Study Guide Exam #2
Study Guide Exam #2 Nurs 3310
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This 14 page Study Guide was uploaded by Christie Kepler on Wednesday February 10, 2016. The Study Guide belongs to Nurs 3310 at Western Michigan University taught by Bergman in Winter 2016. Since its upload, it has received 58 views. For similar materials see Nurs Med Surg in Nursing and Health Sciences at Western Michigan University.
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Date Created: 02/10/16
Study Guide Exam #2 Peripheral Artery Disease of the Lower Extremities Chapter 38 Risk factors: Cigarette smoking Hyperlipidemia Hypertension Diabetes mellitus Clinical Manifestations Produces loss of pressure and deep pain Classic symptom of PAD –intermittent sensations claudication Injuries often go unnoticed by patient S&S: Thin, shiny, and taut skin Intermittent pain due to Loss of hair on the lower legs lack of O2 with mobility. Diminished or absent pedal, popliteal, or Ischemic muscle pain that is caused by femoral pulses a constant level of exercise Pallor of foot with leg elevation Resolves within 10 minutes or less with Reactive hyperemia of foot with dependent rest position Reproducible Pain at rest Occurs in the foot or toes Pain, Pallor, pulslesness and paralysis Aggravated by limb elevation ,paresthesia Occurs from insufficient blood flow Numbness or tingling in the toes or feet Occurs more often at night Complications Complications Atrophy of the skin and underlying Non-healing arterial ulcers and gangrene are muscles most serious complications Delayed healing May result in amputation Wound infection If adequate blood flow is not restored Tissue necrosis If severe infection occurs Arterial ulcers- dry crater ulcers Diagnostic Studies Ankle-brachial index (ABI)- compares BP to Upper and Lower extremities Done using a hand-held Doppler Collaborative Care Drug Therapy ACE inhibitors Clopidogrel (Plavix) Ramipril (Altace) Drugs prescribed for treatment of intermittent ↓ Cardiovascular morbidity claudication Mortality Cilostazol (Pletal) ↑ Peripheral blood flow Inhibits platelet aggregation ↑ ABI ↑ vasodilation ↑ Walking distance Pentoxifylline (Trental) Antiplatelet agents ↑ Erythrocyte flexibility Aspirin ↓ Blood viscosity Treatment: Collaborative Care References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Increase exercise Decrease weight Healthy diet Treatment : Radiology Procedures Treatment : Surgery Procedures Percutaneous transluminal balloon Endarterectomy angioplasty (PTA) Picking away plaque Balloon inflation in vessel Patch graft angioplasty WATCH: deflation occlusion of artery| Putting patch(fake piece) in artery Temp and pulse Amputation Atherectomy Removal of the obstructing plaque Nursing Interventions Performed using a cutting disc, laser, or rotating diamond tip Verify blood flow to peripheral Cryoplasty locations Combines percutaneous transluminal angioplasty and cold therapy Capillary Refill Light touch Liquid nitrous oxide Don’t move the patients into knee-flexed position, except exercise Reynaud's Disease Buerger’s Disease – Vasospasm of small Arteries Thromboangiitis Obliterans Red White and Blue Ischemia (white), cyanosis (blue), and re-perfusion (red) Young men with smoking hx Tx: Inflammatory disorder of smaller arteries and veins Prevention of triggers Thrombosis and fibrosis lead to ischemia Calcium channel blockers- relax vasoconstriction of small Tx: stop smoking arteries Disorders of the Aorta Aorta Largest artery for supplying 02 to all vital organs Aortic Aneurysm Outpouching or dilation of the arterial wall Causes: o Degenerative o Congenital o Mechanical o Penetrating or blunt trauma o Inflammatory o Infectious Risk Factors o Male gender o Age o High blood pressure (BP) References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 thed.). St Louis: Elsevier o Coronary artery disease o Smoking o Family history o Being overweight or obese o High cholesterol o White and Native Americans have o Lower extremity PAD higher risk than African Americans, o Carotid artery disease Hispanics, and American Asians. o Previous stroke True Aortic Aneurysm- Wall of the artery an aneurysm is form, one vessel layer is still intact . Pouchlike with narrow neck connecting bulge to one side of arterial wall. False Aortic Aneurysm- Disruption of all layers of the arterial wall Thoracic aorta aneurysms Often asymptomatic Most common manifestation Deep diffuse chest pain Pain may extend to the interscapular area Ascending aorta/aortic arch Angina Hoarseness If presses on superior vena cava Decreased venous return Distended neck veins Edema of face and arms Abdominal aortic aneurysms (AAA) Often asymptomatic Frequently detected On physical exam When patient examined for unrelated problem (i.e., CT scan, abdominal x-ray) May mimic pain associated with abdominal or back disorders May spontaneously embolize plaque Causing “blue toe syndrome” Patchy mottling of feet/toes with presence of palpable pedal pulses Aortic Aneurysm - Diagnostic Studies X-rays Chest – demonstrate mediastinal silhouette and any abnormal widening of thoracic aorta Abdomen – may show calcification within wall of AAA ECG – to rule out MI Echocardiography Assists in diagnosis of aortic valve insufficiency Ultrasonography Useful in screening for aneurysms Monitors aneurysm size CT scan Most accurate test to determine Anterior-to-posterior length Cross-sectional diameter Presence of thrombus Best type of surgical repair MRI Diagnose and assess the location and severity References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Angiography Anatomic mapping of aortic system using contrast Not reliable method of determining diameter or length Can provide accurate information about involvement of intestinal, renal, or distal vessels Endovascular graft procedure Involves placement of sutureless aortic graft into abdominal aorta inside aneurysm Minimally invasive Done through femoral artery cutdown Benefits ↓ anesthesia and operative time Smaller operative blood loss ↓ morbidity and mortality More rapid resumption of physical activity Shortened hospital stay Quicker recovery Higher patient satisfaction Reduction in overall costs Complications : Intraabdominal hypertension (IAH) Potentially lethal complication in emergency repair Associated with abdominal compartment syndrome (ACS) Reduces blood flow to viscera End-organ perfusion impaired Nursing Assessment Monitor for indications of rupture Diaphoresis Pallor Weakness Tachycardia Hypotension Abdominal, back, groin, or periumbilical pain Changes in level of consciousness Pulsating abdominal mass Aortic Dissection Often misnamed “dissecting aneurysm” Not a type of aneurysm Result of a false lumen through which blood flows Classified by location and duration of onset Clinical Manifestations Depend on location of intimal tear and extent of dissection Pain characterized as Sudden, severe pain in anterior part of chest, or intrascapular pain radiating down spine to abdomen or legs Described as “sharp” and “worst ever” May mimic that of MI Cardiovascular, neurologic, and respiratory signs may be present If aortic arch involved Neurologic deficiencies may be present Complications Cardiac tamponade Severe, life-threatening complication References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Occurs when blood escapes from dissection into pericardial sac Clinical manifestations include Hypotension Narrowed pulse pressure Distended neck veins Muffled heart sounds Pulsus paradoxus Aortic Dissection - Collaborative Care Initial goal ↓ BP and myocardial contractility to diminish pulsatile forces within aorta Drug therapy IV β-adrenergic blocker Esmolol (Brevibloc) Other antihypertensive agents Calcium channel blockers Nitroprusside Angiotensin-converting enzyme inhibitors Morphine Venous Disorders Phlebitis, inflammation of IV site Venous Thromboembolism Venous Thrombosis Can result in PE Superficial or Post thrombotic syndrome From chronic venous hypertension Deep vein thrombosis Venous thromboembolism Aching, heavy, swelling, itching, increased DVT travels to Lungs , PE pigmentation, lipodermatoscerosis (inverted bottle appearance of leg) Virchow’s Triad Superficial Vein Thrombosis Venous stasis- blood stops moving and won’t go back to the heart. Palpable cord like vein Obese, pregnant, heart disease, AF, inactivity Lower leg LMWH 45 days Endothelial damage- damage to inside of blood vessels Small segments do not require treatment Direct, trauma, surgery, vascular access Chronic Venous Insufficiency Indirect, chemo, DM, sepsis Failure of veins and valves to keep blood moving forward Hypercoagulibility of blood Cancers, estrogens, chemo Leathery, brownish skin of lower leg, persistent Superficial Vein Thrombosis edema, stasis dermatitis, venous ulcers of medial maleolus Palpable cord like vein o Treat with compression therapy Lower leg LMWH 45 days o Wound management Small segments do not require treatment Cardiovascular System Chapter 32 References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 thed.). St Louis: Elsevier Mechanical System Cardiac outpu: Amount of blood pumped by each ventricle in 1 minute Normal 4-8 L/min Cardiac inde: CO divided by body surface area Normal 2.8-4.2 L/min2m Factors Affecting Cardiac Output Preload o Volume of blood in ventricles at the end of diastole- How much is coming back to the heart Hydration and volume Contractility Afterload o Peripheral resistance against which the left ventricle must pump Comparison of Artery, Vein, and Capillary Structures and Functions of Cardiovascular System Regulation of the cardiovascular system Autonomic nervous system B-adrenergic receptors Receptor: Norepenephrine Epinephrine Baroreceptors Located in aortic arch and carotid sinus are sensitive to pressure located in the arterial system Chemoreceptors Aortic and carotid bodies and the medulla stimulate the vasomotor center to increase BP. Diagnostic Studies of Cardiovascular System Cardiac Biomarkers Troponin- CARDIAC INJURY C-Reactive protein Marker for inflammation Troponin T (cTnT) Troponin I (cTnI) Risk factor for coronary artery disease Rises within 4-6 hours, peaks 10-24 (CAD) Homocysteine hours, detected for up to 10-14 days Elevated levels increased risk for CAD, Diagnostic Studies of Cardiovascular System peripheral vascular disease (PVD), and stroke Cardiac Biomarkers Cardiac natriuretic peptide markers Creatine kinase (CK) Tells your body to get rid of sodium and fluid Three isoenzymes because ventricle is being stretched and fluid CK-MB cardiac specific, not as specific overloaded as Troponin Three types- CARDIAC FAILURE Rises in 3-6 hours, peaks in 12-24 Atrial natriuretic peptide (ANP) hours, returns to baseline within 12-48 B-type natriuretic peptide hours (BNP) Myoglobin C-type natriuretic peptide Diagnostic Studies of Cardiovascular System Increased levels of BNP levels signify heart failure. Additional blood studies- General marker for inflammation NT-pro-BNP Serum Lipids Triglycerides 150 or below- Low risk of heart disease Electrocardiogram- Diagnostic for heart attack Resting ECG References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Ambulatory ECG monitoring Event monitor or loop recorder Exercise or stress testing Echocardiogram- Ejection fraction and identification of blood clots Ultrasound of heart With or without contrast Provides information regarding structures and motion of heart Measures ejection fraction CT angiography (CTA)- Most popular used to look at blood vessels Computed Tomography Diagnostic Studies of Cardiovascular System Cardiac catheterization Right-sided to measure pressures Left-sided to evaluate coronary arteries Coronary angiography Uses contrast medium to identify coronary blockages Hypertension Chapter 33 Hypertension physiology Definition Persistent elevation of Prehypertension Systolic blood pressure ≥140 mm Hg Definition OR Systolic BP: 120 to 139 mm Hg Diastolic blood pressure ≥90 mm Hg OR OR Diastolic BP: 80 to 89 mm Hg Current use of antihypertensive drug(s) Blood Pressure Classification Isolated systolic hypertension SBP >140 mm Hg with DBP <90 mm Hg Hypertension Stage 1 SBP 140–149 or DBP 90–99 Hypertension Stage 2 SBP >160 or DBP >100 Etiology of Hypertension Primary hypertension Also called essential or idiopathic hypertension Elevated BP without an identified cause Secondary hypertension Elevated BP with a specific cause Clinical findings relate to underlying cause Risk Factors for Primary Hypertension Age Alcohol Tobacco use Diabetes mellitus Elevated serum lipids References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Excess dietary sodium “Silent killer” Gender Symptoms of severe hypertension Family history- greatest risk factor Fatigue Obesity Dizziness Ethnicity Palpitations Sedentary lifestyle Angina Socioeconomic status Dyspnea Stress Clinical Manifestations Lifestyle Modifications Weight reduction Weight loss of 22 lb (10 kg ) may decrease SBP by approx. 5 to 20 mm Hg Calorie restriction and physical activity Recommend Dietary Approaches to Stop Hypertension (DASH) diet Physical activity Avoidance of tobacco products Psychosocial risk factors Low socioeconomic status, social isolation and lack of support, stress, negative emotions Activate SNS and stress hormones Rate of rise more important than absolute Hypertensive Crisis value Hypertensive emergency Clinical Manifestations Hypertensive encephalopathy Occurs over hours to days BP >220/140 with target organ Headache, n/v, seizures, confusion, disease coma Renal insufficiency Hypertensive urgency Occurs over days to weeks Cardiac decompensation BP >180/110 with no clinical evidence MI, HF, pulmonary edema Aortic dissection of target organ disease Hospitalization IV drug therapy: titrated to MAP Nicardipine, Nitro, Nipride Monitor cardiac and renal function Neurologic checks Coronary Artery Disease and Acute Coronary Syndrome Chapter 34 Risk Factors for CAD Non-modifiable risk factors _ Increased catecholamine Age release Gender _ ↑ LDL, ↓ HDL, ↑oxygen Ethnicity radicals Family history _ ↑ Carbon monoxide Genetic predisposition _ Second-hand smoke Modifiable risk factors Obesity Physical inactivity Diabetes Smoking BP control Tobacco use Hypertension References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 thed.). St Louis: Elsevier _ >140/90 mm Hg or >130/80 _ Cholesterol >200 mg/dL (5.2 mm Hg if diabetes or CKD mmol/L) _ Begin lifestyle changes for _ Triglycerides >150 mg/dL (3.7 prehypertension mmol/L) _ Treat stage 1 or 2 _ High-density lipoproteins hypertension with drugs (HDL) Psychological states _ Low-density lipoproteins (LDL) Lipid control _ Treatment according to Elevated serum lipids guidelines based on 10-year risk score Substance abuse Manage high-risk persons by controlling modifiable risk factors Encourage lifestyle changes Education Clarify personal values Set realistic goals Remember: takes a few days to create bad habit and months to change a habit Nutritional therapy ↓ Saturated fats and cholesterol ↑ Complex carbohydrates and fiber ↓ Red meat, egg yolks, whole milk ↑Omega-3 fatty acids (certain fish) Collaborative and Nursing Management: CAD Lipid-lowering drug therapy If diet and exercise ineffective Statins Inhibit cholesterol synthesis, decrease LDL, increase HDL Monitor for liver damage and myopathy Niacin Lowers LDL and triglyceride by inhibiting synthesis Increases HDL Flushing, pruritus, GI side effects, orthostatic hypotension Fibric acid derivatives (Lopid) _ Decrease triglycerides and increase HDL _ GI side effects Bile acid sequestrants (Questran) _ Increase conversion of cholesterol to bile acids _ GI side effects; bind with other drugs Ezetimibe (Zetia) _ Decrease absorption of dietary and biliary cholesterol Antiplatelet therapy ASA Clopidogrel (Plavix) Prasugrel (Effient) References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Angina Progressive Disease O2 demand > O2 supply → myocardial ischemia Angina = reversible ischemia • Occurs when arteries are blocked 75% or more • Hypoxic within 10 seconds of occlusion • Viable for 20 minutes Lack of oxygen and glucose leads to anaerobic metabolism Lactic acid irritates nerve fibers → pain in cardiac nerves Referred pain from transmission to the upper thoracic posterior nerve roots Clinical Manifestations of CAD Angina Pain Pressure/ache Squeezing, heavy, choking, or suffocating sensation Rarely sharp or stabbing Indigestion or burning Various locations Chronic Stable Angina Refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms S&S: Squeezing, heavy, choking, or suffocating sensation Many complain of indigestion or burning sensation in the epigastric region Episodic pain lasting 5-15 min, provoked by exertion, relieved by nitroglycerin Tx: antiplatelet and lipid-lowering drug therapy o Nitrates, Angiotension-coverting enzyme (ACE) inhibitor, B-adrenergic blockers, and calcium channel blockers to optimize myocardial perfusion ACE inhibitors EF < 40 %/ hx of diabetes Vasodilation and reduced blood volume B-adrenergic blockers Left ventricular dysfunction Decrease myocardial contractility, HR, SVR, and BP SE: bradycardia, hypotension, wheezing, and GI symptoms Calcium Channel Blockers 3 effects: 1.) Systemic vasodilation with decreased SVR, 2.) decreased myocardial contractility 3.) Coronary vasodilation Causes smooth muscle relaxation, and relative vasodilation of coronary and systemic arteries, and increasing blood flow Nitroglycerin Dilate peripheral blood vessels Dilate coronary arteries and collateral vessels Sublingual decreases pain in 3 min Sodium current inhibitor Ranolazine (Ranexa) Decrease workload of heart Remove fluid Slow conduction, Prevent vasospasm Silent ischemia References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 thed.). St Louis: Elsevier Ischemia that occurs in the absence of Chest pain that occurs only while lying any subjective symptoms down Associated with diabetic neuropathy Relieved by standing or sitting Confirmed by ECG changes Prinzmetal’s (variant) angina Nocturnal angina Occurs at rest due to a spasm of a major Occurs only at night but not necessarily coronary artery during sleep or lying down Seen in patients with a history of migraine headaches and Raynaud’s phenomenon May occur with or without CAD Not precipitated by increased demand Chest pain with marked, transient ST- segment elevation Microvascular angina Chest pain occurs in the absence of significant coronary atherosclerosis or coronary spasm Myocardial ischemia associated with abnormalities of the coronary microcirculation Coronary microvascular disease (MVD) affects small, distal coronary arteries Angina decubitus Acute Coronary Syndrome Etiology and Pathophysiology Result Partial occlusion of coronary artery: UA or NSTEMI Unstable lesion partially occluded by a thrombus Total occlusion of coronary artery: STEMI Total occlusion by a thrombus Unstable Angina (UA) Chest pain that is new in onset, occurs at rest, or has worsening pattern. Previously stable angina- change in pattern. Increasing frequency, easily provoked w/o exertion, during sleep or even at rest. S&S: Fatigue, SOB, indigestion, and anxiety Myocardial Infarction Due to sustained ischemia r/t thrombus formulation aeb occlusion Cell death occurs after 20 min S&S: Severe Chest pain not relieved by position change or nitrate administration, also described as heaviness, pressure, tightness, burning, constriction or crushing. Epigastric pain r/t indigestion and take antacids w/o relief, pain radiates to neck, lower jaw, and arms or to the back. Catecholamine release – stimulation of SNS Release of glycogen Diaphoresis Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch Cardiovascular Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO) References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Crackles Jugular venous distention, hepatic engorgement, and peripheral edema Abnormal heart sounds S3 or S4 New murmur Nausea and vomiting Reflex stimulation of the vomiting center by severe pain Vasovagal reflex Fever Up to 100.4° F (38° C) in first 24 hours Systemic inflammatory process caused by myocardial cell death Complications: Thrombolytic therapy Dysrhythmia When PCI not available Heart Failure Stops infarction process by Cardiogenic Shock dissolving thrombus Papillary muscle dysfunction Within 6 hours of onset of symptoms Ventricular Aneurysm Ideally within first hour Pericarditis Given IV Dressler Syndrome Patient selection critical Emergent PCI Risk Factor, giving TPA: Treatment of choice for confirmed MI Recent trauma, surgery, head Goal: 90 minutes from door to injury catheter laboratory Coronary surgical revascularization Balloon angioplasty + drug-eluting Failed medical management stent(s) Many advantages over CABG Drug therapy Nutritional therapy IV nitroglycerin Initially NPO Morphine sulfate Progress to: β-adrenergic blockers- decreases Low salt (DASH diet) oxygen need of the heart Low saturated fat Angiotensin-converting enzyme Low cholesterol inhibitors- Vasodilators decrease workload Antidysrhythmia drugs Cholesterol-lowering drugs Stool softeners Sudden Cardiac Death (SCD) Unexpected death from cardiac causes Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow Most commonly caused by ventricular dysrhythmias Structural heart disease Conduction disturbances No warning signs or symptoms if no MI Prodromal symptoms if associated with MI Chest pain, palpitations, dyspnea Death usually within 1 hour of onset of acute symptoms References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Heart Failure Chapter 35 Heart Failure An abnormal clinical syndrome involving inadequate cardiac pumping/filling Insufficient blood supply/oxygen to tissues Used to be called congestive heart failure (CHF) Leads to hypertrophy of the muscles RISK FACTORS: HTN- Hypertension CAD- Coronary Artery Disease Patho Systolic Failure – inability of the heart to pump blood efficiently Diastolic Failure – inability of the ventricles to relax and fill during systole Left-sided Heart Failure- back up in left atrium and pulmonary veins pulmonary congestion & edema Right-sided Heart Failure- Venous congestion in the systemic circulation results in venous distention, hepatomegaly, splenomegaly, vascular congestion, peripheral edema, cor pulmonae(Right ventricular dilation and hypertrophy caused by pulmonary disease) Counter-regulatory Mechanisms Natriuretic peptides Atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP) Released in response to increased blood volume in heart Causes diuresis, vasodilation, and lowered BP Counteracts effects of SNS and RAAS Nitric oxide (NO) Released from the vascular endothelium in response to compensatory mechanisms NO relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload Clinical Manifestations Early → increased pulmonary venous pressure Increase in the respiratory rate Decrease in PaO2 Later → interstitial edema Tachypnea Further progression → alveolar edema Respiratory acidemia S&S: Behavioral Changes Fatigue Chest pain Dyspnea FACES Paroxysmal nocturnal dyspnea- fluid F atigue redistribution during sleep awakes with Limitation ofActivities cough, untreatable. C hest congestion/cough Tachycardia E dema Edema S hortness of breath Nocturia Skin changes References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier Drug Therapy Diuretics Decrease volume overload (preload) Furosemide (Lasix), bumetanide (Bumex) IVP Vasodilators Reduce circulating blood volume and improve coronary artery circulation IV nitroglycerin Sodium nitroprusside (Nipride) Nesiritide (Natrecor) Morphine Reduces preload and afterload Relieves dyspnea and anxiety Positive inotropes β-adrenergic agonists (dopamine [Intropin], dobutamine [Dobutrex]) Phosphodiesterase inhibitors (inamrinone [Inocor], milrinone [Primacor]) Digitalis Nutritional Therapy Low sodium diet Individualize recommendations and consider cultural background (www.nhlbi.nih.gov/health/index.htm#recipes) Recommend Dietary Approaches to Stop Hypertension (DASH) diet Sodium is usually restricted to 2 g/day Fluid restriction not generally required If required, < 2L/day. Ice chips, gum, hard candy, ice pops to help thirst Daily weights important Same time, same clothing each day References : (Bergman, 2016) Lewis et al. (2014). Medical-surgical nursing: Assessment and management of clinical problems(9 ted.). St Louis: Elsevier
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