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Fluid and Electrolyte Disorders

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1 Fluid and Electrolyte Disorders
J.B. Handler, M.D. Physician Assistant Program University of New England

2 Abbreviations ABG- arterial blood gas
SIADH- syndrome of inappropriate ADH ADH- anti-diuretic hormone Cr- creatinine AVP- arginine vasopressin N- nausea HA- headache OSM- osmolality DI- diabetes insipidus ACEI- angiotensin converting enzyme inhibitor HTN- hypertension PE- physical exam HF- heart failure WNL- within normal limits BS- blood sugar RRR- regular rate & rhythm Mg- magnesium AMI- acute myocardial infarction S04- sulfate Ca- calcium Nl- normal DKA- diabetic ketoacidosis ECF- extracellular fluid EF- ejection fraction MR- mitral regurgitation MSE- mental status exam BP- blood pressure UT- urinary tract

3 Alterations of Fluid Volume
Volume overload (e.g. HF): Increase in total body fluid/Na. Findings: weight; edema, ascites. Volume depletion (vomiting, diarrhea): Wt. loss, excessive thirst, postural hypotension and dry mucous membranes; both H2O and salt are lost. Dehydration: Refers to volume depletion with disproportionate water deficit; may lead to Na, osmolality. Most common cause of dehydration worldwide: diarrhea; others- heat related illness, fevers, vomiting. 1. Increased wt over a short time period.

4 Electrolyte Values Na 135-145 meq/L K 3.5-5 meq/L Cl 98-107 meq/L
HCO meq/L (equivalent to total venous *CO2 done via lab testing) Mg mg/dl Ca: total/ionized (see below) Total CO2 is not PCO2, and is about the same as a bicarb measurement. *Total CO2 = dissolved CO2 + (H2CO3) +HCO3 (90-95% of total CO2) Therefore, total venous CO2  HCO3

5 Renal Function Creatinine mg/dL: breakdown product of muscle energy metabolism; lower in women than men, reflects lean muscle mass. Good indicator of glomerular filtration. Blood Urea Nitrogen (BUN) mg/dL- end product of protein metabolism; excreted by kidney. BUN can also be elevated if hypovolemia, and after blood digestion in GI tract

6 Clinical Implications
May be asymptomatic Variety of symptoms (often neuromuscular) depending on the electrolyte disturbance: Hyponatremia: weakness, delerium, seizures Hypokalemia: arrhythmias, muscle weakness, cramps Hyperkalemia: weakness, diarrhea Hypocalcemia: cramps, arrhythmias, seizures Hypercalcemia: polyuria, constipation, lethargy/confusion Measurement of electrolytes is essential in patients with neuromuscular symptoms (including mental status changes). Sx will be either neurologic or muscle, or GI or caridac. GI, GU, neurologic and cardiac.

7 Clinical Evaluation History including Neuro, CV, GI, GU ROS.
Assess neurologic status (including MSE)– may reflect severe electrolyte imbalance, hypoxia, hypoglycemia, etc. Assess volume status- weight, skin turgor, BP, P, postural changes, mucous membranes, edema. Assess metabolic and renal status – glucose, BUN, Cr, electrolytes (Na, K, Cl, HCO3), Ca, Mg, O2 sat.

8 Clinical Evaluation When indicated- serum osmolality, urine Na, O2 sat, ABG’s (acid-base disturbance). Serum Osmolality: Normal mosm/kg. Osm = 2(Na meq/L) + Glucose mg/dl *BUN mg/dl Represents solute [ ]: # particles in solution. *Urea is an ineffective osmole; easily permeates cell membranes

9 Case 1 42 y/o female with HTN- 3 day history of severe N&V; oral intake limited to tea and sips of H2O. Meds: HCTZ 25 mg/daily; not taken in 48 hrs. PE: P-120, BP 90/60 lying, 70/50 upright; weight 5 pounds in last 3 days. Labs: Na-125 meq/L, K-2.8 meq/L, Cl-88meq/L, Cr-1.0 mg/dL, BUN-24 mg/dL, HCO3-35 meq/L, Glu-100 mg/dL; urine Na- 5 meq/L. Describe the abnormal findings and why they have developed. Management? Urine Na usually reflects daily intake. K from diuretic and vomiting/aldosterone gets rid of K for Na

10 Hyponatremia Definition: Na< 130 meq/L
Volume status and osmolality essential for clarification. What change in osmolality is most commonly found….? Most cases of hypoNa result from H2O imbalance (from ADH secretion), not Na imbalance. The result is a relative increase in intravascular free H2O, leading to a dilutional decrease in Na.

11 Hyponatremia and Volume
HypoNa can occur with hypo, hyper and euvolemia (more examples to follow). When hypovolemia is present, important to determine if basis is renal (salt wasting nephropathy, diuretics) or non-renal (GI losses-vomiting/diarrhea, sweating, etc.). Urine Na is useful to differentiate renal vs non-renal etiologies: If < 10 meq/L implies avid Na retention by kidney (in absence of diuretics) non-renal loss (vomiting, etc). If > 20 meq/L indicates renal salt wasting (diuretics, salt wasting nephropathy).

12 ADH/AVP Secretion Very small increases in plasma osmolality (1-2%) result in ADH secretion from the neurohypophysisosmolality & Na maintained. Large changes (5-10%) in volume (with concomitant decrease in BP) also result in ADH release (mediated through baro-receptors in the circulation) free H2O is retainedhypoNa. Marked  in CO and BP can mimic (see below) With hypovolemia both Na/H2O (via RAA) and free H2O (via increased ADH/thirst) will be conserved. Increased free water dilutes Na

13 Case 1 Volume: Decreased Total body Na: Decreased
Serum Osmolality: Decreased ADH secretion: Increased– why? Renal status: preserved Hyponatremia- why? - ADH Hypokalemia- why? – diuretic/ALD Predicted arterial pH- alkalotic …why?  see lecture on Acid-Base disorders.

14 Hypovolemic Hypotonic HypoNa
Decreased Na with decreased ECF volume: Renal (diuretics) or extrarenal (vomiting, diarrhea) volume loss. Total body Na/H2O decreased. ADH secretion is increased to maintain intravascular volume. This drive overrides the need to sustain normal osmolality. Patient often initially unable to take in adequate Na/H2O orally. Rx (Case 1): Isotonic fluids IV (normal saline/0.9% saline or ringers lactate) with KCL. If mild volume  and oral intake intact: Electrolyte drink (“Gatorade”) + KCL.

15 Case 2 55 y/o man with dilated cardiomyopathy (EF 24%) presents with recurrent shortness of breath, wt gain and leg edema. Meds: Furosemide, metolazone*, metoprolol, lisinopril & digoxin. PE: BP 88/60, Lungs- diffuse crackles; Heart- S3 gallop and MR murmur; Ext- 3+ edema. Labs: Na-125 meq/L, K-2.9 meq/L, Cl-100 meq/L, glu- 100mg/dL, Cr-1.5 mg/dL, BUN-60 mg/dL. What is going on? Management? Pre-renal azotemia – mild incr in Cr, sig incr in BUN – kidneys not perfused well. Baroreceptors cause ADH secretion to increase. Body does not have a healthy heart to perfuse baroreceptors, which causes ADH secretion to increase. *thiazide like diuretic used in addition to a loop diuretic for severe HF

16 Case 2 Volume: Increased Total body Na: Increased
Serum Osmolality: Decreased ADH secretion: Increased- why? Renal status: Pre-renal azotemia from renal perfusion Hyponatremia- why? Hypokalemia- why? Mimics hypovolemia b/c baroreceptors are not perfused.

17 Hypervolemic Hypotonic HypoNa
Hyponatremia with increased ECF; edema related disorders (HF, cirrhosis, nephrotic syndrome). Total body Na/H2O are increased but circulating blood volume is sensed as inadequate by baroreceptors because of CO and BP; CO renal perfusion (can lead to pre-renal azotemia). Result: Increased ADH + activation of RAA system. Treatment: Water restriction, diuretics, and treatment of the underlying condition (very difficult to Rx; patient is often end-stage). Ultrafiltration of fluid is another option. This is end stage ht failure – ht can’t perfuse baroreceptors.

18 Case 3 A 55 y/o man with small cell lung cancer presents to the ED following a grand-mal seizure. He has been treated with chemotherapy. PE: P-80, BP-140/80; membranes moist, skin turgor intact; Lungs-clear, Heart-RRR, no murmurs; extremities- no edema, intact pulses. Labs: Na- 116 meq/L, K-4.8 meq/L, Bun 8 mg/dL, Creatinine 0.9meq/L, Glu 100mg/dL. Urine Na-36 meq/L; urine osmolality . What is going on? Management?

19 Case 3 Volume: Euvolemic Total body Na: Normal
Serum Osmolality: Decreased ADH secretion: Increased- why? Renal status: Normal Hyponatremia- why? Increased urine osmolality- why? SIADH – from ca Start getting rid of extra Na into urine. Volume status is maintained b/c RAA is turned off, and you trade Na/H2O for free H2O

20 Euvolemic Hypotonic Hyponatremia
Need urine Na and osmolality to diagnose SIADH is most common cause. Patient is euvolemic with inappropriate ADH secretion. Etiology: Disorders of CNS (stroke), tumors (lung Ca, others), pulmonary lesions (TB), drugs with ADH-like effects (SSRIs, others), post-op pain, etc. Hyponatremia, decreased serum osmolality (<280 mosm/kg), with inappropriately high urine osmolality (>150 mosm/kg).

21 SIADH Absence of cardiac, liver, renal, adrenal or thyroid disease.
Urine Na >20meq/L. Natriuresis (RAAS turned off) compensates for slight increase in volume from ADH. Serum BUN and uric acid are low due to increased clearance (mild volume expansion).

22 Treatment of SIADH (IO)
Symptomatic hyponatremia (Na< 120 meq/L) is a medical emergency. Na correction must be done slowly (<10-12 meq/L/d). Too rapid correction Central Pontine Myelinosisirreversible and disastrous. Hypertonic (3%- 513 meq/L) saline used only for most severe cases. Must monitor serum Na every 2 hrs and Na by no more than meq/L/d. Asymptomatic hyponatremia: H2O restriction or Demeclocyline- inhibits effect of ADH on distal tubule. IO- interest only

23 Psychogenic Polydipsia
Marked excess free H2O intake >10 L/d or more. Seen in patients with psychiatric disease who may be on psychiatric meds (SSRI’s, others) that can interfere with H2O excretion. Euvolemia maintained via renal excretion of H2O and Na (urine Na > 20 meq/L). Serum ADH levels are low. Urine osmolality is low.

24 Post-op Hyponatremia Post-op pain increases ADH secretion. If patient receives inappropriate administration of hypotonic fluids, result can be severe symptomatic hyponatremia (N, HA, seizures, etc.). Treatment: Appropriate pain control with administration of isotonic fluids until patient able to take adequate fluids orally.

25 Hypertonic Hyponatremia
Seen with significant hyperglycemia in diabetics, especially if insulin dependent with an acute rise in BS osmolality. Water is drawn from cells into extracellular space resulting in dilution of Na. Na falls 2-3 meq/l for every 100mg/dL rise in glucose above 200mg/dL; resolves with insulin infusion and volume expansion. A dilutional hyponatremia. Example covered during Acid-Base section.

26 Hyponatremia and HIV/AIDS
Common; 20% ambulatory and 50% hospitalized patients with AIDS have Na. Pathophysiology: multiple mechanisms involved often a combination of GI fluid and electrolyte loss along with inappropriate ADH secretion associated with CNS and/or pulmonary involvement from HIV infection.

27 Hypernatremia with Concentrated Urine
Unusual with intact thirst mechanism and access to H2O. “Stranded in the desert.” Appropriate H2O intake not possible (no H2O available or unconscious). Signs/Sx: Orthostatic hypotension, dehydration; oliguria. Lab: Uosm >400mosm/kg with intact renal function. ADH levels increased. Non-renal H2O losses: e.g. water ingestion fails to keep up with hypotonic losses from excessive sweating, losses from GI or respiratory tracts.

28 Treatment of Hypernatremia
Correct cause of fluid loss and replace volume, water and electrolytes as indicated. Replace water deficit slowly to avoid cerebral edema (brain cell adaptation to serum hyperosmolality). Fluid deficit should be replaced over hours. Type of fluid replacement will vary depending on patient volume status (0.9% saline followed by 0.45% saline).

29 Case 4 A 28 y/o woman presents to the ED with marked dizzyness and a syncopal episode. Marked thirst/polydipsea and urination x 1 week, nauseated without fluid intake the last 24 hours. Meds: started on Lithium for bipolar disease one week ago. PE: P-115, B.P lying 90/60, standing 70/50; Skin turgor  and mucus membranes dry. Na-150 meq/L, K-3.4 meq/L, BUN-40 meq/L, Cr-1.3meq/L. Urine Osm 100 mosm/kg. What is going on? Management? Lithium is blocking reabsorption of H2O Pt has Diabetes Insipidous – problem holding onto free water. She is making ADH but it is not working any more for her kidneys (Lithium is blocking effect of ADH at tubule).

30 Hypernatremia with Dilute Urine
Diabetes Insipidus: thirst, H2O (polydipsia) Urine osmolality < 250 mosm/kg. Central Diabetis Insipidus: Lack of ADH/AVP production by posterior pituitary. Hypernatremia due to free water loss. Rx is with ADH. Nephrogenic DI (Acquired): Renal insensitivity to ADH seen after relief of prolonged UT obstruction; renal interstitial disease; hypercalcemia; lithium or demeclocycline Rx.  response to ADH. Congenital Nephrogenic DI (rare)- absence of renal ADH receptors. Can give synthetic ADH and look for changes to determine which DI.

31 Case 5 44 y/o man with dilated cardiomyopathy presents with syncopal episode and weakness following 3 day history of fever and diarrhea. Meds: Digoxin, lisinopril, furosemide & carvedilol. PE: P-105 (irregular with pauses), BP- 95/70; skin turgor, dry mucus membranes; Heart- Tachycardic with “extra sounds” and pauses, S3 gallop. Na-135 meq/L, K-2.8 meq/L, Cl-104 meq/L, HCO3-22meq/L; Digoxin level 2.2 ng/mL (0.8-2 ng/ml); BUN and CR- WNL; ECG- see below What is going on? Other labs needed? Treatment? Low K in pt with ht problems is a bad thing – can lead to fatal cardiac arrhythmias

32 Hypokalemia K is the major intracellular ion (95% IC)
K regulation: 1. Shifts intra/extracellular 2 Renal K modulation (RAA System) (most important) K uptake by cells stimulated by insulin in the presence of glucose and facilitated by beta adrenergic stimulation. Symptoms/signs: weakness, muscle cramps, fatigue, constipation. ECG: NSST-T* changes and “U” waves; PVC’s Very common b/c we tx pt’s with diuretics. *NSST-T- non-specific ST and T wave changes

33 Pathophysiology of Hypokalemia
Extrarenal K losses: GI via vomiting, diarrhea. Renal K losses: Aldosterone facilitates urinary K excretion; most important regulator of body K content. Most diuretics lead to renal K losses. Treatment: Mild to moderate K losses can be replaced with oral KCL. Severe hypokalemia requires IV administration slowly, with cardiac monitoring. Case 5: Hospitalize, IV fluids/KCL, frequent measurement of K and other parameters until stable; digoxin dose + normal K PVC’s. Get hypokalemic b/c of diuretics or these. ALD is major regulator

34 Case 6 32 y/o man presents to the ED with 7 days of weakness and malaise. In last 24 hours he has become lethargic and developed diarrhea; poor historian. No prior medical problems; no meds. PE: Ill appearing man, moaning. T-38.8, P-125, BP-90/60; lungs- basilar crackles; heart- tachycardic without murmur; ext-2+ edema. ECG done in ED (see below)- wide QRS tachycardia, ?Vtach. Labs: pending; O2 sat-94% on room air. Cardiology consultation requested- Handler called.

35 Case 6, continued Cardiology consult: “I don’t think this is Vtach. The rate slows during carotid message. Is the potassium level back?” (ED doc skeptical). Labs: Na-136 meq/L, K-8.1meq/L*, Cl- 98meq/L, HCO3-17meq/L, BUN-90meq/L, Cr-8.6meq/L CxR: normal size heart; pulmonary congestion. ABG- pH-7.32, PCO2-32mmHg, PO2-68 mmHg on room air. Describe acid-base status? What is going on? Management? Hyperkalemia b/c kidneys shut down. ARF. *Test repeated with same result; no hemolysis

36 Hyperkalemia Important to confirm lab values (hemolysis)
Patients with renal insufficiency are at risk. Mild K may accompany metabolic acidosis due to intra/extra cellular shifts (H/K exchange). Risk factors for developing hyperkalemia: Severe renal insufficiency Renal insufficiency plus K supplements (KCL), K sparing diuretic or ACEI Combination of KCL + K sparing diuretic as Rx of hypokalemia: avoid for most patients Triampterine? Spironolactone, amiloride = K sparring diurtics – know them for exam.

37 Clinical Findings Abnormalities in neuromuscular function: weakness, diarrhea, rarely paralysis. Characteristic ECG findings may occur: Peaked T waves, widening of QRS, increased intervals, loss of p waves, etc. Important to assess renal function.

38 Case 6 Diagnosis- acute renal failure, uncertain etiology.
Severe hyperkalemia, secondary to renal shutdown; acidosis also contributes. Compensated metabolic acidosis secondary to uremia- to be discussed during Acid-Base lecture. Infusion of Insulin/Glucose started; albuterol by nebulizer given. Nephrologist called, dialysis catheter placed at her request. K follow glucose intracellularly.

39 Treatment of Hyperkalemia
In life threatening situations (K> ) an infusion of insulin and glucose will drive K intracellularly, buying time for further Rx. This is potentiated by ß-agonists (albuterol). Eliminate K supplements/K sparing drugs Cation exchange resins orally or rectally exchange Na for K (Kayexelate). Give cautiously in HF. Dialysis required with severe renal failure

40 ECG: Hyperkalemia

41 Calcium Metabolism 1% total body calcium is in solution in body fluid 50% is ionized muscle & nerve function 40% is protein bound (primarily albumin) 10% complexed with anions (citrate, etc) Normal Total Serum Ca is mg/dL Ionized Ca is mg/dL Important to measure serum albumin to determine if Ca levels reflect true deficiency. For every 1 gram of albumin, total Ca s by 0.8meq/L. Ionized Ca is not effected by albumin levels. “Corrected” serum Ca= total serum Ca mg/dL + (0.8 x [4.0-Albumin g/dL]) Important role in muscle and nerve function. Normally don’t get ionized Ca as lab test. Therefore, #3. if albumin drops, total Ca should as well, but ionized should be nl.

42 Hypocalcemia Most common cause is chronic renal failure (decreased Vit D3 and increased PO4). Hypoparathyroidism and malabsorbtion less common Signs/Sx: Increased excitation of nerve and muscle cells; cramps, tetany, paresthesias and convulsions. Chvostek’s sign, Trousseau’s sign ECG: Prolonged Q-T interval/arrhythmias Serum Ca <9.0mg/dL (nl albumin), ionized Ca <4.5mg/dL PO4 binds to Ca and pull it out of circulation. 3. C sign – tap on facial nerve in front of ear, if Ca is low face will twitch on that side. T sign – inflate BP cuff above systolic. Watch for a few minutes, if Ca down hand will cramp and tetany.

43 Treatment: Hypocalcemia
If symptomatic: IV calcium gluconate via bolus and infusion. If asymptomatic: Oral calcium and Vitamin D. Correction of hypomagnesemia if present. 3. Can worsen hypocalcemia.

44 Hypercalcemia *Sounds like?
Etiologies include hyperparathyroidism, malignancy (tumors produce PTH related proteins), milk-alkali syndrome (Ca antacids + Vit D excess). Signs/Sx: Often without sx if mild Ca Renal/GI: polyuria (H2O* reabsorption is blocked by hypercalciuria), nephrolithiasis; nausea, constipation. Neuro changes (drowsiness, weakness, lethargy, stupor/coma) with severe hypercalcemia. ECG findings: Shortened Q-T, PVC’s. Lab: increased Ca with nl. or low PO4. Parathyroid Tumor most common cause. Polyuria – kidneys don’t hold onto free water. Sounds like nephrogenic DI. *Sounds like?

45 Treatment or Hypercalcemia
Treat underlying disease process. Promote Na rich diuresis which will be accompanied by excretion of Ca. Infusion of 0.9% Saline + IV furosemide will expand ECF volume and promote Na/Calcium rich diuresis. Avoid Thiazide diuretics: Can worsen hypercalcemia. Want to promote Na rich diuresis.

46 Hypomagnesemia Very common in hospitalized patients, especially those on diuretics who are receiving continuous IV fluid support. Normal Mg Level: meq/L Symptoms similar to hypocalcemia: weakness, muscle cramps, tremors, neurmuscular and CNS hyperirritability. Often associated with hyopK and hypoCa Low Mg potentiates dangerous (ventricular) cardiac arrhythmias, esp if K is low.

47 Treatment of Hypomagnesemia
Important to order Mg levels in hospitalized cardiac patients (AMI, CHF, etc.). IV therapy with MgSO4, and monitor levels. Oral Mg oxide can be given for supplemental oral use. Know relationship about total Ca and albumin.

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