electrolytes and shock
DESCRIPTION
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, c alcium and phosphorus Discuss the causes of electrolyte derangements - PowerPoint PPT PresentationTRANSCRIPT
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Electrolytes and ShockJanis Rusin APN, MSN, CPNP-ACPediatric Nurse PractitionerLurie Children’s Transport Team
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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
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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)
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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
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Body Type TBW% TBW% TBW%
Adult Male Adult Female Infant
Normal 60 50 70
Lean 70 60 80
Obese 50 42 60
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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
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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
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
• 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
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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
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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
– 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:
– 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• 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
– 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 • 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• 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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