Potassium At risk for hypokalemia (HG)) WORTSOL • • • • • • • • • • aldosterone Cushing syndrome colitis overusing laxatives gastrointestinal suction Diarrhea Vomiting Diuretics Alkalosis Stress Diabetic acidosis and increases At risk for hyperkalemia sodium • • • • • • • • • excretes potassium which lowers the level Clinical manifestation for hypokalemia • Heart is tight and contracted • St elevation, and peaked t waves • severe = v fib or cardiac standing • hypotension, bradycardia • GI tract is tight and contracted • Diarrhea • hyperactive bowel sounds • Muscular is low and slow • Decrease DTR • muscular cramping • paralyzed limbs • GI is low and slow • • • • Neuromuscular is tight and contracted • Paralysis in extremities • increase deep tendon reflex • muscle weakness Decrease motility hypoactive to absent bowel sounds constipation abdominal destination paralytic intestines Nursing consideration for hypokalemia Do not give KCL via IV push or as bolus Always dilute IV KCL Administer oral or iv pot'assium chlo ride supplements and increased dietary intake of potassium Trauma burns sepsis metabolic or respiratory acidosis addisons disease blood transfusions bleeding or hemorrhage ingestion of potassion medications failure to restrict dietary sodium Clinical manifestation for hyperkalemia • Heart is low and slow • Flat T waves, St depression and prominent u waves • • • • • P= potassium P= priority P= pumps the heart and muscles Nursing consideration for hyperkalemia • • • • Stop oral and iV potassium intake increase potassion excretion using loop or thiazide diuretics force potassium from ICF to ECF by a combination ofIV regular insulin with dextrose and B-Adrenergic agonist ECG motoring to detect dysrhythmia Sodium At risk for hyponatremia • • • • • • • Taking diuretics draining wounds diarrhea vomiting primary adrenal insufficiency Pt with psychiatric disorders inappropriate use of sodium free or hypotonic Iv from water excess; may occur after surgery or trauma • giving fluids with renal failure • SIADH caused by abnormal retention of water At risk for hypernatremia • • • • Central diabetes insipidus ingestion of corticosteroids Cushing syndrome decrease in kidney responsiveness to adH • excess sodium intake • iv administration of hypertonic saline or sodium bicarbonate S= sodium S = swells the body to maintain: • Blood pressure • blood volume • pH balance Clinical manifestations of hypernatremia Clinical manifestations of hyponatremia • • • • • • • • • Headache irritability difficulty concentration confusion vomiting seizures coma tachycardia weak & thready pulse • • • • • • • • • • • • • Drowsiness restlessness confusion lethargy to seizures and coma postural hypotension tachycardia weakness excess thirst edema flushed skin swollen dry tongue Nausea and vomiting Increased muscle tone Nursing consideration for hyponatremia • Replace fluid using isotonic sodium-containing solutions • encouraging oral intake • withholding all diuretics • loop diuretics and demeclocycline may be given • if severe, 3% sodium chloride (hypertonic) can restore serum sodium level • vasorépressor antagonist for those who cannot tolerate fluid restrictions • urine output is essential, if no urine output catheter may be placed Nursing consideration for hypernatrenia • in Primary water deficit, Fluid Replacement is given either orally or iv with isotonic solution (0.9% sodium chloride) • if sodium excess, administer 5% dextrose in water and promote sodium excretion with diuretics • quickly reducing levels can cause cerebral edema and neurologic complications Anemia Anemia is a deficiency in the ne number of erythrocytes, the quantity or qualify of hgb, and or volume of packed RBC Anemia is classified by morphology or etiology Causes of anemia: • Blood loss • impaired RBC production • increased RBC destruction Acute • Acute traumas • ruptured aortic aneurysm • Gl bleeding Nursing management of anemia Goals • assume normal aDl • maintain adequate nutrition • prevent complications Interventions • blood transfusion • drug therapy • volume replacement • O2 therapy • dietary and lifestyle changes • assess for safety • energy conservations Blood loss • • • • Chronic Bleeding duodenal ulcer Colorectal cancer Liver disease Increased RBC destruction Hemolysis • Sickle cell disease • Medication • Incompatible blood • 'Trauma Manifestations of anemia that are caused by tissue hypoxia • • • • • • Decreased hgb palpitations Dyspnea fatigue skin changes cardiopulmonary manifestations: • Increase hr and stroke volume Iron deficiency anemia Iron deficiency is the most common nutrition disorder Most susceptible are the very young, those on poor diets and women in their reproductive years Develop from: • Inadequate diet intake • malabsorption - after gi surgery - Iron must be in acidic environment • blood loss - mainly from gi and Gu - dialysis treatment • hemolysis - splenomegaly Clinical Manifestations • • • • • • • early can be asymptomatic pallor (most common) Glossitis ( second most common) inflammation of lips headache paresthesia burning sensation of tongue nursing consideration Goal: • treatment of underlying cause Intervention: • educate proper source of iron • oral and parental iron supplement - parental iron can be given IV or Im; usually for malabsorption, intolerance of Oral iron and in need for beyond oral limits • blood transfusion - acute blood loss; may need packed RBC transfusion • Drug therapy - iron is absorbed best from duodenum and proximal jejenum - best absorbed in acidic environment; take iron an hour before meals with vitamin c - dilute liquid iron and have patient drink it through straw - have patient stay upright after 30 mins of taking oral form - iron will cause stools to be black - constipation is common, pt should be started on stool softener Thalassemia Thalassemia is a group of disease inadequate production of normal hemoglobin, which decreases ABC production Thalassemia has an autosomal recessive genetic basis; can either have heterozygous (thalassemia major) or homozygous(thalassemia minor) form of diseases Commonly found in people at southeastern Asia, Middle East, India, Pakistan, China, southern Russia, and Africa Clinical manifestation for thalassemia minor • often asymptomatic • mild to moderate anemia with microcytosis and hypochromia • mild splenomegaly • bronzed skin color • bone marrow hyperplasia Clinical manifestation for thalassemia major • life threatening • growth and development deficits • pale • jaundice from RBC hemolysis • splenomegaly because spleen continuously tries to remove damage RBC • chronic bone marrow hyperplasia - bone marrow responds to the reduced Oz carrying capacity by increasing RBC production but they are immature RBC that dies • hypercoagulable blood Nursing consideration • thalassemia minor does not need treatment because the body adapts to the reduction of normal hemoglobin • thalassemia major • Blood transfusions or exchange transfusion (less than 7) with chelating agents that bind to iron - chelating agents reduce iron overloading that occurs with chronic infusion therapy Megaloblastic anemia Megaloblastic anemia are characterized by the presence of abnormally large RBC. Macrocytic RBC are easily destroyed because they have fragile cell membranes Megaloblastic anemia are caused by • impaired DNA synthesis, which results in defective RBC maturation. Most result from cobalamin (vitamin bi2) and folic acid deficiency • suppression of DNA synthesis by drugs • inborn error metabolism • erythroleukemia Most common cause of Cobalamin deficiency is pernicious anemia • Caused by an absence of intrinsic factor • Intrinsic factor is required for cobalamin (Extrinsic Factor), so without the intrinsic factor, cobalamin is not absorbed • In pernicious anemia, gastric mucosa does not secrete intrinsic factor because of either gastric mucosal atrophy or autoimmune destructionsa Cobalamin deficiency can occur: • who just had gi surgery or small bowel resection • excess alcohol • hot tea ingestion • smoking • strict vegetarians Nursing consideration of megaloblastic anemia: • without cobalamin administration, pt can die in 1-3 years • parental vitamin b12 • evaluate pt with family history of anemia • early defection and treatment • report s&s to PCP • protect from fall, burns, and trauma • assess for neurologic difficulties • gi cancer screening Folic acid deficiency • Needed for DNA synthesis leading to RBC formation and maturation Causes of Folic acid deficiency • chronic alcohol use • chronic hemodialysis • diet deficiency • increase requirement ( pregnancy) Clinical manifestations • sore red beefy and shiny tongue • anorexia • nausea/ vomiting • abdominal pain • weakness • parasthesia of feet and hands • decrease vibratory and position senses • ataxia • muscle weakness • confusion / dementia Valvular heart disease Functional alteration of one or more values of the heart due to stenosis and regurgitation := Mitral value stenosis Shortening and thickening of the mitral value structures.it blocks the blood flow and create a pressure between the left atrium and left ventricle during diastole; as a result left atrial pressure and volume increase, causing higher pulmonary vasculature pressure Clinical manifestation of mitral stenosis: • Dyspnea • hemoptysis • fatigue (less cardiac output) • a-fib on ECG • palpitations • diastolic murmur Causes of stenosis: • rheumatic heart disease: condition in which the heart values have been permanently damage by rheumatic fever (inflammatory disease) • congenital Stenosis • rheumatoid arthritis • systemic lupus erythematous Clinical manifestation of aortic value stenosis: • angina (due to less oxygenation or clot that blocks) • syncope • dyspnea • Hf • normal or soft S1 or soft or absent S2, • systolic murmur • Prominent S4 Clinical manifestation Tricuspid stenosis • peripheral edema • ascites • hepatomegaly • low pitched diastolic murmur Clinical manifestation of pulmonic stenosis • fatigue • loud midsystolic murmur Mitral value regurgitation ↑ Clinical manifestation of Mitral value regurgitation • pulmonary edema • weakness • fatigue Causes of regurgitation • dyspnea • inflammatory • thready peripheral pulse • Degenerative • systolic murmur • Infective • peripheral edema • Structural/congenital • cool clammy extremities Clinical manifestation of aortic valve regurgitation • Dyspnea • orthopnea • high pitch diastolic murmur Management of valvular heart disease • Prevent recurrent rheumatic fever or infective endocarditis (complete antibiotic therapy) • treatment is prevention of hf, pulmonary edema, and thromboembolism • treatment of CFH, atrial arrhythmia Nursing therapeutic of valvular heart disease • Prevent acquired rheumatic valvular disease • hospitalization due to cHf and arrhythmia • exercise plan to increase cardiac tolerance with periods of rest • smoking cessation • assist in planning for aDl with periods of rest • prophylactic abt to prevent endocarditis Aortic aneurysm Aneurysm: permanenent, localized outputting or dilation of the arterial wall Aortic aneurysm may involve the aortic arch and thoracic and/ or abdominal aorta. 3/4 occur in abdominal aorta Causes of aortic aneurysm • atherosclerosis • genetic predisposition • penetrating or blunt trauma • infection Classification of aortic aneurysm • true aneurysm: one in which the wall of the artery forms the aneurysm, with at least 1 vessel layer still intact • false aneurysm: a disruption of all arterial wall layers with bleeding that is contained by surrounding anatomic structures May result from: • trauma • infection • peripheral artery bypass graft surgery • arterial leakage after removal of cannula Clinical manifestations of aneurysm • often Asymptomatic • deep diffuse chest pain may radiate to interscapular • angina from decreased blood flow to coronary arteries • transient ischemic attacks from decreased blood flow to carotid arteries • coughing • shortness of breath • hoarseness • dysphagia • jugular venous distention and edema of face and head from the decreased venous return due to the aneurysm pressing on superior vena Cava • pulsatile mass in the periumbilical area • audible bruit • pain in abdomen or back • discomfort with or without alteration of bowel elimination Complications of aortic aneurysm • more likely to rupture for those who smoke tobacco - if rupture occurs into retropineal space, bleeding may be controlled by surrounding anatomic structures, preventing exsanguenation and death - patient has severe back pain. And grey turner sign ( blank or flank bruising) may be present • if rupture occurs into thoracic or abdominal, patient can die from massive hemorrhage Collaborative care • goal: prevent rapture of aneurysm Conservative medical treatment < 4cm • risk factor modification (smoking, BP, lipid profile, physical activity) Surgical repair < 5-6cm • recommended in patients with asymptomatic Nursing therapeutic of aortic aneurysm • decrease risk factors associated with atherosclerosis • preop support and teaching • ICU care post surgery • Maintain bp • Oxygen supply • Prevention of infection • Prevent paralytic ileus • Monitor peripheral perfusion status • Monitor renal perfusion • Avoid heavy lifting 4-6 weeks post op • Monitor sign and symptoms of infection Coronary artery disease Coronary artery disease is a type of blood vessel disorder affecting the coronary artery resulting to atherosclerosis or hardening of the arteries due to fatty deposits Theories of atherogenesis: • Endothelial injury - result from tobacco use, hyperlipidemia, hypertension, toxins, diabetes, inflammation, infection • lipid infiltration • aging • thrombogenic • vascular dynamics • inflammation, diabetes Major clinical manifestation of cad • Angina pectoris • Acute coronary syndrome • sudden cardiac death Risk factors for coronary artery disease Nonmodifiable risk factor: • age: highest incidence among middle aged men. Increase risk * Atacit 65, BOTH LENDERS Cardiovascular manifestations for men over 45 and women over 55 (estrogen has RISK ORE HE • elevated hr cardioprotective effects) SAME • decrease bp and urine output • gender: women are more likely than men to die after their • crackles first mi • hepatic engorgement • ethnicity and genetics: black women at rates higher than • peripheral edema white or Hispanic women Modifiable major risk factor • elevated serum lipid levels = above 200 mg/dl - hdl high density lipoprotein = below 35 mg/dl (major risk factor) woop lots liver and metabolizes ares StralA to - LDL low density lipoprotein = above 160 mg/dl ( high risk for cad) BAD BYPUSS A* UveR aptemues • hypertension Damal ARTERY UFEStlE - bp greater than or equal to 140/90 mm hg 130/90 Staitmep Damage • smoking - 2-6 times at risk to develop cad • physical inactivity CALCIFICATION • obesity to anD CDI and stand I ntima LaGE BM1 30 = MODIRABLE CONTRIBUTNG ISR FACTOR - DIABETES MELUAS:aurcose can't Get INTO CALL BECAUSE not Enorult insrun.altiontonellesis MSSVE) FREEZING LIPIDS AYERUPUOMA (destructs aDIPOSE In Apeviation, LEadina to - HOMOCYSTIE:HaHLeVe OF TS (amino and Damane HE InTma LaTER (IRRhtant) STRESS and H & BETACTOR PateRU: INCREASES CORASOL, (SIMPATHETC) WHH constructs and oveRWORK HE HEART TYPE A PERSONALY:PERFECTIONS, anaRY Myocardial infarction Occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation Clinical manifestation of mi Complications of mi • pain is severe, immobilizing, not relieved by rest or • dysrhythmia (most common complication) 80-90% nitrate administration • heart failure: occurs when the right or left ventricle • describe as heaviness, pressure, tightness, burning, pumping action is reduced crushing • cardiogenic shock: occurs when O2 and nutrients supplied • common locations are substernal or epigastric area to the tissues are inadequate and may radiate to neck, lower jaw and arms or to the back • weakness • nausea And vomiting, fever Diagnostic studies of mi • shortness of breath • pt history of pain, risk factors, and health • Mental status changes in older adults • electrocardiogram: primary tool to diagnose unstable angina or mi - changes in ST segment • serum cardiac markers: highly specific indicators of MI - CK-mB band is specific to heart muscle cells and helps quantify myocardial damage - high cardiac troponin test provides more rapid detection of MI, showing quicker diagnosis Nursing consideration of mi • Initial management is best accomplished in ICU • fibrinolytic therapy - produce an open artery by lysis of thrombus to reprefuse the myocardium • cardiac catherization: procedure used to open a narrowed artery in or near the heart • drug therapy - IV nitroglycerin: initial treatment of patient with ACS. Goal of therapy is to reduce angina pain and improve coronary blood flow. Decreases preload and afterload while increasing myocardial O2 supply. Closely monitor bp; hypotension • antiarrhythmic drugs • morphine sulfate (vasodilator ( : drug choice for chest pain that is unrelieved by nitroglycerin • b- adrenergic blockers: decrease myocardial O2 by reducing HR, BP, and Contractility • angiotensin - converting enzyme inhibitors • stool softeners • nutritional therapy: npo except for water until stable advance the diet as tolerated to a low salt, low-saturated fat, and low cholesterol diet Nursing therapeutic of mi Acute intervention (prioritize actions) • Pain • monitoring • rest and comfort • control anxiety • emotional and behavioral reactions Ambulatory/home care • Patient teaching: anticipatory guidance • physical exercise • resumption of sexual activity: use matter of fact approach Angina pectoris Nursing therapeutic of angina • Health promotion: aim to decrease risk factor • ambulatory/home care - patient assurance - health teaching - counseling Types of angina: Angina = pain • Stable angina pectoris : chest pain that is provoked by physical exertion, stress, or emotional upset - can be controlled with angina • Silent ischemia (asymptomatic): likely due to diabetic neuropathy • Prinzmetal angina: occurs at rest without increased physical demand due to spasm of of the coronary artery • Nocturnal angina and angina decubitus: occurs at night, chest pain while lying relieved by standing • Unstable angina: new onset, unpredictable, worsening pattern Nursing consideration of angina • Treatment aimed at decreasing oxygen demand and/or increasing oxygen supply • drug therapy - antiplatelet aggregation therapy (first line of treatment) - nitrates (use of nitrate initial therapeutic intervention); sublingual, ointment, transdermal controlled, long acting, IV - beta-adrenergic blocker: relieve angina symptoms in patients with chronic stable angina. Contraindicated with asthma or severe Bradycardia • calcium channel blocker is used if beta blocker is contraindicated or can't control angina symptoms • Percutaneous coronary intervention: insertion of catheter equipped with an inflatable top to the coronary artery resulting to vessel dilation • Stent placement: expandable mesh like structures designed to maintain vessel patency by compressing the arterial walls and resisting vasoconstriction • Atherectomy • Laser angioplasty • Myocardial revascularization (CABG): recommended for patients who does not respond well to medical management, have left main coronary artery disease, not candidate for PCI, or continue to have chest pain after PCI. A palliative treatment not a cure Acute care (chest pain but unsure of the cause) • position patient upright unless contraindicated and apply supplemental O2 • assess vital signs • apply continuous ECG monitor • obtain 12-lead ECG • provide prompt pain relief of nitroglycerin followed by Iv opioid analgesic • obtain cardiac biomarkers • assess heart and breath sounds • obtain chest X-ray Clinical manifestations of cad • Angina - pain is at substernal, neck, radiate to jaw, shoulder and down to the arm. Feeling of indigestion or burning sensation in epigastric Diagnostic studies of angina pectoris • chest X-ray: shows heart enlargement aortic calcifications, and pulmonary congestion • ECG: detect resting left ventricle wall motion abnormalities, may suggest cad • laboratory test - serum lipids - cardiac markers - c- reactive protein • treadmill exercise testing • nuclear imaging (IV injection of radioisotope); if has physical limitation • pet scan: scan images of blood flow to the heart muscle at rest and stress • coronary angiography Iv solutions Isotonic solution D5W: use to replace Water loss Such are blood loss, trauma or dehydration due to nausea vomiting or diarrhea and to treat hypernitremia Lactated ringers: use to treat hyporolemia, burns and GI fluid loss • cannot be used in patients with alkalosis or lactic acidosis 0.9% normal saline: only solution given with blood products • may cause volume overload in patients with heart or kidney disease Hypertonic solution D10W: use with parental nutrition 3% normal saline: use to treat symptomatic hyponatrema and trauma patients with head injury • give slowly because it may cause volume overload and pulmonary edema 5% in 0.45% ds: used as maintenance solution 5% in 0.9%: use to treat metabolic alkalosis and volume deficits in patient with hyponatremia & Hypotonic solution 0.45% saline: used to treat hypernatremia and controlled hyperglycemia • Do not give hypotonic fluids with patients who has increased intracranial pressure CID;FLUID OVERLOaD maMFeStation: BP HYPOnaReMla:CONFseD LITHAROIC C) SOCTOMG DOHYDRAHON:ORTHOSTATC HYPOteNSION HYPERKALEMA:PIABET KETOUDOSIS IUPHEY DISEASE CRASHMG nasocastuc Suction needs ledto Alolatzemla P5W Suction INJURES aUPOSTERONEINSUFAUENC (isrtomc witen cantana Fots a p+w/ mitical value stenosis, assess FOR Its mostimportantto ~ SHORTNSS OFBRECH ON QXCTION aU vae HYPORensIon NOT URABLE RePAIRS AREPAUlaHVE anD WILL neeD UFALONG HARaPY. MEdtancal In Pt WITH AORA PEGURUIaHON CORDIOUSMC SHOCK may INDICATE values AREMORE DURABLE and cast ronaER NANBIOWGIC VALUES - neeD FREQUENTCAB BLOOD HiSHG It WI DEDRATIONRECelUnG PeRTOMC Following assessments SHOULD BE DONE - Pattent WHO HAD a mtiaL VALVEREPLACEment a mentanical valve With will need prophylactic SocTOn, WHG SOUNDS BLOOD PRISSUM Setm sobium level aUTBIONCS wIeR HavIna Dental PROCEDURES nausea and vomi Patientw/ Dettypiation + WIT WORTC StenosIS Its most important to FLUID IS SHFTED FROM INRSHAL SPACEInto Plasma REPORTTO PIP OF COMPLALMNG OFCEST PRESSURE amBuLatina;caUseD BY CARPlaC saemia witeh LOOP DIURETICS ARE CONTRMM KateD Cause luphex MITRAL VALUE ZEGURUItaTION;IMPORTANTTO REPORT TO PIP IFITHAS BILATERAL WUG CRACKLES OF HTPORALEMA exclett SODIUM anD Potassium Cardiovascular lecture Developmental sthats of CAD FRASTEAR:EARLeSt IISION OFATHROSCLEROSIS (aGE (5) DIABETC:PROBLEM WI vision - ROISITS FIBROUS PLAQUE:NO ONE DOES It STCK BUT As elevated -BEGIUMUG OF PROGRESSIVE CHANGES to TE Intima LAYER, aCOmulatina naipowine toactory COMPUCATED WELL, PlaTELet (TAMBUS FoteD), (aut s0) myocardium, not only UPIDs, Platinet, atocestial BUT also calcium making it calcified (Harpenes chot) ISCHIMA:DEATH OFISSUE LlateRal UIReVIatION: WILL MAKEOTHER UIRCULATION TO RECEIVE OXThen, COMPENSATE act Hal Due to accose, URWLATING I MICROURVLATON · BLOCKED, IS THEVISCOSIT OF BLOOD PREVENTS I FROM aLROODY Has DamanE LESION:DANGEROUS, UAEURCULATION OR COMPLETER Decrease oxyatn in aDHRED OF BLOOD VISOSIT CoLaTIRAL URVIATION AROUND EYFS T MONTOM VISION BUT I GetS MULER - DIABCTIC REMMOPATHY
