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Electrolytes and Shock

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1 Electrolytes and Shock
Janis Rusin APN, MSN, CPNP-AC Pediatric Nurse Practitioner Lurie Children’s Transport Team

2 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

3 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)

4 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% Adult Male Adult Female Infant Normal 60 50 70 Lean 80 Obese 42

5 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

6 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

7 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

8 Hypernatremia Symptoms Management 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

9 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

10 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 mEq/L/hr Na deficit = (0.6) X Wt (kg) X (Na-goal – Na-actual)

11 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 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

12 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

13 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

14 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 

15 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

16 Magnesium Hypermagnesemia Hypomagnesemia 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

17 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

18 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

19 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

20 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

21 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

22 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

23 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

24 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

25 Organ System Involvement
Cardiac: Decreased preload Decreased cardiac output Decreased systemic vascular resistance Decreased coronary blood flow Cardiac ischemia Arrhythmias Progressive heart failure occurs

26 Organ System Involvement
Respiratory: Increased permeability to fluid shifts Pulmonary edema Decreased O2 transport Hypoxia Acidosis Lung damage: ARDS

27 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

28 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

29 Types of Shock Hypovolemic Cardiogenic Obstructive Distributive Septic
Neurogenic Anaphylactic

30 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%

31 Cardiogenic Shock Pump Failure
Inability of the heart to maintain adequate cardiac output SVT, arrhythmias, Cardiomyopathy Support ABC’s Treat the cause

32 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

33 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

34 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

35 Distributive Shock Neurogenic shock: Anaphylactic 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

36 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!

37 Treatment of Shock Circulation Dextrose
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

38 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

39 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

40 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

41 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?

42 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

43 Questions?

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