Module 6: Fluid, Electrolyte, and Acid-Base Imbalances

Question 1

What are electrolytes?

Answer 1

Substances whose molecules dissociate into ions
when placed in water
 Cations: positively charged
 Anions: negatively charged
 Concentration of electrolytes is expressed in
milliequivalents (mEq)/L

Composition
ICF (intracellular fluid)
 Prevalent cation is K+
 Prevalent anion is PO43−

ECF (extracellular fluid)
 Prevalent cation is Na+
 Prevalent anion is Cl−

Question 2

Mechanisms Controlling Fluid/Electrolyte Movement

Answer 2

Diffusion
 Movement of molecules across a permeable
membrane from high to low concentration

Facilitated diffusion
 Uses carrier to help move molecules

Active transport
 Process in which molecules move against
concentration gradient
 External energy is needed for this proces

Osmosis
 Movement of water “down” concentration gradient
* From a region of low solute concentration to one of high solute concentration
* Across a semipermeable membrane
 Requires no outside energy sources

Osmotic pressure
-Amount of pull required to stop osmotic flow of water
 Osmolarity measures the total mOsm/L of solution
 Osmolality measures the number of mOsm/kg of
water

Question 3

Measurement of Osmolality

Answer 3

Calculate the plasma osmolality
 Plasma Osmolality = (2 × Na) + (BUN / 2.8) +
(glucose /18)
 Normal plasma osmolality is between 280 and 295
mOsm/kg
 Greater than 295 mOsm/kg= water deficit
 Less than 275 mOsm/kg= water excess

Question 4

Osmotic Movement of Fluids

Answer 4

The osmolality of the fluid surrounding cells affects
them
 Isotonic—same as cell interior
 Hypotonic—solutes less concentrated than in cells/
hypoosmolar
 Hypertonic—solutes more concentrated than in cells/
hyperosmolar

Question 5

Mechanisms Controlling Fluid and
Electrolyte Movement: Hydrostatic Pressure

Answer 5

-pressure exerted by the blood against the walls of blood vessels or heart chambers. It is a key factor in the movement of fluids and solutes across capillary walls, influencing the exchange between the bloodstream and the interstitial fluid surrounding cells.

Force of Fluid in a Compartment
-Hydrostatic pressure can be thought of as the force that the fluid exerts in a confined space. In blood vessels, this force is exerted by the blood itself, pushing against the vessel walls. This pressure is responsible for driving blood through the circulatory system and facilitating the exchange of nutrients, gases, and waste products between the blood and tissues.

Blood Pressure Generated by Heart’s Contraction
-The heart’s contraction generates the primary hydrostatic pressure within the circulatory system. Each time the heart beats, it pumps blood into the arteries, creating a surge of pressure known as systolic pressure. This is the maximum pressure in the arteries and occurs when the heart’s ventricles contract. The diastolic pressure, the minimum pressure, occurs between heartbeats when the heart is at rest and refilling with blood.
-The hydrostatic pressure decreases as blood moves away from the heart through the arterial system and into the capillaries due to friction and resistance within the vessels. By the time blood reaches the venous system, the pressure has significantly dropped, which is why venous blood is returned to the heart largely through the action of muscle contractions and valves in the veins, rather than hydrostatic pressure.

Role in Capillary Exchange
-The balance between hydrostatic pressure and osmotic pressure (the pressure exerted by proteins, notably albumin, in the blood plasma) determines the movement of water and solutes across capillary walls.

-At the arterial end of a capillary, hydrostatic pressure is higher than osmotic pressure, pushing fluid out of the capillaries into the interstitial space. At the venous end, hydrostatic pressure decreases, and osmotic pressure predominates, drawing fluid back into the capillaries.

Question 6

Oncotic Pressure

Answer 6

Oncotic pressure, also known as colloid osmotic pressure, is a form of osmotic pressure exerted by proteins, notably albumin, in a blood vessel’s plasma. This pressure helps to maintain the balance of fluid between the blood vessels and the surrounding body tissues.

Colloid Osmotic Pressure
Oncotic pressure is termed “colloid” osmotic pressure because it is generated by the presence of large protein molecules (colloids) in the plasma, which are too large to easily cross the capillary walls. These proteins effectively draw water towards themselves.

Osmotic Pressure Caused by Plasma Proteins
The primary plasma protein contributing to oncotic pressure is albumin, although globulins and fibrinogen also play roles. Albumin’s role is critical because it constitutes about 60% of the total plasma proteins and has a significant influence on the blood’s osmotic pressure.

Oncotic pressure is essential for the reabsorption of water from the interstitial fluid back into the capillaries. At the venous end of capillaries, where the hydrostatic pressure has dropped, the oncotic pressure predominates, facilitating the movement of water from the tissue spaces back into the bloodstream, thus preventing excessive fluid loss from the capillaries and edema (swelling due to fluid accumulation in tissues).

Question 7

Fluid Movement in Capillaries

Answer 7

The amount and direction of fluid movement across capillary walls are determined by the interplay of four primary forces, collectively known as Starling forces. These forces include capillary hydrostatic pressure, plasma oncotic pressure, interstitial hydrostatic pressure, and interstitial oncotic pressure. Together, they govern the exchange of water and solutes between the capillaries and the interstitial space surrounding the cells.

Capillary Hydrostatic Pressure (CHP)
Definition: The pressure exerted by the blood within the capillary walls. It tends to push fluid out of the capillaries into the interstitial space.
Role in Fluid Movement: CHP is a major force driving fluid out of the capillaries at the arteriolar end, facilitating the delivery of nutrients and oxygen to the tissues.

Plasma Oncotic Pressure (POP)
Definition: The osmotic pressure exerted by plasma proteins, primarily albumin, which cannot easily cross the capillary wall. It pulls water from the interstitial space back into the capillaries.
Role in Fluid Movement: POP promotes the reabsorption of water into the capillaries at the venous end, helping to maintain blood volume and pressure.

Interstitial Hydrostatic Pressure (IHP)
Definition: The pressure exerted by the fluid in the interstitial space outside the capillaries. It tends to push fluid from the interstitial space back into the capillaries.
Role in Fluid Movement: Generally lower than CHP, IHP can vary in different tissues but usually opposes the outward movement of fluid from capillaries, aiding in reabsorption.

Interstitial Oncotic Pressure (IOP)
Definition: The osmotic pressure exerted by proteins in the interstitial fluid. Since plasma proteins can occasionally leak into the interstitial space, they can exert a small osmotic pressure that draws fluid out of the capillaries into the interstitial space.
Role in Fluid Movement: IOP is typically much lower than POP but works in conjunction with CHP to promote the filtration of fluid from capillaries into the interstitial space.

The net movement of fluid across the capillary wall is determined by the balance of these forces, described by the Starling equation. When the sum of forces pushing fluid out of the capillaries (CHP and IOP) exceeds the sum of forces pulling fluid into the capillaries (POP and IHP), filtration occurs, moving fluid into the interstitial space. Conversely, when the reabsorptive forces (POP and IHP) exceed the filtrative forces (CHP and IOP), fluid moves back into the capillaries from the interstitial space.

This dynamic balance ensures adequate tissue hydration and nutrient delivery while preventing excessive accumulation of fluid in tissues (edema) or within the vascular system. Disruptions in any of these forces can lead to pathological conditions affecting fluid distribution and balance in the body.

Question 8

Edema

Answer 8

Edema is caused by
 Shifts of plasma to interstitial fluid
 Elevation of venous hydrostatic pressure
 Decrease in plasma oncotic pressure
 Elevation of interstitial oncotic pressur

Question 9

Fluid Spacing

Answer 9

First spacing— Normal distribution in ICF and
ECF
 Second spacing— Abnormal accumulation of
interstitial fluid (edema)
 Third spacing— Fluid is trapped where it is
difficult or impossible for it to move back into
cells or blood vessels

Question 10

Regulation of Water Balance: Hypothalamic-pituitary regulation

Answer 10

Osmoreceptors in hypothalamus sense fluid deficit or
increase
 Deficit stimulates thirst and antidiuretic hormone
(ADH) release
 Decreased plasma osmolality (water excess)
suppresses ADH release

Question 11

Regulation of Water Balance: Renal Regulation

Answer 11

Main organ for regulating fluid and electrolyte balance
 Adjusting urine volume
* Selective reabsorption of water and electrolytes
* Renal tubules are sites of action of ADH and
aldosterone

Question 12

Regulation of Water Balance: Adrenal cortical regulation

Answer 12

Releases hormones to regulate water and electrolytes
 Glucocorticoids
* Cortisol
 Mineralocorticoids
* Aldosterone

Question 13

Regulation of Water Balance: Cardiac regulation

Answer 13

Natriuretic peptides are antagonists to the RAAS
 Hormones made by cardiomyocytes in response to
increased atrial pressure
 They suppress secretion of aldosterone, renin, and
ADH to decrease blood volume and pressure

Question 14

Regulation of Water Balance: GI regulation

Answer 14

Oral intake accounts for most water
 Small amounts of water are eliminated by GI tract in
feces
 Diarrhea and vomiting can lead to significant fluid and
electrolyte loss

Question 15

Considerations for Geriatric Population

Answer 15

Structural changes in kidneys decrease ability to
conserve water
 Hormonal changes include a decrease in renin
and aldosterone and increase in ADH and ANP
 Subcutaneous tissue loss leads to increased
moisture lost

Question 16

Fluid Volume Imbalances

Answer 16

Fluid volume deficit (FVD) or hypovolemia
 Abnormal loss of body fluids, inadequate fluid intake,
or plasma to interstitial fluid shift

Dehydration
 Loss of pure water without corresponding loss of
sodium

Correct the underlying cause and replace water and
electrolytes
* Orally
* Blood products
* Isotonic IV solutions

Fluid volume excess (hypervolemia)
 Excess fluid intake, abnormal fluid retention, or
interstitial-to-plasma fluid shift
 Clinical manifestations related to excess volume
* Weight gain is the most common

Remove fluid without changing electrolyte
composition or osmolality of ECF
 Diuretics
 Fluid restriction
 Possible restriction of sodium intake
 Removal of fluid to treat ascites or pleural effusion

Question 17

Sodium

Answer 17

Imbalances typically associated with parallel
changes in osmolality
 Plays a major role in
 ECF volume and concentration
 Generating and transmitting nerve impulses
 Muscle contractility
 Regulating acid-base balance

Question 18

Hypernatremia

Answer 18

-High serum sodium may occur with inadequate
water intake, excess water loss or sodium gain
 Causes hyperosmolality leading to cellular
dehydration
 Primary protection is thirst

Clinical manifestations
 Thirst
 Changes in mental status, ranging from drowsiness,
restlessness, confusion and lethargy to seizures and
coma
 Symptoms of fluid volume deficit

Question 19

Hypernatremia Management

Answer 19

Treat underlying cause
 Primary water deficit—replace fluid orally or IV with
isotonic or hypotonic fluids
 Excess sodium—dilute with sodium-free IV fluids and
promote sodium excretion with diuretic

Question 20

Hyponatremia

Answer 20

Results from loss of sodium-containing fluids and/or
from water excess
 Clinical manifestations
 Mild—headache, irritability, difficulty concentrating.
 More severe—confusion, vomiting, seizures, coma

If the cause is water excess,
 Fluid restriction may be only treatment
 Loop diuretics and demeclocycline
 Severe symptoms (seizures)
* Give small amount of IV hypertonic saline solution (3%
NaCl)

If the cause is abnormal fluid loss,
 Fluid replacement with isotonic sodium-containing
solution
 Encouraging oral intake
 Withholding diuretics
 Drugs that block vasopressin (ADH)
* Convaptan (Vaprisol) IV
* Tolvaptan (Samsca) ora

Question 21

Potassium

Answer 21

Major ICF cation
-Necessary for
 Resting membrane potential of nerve and muscle
cells
 Regulates intracellular osmolality
 Promotes cellular growth
 Maintenance of cardiac rhythms
 Acid-base balance

Sources
 Protein-rich foods
 Fruits and vegetables
 Salt substitutes
 Potassium medications (PO, IV)
 Stored blood
 Regulated by kidneys

Question 22

Hyperkalemia

Answer 22

High serum potassium caused by
 Impaired renal excretion
 Shift from ICF to ECF
 Massive intake of potassium
 Some drugs
 Most common in renal failure

Manifestations
 Life-threatening arrhythmias
 Fatigue, confusion
 Tetany, muscle cramps
 Weak or paralyzed skeletal muscles
 Abdominal cramping or diarrhea

Question 23

Management of Hyperkalemia

Answer 23

Stop oral and IV K+ intake
 Increase K+ excretion (thiazide diuretics, dialysis)
 patiromer (Veltessa), sodium zirconium cyclosilicate
(ZS-9, Lokelma), and/or sodium polystyrene sulfonate
(Kayexalate)

Force K+ from ECF to ICF by IV regular insulin with
dextrose and a -adrenergic agonist or sodium
bicarbonate
 Stabilize cardiac cell membrane by administering
calcium chloride or calcium gluconate IV
 Use continuous ECG monitoring

Question 24

Hypokalemia

Answer 24

Low serum potassium caused by
 Increased loss of K+ via the kidneys or gastrointestinal
tract
 Increased shift of K+ from ECF to ICF
 Decreased dietary K+ (rare)
 Renal losses from loop or potassium depleting
diuresis
 Low magnesium level

Clinical manifestations
 Cardiac most serious
 Skeletal muscle weakness and paresthesia
 Weakness of respiratory muscles
 Decreased GI motility
 Hyperglycemia

Question 25

Management of Hypokalemia

Answer 25

KCl supplements orally or IV  Always dilute IV KCl  NEVER give KCl via IV push or as a bolus  Should not exceed 10 mEq/hr  Use an infusion pump

Question 26

Calcium

Answer 26

Functions  Formation of teeth and bone  Blood clotting  Transmission of nerve impulses  Myocardial contractions  Muscle contractions Major source is dietary intake  Need vitamin D to absorb  Present in bones and plasma  Ionized or free calcium is biologically active  Changes in pH and serum albumin affect levels Balance controlled by  Parathyroid hormone (PTH) * Increases bone resorption, GI absorption, and renal tubule reabsorption of calcium  Calcitonin * Increases calcium deposition into bone, increases renal calcium excretion, and decreases GI absorption

Question 27

Hypercalcemia

Answer 27

High levels of serum calcium caused by  Hyperparathyroidism (two-thirds of cases)  Cancers, especially kidney, breast, prostate, ovarian, hematologic,, and lung cancers Manifestations  Fatigue, lethargy, weakness, confusion  Hallucinations, seizures, coma  Dysrhythmias  Bone pain, fractures, nephrolithiasis  Polyuria, dehydration

Question 28

Hypercalcemia Interventions

Answer 28

 Low calcium diet  Stop medications related to hypercalcemia  Increased weight-bearing activity  Increased fluid intake * 3000 to 4000 ml daily * Cranberry or prune juice  Hydration with isotonic saline infusion  Bisphosphonates—gold standard  Calcitonin

Question 29

Hypocalcemia

Answer 29

Low serum Ca levels caused by  Decreased production of PTH  Multiple blood transfusions  Alkalosis  Increased calcium loss Manifestations  Positive Trousseau’s or Chvostek’s sign Trousseau's Sign Description: Trousseau's sign is elicited by inflating a blood pressure cuff on the upper arm to a pressure greater than the systolic blood pressure and maintaining it for 3 to 5 minutes. A positive Trousseau's sign is indicated by the occurrence of carpal spasm, which involves flexion of the wrist and metacarpophalangeal joints, extension of the fingers, and adduction of the thumb and fingers (a position sometimes referred to as the "obstetrician's hand"). Associated Conditions: Trousseau's sign is most commonly associated with hypocalcemia but can also be seen in patients with hypomagnesemia (low magnesium levels) and alkalosis (increased blood pH). Chvostek's Sign Description: Chvostek's sign is tested by tapping on the facial nerve just in front of the ear and watching for a twitch of the facial muscles, particularly the nose or lips. A positive Chvostek's sign indicates facial muscle contraction in response to the tapping. Associated Conditions: Like Trousseau's sign, a positive Chvostek's sign is commonly associated with hypocalcemia but can also occur in hypomagnesemia and other conditions that cause neuromuscular excitability.  Laryngeal stridor  Dysphagia  Numbness and tingling around the mouth or in the extremities  Dysrhythmias

Question 30

Management of Hypocalcemia

Answer 30

Treat cause  Calcium and Vitamin D supplements  IV calcium gluconate  Rebreathe into paper bag  Treat pain and anxiety to prevent hyperventilation- induced respiratory alkalosis

Question 31

Phosphate

Answer 31

Primary anion in ICF  Essential to function of muscle, red blood cells, and nervous system  Involved in acid-base buffering system, ATP production, cellular uptake of glucose, and metabolism of carbohydrates, proteins, and fats Serum levels controlled by parathyroid hormone  Maintenance requires adequate renal functioning  Reciprocal relationship with calcium

Question 32

Hyperphosphatemia

Answer 32

High serum PO43− caused by  Acute kidney injury or chronic kidney disease  Excess intake of phosphate or vitamin D  Hypoparathyroidism Manifestations  Tetany, muscle cramps, paresthesias, hypotension, dysrhythmias, seizures (hypocalcemia)  Calcified deposits in soft tissue such as joints, arteries, skin, kidneys, and corneas (cause organ dysfunction, notably renal failure)

Question 33

Hyperphosphatemia Management

Answer 33

 Identify and treat underlying cause  Restrict intake of foods and fluids containing phosphorus  Oral phosphate-binding agents  Hemodialysis  Volume expansion and forced diuresis  Correct any hypocalcemia

Question 34

Hypophosphatemia

Answer 34

Low serum PO43− caused by  Malnourishment/malabsorption  Diarrhea  Use of phosphate-binding antacids  Inadequate replacement during parenteral nutrition Manifestations  CNS depression  Muscle weakness and pain  Respiratory and heart failure  Rickets and osteomalacia

Question 35

Hypophosphatemia Management

Answer 35

Increasing oral intake with dairy products  Oral supplements  IV administration of sodium or potassium phosphate * Monitor serum calcium and phosphorus levels every 6 to 12 hours

Question 36

Magnesium

Answer 36

Cofactor in enzyme for metabolism of carbohydrates  Required for DNA and protein synthesis  Blood glucose control  BP regulation  Needed for ATP production Acts directly on myoneural junction  Important for normal cardiac function  50% to 60% contained in bone  30% in cells  Only 1% in ECF  Absorbed in GI tract  Excreted by kidneys

Question 37

Hypermagnesemia

Answer 37

High serum Mg caused by  Increased intake of products containing magnesium when renal insufficiency or failure is present  Excess IV magnesium administration Manifestations  Hypotension, facial flushing  Lethargy  Nausea and vomiting  Impaired deep tendon reflexes  Muscle paralysis  Respiratory and cardiac arrest

Question 38

Hypermagnesemia Management

Answer 38

Prevention first—stop magnesium-containing drugs and limit dietary intake of magnesium-containing foods  IV calcium gluconate if symptomatic  Fluids and diuretics to promote urinary excretion  Dialysis

Question 39

Hypomagnesemia

Answer 39

Low serum Mg caused by  Prolonged fasting or starvation  Chronic alcoholism  Fluid loss from GI tract  Prolonged PN without supplementation  Diuretics, proton-pump inhibitors, some antibiotics  Hyperglycemic osmotic diuresis Manifestations  Resembles hypocalcemia * Muscle cramps, tremors * Hyperactive deep tendon reflexes * Chvostek’s and Trousseau’s signs * Confusion, vertigo, seizures  Dysrhythmias

Question 40

Hypomagnesemia Management

Answer 40

Management  Treat underlying cause  Oral supplements  Increase dietary intake  IV magnesium when severe

Question 41

pH

Answer 41

Measure of H+ ion concentration  Increase H+ concentration= acidity  Decrease H+ concentration= alkalinity  Blood is slightly alkaline at pH 7.35 to 7.45  Less than 7.35 is acidosis  Greater than 7.45 is alkalosis

Question 42

Acid-Base Regulation

Answer 42

3 mechanisms to regulate acid-base balance and keep pH between 7.35 and 7.45  Buffer system  Respiratory system  Renal system

Question 43

Buffer System

Answer 43

Primary regulator of acid-base balance  Act chemically to change strong acids to weak acids or bind acids to neutralize them  Respiratory and renal systems need to be functioning adequately HCl + NaH2CO3  NaCl + H2CO3  Strong acid + strong base is buffered into salt and weak acid  Major buffer system Other Buffer Systems  Phosphate  Protein  Hemoglobin  Cellular  Shifts H+ in and out of cell in exchange for potassium

Question 44

Respiratory System Regulation

Answer 44

CO2 + H2O --> H2CO3 --> H+ + HCO3−  Respiratory center in medulla controls breathing  Increased respirations lead to increased CO2 elimination and decreased CO2 in blood  Decreased respirations lead to CO2 retention

Question 45

Renal System Regulation

Answer 45

Kidneys conserve bicarbonate and excretes some acid - 3 mechanisms for acid excretion  Secrete free hydrogen  Combine H+ with ammonia (NH3)  Excrete weak acids

Question 46

Alterations in Acid-Base Balance

Answer 46

Imbalances occur when compensatory mechanisms fail -Classification of imbalances  Respiratory (CO2) or metabolic (HCO3)  Acidosis or alkalosis  Acute or chronic

Question 47

Blood Gas Values

Answer 47

Arterial blood gas (ABG) values give objective information about  Acid-base status  Underlying cause of imbalance  Body's ability to regulate pH  ABG analysis also shows the partial pressure of arterial O2 (PaO2) and O2 saturation

Question 48

Interpretation of ABGs

Answer 48

1. Look at each of the values Start by reviewing all the values provided in the ABG report, which typically includes: pH: Indicates the acidity or alkalinity of the blood. PaCO2 (Partial Pressure of Carbon Dioxide): Reflects the respiratory component of acid-base balance. HCO3- (Bicarbonate): Represents the metabolic component of acid-base balance. PaO2 (Partial Pressure of Oxygen): Measures the oxygen level in the blood. O2 Saturation (Oxygen Saturation): Indicates the percentage of hemoglobin saturated with oxygen. 2. Look at pH first The pH value will tell you if the blood is acidic, alkaline, or normal: Normal pH: 7.35 - 7.45 Acidemia: pH < 7.35 Alkalemia: pH > 7.45 3. Use ROME to determine respiratory or metabolic ROME stands for "Respiratory Opposite, Metabolic Equal": Respiratory: Changes in PaCO2. If pH and PaCO2 are in opposite directions (pH down, PaCO2 up = acidosis; pH up, PaCO2 down = alkalosis), it indicates a respiratory issue. Metabolic: Changes in HCO3-. If pH and HCO3- move in the same direction (both up or both down), it indicates a metabolic issue 4. Determine if patient is compensating Compensation refers to the body's attempt to restore normal pH: Fully Compensated: pH has returned to normal, but PaCO2 and HCO3- are abnormal. Partially Compensated: pH, PaCO2, and HCO3- are all abnormal, indicating the body is attempting to compensate, but has not yet normalized the pH. Uncompensated: Only one of either PaCO2 or HCO3- is abnormal along with an abnormal pH, indicating no compensation has occurred. 5. Assess the PaO2 and O2 saturation These values provide information about the patient's oxygenation status: PaO2: Normal values range from 75 to 100 mmHg. Values below this range indicate hypoxemia. O2 Saturation: Normal saturation is 95-100%. Values below 95% may indicate insufficient oxygenation.

Question 49

Respiratory Acidosis

Answer 49

Carbonic acid excess caused by  Hypoventilation  Respiratory failure Compensation  Kidneys conserve HCO3– and secrete H+ into urine

Question 50

Respiratory Alkalosis

Answer 50

Carbonic acid deficit caused by  Hypoxemia from acute pulmonary disorders  Hyperventilation Compensation  Rarely occurs when acute  Can buffer with bicarbonate shift  Renal compensation if chronic

Question 51

Metabolic Acidosis

Answer 51

Base bicarbonate deficit caused by  Diabetic ketoacidosis  Lactic acid accumulation (shock)  Severe diarrhea  Kidney disease Compensatory mechanisms  Increased CO2 excretion by lungs * Kussmaul respirations (deep and rapid)  Kidneys excrete acid -Anion gap  = Na+ – (HCO3– + Cl–)  Normal: 8–12 mmol/L  Increased with acid gain

Question 52

Metabolic Alkalosis

Answer 52

Base bicarbonate excess caused by  Prolonged vomiting or gastric suction  Gain of HCO3– Compensatory mechanisms  Renal excretion of HCO3–  Decreased respiratory rate to increase plasma CO2 (limited)

Question 53

ABG Interpretation Guide

Answer 53

ABG Interpretation Guide 1. Evaluate pH: Normal: 7.35-7.45 Acidemia: pH < 7.35 (indicates acidosis) Alkalemia: pH > 7.45 (indicates alkalosis) 2. Analyze PaCO2 & HCO3-: PaCO2 (Respiratory Component): Normal: 35-45 mmHg ↑ PaCO2 suggests respiratory acidosis ↓ PaCO2 suggests respiratory alkalosis HCO3- (Metabolic Component): Normal: 22-26 mEq/L ↑ HCO3- suggests metabolic alkalosis ↓ HCO3- suggests metabolic acidosis 3. Apply ROME: Respiratory Opposite: pH ↓ & PaCO2 ↑ = Respiratory Acidosis pH ↑ & PaCO2 ↓ = Respiratory Alkalosis Metabolic Equal: pH & HCO3- both ↓ = Metabolic Acidosis pH & HCO3- both ↑ = Metabolic Alkalosis 4. Assess Compensation: Uncompensated: Abnormal pH with one other abnormal value (PaCO2 or HCO3-) Partially Compensated: All three values (pH, PaCO2, HCO3-) are abnormal Fully Compensated: Normal pH, but both PaCO2 and HCO3- are abnormal 5. Examine Oxygenation: PaO2 (Oxygen Level): Normal range is 75-100 mmHg. Values below this range suggest hypoxemia. O2 Saturation: Normal saturation is 95-100%. Values below 95% may indicate inadequate oxygenation.

Question 54

Oral Fluid and Electrolyte Replacement

Answer 54

Used to correct mild fluid and electrolyte deficits  Water  Glucose  Potassium  Sodium

Question 55

IV Fluid and Electrolyte Replacement

Answer 55

Purposes  Maintenance * When oral intake is not adequate  Replacement * When losses have occurred or are ongoing  Types of fluids categorized by tonicity

Question 56

IV Fluids: Hypotonic

Answer 56

Hypotonic  Lower osmolality when compared to plasma * Dilutes ECF  Water moves from ECF to ICF by osmosis  Good maintenance fluids  Also used to treat hypernatremia  Monitor for changes in mentation

Question 57

IV Fluids: D5W

Answer 57

Technically isotonic  Dextrose quickly metabolizes  Net result free water  Provides 170 cal/L  Used to replace water losses, helps prevent ketosis

Question 58

IV Fluids: Isotonic

Answer 58

Isotonic  Similar osmolality to ECF * Expands only ECF  No net loss or gain from ICF  Ideal to replace ECF volume deficit

Question 59

IV Fluids: Normal Saline

Answer 59

NS, 0.9% saline, NSS  Isotonic  Slightly more NaCl than ECF  Used when both fluid and sodium lost  Only solution used with blood

Question 60

IV Fluids: Lactated Ringer's

Answer 60

Isotonic  Contains sodium, potassium, chloride, calcium and lactate  Expands ECF—ideal for surgery, burns and GI losses  Contraindicated with liver problems, hyperkalemia, and severe hypovolemia

Question 61

IV Fluids: Hypertonic

Answer 61

Hypertonic  Higher osmolality compared with plasma  Draws water out of cells into ECF  Require frequent monitoring of * Blood pressure * Lung sounds * Serum sodium levels

Question 62

IV Fluids: D5 ½ NS

Answer 62

Hypertonic  Common maintenance fluid  Replaces fluid loss  KCl added for maintenance or replacement

Question 63

IV Fluids: D10W

Answer 63

Hypertonic  Provides 340 kcal/L  Provides free water but no electrolytes  Limit of dextrose concentration that may be infused peripherally

Question 64

IV Fluids: Colloids

Answer 64

Stay in vascular space and increase oncotic pressure  All colloids affect blood coagulation, by interfering with coagulation factor VII Include:  Human plasma products (albumin, fresh frozen plasma, blood)  Semisynthetics (dextran and starches, [Hespan]

Question 65

Remembering IV Fluids

Answer 65

IV Solution Uses Guide: Normal Saline (0.9% NaCl): Used for fluid resuscitation, hydration, and managing shock. Hypertonic Saline: Used to treat cerebral edema and hyponatremia. D5W (5% Dextrose in Water): Used for hypoglycemia, fluid loss, and dehydration. Isotonic Solutions: Used for fluid replacement and electrolyte balance. Lactated Ringer's: Used for burns, fluid loss from third spacing. D5 1/2 Normal Saline (D5 0.45% NaCl): Used for hypotonic hydration and SIADH (Syndrome of Inappropriate Antidiuretic Hormone) treatment. D10W (10% Dextrose in Water): Used for nutritional supplementation and high-calorie fluid replacement. Colloids: Used for volume expansion, managing shock, and compensating for blood loss.

Question 66

CVADs

Answer 66

Catheters placed in large blood vessels  Subclavian vein, jugular vein 3 main types  Centrally inserted catheters  Peripherally inserted central catheters (PICCs)  Implanted ports Permit frequent, continuous, rapid, or intermittent administration of fluids and medications  Allow us to more safely administer drugs that are potential vesicants  Used to administer blood/blood products and PN  Useful for patients with limited peripheral vascular access or need for long-term vascular access  Hemodynamic monitoring  Venous blood samples  Injection of radiopaque contrast media

Question 67

CVADs Advantages/Disadvantages

Answer 67

Advantages  Immediate access  Reduced venipunctures  Decreased risk of extravasation Disadvantages  Increased risk of systemic infection  Invasive procedure

Question 68

Centrally Inserted Catheter (CVC)

Answer 68

Inserted into a vein in the chest or abdominal wall with tip resting in distal end of superior vena cava  Nontunneled or tunneled  Dacron cuff anchors catheter and decreases incidence of infection Single-, double-, or triple-lumen  Examples of long-term (tunneled) catheters  Hickman  Broviac  Groshong

Question 69

PICC

Answer 69

Central venous catheter inserted into a vein in arm  Single- or multi-lumen, nontunneled  For patients who need vascular access for 1 week to 6 months  Cannot use arm for BP or blood draw

Question 70

PICC Advantages/Disadvantages

Answer 70

Advantages  Lower infection rate  Fewer insertion-related complications  Decreased cost Complications  Deep vein thrombosis  Phlebitis

Question 71

Implanted Infusion Port

Answer 71

Central venous catheter connected to an implanted, single or double subcutaneous injection port  Port is titanium or plastic with self-sealing silicone septum  Port is accessed using a special non-coring needle with a deflected tip Drugs are placed in the reservoir of the port through skin by a direct injection or through injection into an established IV line Advantages  Good for long-term therapy  Low risk of infection  Cosmetic discretion

Question 72

Midline Catheters

Answer 72

Peripheral catheters  3 to 8 in long  Single- or double-lumen  Use and care similar to PICC  May stay in place up to 4 weeks

Question 73

Complications

Answer 73

Catheter occlusion  Clamped or kinked catheter  Tip against wall of vessel  Thrombosis  Precipitate buildup in lumen Embolism  Catheter breaking  Dislodgement of thrombus  Entry of air into circulation Infection  Contamination during insertion or use  Migration of organisms along catheter  Immunosuppressed patient Pneumothorax  Perforation of visceral pleura  Catheter migration  Improper suturing  Trauma, forceful flushing  Spontaneous