Turning on the Lytes
in Dialysis
DEBRA CASTNER RN, MSN, APRN, CNN
JERSEY COAST NEPHROLOGY & HYPERTENSION
BRICK, NJ
Objectives

List 2 electrolytes that are adjusted during dialysis

Describe common signs and symptoms of electrolyte shifts in people
on dialysis

Explain how to reduce recovery time after dialysis
So……………. WHAT ARE
ELECTROLYTES?
“Salts and minerals that can conduct electrical impulses in the body.
Common human electrolytes are sodium chloride, potassium, calcium,
and sodium bicarbonate. Electrolytes control the fluid balance of the
body and are important in muscle contraction, energy generation,
and almost every major biochemical reaction in the body.”
http://medical-dictionary.thefreedictionary.com/electrolytes
Why Electrolytes ?

Electrolytes are controlled by the kidneys and hormonally

Provide “electricity” within the body for transport of chemicals and
fluids

All higher forms of life need electrolytes to survive
Ions and Charges

Cations are positively charged ions ++++++

Anions are negatively charged ions - - - - - -
How Do We Apply Them in Dialysis
Hemodialysis
Peritoneal

Uses osmosis as main transport for fluid and solutes
Glu
c
Glu
c
Glu
c
Glu
c
Glu
c
Glu
c
AQP1
Glu
c
peritoneal
Glu
c
Glu
c
small
Glu
c
large
blood
Slide courtesy of Anjali Bahatt Saxena, M.D., Santa Clara Valley Medical Center.
What Lytes Do We Consider in
Dialysis ?

Potassium

Sodium

Calcium

Magnesium

Bicarbonate/Lactate

Glucose

Urea
What Lytes Will We Focus On
Today?

Potassium

Sodium

Calcium

Magnesium

Bicarbonate/Lactate

Glucose

Urea
Potassium







Major intracellular cation in the body
Associated with cardiac and muscle conduction, acid-base
balance, and enzyme reactions
Rapidly reducing potassium can effect the QT interval when
dialyzing a patient against a zero or 1mEq potassium bath
Low dialysate potassium concentration has been associated with
cardiac dysrhythmias, especially in patients receiving digitalis
preparations.
Low post potassiums may cause muscle cramping and fatigue
Higher pre potassium levels of 4.6-5.3 mEq/L have been associated
with better survival
Patients with predialysis potassium levels of less than 4.0 or greater
than 5.6mEq/L were associated with increased mortality
(Palmer, 2009)
Potassium Homeostasis
2 Mechanisms:

Excretion via kidney 90-95% over 6 to 12 hrs
and intestine 5 – 10%

Extracellular to Intracellular compartment shifts
Hypokalemia Causes
Potassium Removal During Dialysis
Hypokalemia vs Potassium
Deficiency/Depletion

Potassium deficiency cause by negative potassium balance, intake
is lower than excretion

Hypokalemia is induced from potassium deficiency or from ECF to
ICF shifts (ketoacidosis, catecholamine release during AMI,
hyperthyroidism)

Can have deficiency without hypokalemia ( low plasma measured
potassium level)
Primer on Kidney Diseases, 2009, Allon,M.
Hypokalemia S & S

Muscle weakness can lead to paralysis

Ileus

Urinary Retention

Inability to concentrate urine

Can lead to AV Block
Hypokalemia Treatment







Multiple small doses of potassium
Oral is safer than IV, not to exceed 40mEq/dose
IV dosing more likely to overcorrect, for levels <3.0meq
IV infusion not greater than 10mmol/hr if not on cardiac monitor, check
levels Q 2 to 3 hrs.
Higher potassium dialysate 3 or 4mEq
Diet instruction
CORRECT Cause
Primer on Kidney Diseases, 2009, Allon,M.
Hyperkalemia Causes

Pseudohypekalemia caused by in vitro release of potassium from
blood cells ( hemolysis, severe leukocytosis or thrombocytosis, “fist
clenching”)

True hyperkalemia caused by high intake, low excretion, or shift from
ECF to ICF ( ACE drugs in moderate CKD, potassium sparing
diuretics, acidosis )

Can occur from prolonged fasting in dialysis patients due to
increased insulin levels
Primer on Kidney Diseases, 2009, Allon,M.
Hyperkalemia S & S

Bradycardia then Ventricular arrhythmias

Muscle weakness as in hypokalemia

Tingling of lips and fingers

Intestinal cramping, diarrhea

LIFE Threatening
Risk Factors for Hyperkalemia

Dialysis dependent

Chronic Kidney Disease Stages 4 & 5 (CKD, eGFR < 30
ml/min/1.73m2)

Nephrotoxic medications (e.g. renin-angiotensin agents, nonsteroidal anti-inflammatory drugs)

Cardiac failure (e.g. renin-angiotensin agents)

Diabetes mellitus (e.g. renin-angiotensin agents, diabetic ketoacidosis)

Liver disease (e.g. spironolactone, hepato-renal failure) Adrenal
insufficiency
http://www.renal.org/guidelines/modules/treatment-of-acute-hyperkalaemia-in-adults#sthash.1D3sBbnO.dpuf
Step Wise Approach
Hyperkalemia Treatment
Recipe for Emergency Treament
1.
Calcium gluconate IV 10ml over 1 minute repeat in 3-5min. If no
improvement in EKG to stabilize the heart does not decrease K+
2.
IV Insulin 10 units in 50 ml of 50% dextrose bolus first then infusion of
5% dextrose at 100cc/hr NEVER dextrose without insulin, potassium
will decrease within 15 minutes
3.
20mg of Albuterol inhaled over 10 minutes, take 30 minutes to see
effect
4.
Sodium Bicarbonate in patients with residual kidney function only,
takes 3 – 4hrs for potassium to decline
5.
Then consider diuretics, kayexalate, hemodialysis
Progression of EKG Changes in
Hyperkalemia
http://www.renal.org/guidelines/modules/treatment-of-acute-hyperkalaemia-in-adults#sthash.1D3sBbnO.dpuf
EKG Changes
Other Treatment

Dialysate 1 or 2K

Diet instruction

Education for patient to understand risks

Careful interviewing to establish cause
Sodium

Major cation of dialysate and the extracellular compartment of
total body water

Associated with cardiac, neuro, muscle conduction, acid-base and
fluid balance

Dialysate sodium concentration lower than plasma sodium
concentration may induce intracellular movement of water and
plasma volume depletion.

Dialysate sodium concentration higher than plasma sodium
concentration may induce extracellular movement of water,
intracellular dehydration, and stimulation of thirst (Daugirdas, 2007)

NKF-KDOQI Clinical Practice Guidelines for Adequacy,(2006)
recommend that high dialysate sodium concentrations and sodium
profiling be avoided.
Hyponatremia

Occurs in 15 – 20% of hospitalized patients

Elderly are most susceptible

Acute cases impact negatively on M&M

Rapid correction can lead to severe neuro deficits

High glucose levels will give false low sodium
CORRECTION: 1.6 meq per each 100 mg/dL glucose above 100 add
that number to serum sodium
So if glucose is 300 and sodium was 130 it actually 133.2
Primer on Kidney Diseases, Verbalis, 2009
Hyponatremia Evaluation
Hypernatremia







Ability to excrete sodium loads can be impaired in kidney disease
Defined as serum sodium over 146mEq/L
Mostly seen in patients who have been restricted access to fluids or
impaired thirst signals
Sodium cannot freely cross into cells
Always a “water problem”
Hypernatremia = Hyperosmolar
Associated with insulin resistance
Primer on Kidney Diseases, Dennen & Linas, 2009
Contemporary Nephrology Nursing Principles and Practice, Molzahn, 2006
Hypernatemia Causes

Hypovolemia/Euvolemic: GI, kidney, or skin, no access to water

Hypervolemia: Intravenous solutions or tube feedings,
hypoaldosterism
Contemporary Nephrology Nursing Principles and Practice, Molzahn, 2006
Hypernatremia S&S

Thirst

Dry mucous membranes, N/V

Flushed skin, fever, oliguria

Irritability, lethargy, altered LOC, seizures

OR No Signs
Sodium Correction



Cannot be done quickly
Too fast a correction can lead to more issues than the disorder
Abnormally high or low sodiums are associated with M&M in CKD
patients (Kovesdy, 2012 Circulation)
Low Sodium
0.5 – 2mEq/L per hour no more than 12mEq/l in frst 24 hours 18mEq/l
over first 48hours of correction
High Sodium
0.5mEq/l per hour, or a decrease of 10 – 12mEq/l in a 24 hour period
Primer on Kidney Diseases, Verbalis,;, Dennen & Linas,, 2009
Sodium Variation: Is it the Right
Approach?
Calcium

Cation associated with bone formation, neuromuscular transmission,
enzyme and intracellular reactions

Bound to plasma proteins (50%)

99% found in bone, 0.9% ICF, 0.1% ECF

Kept in range by GI tract, skeleton, and kidneys

Calcium level is a poor reflection of “true” body calcium

40% available as ionized, the active form
Hypocalcemia Causes

Decreased intake or poor absorption, malabsorption states

Urinary losses

Decreased availability: alkalosis, multi-transfusions, low albumin

Medications: biphosphates, calcitonin, citrated blood, mithramycin

Vitamin D deficiency, hypoparathyroidism

Sepsis
CORRECTION: Add 0.8mg/dL to the ionized calcium for every 1mg
decrease in albumin below 4
So, if albumin is 3, a calcium of 7.8 would be 8.8
Hypocalcemia S&S

Peri-oral numbness or tingling (parasthesias)

Spasms of hands and feet

Intestinal cramping, increased bowel sounds

Tetany, seizure, laryngospasm

Chvostek’s Sign (tap TMJ watch for grimace)

Trousseau’s Sign ( BP cuff x 3 min. watch for hand spasm)
Treatment of Hypocalcemia
Hypercalcemia Evaluation/Causes
Medications:
Vitamin D or A
lithium, thiazides
Hypercalcemia S&S

Severity depends on degree and rate of increase

GI: N/V, constipation, abdominal pain

Neuro: altered mentation, fatigue, muscle weakness

Renal: sodium wasting due to increased urine output
Most Common Causes (80%) are
HYPERPARATHRYOIDISM OR MALIGNANCY
Hypercalcemia Treatment

Remove cause

Fluids & diuretics

IV Biphosphonates (Aredia, Reclast)

Calcitonin

Glucocorticoids

Cinacalcet
EKG Changes
Magnesium

An abundant intracellular cation, 60- 64% is stored in bone

Bound to ATP, ADP, mitochondria, proteins, nucleic acids and
doesn’t move freely to ECF

Absorbed through the small intestine

95% excreted via kidney
Hypomagnesemia S & S/Causes
How It Happens Medications: amphotericin B,
aminoglycosides, cisplastin,
CSA, Prograf, PPI’s, diuretics.
Associated with low K/CA
GI Losses, malnutrition,
alcoholism, gastric bypass,
pancreatitis, ketoacidosis.
Hypomagnesemia treatment
EKG Changes
Hypermagnesemia S & S
Hypermagnesemia Treatment

Remove cause
magnesium containing medications
Laxatives
Antacids
Herbal Remedies
Dialysis
 IV calcium can temporarily shift Mg

Bicarbonate/Lactate/Acetate

Polyatomic anion

A buffer that helps maintains pH of the ECF

Normal pH is 7.35-7.45

Kidney produces and regulates it in the proximal tubule by excretion
or reabsorption. Also produced in the pancreas.

70-75% of CO2 in the body is converted into carbonic acid (H2CO3),
which is turned into bicarbonate

We add it to dialysate based on CO2 levels of patient

Goal is pre dialysis CO2 of 22-24

Use caution with bicarbonate dialysate >35mEq (Handbook of Dialysis 2007)
Metabolic Acidosis

Acids are extracted from dietary carbohydrates and fats which
yields carbon dioxide and water

The lower the pH the worse the acidosis

In renal failure patients become acidotic because hydrogen ions
cannot be excreted and bicarbonate production / reabsorption is
impaired

High pre CO2 levels can indicate inadequate dialysis

Other causes of acidosis: sepsis, starvation, diarrhea, overdoses of
salicylates, ethylene glycol, or methanol
Metabolic Acidosis S & S
Metabolic Alkalosis

Rare in renal disease

Alkalosis is more dangerous to renal patients than acidosis, can lead
to soft tissue calcification, nausea, lethargy and H/A

Mild alkalosis can lead to hypoventilation
(Handbook of Dialysis, 2007)
Relative Risks Associated with K and
Bicarbonate levels – FMC Study 2011
http://graphic8.nytimes.com/packages/pdf/business/fresenius-memo.pdf
Metabolic Alkalosis
Treatment of
Metabolic Acid – Base Disorders

Identify cause

Adjust dialysate

May need to add oral medication

Trend out CO2 levels every month and call for adjustments

Correct severe imbalances gradually
Glucose

In dialysate not used to adjust serum glucose but to avoid
hypoglycemia
Urea

A marker solute for clearance of toxins

Not of itself toxic

Serum levels depend on rate of removal and generation rate

Low levels associated with malnutrition

Post dialysis rebound for urea is highest for smaller patients

Rapid removal associated with Disequilibrium Syndrome (urea >125)
(Daugirdas, 2007)
Fluid Removal

Changes occur in microcirculation before you see hypotension or
other S&S

Dialysis in general is an inflammatory procedure with release of
bradykinins and nitric oxide
Ultrafiltration Rates & Mortality

High UF rates are associated with higher mortality and
hospitalization rates

UF Rates of 10-13ml/kg/hr have statistical significance in pts with HF
N = 1846 Hemodialysis Study: 7 year trial

All pts had risk increase (all-cause and CV) when compared from
lowest group to highest group
Flythe et al, 2011
Recovery Time
How Long Does It Take You To
Recover From A Dialysis Session ?
Recovery Time & Quality of Life
N = 6,040 DOPPS data

32%
less than 2hrs

41%
2 – 6hrs

17%
7 – 12hrs

10%
Longer than 12hrs
There is a correlation of improved QOL with lower recovery time.
Longer recovery time associated with admissions, mortality and poor
QOL
Rayner et al, 2013, AJKD published online February 2013
Adverse Effects of Intradialytic
Hypotension

Life-threatening consequences

Impaired tissue perfusion can lead to inaccurate adequacy

Contributes to loss of residual renal function

Can cause cerebral ischemia
Core Curriculum for Nephrology Nursing, 5th ed. 2008
Cerebral Ischemia

Cerebral blood flow is reduced during dialysis

It gets lower with increased UF

Cerebral compensation is less effective with advanced age,
hypertension, inflammation, vascular injury

Rapid increase in bicarbonate can reduce CBF and increase
cerebral edema

Neuroimaging confirms brain changes in renal patients occurring
within months of starting dialysis Davenport, 2014

There is a link with higher pre dialysis BP and survival
Robinson et al 2012
130-159
Cardiac Stunning
‘delayed recovery of regional myocardial contractile function after
reperfusion despite the absence of irreversible damage and despite
restoration of normal flow’. Braunwald and Kloner , 1982
HD-induced myocardial stunning is common and could be the
predisposing element leading to the increased prevalence of heart
failure and increased mortality in CKD patients with ESRD. Breidthard, 2011
Mechanism of Cardiac Stunning

Loss of high-energy phosphates, impaired microvascular perfusion,
impaired sympathetic neural responses, reactive oxygen species,
leukocyte activation, and disturbances in calcium homeostasis

At the cellular level reactive oxygen species, thrombosis,
ischemia/reperfusion injury, microvascular dysfunction, and
channelopathies may contribute to myocardial stunning

Two main metabolic pathways leading to myocardial stunning
include calcium overload and reactive oxygen species (ROS)
generation.

Cardiac stunning = Sudden Death
Myocardial Stunning with Hemodialysis: Clinical Challenges of the
Cardiorenal Patient, Zuidema et al, 2012
Cardiorenal Med. May 2012; 2(2): 125–133.
Published online Mar 30, 2012. doi: 10.1159/000337476
ANNA Scope and Standards for Care:
Hemodialysis Treatment and Equipment
Related Complications
The patient will:

Receive appropriate and safe HD treatment

Be free of treatment/equipment-induced complications………..
Gomez, N. 2011
Practice Pearls

Always LOOK at the patient

Scan your environment

Communicate

Compare historical measures when “numbers” or “readings”
don’t fit the patient

Your patient chart is your friend

Always “error” on the side of patient safety
Case Study

Joe is an active HD patient enjoying family parties and frequent
travel. He reports feeling “lousy” after dialysis lately and it is taking a
whole day to recover.
He is on:
1K, 138mEq, bicarb 38, sodium 142, glucose 100, Mg 0.8, Dialysate
His labs are:
K 5.5, CO2 27, sodium 137, Mg 2.5

What could be causing issues for this patient?

What would you review to help plan a strategy?
So What Have We Learned?

Fast is not always better

Using lab results and patient trending can help make dialysis more
comfortable for our patients

Recovery Time is linked to QOL
Questions, Comments?