Electrolytes and ShockJanis Rusin APN, MSN, CPNP-ACPediatric Nurse PractitionerLurie 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

4

Body Type TBW% TBW% TBW%

Adult Male Adult Female Infant

Normal 60 50 70

Lean 70 60 80

Obese 50 42 60

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

– 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

7

Hypernatremia• Symptoms

– 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• 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

9

Hyponatremia• Management

– 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

• 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

11

Potassium• 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• 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

– Mg > 2.5mEq/L– Renal Failure– Excess ingestion of Mg antacids– Depressed contraction of

skeletal muscles– Depressed nerve function– Hypotension– Bradycardia– Respiratory depression

• Hypomagnesemia– 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• 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

– Confusion– Parasthesia’s – Muscle spasms to hands and

feet– Hyperreflexia

• Hypercalcemia• Ca > 12 mg/dl• Hyperparathyroidism• Bone Metastasis• Excess Vitamin D• Symptoms

– Fatigue/weakness– Bradycardia and heart block– Lethargy– Anorexia– Nausea– Constipation– Kidney stones

20

Phosphate• Hyperphosphatemia• PO4 > 4.5mg/dl• Chemotherapy resulting in

cell destruction• Hypoparathyroidism• Symptoms

– Same as Hypocalcemia– Chronically, calcification of

lungs, kidneys and joints

• 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

23

Organ System Involvement• Cellular

– 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

24

Organ System Involvement• Cardiac:

– Decreased preload– Decreased cardiac output– Decreased systemic vascular

resistance– Decreased coronary blood flow– Cardiac ischemia– Arrhythmias– Progressive heart failure occurs

25

Organ System Involvement• Respiratory:

– Increased permeability to fluid shifts

– Pulmonary edema– Decreased O2 transport– Hypoxia– Acidosis– Lung damage: ARDS

26

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

27

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

28

Types of Shock• Hypovolemic• Cardiogenic• Obstructive• Distributive

– Septic– Neurogenic– Anaphylactic

29

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%

30

Cardiogenic Shock• Pump Failure• Inability of the heart to

maintain adequate cardiac output

• SVT, arrhythmias,• Cardiomyopathy• Support ABC’s • Treat the cause

31

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

32

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

33

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

34

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

35

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

– 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!

36

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

37

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

38

Phone call • 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

39

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

40

Case Study-Interventions• 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?

41

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

42

Questions?

43