclotted blood in mm/hr. It is non-specific. Less than 50 yrs: male- 0-15, Female-0-20, Greater tha 50 yrs: Male-0-20, Female- 0-30 WBC- for cardiac- elevated with MI, WBC increase during healing process, showing that damage has occurred. 5-10 BUN & Creatinine- evaluates renal. Decreased CO= Decreased urinary output. With decreased urinary output toxins stay in the body increasing levels. BUN-10-20, Creatinine-0.5-1.5. Urea nitrogen/ creatinine ratio will be elevated d/t decreased renal perfusion from decreased CO. normal is 10:1 to 20:1

BNP-evaluate tx of pt with CHF. Assessess ventricular function, if increases pt has CHF, value used to determine treatment. <100 Lipids-HDL and LDL, causes blocking leading to CAD, HDL: 29-77, LDL:60-160 CPK-elevates in 3-6 hours, returns to normal in 3-5 days, male 5-35 female 5-25 LDH-elevates in 24 hours, returns to normal in 10-14 days, 100-190 CKMB- elevates in 2-4 hours, returns to normal in 48-72 hours, 0% Myoglobin- elevates in 1-4 hours, returns to normal in 24 hours, male- 20-90, female-12-75 Triponin levels- first one to elevate, within first hour, returns to normal in 5-14 days, <0.03 *cardiac enzyme labs will be increased if there was damage to the heart* Potassium-Will always affect heart contractility, influences conduction impulses and muscle contractility. 3.5-5.5 *both hypo and hyper lead to v-fib and cardiac standstill. Hypokalemia- increasesed excitability, susceptible to toxic effects of dig, decrease pulse, vision changes, dysrythmias. Caused by vomiting or gastric suctioning. EKG- creation of U wave, ST segment depression. Tx- give potassium Hyperkalemia- T wave elevated, widening QRS, causes depressed action on heart, contracts slowly, muscle weakness, confusion, restlessness. Tx- flush out potassium with kaexilate or for rapid effect glucose mixed with insulin or dialysis. Sodium-135-145 Hyponatremia- loss through sweating, urine, diarrhea, CHF(retaining fluid further dilutes sodium) Tx- add sodium through NG tube or IV Hypernatremia- gain of sodium, thirst, sticky mucous membranes. Tx- give hypotonic electrolyte solution(D5W) EKG interpretations: electrical activity of heart, pattern of electrical impulses. PQRST Sinus Bradycardia- Atropine, pacemaker if it is an electrical issue Sinus Tachycardia- determine cause and tx, If s/s of CHF give dig and diuretics Atrial Flutter- give dig, quinidine, cardio version Atrial Fib- dig, verapimil, quinidine, propanolol, cardio version PVCs- O2 if hypoxic, lidocaine, mg sulfate V- tach-(marching nuns) No P wave, QRS is wide and bizarre, tachycardic. Card overt if pulse, Defib if no pulse V-fib- Heart is quivering, No CO, No heart beat. Defib, CPR, EPi, lidocaine, Bretylium, Vasopressin Asystole- CPR, Epi, Atropine, Pacemaker

ProceduresEchocardiogram- visualizes structures of the heart (valves) Thallium imaging- injecting thallium. Only healthy cells pick up thallium, can determine if area is necrotic from MI. Cardiac Cath- Assesses coronary arteries. Put dye in vessels of heart to determine blockage, Assess BUN and Creatinine. Put through the femoral artery Complications- allergies (ask if allergic to iodine), dysrythmias Before Procedure: obtain consent, tell how long procedure will last, NPO 8-12 hours, give mild sedative or sedation, need to be told that they can feel palpitations d/t dye, may feel urge to cough when going through pulmonary artery. Post Procedure- Assess site for bleeding, assess pedal pulses, temp color, CMS, pain, Monitor for dysrythmias, Assess pain level, Report chest pain immediately, encourage fluids to flush out dye, assist them out of bed for the first time( can experience orthostatic hypotension), elevate ext if pt c/o pain, numbness or tingling Teaching for NTG: pg 870 Instruct the pt to make sure the mouth is moist, tongue is still, and saliva is not swallowed until the nitro has dissolved. If the pain is severe they can crush the tablet between the teeth to hasten the absorption. Must carry meds at all times. Should be stored in dark, glass bottle, explain that it is inactivated by heat, air, moisture, and light. Its only good for 6 months. Medication should be taken in anticipation of pain(before angina producing activity), after 3 sublingual tablets at 5 min intervals and there is still no relief they need to go to the ER (possible MI), discuss SE, advise pt to sit for a few min after taking SE: flushing, throbbing headache, hypotension, tachycardia READ PG 904-911 CARE OF THE PT AFTER CARDIAC SURGERY Tutoring: *if pt has CHF call MD if pt has a weight gain of 2.2 ibs *Know difference of MI and Angina *If fails cardiac stress test pt needs cardiac cath *know pt teaching before cardiac cath and assessment after cardiac cath *If chest pain after cardiac cath- assess pt, look at monitor, give O2, call MD *During an angina attack: 1. Provide immediate rest, 2.take VS. 3.record ECG, 4.Give nitro. You would provide immediate rest first because it will increase O2 to the heart and oxygenation is first priority.

*medical intervention for angina attack- PTCA. It will open up or widen coronary arteries *Cardiogenic shock- pump failure, not effective enough to perfuse tissue. If meds and fluids do not work, the pt needs IABP to increase cardiac output and decrease workload of heart *Digoxin is not appropriate for angina because it is not a vasodilator. In angina the vessels need to be opened up *Inderal is not appropriate for acute angina because it reduces O2 demand. It does not vasodilate. It is a beta blocker. SE- hypotension. Do not stop abruptly *Know CKMB, Myoglobin, and Troponin. Do not need to know values *How to tell thrombolytics are effective in MI- Chest pain will stop because the blockage is gone. Only give throbolytics until the chest pain has stopped *HTN 140/90. Most people fall into primary HTN * in HTN need to monitor serum electrolytes and BUN & creatinine because increased BP can damage the kidneys. Increased BP can damage all organs. *PVD. Know the difference in Raynauds and Bergers. Raynauds- temp changes, color changes from pale to blue to red. Bergers- vasoconstrictive, caused by tobacco. *varicose veins- caused by incompentent valves, can for ulcerations *Pain for PVD- sharp, intermittent claudication(Bergers), pain at rest(ulcers) *Need to watch potassium levels with Thiazide diuretics. Hypokalemia puts pt at risk for dig toxicity. Both hyperkalemia and hypokalemia the pt has dysrythmias and cardiac stand still. *Aldactone is potassium sparing and can cause life threatening hyperkalemia *PAD: arterial- very painful and necrotic, venous- slightly painful, edema *With PAD need to keep ext elevated, do not cross legs, do not wear constrictive clothing, keep ext warm. No heating blankets *Heart failure- inability of heart to pump enough blood to meet tissues O2 demands, decreased CO. Know causes of heart failure, Know the difference in right sided or left sided *A-fib associated with blood clots because blood is sitting in heart and when the pt gets a shock the clots are pushed to the system. They need to get anticoagulants *Amioderone. Know drug. It is the primary drug for ventricular dysrythmias. Pg 101 of HESI *For heart failure- elevate ext while sitting, give diuretics in am. Assess pts urinary output before giving diuretics so you can assess effectiveness of diuretic.

*pt with CHF need to monitor airway and breathing at night because they are lying down and the diuretic has worn off by then because it is given in am *Know Lasix IV and PO onset and durations *To tell the difference between the pericarditis and MI. pericarditis is relieved by sitting forward and sitting up. *ASO titer to find recent infection with Strep. *If pt has endocarditis monitor with hemodynamic monitoring. If not on hemodynamic monitoring, monitor VS, LOC, and urinary output to ensure organs are being perfused. Urinary output- 30ml/hr is sufficient. *must take erythromyacin before dental or GU procedures if has endocarditis or heart murmur *dx valve diseases by echocardiogram *Symptoms of Mitral Valve stenosis- fatigue, dyspnea on exertion, orthopnea, dry cough, hemopytis, pulmonary edema *Common cause for valve disorders is Rheumatic fever. To prevent need to get tested for strep if has sore throat and fever and needs to get antibiotics. *Pt will need lifelong anticoagulant therapy after valve replacement to prevent thrombus formation. Does not need it for valve repair *She said to look at all questions on HESI pg 106 but she specifically went over 1,2, 4, 6, 9, 11, 12, 13, 18.