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Med-Surg
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Fluid & Electrolyte Balance
Fluid balance is closely linked to and affected by electrolyte concentrations
Age, sex, and amount of fat affect the distribution of body fluids
Functions of Water
Transports nutrients, gases, & wastes into and out of cells
Facilitates elimination of wastes via kidneys, gastrointestinal tract, skin, & lungs
Regulates body temperature through evaporation from the skin
Filtration
Movement of water through a cell or membrane because of hydrostatic pressure
Diffusion
Movement of particles across a permeable membrane from an area of higher
concentration to an area of lower concentration
Osmosis
Movement of water through a semipermeable membrane
Water moves by osmosis from a dilute fluid (fewer particles) to a more concentrated fluid until equilibrium is achieved
Osmolarity
Is the number of milliosmoles in one liter of fluid
Normal osmolarity is 270-300 mOsm/L
Osmolality
Is the number of milliosmoles in one kilogram of fluid
1L=1Kg
Aldosterone
Antidiuretic hormone
Natriuretic peptides
What hormones influence fluid output
Renin Angiotensin Aldosterone System
Maintains blood pressure
.1. Renin
Kidneys respond to drop in BP by secreting renin
Low BP & Low circulation is sensed by the kidneys
Angiotensinogen
is produced by the liver, is coverted, by renin into Angiotensin I
Angiotensin I
Angiotensin Coverting Enzyme (ACE)
converts angiotensin I into angiotensin II
5.Angiotensin II
Stimulates peripheral vasoconstriction which increased blood pressure
Stimulates adrenal glands to release aldosterone
Aldosterone
High
Dehydration
Fluid intake or retention is less than what is needed to meet the body’s fluid
needs
Actual decrease in total body water
Vascular dehydration: water shifts from the plasma into the interstitial space (third spacing)
Isotonic dehydration most common type of fluid loss problem
Dehydration is important to know due to: hypovolemia and decreased tissue perfusion
Risk factors of Dehyrdation
Older Adults/pediatrics
Hemorrhage
Vomiting
Diarrhea
Profuse Diaphoresis (sweating)
Burns
Severe Wounds
Fistulas
Long-term NPO
Diuretic Therapy
GI suction
DI (diabetes inspipidus)
Fever
Impaired Motor Function
Manifestations of Dehydration
Decreased blood pressure
Elevated heart rate
Weak peripheral pulses
Orthostatic hypotension
Poor skin turgor
Dry scaly skin
Dry, sticky mucus membranes
Urine output less than 500 ml/day or 20 ml/hour
Weight loss of over half a pound/day
Diagnostic Studies of Dehydration
High Sodium (normal 136-145)
High potassium (normal 3.5-5.0)
Elevated hemoglobin, hematocrit, serum osmolarity, glucose, protein, and BUN
Hemoconcentration
Priority Problems for Dehydration
Disrupted Fluid and Electrolyte Balance
Potential for Decreased Tissue Perfusion
Planning/Implementation for Dehydration
Mild to Moderate:
Oral fluid replacement
Delegate to the UAP 60-120 ml/hr
Oral rehydration solutions with glucose and electrolytes
Severe:
IV Fluid Replacement
Colloids IV Fluids
Includes Albumine, Dextran, Hydroxyethyl starches (HES), Gelatin
Large molecules that stay in intravascular space longer
Fast at expanding intravacular space & amount administered equal to amount lost
Risk: allergic reaction, coagulation problems
Cost More
Crystalloids IV Fluids
Include Hypotonic, Hypertonic, Isotonic solutions
Small molecules that dont stay too long in intravascular space
High amount of fluids needed to equal amount lost (overload: edema)
No allergic reaction or coagulation problems
Cost Less and easier to access
Hypotonic Solutions
IV fluid with osmolarity lower than blood. Moves fluid out of blood vessels into cells nd interstitial spaces
Indications: DKA, HHNS, & Hypernatremia
EX
- 0.45% Sodium Chloride (1/2 Normal Saline)
- 0.33% or 0.2% Sodium Chloride
- 2.5% Dextrose in Water (D2.5W)
- 5% De
Isotonic Solution
IV fluid with osmolarity similar to blood. Expand intravascular fluid volume and do not cause shift in fluid.
Indications: blood loss, surgert, isotonic dehydration, fluid loss, maintenance fluids, npo pts
EX
-- lactated ringers
— 0.9% Sodium Chloride (NS)
— D5W
Hypertonic Solution
IV fluid with osmolarity higher than blood. Moves fluid out of cells and interstitial spaces into blood vessels
Indications: Hyponatremia, Cerebral edema
EX
— 1.5%, 3% or 5% Sodium Chloride
— D5NS
— D5LR
— D10W
Drug Therapy
Antidiarrheal drugs
Antimicrobials
Antiemetics
Antipyretics
Preventing Injury
Monitor Vitals signs
Prevent falls
Evaluating outcomes of Dehydration
Maintains fluid intake of at least 1500 ml or 500 ml more than output
Maintains blood pressure at or near the patient’s normal
Moist mucous membranes and normal skin turgor
Fluid Volume Overload
Excess of body fluid
Caused by: excessive intake or inadequate excretion of
fluids (See Box 13.1)
Hypervolemia
— Excessive fluid in the extracellular fluid space
— Excessive fluid in the vascular space or dilution of electrolytes
Severe FVO → heart failure and pulmonary edema
Dilution of sodium and potassium → seizures, coma, death
Risk Factors for Fluid Overload
Excessive fluid replacement
Kidney Failure
Heart Failure
Long-term steroid replacement
SIADH
Water Intoxication
Psychiatric disorders
Manifestations of Fluid Overload
Increased pulse rate
Bounding pulses
Elevated blood pressure
Distended neck and hand veins
Weight gain
Increased respiratory rate
Shallow respirations
Shortness of breath
Moist crackles
Pitting edema
Pale, cool skin
Diagnostic Studies
Low Sodium (normal:136-145)
Low Potassium (normal:3.5-5.0)
Low Chloride (normal:98-108)
Decreased hemoglobin, hematocrit, serum osmolarity, and protein
Hemodilution
Priority Problems of Fluid Overload
Patient Safety
Restore Fluid Balance
Prevent Future Fluid Overload
Planning/Implementation for Fluid Overload
Drug Therapy:
• Remove excess fluid – diuretics
Nutrition Therapy:
• Fluid and Sodium restriction
• Monitor food labels and keep a record
Monitoring:
• Intake and output
• Rapid Weight gain
Intake & Outpute
Intake:
Oral intake
IVPB intake
Continuous IV fluid
Irrigations
Tube feedings and flushes
IV flushes
Output
Urine output
Emesis
Chest tubes
Surgical drains (JP drains, hemovac, etc.)
Nasogastric tube output
Ostomy output
Key reminders:
Measure all output in mL
Do the math for continuous fluids! (100mL/hr x 8 hours = 800mL)
Add all amounts for intake and output to get shift totals
Intake total - Outtake total = Net I&O Fluid Status (+) or (-)
Sodium (Na)
Major cation in the Extracellular Fluid
Vital for
— Muscle Contraction
— Cardiac Contraction
— Nerve Impulse Transmission
Influences water balance
Often enters the body through foods and fluids
Hyponatremia <136 mEq/L (less than 136)
Hypernatremia >145 mEq/L ( greater than 145)
Na+ = 135-145
Risk factors for Hyponatremia
Loss of body Na
GI fluid loss (V/D)
Diuretics
Severe burns
↓ Aldosterone
Renal disease
Dilution of Na
Excess water intake
Renal failure
Hypotonic fluid irrigations
SIADH
Heart failure
Liver failure/ cirrhosis
Manifestations of Hyponatremia
Cerebral edema
•Altered LOC•
Seizures
•Death
Neuromuscular changes
•Muscle weakness
• ↓ DTR (deep tendon reflex)
Intestinal/ GI changes
• ↑ motility (bowel sounds?)
• N/D
•Cramping
Cardiovascular changes
• *depends on the cause:
Na+Hypovolemia: Weak, thready pulses; ↓BP; dizzy; lightheaded (fluid volume defecit)
Na+Hypervolemia (dilutional): Bounding pulses; normal/high BP
Interventions (Action) for Hyponatremia
Interventions depend on the CAUSE
Drug Therapy: Give slow
Decrease/change diuretics
0.9% sodium chloride infusion
3% sodium chloride**
Vasopressin (ADH) receptor antagonists
Nutrition Therapy
Increased sodium oral intake
Restricting oral fluid intake
Risk factors of Hypernatremia
Actual Na Excess
Excess Na intake (oral or IV)
Renal failure
Hyperaldosteronism
Relative Na Excess (concentration)
Dehydration
Fever
Excessive diaphoresis
Watery diarrhea
Manifestations of Hypernatremia
Cerebral Changes
• Agitation
• Confusion
• Lethargy →stupor →coma
Musculoskeletal changes
• Muscle twitching
• Progressive weakness
• Absent DTR
Cardiovascular changes
• *Depends on the cause
Na+Hypovolemia: Weak, thready pulses; ↓BP; dizzy; lightheaded (fluid volume defecit)
Na+Hypervolemia (dilutional): Bounding pulses; normal/high BP, JVD (fluid volume overload)
Interventions (Actions) for Hypernatremia
Interventions depend on the CAUSE
Drug Therapy:
0.9% sodium chloride infusion
Hypotonic solutions
Diuretics
Nutrition Therapy
Promoting adequate oral water intake
Oral sodium restriction
Potassium (K)
Major cation of the Intracellular Fluid
Vital for excitable tissues
Small changes = significant effect
Regulated by the sodium-potassium pump and
adequate magnesium levels
80% of K is removed by the kidneys
Potassium is Excitable, removed by the kidneys
Hypokalemia < 3.5mEq/L (less than 3.5)
Hyperkalemia >5 mEq/L (greater than 5)
Risk Factors for Hypokalemia
Actual K Deficit
Diuretics
D/V
Gastric suction
Wound drainage
↑ Aldosterone
Inadequate intake
Relative K Deficit
Alkalosis
Hyperinsulinemia and insulin infusions
TPn
Hypomagnesemia
Manifestations of Hypokalemia
Age Impact*
Respiratory changes
Muscle weakness
Shallow respirations
Musculoskeletal changes
Muscle weakness
Flaccid paralysis
Cardiovascular changes
•Weak, thready pulses
•Cardiac dysrhythmias
•ECG changes:
•ST depression
•U wave
•Orthostatic hypotension
Neurological
AMS, irritability, coma
Gastrointestinal changes
↓motility → paralytic ileus
Interventations (Action) for Hypokalemia
Is LIFE THREATENING
Drug Therapy:
Potassium replacement
Oral supplements
IV potassium *HIGH ALERT
K Sparing diuretics
Nutrition Therapy
• Potassium rich foods
Safety
• ECG monitoring
• Fall precautions
• Respiratory monitoring
Risk Factors of Hyperkalemia
Actual K Excess
Excess intake (PO, IV, salt substitutes)
Renal failure*
K-sparing diuretics,ACEi
Relative K Excess
Massive tissue damage (Crush syndrome)
Acidosis
Uncontrolled DM
Manifestations of Hyperkalemia
Age Impact*
Cardiovascular changes**
Bradycardia
Hypotension
Cardiac dysrhythmias
Vfib, asystole
ECG changes:
Tall peaked T waves
Prolonged PR intervals
Wide QRS
Neuromuscular changes
•Muscle twitching → paresthesia
•Weakness → Flaccid paralysis
•Respiratory muscles not impacted until K levels are lethal
Gastrointestinal changes
• ↑motility, diarrhea, frequent stools
Interventions (Actions for Hyperkalemia
is a COMMON CAUSE OF DEATH
Drug Therapy:
• Potassium replacement
• Oral supplements
• IV potassium *HIGH ALERT
• K Sparing diuretics
Nutrition Therapy
• Potassium rich foods
Safety
• ECG monitoring
• Fall precautions
• Respiratory monitoring
Calcium (Ca2)
Important for
— Bone Strength and Density
— Activating Enzymes
— Skeletal and Cardiac Muscle Contraction
— Controlling Nerve Impulses
— Blood Clotting
Enters the body by dietary intake and absorption through the intestine
Requires Vitamin D for absorption
Regulated by the Parathyroid hormone (PTH)
Cell membrane stabilizer
Hypocalcemia < 9mg/dL (less than 9)
Hypercalcemia > 10.5mg/dL (greater than 10.5)
Risk factors for Hypocalcemia
Actual Ca Deficit
• Inadequate intake
• Inadequate VitD intake
• ESRD
• Diarrhea
Relative Ca Deficit
• Alkalosis
• ↑ Phosphorus
• Acute pancreatitis
• ↓ PTH
Manifestations for Hypocalcemia
Neuromuscular changes
•Paresthesia hands and feet
•Muscle twitching, spasms, tetany
•Seizures*
•Trousseau sign (hand)
•Chvostek sign (cheek)
Cardiovascular changes**
• HR
• Weak, thready pulses
• Severe hypotension
•ECG changes:
•Prolonged ST interval
•Prolonged QT interval
Gastrointestinal changes
• ↑motility, diarrhea, cramping
Skeletal changes
• ↓ bone density
• Brittle, fragile bones; ↓ height
Interventions (Action) for Hypocalcemia
Drug Therapy:
• Calcium replacement (PO, IV)
• Vitamin D supplementation
Nutrition Therapy
• Ca and VitD rich foods
• Low phosphorus diet (low red meats)
Safety
• ECG monitoring**
• Low stimulation room
Risk Factors for Hypercalcemia
Actual Ca Excess
• Excess intake
• CKD
• Thiazide diuretics
Relative Ca Excess
• Hyperparathyroidism
• Malignancy
• Immobility**
• Dehydration
Manifestations for Hypercalcemia
Cardiovascular changes**
• Mild: ↑ HR & BP
• Severe: bradycardia
• Poor perfusion
• Thrombosis
Neuromuscular changes
•Muscle weakness
•↓DTR
•Confusion and lethargy
Gastrointestinal changes
• ↓motility
•Nausea, vomiting, constipation,
distention
Intervnetions (Actions) for Hypercalcemia
Drug Therapy:
• Stop all contributing meds
• Fluid replacement (NS)**
• Diuretic (Loops)**
Prevention meds:
• Calcitonin, bisphosphonates,and prostaglandin synthesis inhibitors
Safety
• ECG monitoring**
• Fall risk
Magnesium (Mg)
Mostly stored in bones and cartilage
Important for
— Skeletal muscle contraction
— Carbohydrate metabolism
— Generation of energy stores
— Vitamin activation
— Blood coagulation
— Cell growth
—Health and maintenance of cardiac muscle
Regulated by potassium and calcium levels
Magnesium is a relaxant*
Hypomagnesmia < 1.3 mEq/L (less than 1.3)
Hypermagnesemia > 2.1 mEq/L (greater than 2.1)
Risk Factors for HypoMagnesemia
Inadequate intake
Mg wasting diuretics
When Mg is low, Ca and K are often also low.
— This further increases the risk for cardiac dysrhythmias
Assessments for Hypomagnesemia
Cardiovascular changes
• HTN
• Cardiac dysrhythmias
• Ventricular fibrillation
• Long QT intervals
Neuromuscular changes
• Numbness, tingling, spasms
• Hyperactive reflexes
• Tetany and seizures
Intestinal changes
• ↓ motility
• Constipation
Implementation for Hypomagnesemia
Discontinue causative agent
• Mg wasting diuretics
Drug therapy
• Magnesium replacement (PO, IV)
• Ca and K correction
Risk Factors of Hypermagnesemia
Rare**
Excessive intake (PO, IV)
Renal failure
Assessment for Hypermagnesemia
Symptoms begin > 4.0
Cardiac changes
• Bradycardia
• Vasodilation
• Hypotension
• Cardiac Arrest
Central Nervous System
• Drowsiness →lethargy →coma
Neuromuscular
• Absent reflexes
• Weak respiratory muscles
• Respiratory failure
Implementations for Hypermagnesemia
Discontinue all Mg Drug Therapy
IV fluids
Diuretics (loops)
Calcium replacement
Acid Base Balance
If a lung problem causes retention of carbon dioxide, the kidney compensates by increasing the amount of bicarbonate that is produced and retained
Acidosis decreases the excitability of the cardiovascular muscles, neurons, skeletal muscle, and GI smooth muscles
Alkalosis increases the sensitivity to excitable tissues, overresponding to normal stimuli
Acidosis
is caused by too much acid (pH < 7.35) not enough base
Acid Excess
- Older adults with chronic health problems DKA, prolonged seizures, severe hypoxia
Respiratory and renal failure
Base Deficit
- Pancreatitis
- Dehydration
- Diarrhea
Acidosis leads to hyperkalemia which triggers: Musculoskeletal, cardiac, respiratory, and CNS symptoms
Risk Factors for Respiratory Acidosis
Respiratory depression
Anesthetics
Opioids
Electrolyte imbalance
Muscle weakness
Airway obstruction
Alveolar-capillary block
Manifestations of Respiratory Acidosis
Cardiovascular changes
↑HR and CO → ↓HR, ↓BP,
vasodilation
CNS changes
Lethargy, confusion → unresponsive
Neuromuscular changes
Muscle weakness → paralysis
Respiratory changes
Ineffective, shallow, rapid
Skin Changes
Pale and cyanotic
Laboratory Studies for Respiratory Acidoses
ABGs
pH < 7.35
PaO2 < 90
PaCo2 > 50
Bicarbonate 21-28
K ↑ ↓ OR Normal
Respiratory Acidosis Improve Gas Exchange Implementation
Drug Therapy
• Bronchodilators, anti-inflammatories, and mucolytics
Oxygen Therapy & Ventilatory Support
Monitoring
• Breathing status, breath sounds, and accessory muscles
• Nail beds, cyanosis
Risk factors for Metabolic Acidosis
Overproduction of hydrogen ions
• DKA
• Starvation
Hypermetabolism
• Excessive ingestion of acids
Under elimination of hydrogen ions
• Kidney Failure
Underproduction of bicarbonate
• Kidney Failure
Over elimination of bicarbonate
• Diarrhea
Manifestations for Metabolic Acidosis
Same as Respiratory Acidosis…Plus
• Kussmaul respirations (deep breaths releasing CO2)
• Warm and dry with reddish undertones
Laboratory Studies for Metabolic Acidosis
ABGS
pH < 7.35
PaO2 80-100
paCO2 35-40
Bicarbonate 15-20
K ↑
Metabolic Acidosis Planning and Implementation
Hydration
Drug Therapy to control the underlying problem
IV Bicarbonate for pH < 7.2
Cardiovascular and Musculoskeletal System monitoring
Interpret ongoing ABGs
Interpreting Arterial Blood Gases (ABGs) Respiratory Opposite Metabolic Equal (R.O.M.E)
Normal
Assess pH: 7.35-7.45
Evaluate PaCO2: 35-45
Evaluate HCO3: 22-26
Acidosis
Assess pH: <7.35 (less than)
Evaluate PaCO2: >45 (greater than)
Evaluate HCO3: <22 (less than)
Alkalosis
Assess pH: >7.45 (greater than)
Evaluate PaCO2: <35 (less than)
Evaluate HCO3: >26 (greater than)
Determine Compensation: Is the opposite system trying to correct the imbalance?
Assess PaO2 & SaO2: What is the O2 status?
Alkalosis
pH > 7.45; is caused by too much base or not enough acid
Base Excess
— Oral ingestion: Antacids
— Parenteral infusions – TPN, sodium bicarb
Excessive CO2 Losses
— Hyperventilation
— High altitude
Acid Deficit
— Prolonged vomiting
— NG tube suctioning
—Diuretics
Metabolic Alkalosis
Increase in bases or decrease in acids
ABG
pH >7.45 and HCO3 > 26
Respiratory Alkalosis
Excessive loss of CO2
ABG
pH > 7.45 and CO2 < 35
Symptoms of Alkalosis
CNS Symptoms
— Anxiety, irritability, tetany, seizures
Neuromuscular Symptoms
— Hyperreflexia, muscle cramping, and muscle weakness
Cardiovascular Symptoms
— Increased heart rate, low blood pressure
Respiratory Symptoms
— Hyperventilation (respiratory alkalosis)
— Decreased respiratory efforts (metabolic alkalosis)
Symptoms result from hypocalcemia and hypokalemia
Alkalosis Planning and Implementation
Prevent further loss of H+, K+, Ca²+, and Cl- ions
• Stop therapies
• Breathe into a paper bag
• Oxygen therapy
Restore fluid balance
• IV fluids
• Antiemetics
Monitor for changes
• Electrolytes
Patient Safety
• Fall Precautions