ࡱ>  @ 7bjbj{{ +G/       EEE8EFt}2HHHHHHHH*},},},},},},}$~R/LP} 7LHH7L7LP}  HHe}%V%V%V7LP H H*}%V7L*}%V%V6u  JxH H P>ܝEQdvx4{}0}v{QR{8Jx    { JxH:PI%V0JJSHHHP}P}CE=UEPathoNormal RangeCausesTreatmentsNsg ConsiderationsI. Blood Chemistries Sodium: Hyponatremia*Most abundant cation in extracellular fluid *Maintainsosmotic pressure of extracellular fluid *Regulates renal retention & excretion of water *Responsible for stimulation of neuromuscular reactions & maintains SBP Serum below 135mEq/Lcritical <120 *Excess sodium loss through N-V-D, skin and kidneys *Excess diuretic dosage *Liver Failure *CHF *Increased hypotonic IV fluids *Sodium containing fluids *Isotonic Ringers *NS 0.9% or 3% THINK VOLUME *Monitor electrolytes *Monitor vital signs *Monitor neurological responses *Mental Status *Headaches *Monitor fluids/I&O for overload *Weight *Cardiac overload-CHF *Monitor musculoskeletal-*Cramps *Weakness-Tremor Sodium: HypernatremiaSerum above 145mEq/Lcritical >160 *Dehydration-fluid loss through N-V-D (water loss in excess of salt loss) or excessive sweating *Diabetes-DKA *Fever *Replace fluids *D5%W *Diuretics- Excrete excess volume and excreteTHINK VOLUME *Monitor electrolytes *Monitor vital signs *Mental Status *Weight/I&O *Monitor for seizures Potassium: Hypokalemia*Most abundant intracellular cation and is essential for transmission of electrical impulses in cardiac and skeletal muscle *Helps maintain acid-base balance and has inverse relationship to metabolic pHdecrease in pH of 0.1 (acidosis) increases K+ by 0.6 mEq/L *80-90% K+ filtered through the kidney Serum below 3.5 mEq/Lcritical <2.5 *Inadequate intake of K+ *ETOH abuse *CHF/HTN *GI Loss-V&D *Renal Loss *Diuretics-Loop (Lasix/Bumex) *Oral or Parenteral Potassium *Diet high in potassium *Balanced electrolyte solutions *Pedialyte *Sports drinks THINK ELECTRICITY *Monitor electrolytes *Monitor vital signs-low BP *Monitor cardiac responses *Irregular heart rate and rhythm for increased ectopy-PVCs/VT Potassium: HyperkalemiaNormal Range Serum above 5.0 mEq/Lcritical >6Causes *Metabolic acidosis *Dehydration *Excess Potassium intake *Potassium Sparing Diuretics *Tissue damage= *Burns (K goes out of cell) *Renal Failure Treatments *Insulin- Moves K into the cell *D50- Prevents hypoglycemia caused by the infusion of Insulin *IV Calcium Gluconate = ER measure to counteract cardiac effects of Potassium *Sodium Bicarbonate- Treats the acidosis caused when K moves into the cell and pushes hydrogen ion into the serum Nsg Considerations THINK ELECTRICITY *Monitor electrolytes *Monitor cardiac responses *Monitor musculoskeletal cramps, weakness, parathesias *Peaked T wave/ wide QRS *Monitor Neurological responses, mental status, headache *Irregular heart rate and rhythm for increased ectopy-PVCs/VT Magnesium: Hypomagnesemia *Second most abundant intracellular cation *Required for transmission of nerve impulses and muscle relaxation *Controls absorption of sodium, potassium, calcium, and phosphorus *Magnesium.Potassium and Calcium all go low or high together! Serum below 1.8 mEq/Lcritical <1.2*Chronic Alcoholism *GI Loss-V&D *Impaired absorption *Renal Disease *Pancreatitis *Treat underlying cause *GI Loss *Give Magnesium replacement THINK NEUROMUSCULAR TRANSMISSION THINK CARDIAC RESPONSE *Monitor electrolytes *Monitor vital signs *Tachycardia *Hypertension *Tremors, tetany, paresthesias *Muscle weakness Magnesium: Hypermagnesemia Serum above 2.6 mEq/Lcritical >6.1*Dehydration *Severe metabolic acidosis *Renal Failure *Tissue trauma *Treat underlying cause *Renal patients treat with dialysis *Monitor cardiac effects of magnesium-increased PVCs-VT *Give Calcium Gluconate THINK NEUROMUSCULAR TRANSMISSION THINK CARDIAC RESPONSE *Monitor electrolytes *Monitor vital signs *Bradycardia *Hypotension *Muscle weaknessPathoNormal RangeCausesTreatmentsNsg ConsiderationsCalcium: Hypocalcemia *Most abundant cation in body and necessary for almost all vital processes *Half of total body calcium circulates as free ions that participate in coagulation, neuromuscular conduction, intracellular regulation, control of skeletal and cardiac muscle contractility *98-99% calcium reserves stored in teeth and skeleton Serum below 8.5 mEq/Lcritical <7 *ETOH abuse *Pancreatitis *Chronic renal failure Inadequate intake *Decreased Vitamin D (Sunshine) *Lack of weight bearing *Loop Diuretics *Hypomagnesemia Oral Calcium carbonate/gluconate Calcium chloride (more irritating to the vein) Watch for extravasate into subcutaneous tissue THINK MUSCLE RESPONSE *Monitor electrolytes *Monitor vital signs *Cardiac Output decreased *Hypotension *Dysrhythmias *Monitor neuromuscular responses: seizures, tetany, paresthesias, muscle spasmsCalcium: HypercalcemiaSerum above 10.5 mEq/Lcritical >12*Prolonged immobilization *Dehydration *Cancer *Excess Antacid Intake *Eliminate Calcium through kidneys through IV fluids *Loop diuretic to promote elimination of calcium THINK MUSCLE RESPONSE *Monitor electrolytes *Monitor vital signs Hypertension *Monitor GI: N&V-anorexia *Dysrhythmias Creatinine*End product of creatine metabolism which is performed in skeletal muscle *Small amount of creatine is converted to creatinine which is then secreted by kidneys *Amount of creatinine generated proportional to mass of skeletal muscle Patho0.5-1.3 mg/dl *Gold standard for kidney function because creatinine is produced in consistent quantity and rate of clearance reflects glomerular filtration Normal RangeDecreased in: Decreased skeletal muscle Inadequate protein intake Increased in: CHF Dehydration Acute & chronic renal failure Shock CausesCorrect underlying problem Fluid resuscitation to keep SBP>90 Dialysis TreatmentsTHINK FLUID BALANCE *Assess I&O closely *Fluid restriction *Assess for signs of fluid retention/edema Nsg ConsiderationsBlood Urea Nitrogen (BUN)Urea represents end product of protein metabolism performed in the liver Urea diffuses freely in intra/extracellular fluid and then excreted by kidneys BUN reflects balance between production and excretion of urea Ratio to creatinine is 15-24:1 (if creatine 1.0 expected BUN should be 15-24) Is indirect measurement of renal function but does not reflect glomerular filtration 10-20 mg/dl critical >100 Decreased in: Poor protein intake/malnutrition Liver disease Malabsorption syndromes Increased in: Acute renal failure CHF Hypovolemia-dehydration Pyelonephritis Hyperalimentation/TPN *Fluid resuscitation-HIGH *Dialysis-HIGH *Improve nutritional intake/Failure to thrive-LOW THINK FLUID BALANCE *Assess I&O closely *Fluid restriction *Assess for signs of fluid retention/edema *Assess for agitation, confusion, fatigue, *N&V-HIGH *Assess liver profile labs for correlating liver damage II.Hematology Hemoglobin-HGB *Primary protein of erythrocytes that is composed of heme (iron) and globin (protein) *Carries O2 to cells and CO2 back to lungs *Parallels Hematocrit which is the % of RBC in proportion to total plasma volume *GOLD Standard for evaluating blood/RBC adequacy (anemia, blood loss) Adult- 13-17 g/dlcritical <6 or >18 Range of Anemias: Mild Hgb 10-12 g/dl-asymptomatic Moderate: Hgb 6-10 g/dl weakness, fatigue, palpitations, SOB, decreased tol to activity-orthostatic hypotension Severe: Hgb < 6 g/dl Hypoxia: confusion, SOB,skin pallor- MM/nailbeds, dizziness, weakness, tachycardiaClinical Uses: Detect blood loss, anemia and response to treatment Detect any possible blood disorder Decreased in: Anemia Cancer Fluid retention/overload Hemorrhage Increased in: COPD CHF Dehydration Polycythemia *Correct underlying problem *Blood transfusions if symptomaticTHINK BLOOD LOSS/ANEMIA *Identify early signs of blood loss: tachycardia, then hypotension *Transfuse as needed-assess closely in first 30 for transfusion reactions *Assess for signs of tissue hypoxia (see above) PathoNormal RangeCausesTreatmentsNsg ConsiderationsWhite Blood Cell Count (WBC)*WBC represent primary defense against invading infections *This is a total count of all 5 leukocytes: neutrophils, lymphocytes, eosinophils, basophils, and monocytes *Indicates overall degree of bodys response to pathology, but must be evaluated and correlated through differential count *Elevated WBC due to significant increase in one differential-usually the neutrophil *Physiologic stress or steroids will increase WBC 4,500-11,000 mm3critical <2500 or >15,000 Decreased in: ETOH abuse Anemia Bone marrow depression Viral infections Increased in: Infection Anemia Inflammatory disorders Steroid use (acute or chronic) *Identify infectious process *Confirm bone marrow depression in chemo/radiation therapy THINK INFECTION *Low or elevated WBC can represent sepsis *Assess closely for hypotension with known infection (septic shock) *Assess closely for any change in temperature trend-hypothermia or febrile can both represent sepsis especially in elderly Neutrophils*Most predominant differential WBC-comprise 50-70% of all WBCs *First line of defense against bacterial infection through phagocytosis (think pacman) *BANDS- if present on differential-correlate with overwhelming sepsis.Immature neutrophils body is kicking into circulation before they are ready because of the severity of infection/sepsis 50-70% of differentialcritical or clinical concern >80% Increased in: Infection Acute hemorrhage Physical stress Tissue necrosis/injury Decreased in: Bone marrow depression (chemo/radiation therapy) Viral infection (due to increased lymphocytes)*Identify infectious process *Confirm bone marrow depression in chemo/radiation therapyTHINK INFECTION *Low or elevated WBC can represent sepsis *Assess closely for hypotension with known infection (septic shock) *Assess closely for any change in temperature trend-hypothermia or febrile can both represent sepsis especially in elderly PathoNormal RangeCausesTreatmentNsg ConsiderationsIII. Cardiac Troponin*Contractile protein found in cardiac muscle that will be released into systemic circulation with cardiac ischemia or acute MI *Levels will rise 2-6 hours after injury-peak 16-24 hours and then remain elevated for several days *If acute onset CP to r/o MI they will be done every 6 hours x3 to determine pattern of abnormal elevation <0.05 ng/ml This may vary depending on each hospital lab If elevated this establishes diagnosis of acute MI *If positive MI, the degree of elevation provides general barometer of degree of heart muscle damage Increased in: Acute MI Unstable angina Minor myocardial damage after CABG or PTCA/stent placement*Standards of cardiac care include continuous telemetry, b-blockers to decrease cardiac workload, heparin or nitroglycerin gtts. *Definitive treatment of MI includes PTCA/stent or CABGTHINK CARDIAC-MI *Assess closely for recurrent or new onset of chest pain *Assess cardiac rhythm for any changes such as PVCs, VT or atrial fibrillation *Assess HR and SBP carefully to promote decreased cardiac workload (maintain heart rate <80 and SBP <140 *Assess tolerance to activity closely Brain Natriuretic Peptide (BNP)*Hormone that is stored in the ventricle of the heart *When left ventricle is distended and stretched due to CHF exacerbation BNP is released into circulation Inhibits the release of renin by kidneys which promotes water and sodium loss as well as increases glomerular filtration rate (Bodys own ACE inhibitor!) <100 normal 100-500 abnormal but not critical for ventricular strain (mild) >500 critical for positive correlation of CHF exacerbation *CHF exacerbation *Ventricular hypertrophy (cardiomyopathy) *Severe hypertension *Aggressive diuresis for fluid overload *May be on NTG gtt or po Nitrates to decrease preload which decreases workload of heartTHINK CARDIAC-CHF *Assess respiratory status for tachypnea and breath sounds closely for basilar or scattered crackles *Assess HR and SBP carefully to promote decreased cardiac workload (heart rate <80 and SBP <140 *Assess tolerance to activity closely *Assess I&O closely *Assess K+ closely with loop diuretics      Most Common & Relevant Clinical Lab Values w/Significance to Patient Care: Copyright 2011, Keith Rischer/www.KeithRN.com 9:NPVWe; < R _    + , ˹݃݃݃r^L#hlRhLdCJOJQJ\^JaJ&hlRh=5CJOJQJ\^JaJ hlRhnCJOJQJ^JaJ#hlRh=6CJOJQJ^JaJ#hlRhn5CJOJQJ^JaJ#hlRh=5CJOJQJ^JaJ#hlRhxF5CJOJQJ^JaJ#hlRhxF5CJ$OJQJ^JaJ$#hlRh=5CJOJQJ^JaJ hlRh=CJOJQJ^JaJ&9 $$Ifa$gdlR$IfG779:OPXe8//// $Ifgd=kd$$Iflֈ N&/<9  - a _  t0644 lae< = ` a    + A V v $7$8$H$Ifgdn $7$8$H$Ifgd=$If $Ifgd=, A B V W u w      / < = > ʸʃqʃʃ#hlRhLd5CJOJQJ^JaJ hlRhLdCJOJQJ^JaJ#hlRh=5CJOJQJ^JaJ#hlRhLd5CJOJQJ^JaJ#hlRhn5CJOJQJ^JaJ hlRh=CJOJQJ^JaJ#hlRhLdCJOJQJ\^JaJ#hlRh=CJOJQJ\^JaJ&   $If $7$8$H$Ifgd=    8222$Ifkd$$Iflֈ N&/<9  - a _  t0644 la = >   0 ? 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