Editing Reduction of Risk Potential – RN Flashcards (section)

== Laboratory Interpretation ==

;Normal serum potassium range, and why it dominates cardiac safety
:3.5 to 5.0 mEq/L. Both hypokalemia and hyperkalemia alter myocardial repolarization. Hypokalemia flattens T waves, depresses ST segments, and produces U waves; hyperkalemia peaks T waves and widens the QRS toward cardiac arrest.

;Two absolute rules for intravenous potassium administration
:Never give it by intravenous push or bolus and never intramuscularly. Always dilute and infuse by pump, generally no faster than 10 mEq per hour on a general unit, after confirming adequate urine output.

;Why a client on digoxin with a "therapeutic" digoxin level can still be toxic
:Hypokalemia, hypomagnesemia, hypercalcemia, renal impairment, and advanced age all increase myocardial sensitivity to digoxin, so toxicity can occur within the 0.5 to 2.0 ng/mL range.

;How a low serum albumin changes the interpretation of a total calcium
:Total calcium is largely albumin bound, so hypoalbuminemia falsely lowers the total value while the physiologically active ionized calcium may be normal. Confirm with an ionized calcium.

;Hypokalemia that will not correct despite repletion suggests what
:Untreated hypomagnesemia. Magnesium must be replaced for potassium to normalize.

;Interpretation of pH 7.50, PaCO2 30 mm Hg, HCO3 24 mEq/L
:Uncompensated respiratory alkalosis. The pH is alkalemic, the PaCO2 is low and explains it, and the bicarbonate has not yet shifted.

;Interpretation of pH 7.30, PaCO2 38 mm Hg, HCO3 16 mEq/L
:Uncompensated metabolic acidosis. Expect deep, rapid Kussmaul respirations as the body attempts respiratory compensation.

;What a rise in serum creatinine from 0.9 to 1.8 mg/dL signifies
:A doubling of creatinine represents a substantial drop in glomerular filtration, even though both numbers look small. Reassess nephrotoxic drugs, contrast exposure, and volume status.

;A blood urea nitrogen to creatinine ratio well above 20 to 1 suggests what
:A prerenal cause such as dehydration, hypovolemia, or gastrointestinal bleeding rather than intrinsic renal injury.

;Which count, not the total white blood cell count, determines infection risk in neutropenia
:The absolute neutrophil count. Below 500/mm3 is severe neutropenia, and fever in that setting is an emergency requiring immediate cultures and broad-spectrum antibiotics.

;Platelet thresholds for procedural bleeding risk and spontaneous bleeding risk
:Roughly below 50,000/mm3 for bleeding with trauma or procedures, and roughly below 20,000/mm3 for spontaneous bleeding.

;Laboratory test, therapeutic range, and antidote for warfarin
:International normalized ratio, usually 2.0 to 3.0 for atrial fibrillation and venous thromboembolism and 2.5 to 3.5 for many mechanical valves. Antidote is vitamin K (phytonadione).

;Laboratory test, therapeutic range, and antidote for unfractionated heparin
:Activated partial thromboplastin time, therapeutic at 1.5 to 2.5 times the control. Antidote is protamine sulfate.

;Pattern that suggests heparin-induced thrombocytopenia and the required response
:A marked platelet fall roughly five to ten days into heparin exposure, often with new thrombosis rather than bleeding. Stop all heparin including flushes and coated catheters, do not substitute low molecular weight heparin, and anticipate a non-heparin anticoagulant.

;Why troponin is preferred over creatine kinase MB for a client presenting two days after chest pain
:Troponin rises within a few hours of myocardial injury and remains elevated for several days, so it still detects a late presentation, while creatine kinase MB normalizes much sooner.

;Signs of lithium toxicity and the conditions that precipitate it
:Nausea, diarrhea, fine tremor, and drowsiness early; coarse tremor, ataxia, confusion, and seizures when severe. Precipitated by dehydration, sodium restriction, vomiting, diarrhea, heavy sweating, thiazide diuretics, and nonsteroidal anti-inflammatory drugs.