NOTES. Lott HYPERKALEMIA & HYPOKALEMIA —— GENERALLY, WHAT ARE THEY? ——— PATHOLOGY & CAUSES TREATMENT + Imbalances of potassium levels in blood + Elologies influence potassium intake, excretion, transcellular shit SIGNS & SYMPTOMS + Mid variations usually asymptomatic, Severe imbalances may be fatal LAB RESULTS + Blood potassium levels; further tests useful to establish underlying cause MEDICATIONS. * Discontinue madication that aggravates potassiurn homeostasis, * Low serurn K* += Oral K* can be supplemented + High serum K: = Agents/procedures that remove ‘extracellular K’, into cel's/t secretion from body HYPERKALEMIA PATHOLOGY & CAUSES + High potassium levels in blood > 5.5 millequivalentsiter (mEq/L) CAUSES Decreased kidney excretion + Decreased glomerular filtration rate in acutelchronic kidney disease + Adrenal insufficiency —+ primary hhypoaldosteronism « Principal cells secrete less potassium + Drugs 800 OSMOSISORG + Renin inhibitors, angiotensin converting lenzyme (ACE) inhibitors, angiotensin I receptor antagonists, potassium-sparing ureties, nonsteroidal ant inflammatory «tugs (NSAIDs), cyclosporine, ‘rimethoprim-sulfamethoxazole ‘Transcellular shift + Uncontrolled Type | diabetes = Lack of insulin —» decreases sodium! potassium pump action + Acidosis © Excess hydrogen ions move into calls, via ion transporters that exchange hydrogen ions for potassium ions + Respiratory acidosis: metabolic acidosis, (Osmosis.orgfrom organic acids are two exceptions + Hyperosmolsrity * Gradient pul's water out of cells > intracellular concentration potassium goes up —+ potassium pushed out + Massive cal sis + Eg. tumor lysis syndrome, rhabdomyolysis, massive hemolysis, + Intracellular potassium released into bloodstream (98% of "found within cells) + Drugs + Beta2-adrenergic antagon'sts digoxin toxicity = Exercise + Cellular ATP consumed —> potassium crannels open = Shift usually small, can exacerbate condition in individuals with hyperkalemia Increased intake + Excessive potassium oval intake «Unusual, can exacerbate condition in individuals with hyperkalernia + Rapid, excessive potassium infusion {rare} SIGNS & SYMPTOMS + Mostly asymptomatic + Severeirapid-onset hyperkalemia = Muscle weakness, flaccid paralysis {starts in lower extremities, moves Upward) —+ respiratory falure + Decreased deep tendon reflexes » Arrhythmias, cardiac arrest = Nausea, vomiting, intestinal colic diarrhea Chapter 112 Hyperkalemia & Hypokalemia MNEMONIC: MURDER Signs & symptoms of Hyperkalemi Muscle weakness Urine: oliguria, anuria Respiratory distress Decreased cardiac contractility EKG changes: peaked T waves: QRS widening Reflexes: hyperreflexia or areflexia laced) LAB RESULTS * Potassium levels in blood > 5.SmEail. OTHER DIAGNOSTICS ECG + Prolonged PR interval, tall, peaked T-waves with narrow base, shortened QT interval, depressed ST segment + Severe += Smallindiscernible P wave, widened QRS complex — strip mimics sine wave Baa AAA RU Mase at Sanaa Figure 1124 An ECG demonstrating the changes of hyperkalemia, including elevated T waves, bizare, broad QRS complexes and a prolonged QT interval OSMOSISORG 801 OSMOSIS.org802 OSMOSISORG TREATMENT “Ins exo ets2-arenerae MEDICATIONS * Increase potassium shift into cells + Kayexalate + Initial teatment individuals with ECG changes) * Bind potassium ~+ decrease potassium + Calcium to stabilize myocardial cell absorbed from gastrointestinal {Gi tract membranes + Loop dreties «Increase potassium excretion in kidneys \) MNEMONIC: © BIG K DROP OTHER INTERVENTIONS 7 = Treatment of Hyperkalemia + Severe hyperkslemiatenalfalure P) Calcium gluconate = Hemedalyss (most rapid, effective way Beta 2 agonist to ower serum K) Insulin + Glucose Koyexalate Diuretcs/Dialysis Dinanosis * TE)» Broop ~ > 5.5 wegie < ELECTROCARDIOGRAM * SEVERE + Peaenaee cane PR INTERVAL ST Seoment DEPRESSION pssenr P wave SHORT OT WvTERVAL wide QPS ComPLex Figure 112.2 The ECG features found in hyperkalemia, (Osmosis.orgChapter 112 Hyperkalemia & Hypokalemia HYPOKALEMIA ee PATHOLOGY & CAUSES * Low potassium levels in the blood < 3.5meqiL CAUSES + Increased kidney excretion = Hyperaldasteronism; drugs (e@. aoe, thiazide diuretics, amphoterin B, splatin); renal tubular defects eg. Bartter syndrome); hypomagnesemia + Increased gastrointestinal excretion = Vomiting {direct loses minimal, causes metabolic akalasis); diarrhea + Increased sweat production + Relevant for individuals who exercise in hot climate + Shift from extracellular to intracellular space + Insulin overdose in Type | diabetes; ‘excess insulin — increases sodium! potassium pump action Alka = Hydragens move out of calls using jon transporter that exchanges with potassium fons + Respiratory alkalosis an exception = Drugs + Beta2-adrenergic agonists Other causes + Low dietary intake (e.g. prolonged fasting, anorexia, ketogenic diet) + Insulin administration + Antibiotics (TMP-SMX/amphotericin B) + Epinephrine (beta 2-agonists) * Slightly more than half of trauma cases present with hypokalemia (increased epinephrine levels) SIGNS & SYMPTOMS + Mostly asymptomatic + Severeirapid-onset hypokalernia + Constipation, paralytic ileus = Muscle weakness, cramas, flaccid paraiysis = Decreased deep tendon reflexes + Arrhythmias forolong cardiac conduction) cardiac arrest + Polvuria, polydipsia, nausea, voriting = Exacerbates digital’s toxicity LAB RESULTS + Blood potassium level < 3.5mEqi OTHER DIAGNOSTICS Ec + Flationediinverted T waves, U waves, ST depression, prolonged PR interval * Prominent U waves fused to T waves, ‘mimic prolonged QT + Atrial, ventricular tachyarrhythmias, TREATMENT MEDICATIONS + Replenish potassium with supplementation In acute coronary ischemia, active arrhythmias + Oral KCl administration (safest) + IV administration for individuals taking rit peros = 10mEq KCl increases K° by O.AMEalL. += Magnesium replacement + If diuretic therapy needed + Potassium-sparing diuretic, OSMOSISORG 803 OSMOSIS.org