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

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

2 2 Abbreviations ABG- arterial blood gasABG- arterial blood gas SIADH- syndrome of inappropriate ADHSIADH- syndrome of inappropriate ADH ADH- anti-diuretic hormoneADH- anti-diuretic hormone Cr- creatinineCr- creatinine AVP- arginine vasopressinAVP- arginine vasopressin N- nauseaN- nausea HA- headacheHA- headache OSM- osmolalityOSM- osmolality DI- diabetes insipidusDI- diabetes insipidus ACEI- angiotensin converting enzyme inhibitorACEI- angiotensin converting enzyme inhibitor HTN- hypertensionHTN- hypertension PE- physical examPE- physical exam HF- heart failureHF- heart failure WNL- within normal limitsWNL- within normal limits BS- blood sugarBS- blood sugar RRR- regular rate & rhythmRRR- regular rate & rhythm Mg- magnesiumMg- magnesium AMI- acute myocardial infarctionAMI- acute myocardial infarction S0 4 - sulfateS0 4 - sulfate Ca- calciumCa- calcium Nl- normalNl- normal DKA- diabetic ketoacidosisDKA- diabetic ketoacidosis ECF- extracellular fluidECF- extracellular fluid EF- ejection fractionEF- ejection fraction MR- mitral regurgitationMR- mitral regurgitation MSE- mental status examMSE- mental status exam BP- blood pressureBP- blood pressure UT- urinary tractUT- urinary tract

3 3 Alterations of Fluid Volume Volume overload (e.g. HF): Increase in total body fluid/Na.Volume overload (e.g. HF): Increase in total body fluid/Na. –Findings:  weight; edema, ascites. Volume depletion (vomiting, diarrhea):Volume depletion (vomiting, diarrhea): –Wt. loss, excessive thirst, postural hypotension and dry mucous membranes; both H 2 O and salt are lost. Dehydration: Refers to volume depletion with disproportionate water deficit; may lead to  Na, osmolality.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.

4 4 Electrolyte Values Na meq/LNa meq/L K meq/LK meq/L Cl meq/LCl meq/L HCO meq/L (equivalent to total venous *CO 2 done via lab testing)HCO meq/L (equivalent to total venous *CO 2 done via lab testing) Mg mg/dlMg mg/dl Ca: total/ionized (see below)Ca: total/ionized (see below) *Total CO 2 = dissolved CO 2 + (H 2 CO 3 ) +HCO 3 (90-95% of total CO 2 ) Therefore, total venous CO 2  HCO 3

5 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.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) 8-20 mg/dL- end product of protein metabolism; excreted by kidney.Blood Urea Nitrogen (BUN) 8-20 mg/dL- end product of protein metabolism; excreted by kidney.

6 6 Clinical Implications May be asymptomaticMay be asymptomatic Variety of symptoms (often neuromuscular) depending on the electrolyte disturbance: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).Measurement of electrolytes is essential in patients with neuromuscular symptoms (including mental status changes).

7 7 Clinical Evaluation History including Neuro, CV, GI, GU ROS.History including Neuro, CV, GI, GU ROS. Assess neurologic status (including MSE)– may reflect severe electrolyte imbalance, hypoxia, hypoglycemia, etc.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 volume status- weight, skin turgor, BP, P, postural changes, mucous membranes, edema. Assess metabolic and renal status – glucose, BUN, Cr, electrolytes (Na, K, Cl, HCO 3 ), Ca, Mg, O 2 sat.Assess metabolic and renal status – glucose, BUN, Cr, electrolytes (Na, K, Cl, HCO 3 ), Ca, Mg, O 2 sat.

8 8 Clinical Evaluation When indicated- serum osmolality, urine Na, O 2 sat, ABG’s (acid-base disturbance).When indicated- serum osmolality, urine Na, O 2 sat, ABG’s (acid-base disturbance). Serum Osmolality: Normal mosm/kg. Osm = 2(Na meq/L) + Glucose mg/dl + 18 *BUN mg/dl 2.8 Represents solute [ ]: # particles in solution.Serum Osmolality: Normal mosm/kg. Osm = 2(Na meq/L) + Glucose mg/dl + 18 *BUN mg/dl 2.8 Represents solute [ ]: # particles in solution. *Urea is an ineffective osmole; easily permeates cell membranes

9 9 Case 1 42 y/o female with HTN- 3 day history of severe N&V; oral intake limited to tea and sips of H 2 O.42 y/o female with HTN- 3 day history of severe N&V; oral intake limited to tea and sips of H 2 O. Meds: HCTZ 25 mg/daily; not taken in 48 hrs.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.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, HCO meq/L, Glu-100 mg/dL; urine Na- 5 meq/L.Labs: Na-125 meq/L, K-2.8 meq/L, Cl- 88meq/L, Cr-1.0 mg/dL, BUN-24 mg/dL, HCO meq/L, Glu-100 mg/dL; urine Na- 5 meq/L. Describe the abnormal findings and why they have developed. Management?Describe the abnormal findings and why they have developed. Management?

10 10 Hyponatremia Definition: Na< 130 meq/LDefinition: Na< 130 meq/L Volume status and osmolality essential for clarification. What change in osmolality is most commonly found….?Volume status and osmolality essential for clarification. What change in osmolality is most commonly found….? Most cases of hypoNa result from H 2 O imbalance (from  ADH secretion), not Na imbalance. The result is a relative increase in intravascular free H 2 O, leading to a dilutional decrease in Na.Most cases of hypoNa result from H 2 O imbalance (from  ADH secretion), not Na imbalance. The result is a relative increase in intravascular free H 2 O, leading to a dilutional decrease in Na.

11 11 Hyponatremia and Volume HypoNa can occur with hypo, hyper and euvolemia (more examples to follow).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: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 20 meq/L indicates renal salt wasting (diuretics, salt wasting nephropathy).

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

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

14 14 Hypovolemic Hypotonic HypoNa Decreased Na with decreased ECF volume: Renal (diuretics) or extrarenal (vomiting, diarrhea) volume loss. Total body Na/H 2 O decreased.Decreased Na with decreased ECF volume: Renal (diuretics) or extrarenal (vomiting, diarrhea) volume loss. Total body Na/H 2 O 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/H 2 O orally.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/H 2 O 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.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 15 Case 2 55 y/o man with dilated cardiomyopathy (EF 24%) presents with recurrent shortness of breath, wt gain and leg edema.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.Meds: Furosemide, metolazone*, metoprolol, lisinopril & digoxin. PE: BP 88/60, Lungs- diffuse crackles; Heart- S 3 gallop and MR murmur; Ext- 3+ edema.PE: BP 88/60, Lungs- diffuse crackles; Heart- S 3 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.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?What is going on? Management? *thiazide like diuretic used in addition to a loop diuretic for severe HF

16 16 Case 2 Volume: IncreasedVolume: Increased Total body Na: IncreasedTotal body Na: Increased Serum Osmolality: DecreasedSerum Osmolality: Decreased ADH secretion: Increased- why?ADH secretion: Increased- why? Renal status: Pre-renal azotemia from  renal perfusionRenal status: Pre-renal azotemia from  renal perfusion Hyponatremia- why?Hyponatremia- why? Hypokalemia- why?Hypokalemia- why?

17 17 Hypervolemic Hypotonic HypoNa Hyponatremia with increased ECF; edema related disorders (HF, cirrhosis, nephrotic syndrome).Hyponatremia with increased ECF; edema related disorders (HF, cirrhosis, nephrotic syndrome). Total body Na/H 2 O 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.Total body Na/H 2 O 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.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.

18 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.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.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 .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?What is going on? Management?

19 19 Case 3 Volume: EuvolemicVolume: Euvolemic Total body Na: NormalTotal body Na: Normal Serum Osmolality: DecreasedSerum Osmolality: Decreased ADH secretion: Increased- why?ADH secretion: Increased- why? Renal status: NormalRenal status: Normal Hyponatremia- why?Hyponatremia- why? Increased urine osmolality- why?Increased urine osmolality- why?

20 20 Euvolemic Hypotonic Hyponatremia Need urine Na and osmolality to diagnoseNeed urine Na and osmolality to diagnose SIADH is most common cause. Patient is euvolemic with inappropriate ADH secretion.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.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 ( 150 mosm/kg).Hyponatremia, decreased serum osmolality ( 150 mosm/kg).

21 21 SIADH Absence of cardiac, liver, renal, adrenal or thyroid disease.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.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).Serum BUN and uric acid are low due to increased clearance (mild volume expansion).

22 22 Treatment of SIADH (IO) Symptomatic hyponatremia (Na< 120 meq/L) is a medical emergency.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.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.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: H 2 O restriction or Demeclocyline- inhibits effect of ADH on distal tubule.Asymptomatic hyponatremia: H 2 O restriction or Demeclocyline- inhibits effect of ADH on distal tubule. IO- interest only

23 23 Psychogenic Polydipsia Marked excess free H 2 O intake >10 L/d or more.Marked excess free H 2 O 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 H 2 O excretion.Seen in patients with psychiatric disease who may be on psychiatric meds (SSRI’s, others) that can interfere with H 2 O excretion. Euvolemia maintained via renal excretion of H 2 O and Na (urine Na > 20 meq/L).Euvolemia maintained via renal excretion of H 2 O and Na (urine Na > 20 meq/L). Serum ADH levels are low.Serum ADH levels are low. Urine osmolality is low.Urine osmolality is low.

24 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.).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.Treatment: Appropriate pain control with administration of isotonic fluids until patient able to take adequate fluids orally.

25 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.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.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.A dilutional hyponatremia. Example covered during Acid-Base section.

26 26 Hyponatremia and HIV/AIDS Common; 20% ambulatory and 50% hospitalized patients with AIDS have  Na.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.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 27 Hypernatremia with Concentrated Urine Unusual with intact thirst mechanism and access to H 2 O. “Stranded in the desert.”Unusual with intact thirst mechanism and access to H 2 O. “Stranded in the desert.” Appropriate H 2 O intake not possible (no H 2 O available or unconscious).Appropriate H 2 O intake not possible (no H 2 O available or unconscious). Signs/Sx: Orthostatic hypotension, dehydration; oliguria.Signs/Sx: Orthostatic hypotension, dehydration; oliguria. Lab: Uosm >400mosm/kg with intact renal function. ADH levels increased.Lab: Uosm >400mosm/kg with intact renal function. ADH levels increased. Non-renal H 2 O losses: e.g. water ingestion fails to keep up with hypotonic losses from excessive sweating, losses from GI or respiratory tracts.Non-renal H 2 O losses: e.g. water ingestion fails to keep up with hypotonic losses from excessive sweating, losses from GI or respiratory tracts.

28 28 Treatment of Hypernatremia Correct cause of fluid loss and replace volume, water and electrolytes as indicated.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.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).Type of fluid replacement will vary depending on patient volume status (0.9% saline followed by 0.45% saline).

29 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.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.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.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.Na-150 meq/L, K-3.4 meq/L, BUN-40 meq/L, Cr-1.3meq/L. Urine Osm 100 mosm/kg.Urine Osm 100 mosm/kg. What is going on? Management?What is going on? Management?

30 30 Hypernatremia with Dilute Urine Diabetes Insipidus:  thirst,  H 2 O (polydipsia)Diabetes Insipidus:  thirst,  H 2 O (polydipsia) Urine osmolality < 250 mosm/kg.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.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.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.Congenital Nephrogenic DI (rare)- absence of renal ADH receptors.

31 31 Case 5 44 y/o man with dilated cardiomyopathy presents with syncopal episode and weakness following 3 day history of fever and diarrhea.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.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, S 3 gallop.PE: P-105 (irregular with pauses), BP- 95/70;  skin turgor, dry mucus membranes; Heart- Tachycardic with “extra sounds” and pauses, S 3 gallop. Na-135 meq/L, K-2.8 meq/L, Cl-104 meq/L, HCO meq/L; Digoxin level 2.2 ng/mL (0.8-2 ng/ml); BUN and CR- WNL; ECG- see belowNa-135 meq/L, K-2.8 meq/L, Cl-104 meq/L, HCO meq/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?What is going on? Other labs needed? Treatment?

32 32 Hypokalemia K is the major intracellular ion (95% IC)K is the major intracellular ion (95% IC) K regulation: 1. Shifts intra/extracellular 2 Renal K modulation (RAA System) (most important)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.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.Symptoms/signs: weakness, muscle cramps, fatigue, constipation. ECG: NSST-T* changes and “U” waves; PVC’sECG: NSST-T* changes and “U” waves; PVC’s *NSST-T- non-specific ST and T wave changes

33 33 Pathophysiology of Hypokalemia Extrarenal K losses: GI via vomiting, diarrhea.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.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.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.Case 5: Hospitalize, IV fluids/KCL, frequent measurement of K and other parameters until stable;  digoxin dose + normal K  PVC’s.

34 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.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.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. ECG done in ED (see below)- wide QRS tachycardia, ?Vtach. Labs: pending; O 2 sat-94% on room air.Labs: pending; O 2 sat-94% on room air. Cardiology consultation requested- Handler called.Cardiology consultation requested- Handler called.

35 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).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, HCO 3 -17meq/L, BUN-90meq/L, Cr-8.6meq/L CxR: normal size heart; pulmonary congestion.Labs: Na-136 meq/L, K-8.1meq/L*, Cl- 98meq/L, HCO 3 -17meq/L, BUN-90meq/L, Cr-8.6meq/L CxR: normal size heart; pulmonary congestion. ABG- pH-7.32, PCO 2 -32mmHg, PO mmHg on room air. Describe acid-base status?ABG- pH-7.32, PCO 2 -32mmHg, PO mmHg on room air. Describe acid-base status? What is going on? Management?What is going on? Management? *Test repeated with same result; no hemolysis

36 36 Hyperkalemia Important to confirm lab values (hemolysis)Important to confirm lab values (hemolysis) Patients with renal insufficiency are at risk.Patients with renal insufficiency are at risk. Mild  K may accompany metabolic acidosis due to intra/extra cellular shifts (H/K exchange).Mild  K may accompany metabolic acidosis due to intra/extra cellular shifts (H/K exchange). Risk factors for developing hyperkalemia: 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

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

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

39 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).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 drugsEliminate K supplements/K sparing drugs Cation exchange resins orally or rectally exchange Na for K (Kayexelate). Give cautiously in HF.Cation exchange resins orally or rectally exchange Na for K (Kayexelate). Give cautiously in HF. Dialysis required with severe renal failureDialysis required with severe renal failure

40 ECG: Hyperkalemia Images.google.com

41 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)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/dLNormal Total Serum Ca is mg/dL Ionized Ca is mg/dL Important to measure serum albumin to determine if Ca levels reflect true deficiency.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])

42 42 Hypocalcemia Most common cause is chronic renal failure (decreased Vit D 3 and increased PO 4 ).Most common cause is chronic renal failure (decreased Vit D 3 and increased PO 4 ). –Hypoparathyroidism and malabsorbtion less common Signs/Sx: Increased excitation of nerve and muscle cells; cramps, tetany, paresthesias and convulsions. Signs/Sx: Increased excitation of nerve and muscle cells; cramps, tetany, paresthesias and convulsions. Chvostek’s sign, Trousseau’s signChvostek’s sign, Trousseau’s sign ECG: Prolonged Q-T interval/arrhythmiasECG: Prolonged Q-T interval/arrhythmias Serum Ca <9.0mg/dL (nl albumin), ionized Ca <4.5mg/dLSerum Ca <9.0mg/dL (nl albumin), ionized Ca <4.5mg/dL

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

44 44 Hypercalcemia Etiologies include hyperparathyroidism, malignancy (tumors produce PTH related proteins), milk-alkali syndrome (Ca antacids + Vit D excess).Etiologies include hyperparathyroidism, malignancy (tumors produce PTH related proteins), milk-alkali syndrome (Ca antacids + Vit D excess). Signs/Sx: Often without sx if mild  CaSigns/Sx: Often without sx if mild  Ca –Renal/GI: polyuria (H 2 O* 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.ECG findings: Shortened Q-T, PVC’s. Lab: increased Ca with nl. or low PO 4.Lab: increased Ca with nl. or low PO 4. *Sounds like?

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

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

47 47 Treatment of Hypomagnesemia Important to order Mg levels in hospitalized cardiac patients (AMI, CHF, etc.).Important to order Mg levels in hospitalized cardiac patients (AMI, CHF, etc.). IV therapy with MgSO 4, and monitor levels.IV therapy with MgSO 4, and monitor levels. Oral Mg oxide can be given for supplemental oral use.Oral Mg oxide can be given for supplemental oral use.


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