6. Fluid + Electrolyte K+ Flashcards
Describe K+ distribution in the body
K+ = the major intracellular cation (98% intracell)
- ICF K+ conc ~20x greater than ECF
- only 2% total K+ present in plasma
Many cell functions require maintenance of low ECF K+ conc
How is K+ regulated?
K+ not as closely regulated as Na+
Kidneys have important role in K+ regulation;
- prox tubules reabsorb nearly all K+
Aldosterone from RAAS or directly from adrenal cortex stimulates additional K+ secretion into the urine in exchange for Na+
K+ uptake from ECF to ICF important - acts to normalise acute rise in K+ due to increased intake
In healthy pop these mechanisms robust + cope with wide variations in K+ intake
What are the K+ reference ranges? And what do they indicate about total body K+?
Serum/plasma ref range = 3.5-5.0mmol/L
Intracellular concentration = ~130mmol/L
Serum level = late indicator of total body depletion/excess
What are the functions of K+?
Integral component of electrochemical gradient across cell membranes;
- created by Na+/K+ ATPase pump
Responsible for correct function of all human cells;
- maintains electrical neutrality + osmolality of cells
- regulates neuromuscular excitability
- contraction or skeletal, cardiac + smooth muscles
- maintenance of ICF volume
- BP control
- acid-base balance (through K+, H+ exchange)
List the sources of K+ intake
Obtained from diet: beans, dark green leafy veg, potatoes, bananas, melon, fish, yoghurt, avocados, mushrooms
What influences the distribution of K+ between ICF + ECF?
- K+ loss due to inhibition of Na+/K+-ATPase pump (hypoxia)
- Insulin promotes acute entry of K+ into skeletal muscle + liver;
- increases ATPase pump activity - Catecholamines, e.g. adrenaline, promote cellular entry of K+/ propanolol impairs entry of K+ into cells
Others;
Exercise: K+ released during, changes reversed after several mins rest
Hyperosmolality: causes H20 to diffuse into cells carrying K+ with it
Cellular breakdown: release K+ into ICF, e.g. trauma, tumour lysis syndrome, blood transfusion
How is K+ measured?
Serum, plasma + urine used for analysis
ISE for K+ = valinomycin membrane;
- selectively binds K+ = impedence that correlates with K+ conc
- KCl used as inner electrode ref solution
Ref ranges;
Serum: 3.5-5.1mmol/L
Plasma: (male) 3.5-4.5/ (female) 3.4-4.4mmol/L
Urine 24H: 25-125mmol/day
What are the common problems with K+ analysis?
Due to low conc dilutional errors (like with Na+) do not tend to arise even with indirect ISEs
Leakage from cells;
- hemolysis: lysis of RBCs + release of contents into surrounding fluid, e.g. blood plasma w/ delayed processing
- Abn cellularity
K+ EDTA contamination from vacutainer tube
When should problems with K+ measurements be suspected?
Sample visibly hemolysed Sample dated previous day Grossly abn result Urea/creatinine normal Doctor reports no accompanying ECG changes
Describe the relationship between K+ and acid-base balance
Acid-base disturbances cause K+ to shift in and out of cells
Hyperkalemia linked to acidosis;
- acidosis causes K+: ICF > ECF (plasma) in exchange for H+ ions
- H+ ions moved into cells to decrease pH
Hypokalemia linked to alkalosis;
- reverse movement
- cells release H+ into blood to increase acidity
What is hyperkalemia?
Increased plasma K+ >4.5mmol/L (male)/ >4.4mmol/L (female)
Pts usually have underlying disorders;
- renal insufficiency, diabetes mellitus, metabolic acidosis
- most common in hosp pts = therapeutic K+ admin
Describe the steps of K+ metabolism
Primary events;
- K+ intake = transient increase in plasma K+
- alpha + beta pancreas cells sense increased plasma K+
Initial response;
- pancreas secretes;
- insulin = increased K+ storage in muscle
- glucagon = increased K+ secretion at renal tubules = increased urinary K+ excretion
- overall decrease in plasma K+
Associated responses;
- decrease in plasma K+ induces;
- K+ release from muscle
- muscle + plasma K+ values return to normal
List the broad causes of hyperkalemia
- Decreased renal excretion
- Cellular shift
- Increased intake
- Artefactual (pseudo)
What are the causes of decreased renal K+ excretion?
Acute/chronic renal failure (GFR<20ml/min) Hypoaldosteronism Addison's Diuretics Adrenal failure Drugs (some anti-hypertensives)
What are the causes of cellular shift leading to hyperkalemia?
Acidosis, e.g. lactic acidosis Muscle/cell injury Chemo Leukemia Hemolysis
What are the causes of increased K+ intake?
Oral/IV K+ replacement therapy, e.g. iatrogenic disease
What are the causes of artefactual hyperkalemia?
Sample hemolysis
Delayed processing
Incorrect processing e.g. EDTA contamination
Exposure to cold
Abn cells
Thrombocytosis
Prolonged tourniquet use/excessive fist clenching
Describe artefactual hyperkalemia caused by hemolysis
Degree of hemolysis varies: faint pink tinge >strawberry jam
Analysers: inbuilt detector for Hb
May still be able to report result if only slightly hemolysed (rules vary b/n labs)
Describe artefactual hyperkalemia caused by delayed processing
Serum must be separate from cells on 1st day of sample collection
No visible signs of problem in sample
IT system may flag up date if entered correctly
Check PO4 (also high) + glucose: cells left overnight will consume glucose giving abn low result
Describe artefactual hyperkalemia caused by incorrect processing
EDTA used as anticoagulant for CBCs
Nurse/clinician may try to transfer blood from this tube to proper tube
Often causes spurious results;
- severe hyperkalemia
- hypocalcemia
- hypomagnesemia
Describe artefactual hyperkalemia caused by exposure to cold
Cells exposed to cold = damaged = leak K+/Mg2+/phosphate
E.g. put in fridge/transported in van in winter
Difficult to prove - usually affects no of samples from same GP practice
Describe artefactual hyperkalemia caused by abn cells
Pts with unusually high WBCs/PLTs, e.g. leukemia, may release unusual quantities of K+ on clotting
Check full blood picture
Check K+ in heparinised blood sample (green bottle);
- obv not a K+-EDTA sample
What are the symptoms of hyperkalemia?
Muscle weakness, twitches, numbness + cramps Irritability + anxiety Decreased BP Dysrhythmias, ECG changes Abdominal cramps Diarrhea
What is the treatment for hyperkalemia?
Admin of calcium gluconate - stabilises heart muscle
IV insulin + dextrose - promotes K+ entry into cells
Other meds e.g. nebulised B agonists
Correction of underlying cause of increased K+
What is important for the testing BMS to know when hyperkalemia discovered in a pt?
Pt may have no specific symptoms but is at risk of cardiac arrest
BMS is first to know;
- reqs immediate treatment
- if result >6.5mmol/L obtained + verified BMS must contact ward immediately
What is hypokalemia?
Plasma K+ <3.5-5.0mmol/L
What do the serum values for hypokalemia indicate?
Late indicator of total body K+ depletion
Usually a genuine result
What are the symptoms of hypokalemia?
Non-specific, become more apparent as K+ drops below 3mmol/L;
- muscle weakness/fatigue
- constipation
- cardiac arrhythmias
What are the causes of hypokalemia?
GI loss;
- vomiting/diarrhea
- gastric suction
- intestinal tumour
- malabsorption
- cancer therapy, e.g. chemo/radio
- large doses laxatives
Renal loss;
- diuretics, e.g. thiazides, MCs
- nephritis
- renal tubular acidosis (RTA)
- hyperaldosteronism
- Cushing’s
- hypomagnesemia
- acute leukemia
Cellular shift;
- alkalosis
- insulin OD
Decreased intake
What does the BMS need to know when detecting hypokalemia in a pt?
If K+ conc <2.5mmol/L phone ward
What is the treatment for hypokalemia?
Oral KCl replacement of K+ over several days
IV K+ replacement
Dietary correction (bananas, OJ, nuts)
May take several days to restore intracellular K+ pool
Treatment guided by repeat K+ measurements
