Electrolyte imbalance

Serum sodium
Hyponatremia <135meq/l

Normal (135-145 meq/l) Hypernatremia

> 145 meq/l

Regulation of Sodium

It is affected by hormones: Aldosterone Renin/angiotensin Atrial Natriuretic Peptide (ANP) ADH

Serum sodium
Hyponatremia Normal (135-145 meq/l) Hypernatremia <135meq/l > 145 meq/l

Causes of hyponatremia Hypovolaemic Hyponatraemic states

Diuretic therapy.

Mineralocorticoid deficit (Addison's disease). GIT losses (diarrhea or vomiting). Fluid loss in third space (peritonitis, burn).

Na

H2O

Euvolaemic (Normal volume) Hyponatraemic States:

Hormonal (Myxoedema, glucocorticoid deficiency). Massive water load (psychogenic polydipsia, parenteral fluid). Syndrome of inappropriate secretion of ADH (SIADH):
H2O

Hypervolaemic (oedematous) Hyponatraemic states

Liver cirrhosis Congestive heart failure. Nephrotic syndrome Renal failure with water overload.
Na H2O

Treatment Modalities
All forms of restriction. hyponatremia will respond to water

Primary polydipsia Renal failure: Dialysis Volume depletion: Normal saline Thyroid, cortisol: replacement SIADH Asymptomatic/chronic: Acute/Mental Hypertonic saline

Major Intravenous Solutions

Name D5W Content 5% Dextrose Water 300 mOsm NaCl 150 mM (0.9%) 280 mOsm 2/3 D5W: 1/3 Isotonic Saline Distribution ICF: ECF 2 : 1

Isotonic (normal) Saline

ECF 100%

2/3:1/3

ICF:ECF 1:1 440: 550

Major Intravenous Solutions

Name Half-Normal Saline Contents NaCl 75 mM 0.45% 140 mOsm Distribution ICF: ECF 1 : 2

Hypertonic Saline

NaCl 450 mM ECF 3% NaCl 840 mOsm 100% Water shifts from ICF

Strategies for Safe Correction of Hyponatremia

General principle:
-Do not exceed 10-12 mEq/L rise in PNa in first 24; and 20 mEq/L rise in PNa after 48 - If seizures or severe neurological abnormalities present, then correct more rapidly initially.

Danger of rapid correction

Central Pontine Myelinolysis (osmotic demyelination)

A 56 years old female patient coming to ER complaining

from 3 days of persistent watery diarrhea.

By examination she was conscious with BP 110/70 and heart rate 90/min week pulse, dry tongue, sunken eyes. Serum Na 118 meq/l (135-142) Serum K 3.1 meq/l (3.5-5.5) S. creatinine 1.7mg/dl, (0.8-1.3) blood urea 70 mg/dl (20-40)

She was treated by Normal saline solution 0.9%

Causes of hyponatremia Hypovolaemic Hyponatraemic states

Diuretic therapy.

Mineralocorticoid deficit (Addison's disease). GIT losses (diarrhea or vomiting). Fluid loss in third space (peritonitis, burn).

Euvolaemic (Normal volume) Hyponatraemic States:

Hormonal (Myxoedema, glucocorticoid deficiency). Massive water load (psychogenic polydipsia, parenteral fluid). Syndrome of inappropriate secretion of ADH (SIADH):

Hypervolaemic (oedematous) Hyponatraemic states

Liver cirrhosis Congestive heart failure. Nephrotic syndrome Renal failure with water overload.

Case A 71 year old woman presented with fatigue

and forgetfulness over last 2 weeks. She is known Hypertensive on thiazide diuretics. Physical exam: Systolic BP drop > 20mmHg on standing. Serum Na:119meq/l Serum potassium 3.1meq/l Blood urea 55 mg/dl S creatinine 1.5 mg/dl (135-142) (3.5-5.5) (25-40) (0.8-1.3)

Causes of hyponatremia Hypovolaemic Hyponatraemic states

Diuretic

therapy.

Mineralocorticoid deficit (Addison's disease). GIT losses (diarrhea or vomiting). Fluid loss in third space (peritonitis, burn).

Euvolaemic (Normal volume) Hyponatraemic States:

Hormonal (Myxoedema, glucocorticoid deficiency). Massive water load (psychogenic polydipsia, parenteral fluid). Syndrome of inappropriate secretion of ADH (SIADH):

Hypervolaemic (oedematous) Hyponatraemic states

Liver cirrhosis Congestive heart failure. Nephrotic syndrome Renal failure with water overload.

Case A 65 year old man with history of chronic

heavy cigarette smoking. He was admitted with unresponsiveness over last two days. Physical exam is normal. Normal CT brain. Normal sugar/urea, s.creatinine. 1.3 mg/dl. PNa+ = 115.

Causes of hyponatremia Hypovolaemic Hyponatraemic states

Diuretic

therapy.

Mineralocorticoid deficit (Addison's disease). GIT losses (diarrhea or vomiting). Fluid loss in third space (peritonitis, burn).

Euvolaemic (Normal volume) Hyponatraemic States:

Hormonal (Myxoedema, glucocorticoid deficiency). Massive water load (psychogenic polydipsia, parenteral fluid). Syndrome of inappropriate secretion of ADH (SIADH):

Hypervolaemic (oedematous) Hyponatraemic states

Liver cirrhosis Congestive heart failure. Nephrotic syndrome Renal failure with water overload.

A Typical Nephron

ADH

Human Anatomy, 3rd edition Prentice Hall, 2001

Hypertonic saline- dose calculation

Current PNa+ = 115 Target PNa+ = 125 Na+deficit= 10 meq/liter

Infusion on 10/0.5 = 20
Total body Na+ deficit= 5 x total body water = 10 x 0.6 x body wt (75kgs) =500 Amount of 3% NaCl needed (Na=513meq/L)= 1000ml Rate of infusion=500/ 20=50ml/hour

Pathogenesis of Hypernatremia
Decreased free water supply Water loss Osmotic diuresis, D.I. Osmotic diarrhea Solute load

Serum Potassium
Normal (3.5-5.5 meq/l)
Hypokalemia < 3.5 meq/l

Hyperkalemia > 5.5 meq/l

Hyperkalaemia
It is plasma K+ concentration which is more than 5.5 mmol/litre. A- Increased Potassium Intake Dietary excess (Banana, citrus fruits...) Intravenous load with K+ containing fluids B- Shift of Intracellular K+ to extracellular Acidosis Cell damage (cancer chemotherapy). Convulsions, myositis

Compartment

C- Decreased excretion of K+ by the kidneys Renal failure Mineralocorticoid deficiency Drug interference as ACEI and K+ sparing diuretics. D- Factitious: Haemolysis of blood sample

ECG tracing in hyperkalaemia may show:

Tall T waves Prolongation of the PR interval Widening of the QRS complex Finally cardiac arrest in diastole

ECG Changes
Note the tented or pinched shape to Twaves

Code Blue

Treatment of Hyperkalemia

Antagonism of membrane action

Intravenous calcium

Intracellular shift
Insulin (Dextrose) NaHCO3 -2 agonists

Removal
Diuretics Cationexchange resin Dialysis

Treatment:
A- Immediate correction (Emergency) of hyperkalaemia
Caclium gluconate slow I.V. (5ml of 10% solution) } It acts as a Physiologic anatagonist of K+ on cardiac cell membrane Correct acidosis with I.V. NaHCO3 8.4%(25 100ml) B adrenergic agonists(e.g. salbutamol) 50 ml of I.V. 50% glucose 20 units soluble insulin every 30 min.

Shift K+ into cell

B- Increase renal excretion of K+

Diuresis with saline and furosemide

C- Potassium exchange resin

e.g. sorbosterit They will increase faecal K+.

D- Dialysis:
Preferably K+ low Dialysate haemodialysis for patients with renal failure. The condition is considered medical emergency if ECG abnormalitiesare present.

50 year old male with type 2 DM/ chronic kidney disease has been prescribed an ACEI (Capotopril) for HTN. He presents to the ER with marked flaccid weakness of both lower limbs.

Labs Serum Na 136 Serum K 7.4 Serum creatinine 2.0

(135-142) (3.5-5.5) (0.8-1.2)

Hyperkalaemia
It is plasma K+ concentration which is more than 5.5 mmol/litre. A- Increased Potassium Intake Dietary excess (Banana, citrus fruits...) Intravenous load with K+ containing fluids B- Shift of Intracellular K+ to extracellular Acidosis Cell damage (cancer chemotherapy). Convulsions, myositis C- Decreased excretion of K+ Renal failure Mineralocorticoid deficiency

Compartment

by the kidneys

Drug interference as ACEI and K+ sparing diuretics. D- Factitious: Haemolysis of blood sample

50 year old male with type 2 DM/ chronic kidney disease has been prescribed an ACEI (Capotopril) for HTN. He presents to the ER with marked flaccid weakness of both lower limbs.

Labs Serum Na 136 Serum K 7.4 Serum creatinine 2.0

(135-142) (3.5-5.5) (0.8-1.2)

Treatment of Hyperkalemia

Antagonism of membrane action

Intravenous calcium

Intracellular shift
Insulin (Dextrose) NaHCO3 -2 agonists

Removal
Diuretics Cationexchange resin Dialysis

A 54 years old female with chronic renal failure and stopped hemodialysis for 1 week because of closure of her AV fistula. He presents to the ER with marked dyspnea, orthopnea, and bradycardia 45/min. Labs Serum Na 136 (135-142) Serum K 7.4 (3.5-5.5) Serum creatinine 2.3 (0.8-1.2)

A 54 years old female with chronic renal failure and stopped hemodialysis for 1 week because of closure of her AV fistula. He presents to the ER with marked dyspnea, orthopnea, and bradycardia 45/min. Labs Serum Na 136 (135-142) Serum K 7.4 (3.5-5.5) Serum creatinine 2.3 (0.8-1.2)

Hemodialysis

45 year old female with type 2 DM and HTN. She presents to the ER with marked tachypnea, dehydration, BP 110/60 .
Labs Random blood glucose 540 mg/dl Acetone in urine Blood gases PH 7.12 pO2 98, pCO2 Serum Na 138 (135-142) Serum K 6.5 (3.5-5.5) Serum creatinine 1.6 (0.8-1.2)

22, Hco3 9.0

DKA

HypokalemiaDecrease intake(never alone)

Intracellualar Shift 1. Treatment with insulin 2. Alkalosis 3. -2 stimulation

Increased Excretion 1) GI 2) Renal 3) Hyperaldosteronism 4) Diuresis 5) Ampho-B 6) Hypomagnesemia

Clinical Consequences of hypokalemia Cardiac arrhythmias Muscle weakness Rhabdomyolysis Renal dysfunction Glucose intolerance

Hypokalemia-Treatment
Estimate of deficit is difficult
~100-200 meqfor 1 meq/liter

PO therapy usually adequate

IV therapy if severe/symptomatic
Max conc. 40meq/liter Max rate 20meq/hour Use in saline (not dextrose)

Case
A 58 yr old cirrhotic is admitted with worsening ascites - Meds: Lasix40mg bid, Lactulose - EKG: Unifocal VPCs, prominent U waves -Admission labs: Na 125 Bl glucose 87 K 2.2 Urea 40 creat 2.0
How would you treat her hypokalemia?

Thanks