Fluids and Electrolytes Flashcards
Average Fluid Input/Output per day
2500mL
Adult normal urine output
0.5-1mL/kg/hr
Peds normal urine output
1-2mL/kg/hr
Fluid Distribution
60% water: 2/3 intracellular, 1/3 extracellular
Extracellular Fluid Distribution
80% interstitial
20% intravascular
Law of Capillaries
Two vectors determine water exchange between plasma and interstitial fluid
Blood hydrostatic Pressure
Forces fluid out of capillaries into interstitial fluid
Interstitial Fluid Colloid Osmotic Pressure
Pulls fluid out from capillaries into interstitial fluid
Blood Colloid Osmotic Pressure
Pulls fluid from interstitial space into capillaries
Interstitial Fluid Hydrostatic Pressure
Forces fluid from interstitial space into capillaries
Osmosis
Dissolved particles pull water across membranes to equalize particle concentration on each side
Osmolarity
Measure of how many dissolved particles are in a L of blood
Plasma proteins, glucose, electrolytes
Causes of low serum osmolarity
Fluid overload
Low levels of plasma protein, albumin (anemia)
Causes of higher serum osmolarity
Dehydration
Hyperglycemia
Hypotonic Solution
Moves fluid from vascular space to interstitial and intracellular space
Cell swells
D5W
Hypertonic Solution
Moves fluid from intracellular to interstitial and vascular
Cell shrinks
3% NS or Mannitol
Isotonic Solution
1/3 stays in vascular space
2/3 drawn into interstitial space
0.9% NS
Potassium
Main intracellular electrolyte
Potassium Serum Levels
3.5-5
Sodium
Main extracellular electrolyte
Sodium Serum Levels
136-145
Cation
Ion which loses an electron and takes a positive charge
Na (outside) + K (inside)
Anion
Gains an electron and takes a negative charge
Chloride
Sodium Potassium Pump
Maintains concentration gradient of Na and K across cell membrane
3 Na Out
2 K in
1 ATP used
Moderate hypernatremia
146-159 mmol/L
Severe Hypernatremia
> 160mmol
Causes of Hypernatremia
Dehydration
Water loss (burns, vomiting/diarrhea, hyperglycemias, heat/sweat)
Increased Na intake (less common): salt, hypertonic solution, aldosterone excess, cushing syndrome
Hypernatremia + Brain
Leads to shrinkage secondary to water loss
Treatment for ICP
Mild Hyponatremia
130-135
Moderate Hyponatremia
120-130
Severe hyponatremia
<120
Hyponatremia
Excess of water in relation to sodium in the ECF
Most common electrolyte derangement in hospitalized pts
Hyponatremia
**especially post-op
Role of ADH
Maintains BP, blood volume and tissue water contents
Inappropriate ADH secretion
Possible development of hyponatremia
ADH secretion stimulation
Hypovolemia
Fever
Pain/Stress
Respiratory distress/failure/infection
Head trauma
CNS infections
Medications (thiazides, SSRI, PPI, ACE inhibitors, loop diuretics)
Increase ADH
Fluid retention
Decrease ADH
Fluid excretion
Osmotic Demyelination Syndrome
Neurologic manifestation associated with overly rapid correction of hyponatremia using hypertonic solutions
Rapid correction of hyponatremia >48 causes pons and CNS structures to demyelinate.
Permanent neurological impairment
Importance of K in the body
Regulates fluid and electrolyte balance in the cell
Maintain BP
Helps to transmit nerve impulses
Helps control muscle contraction, in heart especially
Maintains healthy bonesn
Mild Hyperkalemia
5.5-6
Moderate Hyperkalemia
6.1-7
Severe Hyperkalemia
> 7
Causes of Hyperkalemia
Increased K intake
Decreased K excreted by kidneys
Increased K released from cells
Causes of cells to release K
Rhabdomyolysis
Tumor lysis
Crush injury
Acidosis
Succinylcholine/burns/trauma
Old PRBCs
Digoxin toxicity
Severe Hyperkalemia
Hypotension, decreased LOA, ECG changes
MURDER Hyperkalemia
Muscle cramps
Urine abnormalities
Respiratory distress
Decreased cardiac contractility
EKG changes
Reflexes
Moderate Hypokalemia
2.5-3
Severe Hypokalemia
<2.5
Causes of Hypokalemia
Inadequate K in diet or IV fluids
Inappropriate diuresis of K from osmotic diuresis or diuretic use
GI loss from diarrhea/vomiting
Transcellular shift of K from serum because of alkalosis
K Acid-Base Disturbances
Metabolic Acidosis: hyperkalemia
Metabolic alkalosis: hypokalemia
pH and K
pH inversely correlate with K
Aldosterone
Maintains salt and water balance by increasing sodium + water reabsorption in kidneys
Promotes potassium excretion in urine
Role of Magnesium
Growth + maintenance of bones
Nerve, muscle, cardiac muscle function
Co-factor in enzymatic reactions
Magnesium range
0.74-1.07
Hypomagnesemia Levels
<0.74
Hypermagnesemia Level
> 2
Hypomagnesemia causes
Diuretics
Malabsorption from GI tract or significant diarrhea depletes Mg
Acs and IDDM
Malnutrition
Alcoholism
Hypermagnesemia Causes
Less common
Impaired renal function
Excessive intake
Hypermagnesemia S/Sx
N/v
Loss of deep tendon reflexes
AV nodal block
Bradycardia
Hypotension
Cardiac arrest
Treatment of hypermagnesemia
IV calcium gluconate or calcium chloride and hemodialysis
Calcium regulation
Thyroid gland and Parathyroid hormone stimulates release from bone
Vitamin D utilized to assist in uptake of Ca in GI tract + kidneys
Normal Calcium Ranges
2.1-2.6
Causes of hypocalcemia
Hypoparathyroidism
In-hospital causes
In-hospital causes of hypocalcemia
Blood transfusions
Mg depletion
Renal insufficiency
Sepsis
Pancreatitis
Alkalosis
S/Sx of Hypocalcemia
tetany
Hyperreflexia
Paresthesias
Seizures
Hypotension
ventricular ectopy
Hypercalcemia Causes
Hyperparathyroidism or malignancy
ECG changes hypercalcemia
Shortening of ST segment and QT interval
S/Sx of Hypercalcemia
N/v
Constipation
Polyuria
Confusion
Altered LOC
Chloride
Main extracellular anion
Maintains osmotic pressure and water balance
Maintains balance between cations and anions
Normal Chloride
98-106
Anion Gap
Balance between cations and anions in serum
High anion gap
Unmeasured anions in the serum
Ketoacidosis, lactic acidosis, renal failure, toxic ingestions
Normal anion gap
Hyperchloremic metabolic acidosis, loss of bicarb
Anion Gap equation
(Na + K) – (Cl + HCO3)
Purpose of IV therapy
Gain access to body circulation
Drug administration
Fluid administration and fluid balance
Nutrition and nutrient replacement
Local Complications of IV therapy
Pain and irritation
Infiltration and extravasation
Phlebitis
Hematoma
Venous spasm
Vessel collapse
Infection
Nerve, tendon, ligament damage
Systemic Complications of IV therapy
Sepsis
Hypersensitivity reactions
Pulmonary edema
Emboli
Causes of Infiltration
Dislodged catheter during venipuncture
Puncture through distal vein wall
Leaking solution from insertion site
Poorly secured IV
Poor vein site
Irritating solution or medication
Improper cannula size
Pressure or high rate of delivery
S/Sx of Infiltration
Coolness of skin around IV site
Swelling at site
Sluggish/absent flow
Infusion when pressed applied above tip of cannula
No back flow
Approved medications in minibag
Benadryl, Gravel, Morphine, Fentanyl, Amiodarone, Calcium gluconate
Shock trauma IO
Paediatric + adult shock
Burns
Drug overdose
RSI
Post part hemorrhage
Shock trauma IO
Paediatric + adult shock
Burns
Drug overdose
RSI
Post part hemorrhageC
Cardiac IO
VSA
Arrhythmia
MI
CHF
Chest pain
Neurological IO
Status seizure
Stroke
Coma
Head injury
Respiratory IO
Respiratory arrest
Status asthmaticus
Systemic IO
Hemophilic crisis
Sickle cell crisis
Dehydration
DKA
Renal disease
Dialysis
IO Contraindications
Prosthesis
Trauma to bone
No anatomical landmarks
Local infections
Recent IO in same bone (<48hrs)
IO Sites
Proximal Humerus
Proximal Tibia
Distal Tibia
Complications of IO
Fracture of target bone
Physeal plate injury
Infection
Extravasation
Subperiosteal infusion
Embolism
Compartment syndrome
Pain on use
Dislodgement
Necrosis`
pH range
7.35-7.45
Dangerous pH levels
below 6.8 or above 7.8
Physiological Buffer System
Chemical buffer rely on physiochemical action to minimize pH changes in kidneys
Respiratory and renal systems are physiological mechanisms which excrete H
Chemical Buffer System
First 2 respond to changes
Fast
Protein buffer
Phosphate buffer
Bicarbonate-Carbonic Acid Buffer
Bicarbonate Carbonic Acid buffer System
Largest chemical buffer system
CO2 + H20 <–> H2CO3 <–> H + HCO3
Respiratory buffer system
Mid speed
Takes 1-3 mins
Compensates until renal kicks in
Renal Buffer system
Slowest but most effective
Hours to days
Kidneys excrete or retain bicarbonate and hydrogen
Respiratory Acidosis
Conditions causing hypoventilation
CNS depression
Impaired respiratory muscle function from SCI, neuromuscular disease, drugs
Pulmonary disorders
PE
Hypoventilation due to pain, injury, abdominal distension
Respiratory Alkalosis
Hyperventilation
Psychological
Pain
Metabolic demand increase
Medications
CNS lesions
Metabolic Acidosis
Deficit of base in blood stream or excess acids other than CO2
Renal failure
DKA
Anaerobic metabolism
Starvation
Salicylate intoxication
Alkalosis
Excess base or loss of acid in the body
Loss of acids
Oxygenation normal values
PaO2: 80-100mmHg
SaO2: >95%
Acid Base Normal Values
pH: 7.35-7.45
PaCo2: 35-45mmHg
HCO3: 22-26mEq/L
ETCO2 Changes
Ventilation: air in/out of lungs
Diffusion: exchange
Perfusion: circulation
Phase 1 ETCO2
Dead space ventilation
Beginning of exhalation
No gas exchange
Air from trachea, posterior pharynx, mouth and nose
Phase 2 ETCo2
Ascending Phase
CO2 from alveoli reaches upper airway and mixes with dead space air causing rapid rise in CO2
Phase 3 End-Tidal
End-Tidal
End of exhalation containing the highest concentration of CO2
Phase 3: Alveolar Plateau
Co2 rich gas constitutes majority of exhaled air
Phase 4 ETCO2
Descending phase
Inhalation begins
Oxygen fills airway
Co2 levels drop
Ventilation changes to waveform
Frequency
Duration
Height
Shape
Hyperventilation
Hypoventilation
Physiologic Factors trending ETCO2 up
Increased muscular activity
Malignant hyperthermia/fever
Increased CO
Bicarbonate infusion
Tourniquet release
Drug therapy for bronchospasm
Hypoventilation