Electrolytes and Shock
Janis Rusin APN, MSN, CPNP-AC
Pediatric Nurse Practitioner
Lurie Children’s Transport Team
Objectives
• Discuss the function of each of the following electrolytes;
sodium, potassium, magnesium, calcium and phosphorus
• Discuss the causes of electrolyte derangements
• Discuss the definition and management of compensated and
decompensated shock
• Discuss the types of shock
• Identify the interventions on transport to manage electrolyte
derangements and shock
2
Body Fluids and Total Body
Water
• Bodily fluids are divided between two compartments
– Intracellular Fluid (ICF)-Fluid within the cells
– Extracellular Fluid (ECF)-All the fluid outside of the cells including the
bloodstream
• Subdivided into Interstitial and Intravascular Fluids
• Water travels back and forth between these compartments
• Primarily driven by osmosis
• The integrity and proper functioning of the cell membranes
also contribute to the movement of water
• The amount of the fluid in both compartments together is
referred to as the Total Body Water (TBW)
3
Total Body Water
• Infants have the highest percentage of TBW
• Adults have the least
• The higher the percentage of body fat, the lower the
percentage of TBW
• Males have more TBW than females
Body Type
TBW%
TBW%
TBW%
Adult Male
Adult Female
Infant
Normal
60
50
70
Lean
70
60
80
Obese
50
42
60
4
Electrolytes
• An electrolyte is an element or compound that when
dissolved in water dissociates into ions and conducts an
electrical current
• Sodium primarily exists in the ECF and maintains the osmotic
balance of the ECF
• Potassium primarily exists in the ICF and maintains the
osmotic balance of the ICF
• These two electrolytes tend to repel each other.
• If one increases in one space the other will be driven to the
opposite space
• Water follows salt
5
Sodium
• My Favorite condiment!
• Maintains the osmolality of the ECF
• Interacts with potassium and calcium to maintain electrical
nerve impulses
• Sodium balance is regulated by the hormone Aldosterone
• Aldosterone:
– Produced by the adrenal cortex
– Acts on the distal tubule to reabsorb Na and H2O
– Potassium is then excreted from the Distal tubule
6
Sodium Imbalance
• Hypernatremia
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Serum Na > 147mEq/L
Dehydration/hypovolemia
Diabetes Insipidus
Hyperaldosteronism
• Hypertension
– Iatrogenic
• Excessive administration of hypertonic saline solutions
– Cushings syndrome
• Increased secretion of ACTH
• Also stimulates aldosterone production
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Hypernatremia
• Symptoms
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Thirst
Dry mucous membranes
Weight loss
Concentrated urine (except in DI)
Tachycardia
Hypotension-due to volume depletion
• Management
– Determine the cause
– Rehydrate with isotonic free water solution
• D5W
– Monitor Na levels closely
8
Hyponatremia
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Serum Na < 135mEq/L
Diuretics
SIADH
Dilutional hyponatremia
– Excess water intake
– Dilution of infant formula
– Administration of mannitol
• Causes osmolar shifts of free water into cells leading to
cellular edema
• Symptoms:
– Lethargy, Headache, Seizures, Weight gain, Edema, Ascites
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Hyponatremia
• Management
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Determine the cause
Fluid restrictions
Sodium correction with hypertonic solution (3% NaCl)
Determine the sodium deficit and replaces slowly
Symptomatic patients
• Replace 3-5 mEq/L/hr
– Asymptomatic patients
• Replace 0.5-1 mEq/L/hr
– Na deficit = (0.6) X Wt (kg) X (Na-goal – Na-actual)
10
Sodium correction
• Patient with serum sodium of 125 mEq/L who weighs 20 kg
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0.6 X 25 X (136 – 125) = 165 mEq/L
3% Saline contains 513 mEq/L which is 0.513 mEq/ml
Replace 5mEq/L/hr
165 divided by 5 = 33 hours
5mEq/hr divided by 0.513mEq/ml = 9.7 ml/hr for 33 hours
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Potassium
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Major intracellular electrolyte
Maintains ICF osmolality
Maintains the resting cell membrane potential
Along with Na, contributes to the electrical conduction of
nerve impulses in cardiac, skeletal and smooth muscle
12
Hyperkalemia
• Serum K level > 5.5 mEq/L
• Often caused by movement of K from the ICF to the ECF
– Cellular trauma
• Burns, Crush injuries
– Acidosis
• H ions shift into the cells and K shifts out
– Change in cell membrane permeability
– Insulin deficiency
– Renal failure
13
Hyperkalemia
• Management
– Calcium Gluconate stabilizes cell membranes in the presence of
dangerously high K levels
• Should be given to prevent cardiac arrhythmias while K is being
corrected
– Administration of glucose and insulin
• Glucose stimulates insulin production
• Insulin drive K back into the cell
– Sodium Bicarbonate
• Correction of metabolic acidosis
– Rectal cation exchange resins
• Kayexalate
• Not a popular treatment on transport 
14
Magnesium
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Major intracellular ion
Mostly stored in muscle and bone
Very small amounts in the serum
Contributes to intracellular enzyme reactions
Protein synthesis
Neuromuscular responsiveness to electrical impulses
15
Magnesium
• Hypermagnesemia
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Mg > 2.5mEq/L
Renal Failure
Excess ingestion of Mg antacids
Depressed contraction of skeletal
muscles
Depressed nerve function
Hypotension
Bradycardia
Respiratory depression
• Hypomagnesemia
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Mg < 1.5 mEq/L
Malnutrition/malabsorbtion
Alcoholism
Diuretics
Metabolic acidosis
Increased neuromuscular excitability
Tetany
Ataxia
Nystagmus
Seizures
16
Calcium
• Primarily (99%) located in the bone
• In serum, 50% is bound to proteins, 40% is in the
free/ionized form
• Major cation for the maintaining the structure of bones and
teeth
• Contributes to blood clotting
• Maintains plasma membrane
stability and permeability
• Contributes to muscle contraction and
nerve impulses
17
Phosphate
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•
•
•
Also found primarily in bone
Exists in cells as creatanine phosphate and ATP
Provide energy for muscle contration
Acts as an intracellular buffer to maintain acid base balance
within the cell
18
Calcium and Phosphate
• They have a synergistic relationship
• If the concentration of one increases, the other decreases
• They are regulated by parathyroid hormone, vitamin D and
calcitonin
• Parathyroid (PTH) is sensitive to Ca levels
• When Ca levels are low, PTH is stimulated
• PTH stimulates the kidney to reabsorb Ca and excrete PO4
• The kidney also activates Vitamin D which stimulates the
absorbtion of Ca from the small intestine
• Vitamin D also enhances bone absorption of Ca
• In renal failure, Vitamin D is not activated, Ca decreases and
PO4 increases
19
Calcium
• Hypocalcemia
• Serum Ca < 8.5 mg/dl
• Nutritional deficiencies
– Inadequate Ca or Vit D intake
• Decreased PTH
• Symptoms
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Confusion
Parasthesia’s
Muscle spasms to hands and feet
Hyperreflexia
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Hypercalcemia
Ca > 12 mg/dl
Hyperparathyroidism
Bone Metastasis
Excess Vitamin D
Symptoms
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Fatigue/weakness
Bradycardia and heart block
Lethargy
Anorexia
Nausea
Constipation
Kidney stones
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Phosphate
• Hyperphosphatemia
• PO4 > 4.5mg/dl
• Chemotherapy resulting in cell
destruction
• Hypoparathyroidism
• Symptoms
– Same as Hypocalcemia
– Chronically, calcification of lungs,
kidneys and joints
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Hypophosphatemia
PO4 < 2.0
Intestinal malabsorption
Vitamin D deficiency
Alcohol abuse
Hyperparathyroidism
Symptoms:
– Decreased cellular metabolism
– Reduced capacity for oxygen
transport (requires ATP)
– Bradycardia and MI
– Clotting disorders
21
Shock
• Shock is defined as an abnormal condition of inadequate
blood flow to the body tissues, with life threatening cellular
dysfunction
• Basically it is supply and demand: O2 supply is down and
demand is up
• Remember: CO = HR X SV
• Oxygen delivery to the tissues is the product of cardiac output
and the oxygen content of arterial blood
• Mortality rate varies from 25-50%
• Most patients do not die in the initial stages
22
Shock
• Primary cardiac arrest in infants and children is rare
• Pediatric cardiac arrest is often preceded by respiratory failure
and/or shock and it is rarely sudden
• Early intervention and continued monitoring can prevent
arrest
• The terminal rhythm in children is usually bradycardia that
progresses to PEA and asystole
• Septic shock is the most common form of shock in the
pediatric population
• 80% of children in septic shock will require intubation and
mechanical ventilation within 24 hours of admission
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Organ System Involvement
• Cellular
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Decreased perfusion leads to anaerobic cellular metabolism
Increased lactic acid production: metabolic acidosis
Increased permeability of cell wall
Fluid shifts
Activation of clotting cascade (DIC)
Failure of the Na/K pump
Impaired glucose delivery
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Organ System Involvement
• Cardiac:
– Decreased preload
– Decreased cardiac output
– Decreased systemic vascular
resistance
– Decreased coronary blood flow
– Cardiac ischemia
– Arrhythmias
– Progressive heart failure occurs
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Organ System Involvement
• Respiratory:
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Increased permeability to fluid shifts
Pulmonary edema
Decreased O2 transport
Hypoxia
Acidosis
Lung damage: ARDS
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Organ System Involvement
• Renal
– Decreased renal blood flow
– Renin-Angiotension system kicks in
– Aldosterone causes Na and water
retention
– Persistent decreased renal perfusion
leads to kidney failure
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Organ System Involvement
• Neurologic
– Cerebral perfusion decreases
– Patient becomes obtunded
– Vasomotor area of the brain
becomes less active
– Vascular tone cannot be maintained
– Vascular collapse occurs
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Types of Shock
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Hypovolemic
Cardiogenic
Obstructive
Distributive
– Septic
– Neurogenic
– Anaphylactic
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Hypovolemic Shock
• Occurs from loss of blood or
body fluid volume from the
intravascular space
• Traumatic injury
• Vomiting or diarrhea
• Classes of hemorrhage:
• Class I: <15% blood loss
• Class II:15-25%
• Class III: 26-39%
• Class IV: >40%
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Cardiogenic Shock
• Pump Failure
• Inability of the heart to
maintain adequate cardiac
output
• SVT, arrhythmias,
• Cardiomyopathy
• Support ABC’s
• Treat the cause
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Obstructive Shock
• Inadequate cardiac output due
to an obstruction of the heart or
great blood vessels
• Cardiac tamponade
• Tension Pneumothorax
• Mediastinal mass
• Support ABC’s, but fluids may
not be the best option. The
obstruction must be relieved
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Distributive Shock
• Septic shock
• Systemic infection as evidenced
by a positive blood culture
• Patient in early septic shock will
have bounding pulses and warm
extremities
• Also known as warm shock
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Distributive Shock
• Septic shock:
– Bacterial organisms release toxins, which results in an
inflammatory response and cellular damage
– Massive vasodilation-sometimes called “warm shock”
– Increased capillary permeability
– Fluid shifts to extracellular space
– Hypotension may not respond to fluid resuscitation
– Inotropic support
– 80% of children in septic shock will require intubation and
mechanical ventilation within 24 hours of admission
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Distributive Shock
• Neurogenic shock:
– Severe head or spinal injury
– Decreased sympathetic output from the CNS
– Decreased vascular tone
• Anaphylactic shock:
– Antibody-antigen reaction stimulates histamine release
– Histamine is a powerful vasodilator
– Loss of vascular tone
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Treatment of Shock
• Early goal directed treatment improves outcomes
– Needs to begin with the local emergency departments and continue
with the transport team
– Early aggressive interventions to reverse shock can increase survival by
9 fold if proper interventions are done early!
– Hypotension and poor organ perfusion worsens outcomes
• Shock can progress very quickly into refractory shock which is
irreversible
• Airway and Breathing
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Have suction and airway adjuncts available
100% O2 until more stable, then weaning can begin
Assess breathing effectiveness
If patient cannot protect their own airway, intubate!
Intubate for GSC of 8 or less!
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Treatment of Shock
• Circulation
– Venous access: Ideally 2 large bore IV’s
• Fluid resuscitation: 20ml/kg bolus of NS or LR
• Reassess patient after each bolus
• Convert to blood bolus if patient is bleeding
– Saline cannot carry oxygen
• Inotropic support for hypotension that persists despite fluid
resuscitation-Beware of catecholamine resistant shock!
• Treat hypothermia
• Correct F/E imbalances
• Find the cause and fix it!
• Dextrose
– Treat hypoglycemia and monitor closely
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Case Study
• 8 week old infant s/p cardiac
arrest at home
• Paramedics initiated CPR and
continued CPR for 10
minutes until arrival in ED
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Phone call
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Patient arrived in ED with CPR in progress
Intubated with 3.0 ETT and being bagged
Epinephrine given X 2
Atropine given X 2
Heart rate resumed
Sodium Bicarb given X 2
Vent settings: FiO2 1.0, Rate 40, PIP 20 PEEP 3
Pupils 3mm and sluggish
Cap refill 5 seconds
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Case Study-On arrival
Current vitals: HR-140 RR-40 BP-52/11 Temp- 90F
Vent settings: FiO2 1.0, Rate 40, PIP 20 PEEP 3
Cap refill 5 seconds
ABG 6.93/74.4/259/14.8/-16.9
2 tibial IO’s in place bilaterally and one PIV with maintanance
and dopamine infusing at 5 mcg/kg/min
• Glucose-47, K-7.0 non-hemolyzed
• Succinylcholine given by ED staff but patient with gasping
respiratory effort
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Case Study-Interventions
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Re-tape and pull back ETT 1 cm
Increase PEEP to +5
Sedation with Fentanyl 1-2 mcg/kg
Treat hypoglycemia-2ml/kg of D10W
Provide adequate paralysis with pavulon
Give Calcium Chloride-Why?
Give dextrose to increase accucheck to 100, then give regular
insulin 0.1u/kg-Why?
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Case Study-What happened?
Patient sedated and paralyzed appropriately
CaCl and bicarb given as ordered
Recheck of accucheck after dextrose =112
Insulin given as ordered
Accucheck dropped to 42 so D10W repeated
One IO was infiltrated so new PIV started
Repeat ABG 6.94/92.1/233/18.8/-13.1
BP dropped after pavulon, so dopamine titrated up-to
20mcg/kg/min
• Pt diagnosed with Influenza
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Questions?
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