NCMB312 LEC MIDTERM FLUID & ELECTROLYTES PDF

***-- 1^ST^ SEM MIDTERM WEEK 7 --*** -------------------------- **FLUID & ELECTROLYTES** -------------------------- -- ----------------------------- **BODY FLUID COMPARTMENTS** -- ----------------------------- - The body has two main fluid compartments: intracellular and extr...

***-- 1^ST^ SEM MIDTERM WEEK 7 --*** -------------------------- **FLUID & ELECTROLYTES** -------------------------- -- ----------------------------- **BODY FLUID COMPARTMENTS** -- ----------------------------- - The body has two main fluid compartments: intracellular and extracellular. ------------------------------- ---------------------------------------------------------------------------------- **Intracellular fluid (ICF)** fluid inside the cells, making up approximately 70% of the body\'s total fluid. **Extracellular fluid (ECF)** fluid outside the cells, making up approximately 30% of the body\'s total fluid. ------------------------------- ---------------------------------------------------------------------------------- -- -------------------------------------- **Extracellular Fluid Compartments** -- -------------------------------------- ------------------------------------------- ----------------------------------------------------------------------------------- ---------------------------------------------------------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Compartment** **Description** **Volume (Adult)** **Interstitial fluid** **fluid surrounding cells, including lymph** **11-12 liters** **Intravascular fluid** **fluid inside blood vessels** **6 liters (3 liters plasma, 3 liters formed elements)** **Transcellular fluid** **fluid in specialized compartments (e.g., cerebrospinal fluid, synovial fluid)** **1 liter** ------------------------------------------- ----------------------------------------------------------------------------------- ---------------------------------------------------------- -- ----------------------------- **Third Space Fluid Shift** -- ----------------------------- - Occurs when fluid moves from the intravascular space to the interstitial space but is not available for use by the body. - This can lead to decreased urine output, increased heart rate, decreased blood pressure, and edema. -- -------------------------------------- **Signs of Third Space Fluid Shift** -- -------------------------------------- - Decreased urine output - Increased heart rate - Decreased blood pressure - Edema - Increased body weight - Imbalances in intake and output due to decreased tissue perfusion -- ---------------------------------------- **Examples of Third Space Fluid Loss** -- ---------------------------------------- - **Intestinal obstruction** - **Pancreatitis** - **Crushing injuries** - **Bleeding due to trauma or dissecting aortic aneurysm** - **Major venous obstructions** -- -------------------- **Electrolytes 💡** -- -------------------- - Are active chemicals found in body fluids that carry positive or negative charges. -- --------------------------- **Types of Electrolytes** -- --------------------------- ------------- -------------------------------------------------------------------------------------------------------- **Cations** positively charged electrolytes (e.g., sodium, potassium, calcium, magnesium, hydrogen ion) **Anions** negatively charged electrolytes (e.g., chloride, sodium bicarbonate, potassium, sulfate, protein ions) ------------- -------------------------------------------------------------------------------------------------------- -- ------------------------------- **Electrolyte Concentration** -- ------------------------------- - The concentration of electrolytes in the intracellular fluid (ICF) differs from that in the extracellular fluid (ECF). However, electrolyte levels in the ECF are typically measured due to their accessibility  -- ---------------------------------- **Osmosis and Fluid Movement 🌈** -- ---------------------------------- - **Osmosis** is the movement of solvent (usually water) from an area of lower to higher concentration of solute. A diagram of a solution Description automatically generated -- ------------------------------- **Factors Affecting Osmosis** -- ------------------------------- - Concentration of solute - Osmotic pressure (the amount of hydrostatic pressure needed to stop the flow of water by osmosis) - Oncotic pressure (the pressure exerted by proteins in the blood) -- ------------------------- **Examples of Osmosis** -- ------------------------- - Water movement from an area of lower sodium concentration to an area of higher sodium concentration - Water movement from the intravascular space to the interstitial space in response to increased sodium concentration in the ECF -------------------------------- ---------------------------------------- **INFO** Solute Concentration Water Movement **High solute concentration** **Water moves into the compartment** **Low solute concentration** **Water moves out of the compartment** **Equal solute concentration** **No water movement** -------------------------------- ---------------------------------------- -- ---------------------- **Osmotic Pressure** -- ---------------------- - Pressure exerted by the concentration of solutes in a plasma. - Osmotic pressure pulls fluid into the capillary from the ICF. -- ---------------------- **Oncotic Pressure** -- ---------------------- - **Colloid oncotic pressure or Colloid osmotic pressure**. - Pressure exerted by proteins, particularly albumin, in a bloodstream. - **Colloid** is fluid consisting of no-soluble substances that are evenly distributed within a solvent. - Which fluid in the body moves based on the concentration of protein, particularly albumin. Protein attracts fluid, tubing, or water. - **Blood is an example of a colloid solution.** -- ------------------------------------------ **Crystalloid versus Colloid Solutions** -- ------------------------------------------ - **Crystalloid or colloid solutions** can be used to temporarily replace blood or replenish fluid losses from the body. - **Crystalloid solutions** are mineral ions dissolved in water. - **Examples:** normal saline (0.9% NaCl), half normal saline (0.45% NaCl), and lactated Ringer's solution (Plasma-Lyte). - Commonly used to replace fluid in hypovolemia. - **Colloid solutions** are commonly used as temporary blood replacement until the correct type of blood is available for infusion - **Examples:** albumin solutions, hyper-oncotic starch, and dextran. -- --------------- **Diffusion** -- --------------- - Movement of solute from an area of higher concentration to an area of lower concentration. - Example: diffusion of carbon dioxide and oxygen between the alveoli and pulmonary capillaries.  ------------------------------------------- ------------------------------------------------------- -------------------------------------------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Gases** **Concentration** **Movement** **Carbon Dioxide** **Higher in venous blood, lower in alveoli** **From pulmonary capillaries to alveoli** **Oxygen** **Higher in alveoli, lower in pulmonary capillaries** **From alveoli to pulmonary capillaries)** ------------------------------------------- ------------------------------------------------------- -------------------------------------------- -- -------------------------- **Hydrostatic Pressure** -- -------------------------- - Also called hydraulic pressure - Pressure exerted by a fluid on the wall of a blood vessel. - Example: fluid movement from blood vessels to interstitial fluid space in cases of obstruction or right-sided heart failure. - Hydrostatic pressure pushes fluid out of the capillary toward the ICF. A diagram of a diagram of a pressure Description automatically generated -- ---------------- **Filtration** -- ---------------- - Movement of water from an area of higher hydrostatic pressure to an area of lower hydrostatic pressure. - The kidneys filter approximately **180 L of plasma per day.** - **Example:** - Movement of fluid from intravascular compartment to interstitial compartment. - The passage of water and electrolytes from the capillary bed to the interstitial fluid**hydrostatic pressure** results from the pumping action of the heart -- ------------------------------- **Osmolality and Tonicity 🧬** -- ------------------------------- -- ---------------- **Osmolality** -- ---------------- - Number of dissolved particles in a unit of fluid. - The number of milliosmoles of solute (the standard unit of osmotic pressure) per kilogram of solvent - Measure of a solution\'s ability to create osmotic pressure and affect the movement of water between compartments. - Expressed as **milliosmoles per kilogram (mOsm/kg).** ------------------------------------------- --------------------- ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Normal Range** **Serum Osmolality** **275-290 mOsm/kg** **Urine Osmolality** **200-800 mOsm/kg** ------------------------------------------- --------------------- ---------- -- ---------------- **Osmolarity** -- ---------------- - **The number of milliosmoles (the standard unit of osmotic pressure) per liter of solution** - **Expressed as milliosmoles per liter (mOsm/L).** -- -------------- **Tonicity** -- -------------- - Ability of all solutes to cause an osmotic driving force that promotes water movement from one compartment to another. - It determines the normal state of cellular hydration and cell size. - Most commonly refers to the **NaCl content of the solution.** ------------------------------------------- ----------------------------------------------------------------------------------------------------------- ---------------------------------------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Tonicity** **Uses** **Examples** **Isotonic** **- Used to replace fluid loss, increase extracellular fluid volume without causing cellular shifts.\ **- 0.9% Normal Saline (NS)\ - Commonly used in dehydration, blood loss, or surgery.** - Lactated Ringer\'s (LR)\ - 5% Dextrose in Water (D5W)** **Hypotonic** **- Shifts fluids into cells, causing them to swell.\ **- 0.45% Normal Saline (1/2 NS)\ - Used in cases of intracellular dehydration (e.g., diabetic ketoacidosis, hyperosmolar hyperglycemia).** - 0.33% Normal Saline\ - 2.5% Dextrose in Water** **Hypertonic** **- Draws water out of cells, causing them to shrink.\ **- 3% Normal Saline\ - Used in severe hyponatremia, cerebral edema, or to stabilize blood pressure.** - 5% Dextrose in Normal Saline (D5NS)\ - 10% Dextrose in Water (D10W)** ------------------------------------------- ----------------------------------------------------------------------------------------------------------- ---------------------------------------- -- ----------------------- **Effective Osmoles** -- ----------------------- - Are solutes that are capable of affecting water movement. - Examples: sodium, mannitol, glucose, and sorbitol. - **Osmotic diuresis** is the increase in urine output caused by the excretion of solutes, such as glucose or mannitol. - In high concentrations, glucose or mannitol can act as solutes within the bloodstream that cause a force that pulls water out of the ICF and brings it into the ECF (bloodstream). - Then is filtered out of the bloodstream at the kidneys and excreted into the urine. -- --------------------------- **Fluid Gain and Loss 💧** -- --------------------------- -- ---------------- **Fluid Gain** -- ---------------- - Gained through eating and drinking. - Average daily intake and output of water are approximately equal. -- ---------------- **Fluid Loss** -- ---------------- - Fluid is lost through: - Kidneys (urine output) - Skin (insensible losses through sweating and evaporation) - Lungs (insensible losses through respiration) - GI tract (stool) ------------------------------------------- ------------------------------------------------- ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Average Daily Loss** **Kidneys** **1-2 liters** **Skin** **500 ml (insensible perspiration)** **Lungs** **300 ml (insensible loss during respiration)** **GI tract** **100-200 ml (stool)** ------------------------------------------- ------------------------------------------------- ----------  -- ------------------------------------ **Laboratory Diagnostic Values 📊** -- ------------------------------------ -- ---------------------------------- **Urine Specific Gravity (USG)** -- ---------------------------------- - Measures the ability of the kidneys to excrete or conserve water. - Normal range: **1.010-1.025**. -- ------------------------------- **Blood Urea Nitrogen (BUN)** -- ------------------------------- - Product of protein metabolism. - **Normal circumstances**: protein is broken down into amino acids, which are then broken down into ammonia molecules, which are converted to urea. - A waste product that is produced by the liver and excreted by the kidneys. -  It is a measure of the amount of urea in the blood. - **Urea** is a waste product that is produced when the body breaks down protein. - The normal range for BUN is **10-20 mg/dL.** - Factors that can increase BUN include: - Decreased renal function - Dehydration - GI bleeding - Increased protein intake - Fever - Sepsis - Factors that can decrease BUN include: - End-stage liver disease - Low protein diet - Starvation or malnutrition - Expanded fluid volume (e.g. during pregnancy) -- ----------------- **Creatinine ** -- ----------------- - Waste product that is produced by the muscles and excreted by the kidneys. - It is a measure of muscle metabolism. - Product of muscle metabolism and is used as an indicator of renal function. - The normal range for creatinine is **0.7-1.4 mg/dL.** - Creatinine is a better indicator of renal function than BUN because it is not affected by protein intake and metabolic state. ------------------------------------------- ----------------- ------------------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **BUN** **Creatinine** **Normal Range** **10-20 mg/dL** **0.7-1.4 mg/dL** **Affected by Protein Intake** **Yes** **No** **Affected by Metabolic State** **Yes** **No** ------------------------------------------- ----------------- ------------------- -- ---------------- **Hematocrit** -- ---------------- - Percentage of red blood cells in the blood. - The normal range for hematocrit is: - 42-52% for males - 35-47% for females - Factors that can increase hematocrit include: - Dehydration - Polycythemia (a condition that results in an increased level of circulating RBCs) - Factors that can decrease hematocrit include: - Overhydration - Anemia (a condition that results in a decreased level of RBCs) -- ------------------- **Homeostasis 🌎** -- ------------------- - The ability of the body to maintain a stable internal environment despite changes in the external environment. - [The organs involved in homeostasis include:] - Kidneys - Heart - Lungs - Pituitary glands - Adrenal glands - Parathyroid glands -- ----------------------------------------------------- ***🌊* Regulation of Water and Electrolyte Balance** -- ----------------------------------------------------- A diagram of a flowchart Description automatically generated -- ----------------------- **Kidney Function 🌟** -- ----------------------- - The kidneys play a vital role in maintaining fluid and electrolyte balance. They: - Regulate extracellular fluid volume and osmolality - Remove fluid and waste products from the body - Regulate electrolyte levels in the extracellular fluid - Regulate pH levels in the extracellular fluid - Excrete metabolic waste and toxic substances -- -------------------------------- **Heart and Blood Vessels ❤️** -- -------------------------------- - The heart and blood vessels play a role in maintaining fluid and electrolyte balance by: - Pumping oxygenated blood to the kidneys - Maintaining sufficient pressure in the systemic circulation -- ------------- **Lungs 👅** -- ------------- - The lungs play a role in maintaining fluid and electrolyte balance by: - Removing water through exhalation - Maintaining acid-base balance -- ------------------------ **Pituitary Glands 🧠** -- ------------------------ - The pituitary glands play a role in maintaining fluid and electrolyte balance by: - Releasing antidiuretic hormone (ADH) to conserve water - Regulating blood volume and serum osmolality -- -------------------------------- **Antidiuretic Hormone (ADH)** -- -------------------------------- - Hormone produced by the hypothalamus that plays a crucial role in regulating water and electrolyte balance in the body. - **Functions:** maintain the osmotic pressure of the cells by controlling the retention and excretion of water by the kidneys. - Stimulates the reabsorption of water in the kidneys, which helps to maintain blood volume and serum osmolality. - **Mechanism of Action:** - ADH is released in response to decreased blood volume and serum osmolality. - ADH activates proteins and enzymes that increase the permeability of the distal convoluted tubules (DCT) to water. - Water is reabsorbed from the DCT back into the circulation, increasing blood volume and decreasing urine excretion. - **Effects of ADH on the Body:** - Increased blood volume - Decreased urine excretion - Increased potassium loss - Decreased serum osmolality -- ----------------- **Isotonicity** -- ----------------- - Refers to the balance of water and electrolytes in the body. - It is achieved when the concentration of solutes in the blood is equal to the concentration of solutes in the cells. -- ---------------------- **Thirst Mechanism** -- ---------------------- - **Thirst** is a mechanism that helps to regulate fluid balance in the body. - Thirst is stimulated by increased serum osmolality and decreased blood volume. - Thirst causes the body to drink more water, which helps to dilute the blood and increase blood volume. -- ------------------- **Baroreceptors** -- ------------------- - Specialized sensors that detect changes in blood pressure. - Located in the left atrium, carotid arteries, and aortic arches. - **Functions of Baroreceptors:** - Detect changes in blood pressure - Regulate sympathetic and parasympathetic neural activity - Maintain stable blood pressure levels and homeostasis -- ------------------------------------------------- **Renin-Angiotensin-Aldosterone System (RAAS)** -- ------------------------------------------------- - Complex system that helps to regulate blood pressure and fluid balance. ------------------------------------------- ------------------------------------------------------------------ ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Hormone** **Function** **Renin** **Stimulates the formation of angiotensin I and angiotensin II** **Angiotensin I** **Causes vasoconstriction and increases blood pressure** **Angiotensin II** **Stimulates the release of aldosterone** **Aldosterone** **Increases sodium and water reabsorption in the kidneys** ------------------------------------------- ------------------------------------------------------------------ ---------- -- -------------------- **Adrenal Glands** -- -------------------- - Located on top of each kidney and play a crucial role in regulating fluid balance and blood pressure. - Secrete aldosterone, which increases sodium and water reabsorption in the kidneys. - **Functions of Aldosterone:** - Increases sodium and water reabsorption in the kidneys - Increases blood pressure - Causes potassium loss -- ------------------------ **Parathyroid Glands** -- ------------------------ - Located in the thyroid gland plays a crucial role in regulating calcium and phosphate balance. - Secrete parathyroid hormone, which increases calcium reabsorption in the kidneys and bones. - **Functions of Parathyroid Hormone:** - Increases calcium reabsorption in the kidneys and bones - Increases bone resorption - Regulates calcium and phosphate balance -- ------------------------------------------------------- **🌊 Regulation of Fluid Volume and Blood Pressure 🌊** -- ------------------------------------------------------- -- ------------------------------------------------------ **Baroreceptors and the Sympathetic Nervous System** -- ------------------------------------------------------ - Baroreceptors play a crucial role in regulating fluid volume and blood pressure. - **Upon stimulation of the baroreceptors, the sympathetic nervous system is activated, leading to:** - Constriction of renal arterioles - Reduction of blood flow to the kidneys - Decrease in glomerular filtration rate (GFR) - **Release of enzymes and hormones involved in fluid volume and blood pressure regulation, including:** - Renin - Angiotensin 1 and 2 - Aldosterone - *These hormones promote sodium and water reabsorption from the renal tubules, increasing blood pressure and circulating blood volume.* -- ------------------------------------------------- **Renin-Angiotensin-Aldosterone System (RAAS)** -- ------------------------------------------------- - Complex system that responds to low circulating blood volume and low blood pressure. - It is a critical regulator of fluid balance and blood pressure. - **The RAAS is activated by the sympathetic nervous system, leading to:** - Decreased renal perfusion - Decrease in GFR - Release of renin, an enzyme that converts angiotensin 1 to angiotensin 2 - Angiotensin 2 acts on the renal tubules to increase sodium and water reabsorption - Release of aldosterone, which increases sodium and water reabsorption and promotes potassium excretion  -- -------------------------- **Natriuretic Peptides** -- -------------------------- - Hormones that affect fluid volume and cardiovascular function through the excretion of sodium, direct vasodilation, and opposition of the RAAS. - **There are four types of natriuretic peptides:** ------------------------------------------- ---------------------------------------------- ------------------------------------------------------------------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Peptide** **Tissue Distribution** **Function** **Atrial Natriuretic Peptide (ANP)** **Atrial myocardium** **Decreases blood pressure, promotes sodium and water excretion** **Brain Natriuretic Peptide (BNP)** **Ventricular myocardium, brain** **C-type Natriuretic Peptide (CNP)** **Brain, ovary, uterus, testes, epididymis** **D-type Natriuretic Peptide (DNP)** **Like ANP, BNP, and CNP** ------------------------------------------- ---------------------------------------------- ------------------------------------------------------------------- -- -------------------------------------- **Atrial Natriuretic Peptide (ANP)** -- -------------------------------------- - Peptides are produced by the atrial myocardium in response to increased atrial blood pressure, angiotensin 2 stimulation, endothelin release, and sympathetic nervous system discharge. - **FUNCTIONS:** - Decreases water and sodium loads in the circulatory system - Promotes water and sodium excretion through urination - Stimulates lipolysis (breakdown of fats) - Opposes the RAAS, decreasing blood pressure - **Release of ANP in response to:** - Increased sodium chloride concentration - Increased blood volume - Increased blood pressure - Stretching of the atrial wall of the heart - **ANP works in four ways to decrease blood pressure and maintain fluid and electrolyte balance:** - Suppresses the RAAS - Decreases the release of aldosterone - Increases sodium and water excretion - Stimulates lipolysis - Normal ANP levels in plasma are **20-77 pg/mL.** - Levels increase with increased blood volume and blood pressure and decrease in chronic heart failure and with the use of medications such as enalapril. A diagram of a flowchart Description automatically generated -- ------------------------------------ **🌊 Fluid Balance and Regulation** -- ------------------------------------ -- ------------------------- **Aldosterone and ANP** -- ------------------------- - Aldosterone and Atrial Natriuretic Peptide (ANP) play crucial roles in regulating fluid balance in the body. - **Aldosterone**: A hormone produced by the adrenal glands that helps regulate sodium and potassium levels in the body. - **ANP**: A hormone produced by the heart that helps regulate blood pressure and fluid balance. - **When aldosterone levels decrease, it can lead to:** - Decreased blood pressure - Decreased sodium retention - Decreased blood volume - Decreased potassium excretion - **ANP has the following effects:** - Suppresses the production of Antidiuretic Hormone (ADH) by the posterior pituitary gland - Increases the rate of urine production and water excretion - Decreases blood pressure, sodium retention, and blood volume  **ANP & RAAS PHYSIOLOGY** -- --------------------------- **Osmoreceptors and ADH** -- --------------------------- - **Osmoreceptors **are specialized sensors located on the surface of the hypothalamus that detect changes in sodium concentration. - Stimulated as osmotic pressure increases, leading to an increase in serum osmolality and dehydration of neurons, prompting a quick release of impulses to the hypothalamus to release ADH. - **ADH (Antidiuretic Hormone)** is a hormone produced by the posterior pituitary gland that helps regulate water balance in the body. - ADH increases water reabsorption in the kidneys, leading to decreased urine output and increased blood volume. - ADH is released in response to increased serum osmolality and dehydration. -- ------------------------------- **🌊 Fluid Volume Imbalances** -- ------------------------------- -- ---------------------------------------- **Hypovolemia (Fluid Volume Deficit)** -- ---------------------------------------- - A condition where the loss of extracellular fluid (ECF) volume is greater than the fluid intake. - Is not the same as dehydration, as **dehydration** refers to the loss of water alone with increased serum sodium levels. - **Causes: "DRAINED" (DUE TO LOSS OF FLUIDS)** - **D**iabetes insipidus - **R**educed fluid intake - **A**bnormal fluid loss (vomiting, diarrhea, GI suctioning, sweating) - **I**nsufficient adrenal function - **N**ausea or no access to fluids - **E**dema formation in burns or ascites (third space fluid shift) - **D**ysfunction in liver **Manifestations: \"THIRSTY WOLFCUB\"** - **T**hirst - **H**ypotension (Decreased blood pressure) - **I**ncreased heart rate - **R**educed urine output (Oliguria) - **S**unken neck veins (Flat neck veins) - **T**ime (Prolonged capillary filling time) - **Y**earning for water (Weight loss) - **W**eakness (Muscle weakness) - **O**utput of urine concentrated - **L**ethargy or confusion - **F**eel cool, clammy skin - **C**ollapse (Shock) - **U**rine concentrated - **B**rain fog (Confusion) - **Diagnostic Tests:** ------------------------------------------- -------------------------- --------------------------------------------------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Test** **Result** **Interpretation** **BUN (Blood Urea Nitrogen)** **Elevated** **Indicates dehydration or fluid volume deficit** **Creatinine** **Elevated** **Indicates kidney dysfunction** **BUN/Creatinine ratio** **\> 20:1** **Indicates fluid volume deficit** **CBC ** **Elevated hct and hgb** **Indicates hemoconcentration** **Urine specific gravity** **Elevated** **Indicates water loss and concentrated urine** **Urine osmolality** **Increased** **Serum osmolality** **Increased** **Indicates water loss and concentrated serum** **Urine sodium** **Decreased** **Indicates kidney conservation of sodium** ------------------------------------------- -------------------------- --------------------------------------------------- - **Medical management includes:** - **GOAL:** correct the fluid deficit and restore fluid balance. - Oral route is preferred for mild cases, with increased oral fluid intake. - IV route is initiated for acute or severe cases, with parenteral fluid resuscitation using isotonic electrolyte solutions (e.g. lactated Ringer\'s solution or normal saline solution). - Hypotonic electrolyte solutions (e.g. 0.45% sodium chloride) may be prescribed to provide both electrolytes and water and promote renal excretion of metabolic waste. - **Nursing management includes:** - Frequent and accurate assessment of intake and output - Use of fluid balance charts or IO record forms to track fluid status - Monitoring of vital signs and laboratory results to adjust treatment as needed. - **In patients with hypovolemia, expect the following changes in vital signs:** - Decreased blood pressure - Decreased cardiac output - Tachycardia (increased heart rate) - Decreased peripheral pulses - Increased respiratory rate (tachypnea) due to decreased lung tissue perfusion - *These changes are compensatory mechanisms to maintain blood pressure and oxygen delivery to tissues.* -- ---------------------------------------- **Hypervolemia (Fluid Volume Excess)** -- ---------------------------------------- - Isotonic expansion of the extracellular fluid (ECF) caused by abnormal retention of water and sodium. - **Causes:** - **Congestive heart failure**: inability of the heart to circulate fluid properly - **Renal failure or kidney injury**: inability of the kidneys to filter blood, leading to water and sodium retention - **Liver cirrhosis**: liver failure leading to fluid volume excess in two ways: - Affected liver sends signals to kidneys to retain excess sodium and water - Liver failure leads to decreased production of albumin, a protein that maintains stable blood volume - Excessive consumption of table salts or sodium-containing fluids - Excessive administration of sodium-containing fluids - **Clinical Manifestations of Hypervolemia:** - Distended neck veins due to fluid volume overload - Edema (third spacing) due to fluid shifting out of the intravascular system and into tissues. - Crackles, shortness of breath (SOB), or wheezing due to pulmonary edema. - Weight gain due to fluid retention - Elevated blood pressure due to increased blood volume - Increased urine output - **Diagnostic Tests:** ------------------------------------------- ------------------------------------------------------------------------------------------------------------------------------------------------------ ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Laboratory Test** **Expected Result** **BUN (Blood Urea Nitrogen)** **Decreased due to plasma dilution** **Hematocrit** **Decreased due to plasma dilution** **Urine Sodium** **Elevated if kidneys are attempting to excrete excess volume, but decreased in conditions such as cirrhosis, heart failure, or nephrotic syndrome** ------------------------------------------- ------------------------------------------------------------------------------------------------------------------------------------------------------ ---------- - **Pharmacologic Therapy:** - Diuretics to inhibit reabsorption of sodium and water by the kidneys. - Furosemide (loop diuretic) for severe hypervolemia - Thiazide diuretics (e.g., hydrochlorothiazide) for mild to moderate hypervolemia - **Nursing Management:** - Monitor intake and output at irregular intervals to identify excessive fluid retention. - Weigh patient daily and note any rapid weight gain. - Monitor breath sounds and degree of edema. - Assess for pitting edema by measuring circumference of extremities daily. - Encourage adherence to prescribed diet and sodium restriction. - Instruct patient to avoid over-the-counter medications that may contain sodium. - **Medical Management:** - **Hemodialysis or peritoneal dialysis** may be used to remove excess fluid, nitrogenous waste, and control potassium and acid-base balance in patients with severely impaired renal function. -- ------------------------------------- **🌊 Electrolyte Volume Imbalances** -- ------------------------------------- - Disturbances in electrolyte balances are common in clinical practice and may need to be corrected based on history, physical examination findings, and laboratory values (with comparison to previous values). -- ----------------------- **Sodium Imbalances** -- ----------------------- - **Sodium (Na+)** is the most abundant electrolyte in the extracellular fluid (ECF) - Its concentration ranges from **135 to 145 mEq/L** **(135 to 145 mmol/L)** - The primary determinant of ECF volume and osmolality - **Major Function:** - Controlling water distribution throughout the body, because it does not easily cross the plasma membrane and because of its abundance and high concentration in the body - **Sodium is regulated by:** - ADH (Antidiuretic Hormone) - Thirst - Renin-Angiotensin-Aldosterone System -- ------------------------------------------------------------------------- **Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)** -- ------------------------------------------------------------------------- - SIADH may be associated with sodium imbalance. - When there is a decrease in the circulating plasma osmolality, blood volume, or blood pressure, ADH (also called arginine vasopressin \[AVP\]) is released from the posterior pituitary.  - Over secretion of ADH can cause SIADH. - **Patients at risk for SIADH:** - Older adults - Those who have had brain surgery or have a brain tumor, pulmonary malignancy, or acquired immune deficiency syndrome (AIDS) - Those on mechanical ventilation - Those taking selective serotonin reuptake inhibitors (SSRIs) -- ----------------------------------- **Sodium Deficit (Hyponatremia)** -- ----------------------------------- - **Hyponatremia** refers to a serum sodium level that is **less than 135 mEq/L (135 mmol/L).** +-----------------------+-----------------------+-----------------------+ | **TABULAR NOTES ( | | | | Insert Tab \> Table | | | | )** | | | +-----------------------+-----------------------+-----------------------+ | | **INFO** | **INFO** | +-----------------------+-----------------------+-----------------------+ | **Type of | **Description** | | | Hyponatremia** | | | +-----------------------+-----------------------+-----------------------+ | **Acute | **- Commonly the | | | Hyponatremia** | result of a fluid | | | | overload in a | | | | surgical patient.** | | | | | | | | **- This is a | | | | dilutional | | | | hyponatremia because | | | | the excess water | | | | dilutes the sodium in | | | | the bloodstream.** | | +-----------------------+-----------------------+-----------------------+ | **Chronic | **- Seen more | | | Hyponatremia** | frequently in | | | | patients outside the | | | | hospital setting, has | | | | a longer duration, | | | | and has less serious | | | | neurologic | | | | sequelae.** | | +-----------------------+-----------------------+-----------------------+ | **Exercise-Associated | **- More frequently | | | Hyponatremia** | found in women and | | | | those of smaller | | | | stature.** | | | | | | | | **- It can occur | | | | during extreme | | | | temperatures, because | | | | of excessive fluid | | | | intake before | | | | exercise, or | | | | prolonged exercise | | | | that results in | | | | excess loss of sodium | | | | through | | | | perspiration.** | | +-----------------------+-----------------------+-----------------------+ - **Clinical Manifestations: \"DROPS VAN\"** - Dry mucosa - Reduced saliva production - Orthostatic fall in blood pressure - Poor skin turgor - Severe headache - Vomiting - Abdominal cramping - Neurologic changes (Altered mental status, status epilepticus, coma) - **Assessment and Diagnostic Findings:** +-----------+-----------+-----------+-----------+-----------+-----------+ | | | | **TABULAR | | | | | | | NOTES ( | | | | | | | Insert | | | | | | | Tab \> | | | | | | | Table )** | | | +-----------+-----------+-----------+-----------+-----------+-----------+ | | **INFO** | | | | **INFO** | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Paramet | **Normal | **Hyponat | **Hyponat | **Hyponat | | | er** | Range** | remia | remia | remia | | | | | (General) | due to | due to | | | | | ** | SIADH** | Sodium | | | | | | | Deficienc | | | | | | | y** | | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Serum | **135-145 | -- | **Often | **Less | | | Sodium** | mmol/L** | -- | \< 100 | than 135 | | | | | | mEq/L** | mEq/L** | | | | | **Less | | | | | | | than 135 | | | | | | | mEq/L** | | | | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Serum | **275-295 | **Decreas | **Decreas | **Decreas | | | Osmolalit | mOsm/kg** | ed** | ed** | ed** | | | y** | | | | | | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Urinary | **Varies, | **Variabl | **Greater | **Less | | | Sodium** | but | e, | than 20 | than 20 | | | | generally | depends | mEq/L** | mEq/L** | | | | \> 20 | on | | | | | | mEq/L** | cause** | | | | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Urine | **1.010-1 | **Low to | **Greater | **Low | | | Specific |.030** | normal** | than | (1.002 to | | | Gravity** | | | 1.012** | 1.004)** | | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Periphe | **None** | **Absent* | **Absent* | **Sometim | | | ral | | * | * | es | | | Edema** | | | | absent, | | | | | | | but may | | | | | | | show | | | | | | | pitting | | | | | | | edema** | | +-----------+-----------+-----------+-----------+-----------+-----------+ | **Fluid | **Normal* | **Water | **Water | **None** | | | Distribut | * | retention | retention | | | | ion** | | inside | inside | | | | | | cells (no | cells | | | | | | edema)** | (pitting | | | | | | | edema)** | | | +-----------+-----------+-----------+-----------+-----------+-----------+ - **Medical Management:** - **Sodium Replacement**---the most common treatment for hyponatremia - **Sodium-rich foods or sodium supplements** for patients who can eat and drink. - **Lactated Ringer's solution** or **Isotonic saline (0.9% sodium chloride)** for patients who cannot consume sodium orally. - slowly through IV infusion - **Hypertonic Saline (3% sodium chloride)** may be administered in more severe cases, particularly in patients with SIADH. - Administered under close monitoring - **Parenteral Sodium Replacement** via NGT ------------------------------------------- ---------------------------------------------------------------------------------------------------------------------------------------------------------------- ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Treatment** **Description** **AVP Receptor Antagonists** **blocking the effect of ADH at the nephron, which in turn allows diuresis to occur and leads to water excretion.** **Conivaptan HCl** **AVP receptor antagonist that is limited to the treatment of hospitalized patients.** **Tolvaptan** **Oral medication indicated for clinically significant hypervolemic and euvolemic hyponatremia that must be initiated and monitored in the hospital setting.** ------------------------------------------- ---------------------------------------------------------------------------------------------------------------------------------------------------------------- ---------- - **Nursing Management:** - **Monitor the patients: "I WEIGH"** - I - I&O (Intake and Output) - W - Weight (Daily body weight) - E - Evaluate for excess water input or insufficient output - I - Identify patients at risk - G - GI symptoms (Anorexia, nausea, vomiting, abdominal cramping) - H - Hyponatremia (Monitor sodium levels) - **Detect early and control the signs of: "SALTS"** - S - Sodium levels (Monitor labs) - A - Assess fluid intake and output (I&O) - L - Look for GI symptoms (Anorexia, nausea, vomiting, abdominal cramping) - T - Track daily body weight - S - Start interventions early to prevent serious consequences - **Nursing Considerations:** - Fluid restriction - Assess for dehydration - **In using hypertonic solution,** careful monitoring for symptoms of rapid sodium increase, such as altered cognition, ataxia, pseudobulbar palsy, or coma, which can lead to **osmotic demyelination**. - Sodium levels should not be raised by more than 12 mEq/L in 24 hours. - Review the patient's current medications (e.g., SSRIs, anticonvulsants) as they may increase the risk of hyponatremia. - If hyponatremia is severe, place the patient on seizure precautions (e.g., padded side rails, monitoring) as a drop in sodium can lead to seizures or coma. - **Sodium Content of Common Foods and Fluids** ------------------------------------------- ------------------------- ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Food/Fluid** **Sodium Content (mg)** **Broth made with one beef cube** **900** **8 oz of tomato juice** **700** ------------------------------------------- ------------------------- ---------- -- ----------------------------------- **Sodium Excess (Hypernatremia)** -- ----------------------------------- -  A condition where the serum sodium level is **higher than 145 mEq/L (145 mmol/L).** - It can be caused by a gain of sodium more than water or by a loss of water more than sodium. - **Causes: "FEDS IN"** - **F** - Fluid deprivation - **E** - Excessive sodium intake - **D** - Diuretics - **S** - Sodium-rich diet - **I** - Insufficient water intake - **N** - Diabetes insipidus - **Clinical Manifestations: "THIRSTY"** - **T** - Thirst - **H** - Headache - **I** - Increased fatigue (Fatigue) - **R** - Reduced saliva (Dry mouth) - **S** - Seizures (in severe cases) - **T** - Tremors (may also occur) - **Y** - Yawn (indicates fatigue or drowsiness) - **Assessment and Diagnostic Findings:** ------------------------------------------- ---------------------------------------------------------------------- ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Parameters** **Sodium Content (mg)** **Serum Sodium Level** **Exceeds 145 mEq/L** **Serum Osmolality** **Exceeds 300 mOsm/kg** **Urine Specific Gravity** **Increased (indicates concentrated urine)** **Urine Osmolality** **Increased (if water loss is from a route other than the kidneys)** **Diabetes Insipidus (Urine Osmolality)** **Less than 250 mOsm/kg (very dilute urine)** ------------------------------------------- ---------------------------------------------------------------------- ---------- - **Medical Management: "SLOW HYPE"** - **S** - Slow sodium reduction (Gradual reduction to avoid complications) - **L** - Lactated or hypotonic saline (0.45% NaCl) (Preferred for fluid balance) - **O**- Osmolality management (Avoid rapid changes to prevent cerebral edema) - **W** - Water replacement with D5W (When water needs to be replaced without sodium) - **H** - Hyperglycemia correction with 0.45% NaCl (Used in severe cases) - **Y** - Yes to diuretics (May be used to eliminate excess sodium) - **P** - Prescribe Desmopressin (Synthetic ADH for diabetes insipidus) - **E** - Electrolyte balance (Monitor and adjust carefully) - **Nursing Management: \"F.L.U.I.D.S. C.A.R.E.\"** - **F** - Fluid Monitoring (Track intake and output carefully) - **L** - Look for behavior changes (Restlessness, disorientation, lethargy) - **U** - Understand water intake (Ensure patients can drink or receive fluids) - **I** - Intervene with appropriate fluids (Consult for enteral or parenteral routes if needed) - **D** - Daily sodium checks (Monitor serum sodium levels regularly) - **S** - Sodium sources (Review medications and diet for high sodium content) - **C** - Check thirst levels (Evaluate patient\'s ability to perceive thirst) - **A** - Alert for neurological changes (Watch for confusion and neurologic status) - **R** - Rehydrate slowly (Avoid rapid sodium reduction to prevent cerebral edema) - **E** - Ensure water balance (Prevent hypernatremia through regular fluid provision) -- -------------------------- **Potassium Imbalances** -- -------------------------- - Major intracellular electrolyte: 98% of the body's potassium is inside the cells. - Extracellular Potassium (2%): Critical for neuromuscular and cardiac function. - **Influences on skeletal and cardiac muscles**: Alters **myocardial irritability** and **rhythm**. - Normal serum potassium concentration: **3.5 - 5 mEq/L (mmol/L)** - **Potassium Physiology:** - Sodium-potassium pump: Actively pumps potassium into cells, maintaining intracellular concentration. - Potassium imbalances affect neuromuscular and cardiac activity. - **Potassium Regulation:** - Kidneys: Play a major role, excreting 80% of daily potassium through urine. - Potassium is also lost via the bowel and sweat (20%). - Kidneys regulate potassium balance by adjusting excretion through urine, facilitated by the potassium concentration gradient. - Aldosterone: Increases potassium excretion. - Serum potassium increase: Leads to increased excretion through the renal tubules. - In case of potassium deficit, kidneys may continue to lose potassium through urine since they conserve sodium more efficiently than potassium -- ------------------------------------- **Potassium Deficit (Hypokalemia)** -- ------------------------------------- - A condition where the serum potassium level is **less than 3.5 mEq/L (3.5 mmol/L).** - Can cause death through cardiac or respiratory arrest.  - **Causes: \"V.D.I.L.V.H.I.D.\"** - **V** - Vomiting and gastric suction - **D** - Diarrhea - **I** - Intestinal suctioning (prolonged) - **L** - Recent ileostomy - **V** - Villous adenoma (intestinal tumor) - **H** - Hyperaldosteronism - **I** - Insulin hypersecretion - **D** - Diabetic ketoacidosis (DKA) - **Clinical Manifestations: \"FAM DAP\"** - **F** - Fatigue (Feeling weak and tired) - **A** - Anorexia (Loss of appetite) - **M** - Muscle weakness (Weakness in the muscles) - **D** - Decreased bowel motility (Slowed movement of food through the digestive system) - **A** - Arrhythmias (Abnormal heart rhythms) - **P** -- Paresthesia (Numbness or tingling sensations) - **Assessment and Diagnostic Findings** - Serum potassium concentration is **less than 3.5 mEq/L (3.5 mmol/L)** - **Electrocardiographic (ECG) changes:** - Flat T waves - Inverted T waves - Depressed ST segments - Elevated U wave  - **Medical Management** - Oral potassium supplements - IV potassium replacement therapy (in severe cases) - **Dietary intake of potassium-rich foods:** - Fruits (bananas, melon, citrus fruits) - Vegetables (fresh and frozen) - Lean meats - Milk - Whole grains -- ------------------------------------- **Potassium Excess (Hyperkalemia)** -- ------------------------------------- - A condition where the serum potassium level is **greater than 5 mEq/L (5 mmol/L).** - It is usually more dangerous because cardiac arrest is more frequently associated with high serum potassium levels.\" - **Causes: \"DREAM UP\"** - **D** - Decreased renal excretion of potassium - **R** - Rapid administration of potassium - **E** - Extracellular movement of potassium from ICF - **A** - Administration of certain medications (e.g., KCl, heparin, ACE inhibitors, NSAIDs, beta-blockers, cyclosporine, tacrolimus, potassium-sparing diuretics) - **M** - Medications (to emphasize the impact of various drugs) - **U** - Upward shift of potassium from cells (movement to ECF) - **P** - Potassium overload or excess intake - **Clinical Manifestation:** - Muscle weakness - Fatigue - Palpitations - Shortness of breath - Abdominal cramps - **Assessment and Diagnostic Findings:** - Serum potassium concentration is **greater than 5 mEq/L (5 mmol/L)** - **Electrocardiographic (ECG) changes:** - Peaked T waves - Widened QRS complex - Prolonged PR interval - **Arterial blood gas (ABG) values:** - Elevated bicarbonate levels - Elevated pH levels A graph of a heart beat Description automatically generated with medium confidence - **Medical Management:** - Restriction of dietary potassium and potassium-containing medications - Administration of potassium-lowering medications (e.g. calcium gluconate, insulin, glucose) - Hemodialysis (in severe cases) - **Causes of Pseudohyperkalemia:** - Potassium leaks out of red blood cells (RBCs) while the blood is awaiting analysis - Lack of awareness of these causes can lead to aggressive treatment of a nonexistent hyperkalemia - **Clinical Manifestations:** - [Cardiac effects:] - Peaked, narrow T waves - ST-segment depression - Shortened QT interval - Prolonged PR interval - Disappearance of P waves - Decomposition and widening of the QRS complex - Ventricular arrhythmias and cardiac arrest may occur - **Assessment and Diagnostic Findings:** ------------------------------------------- -------------------------------------------------------------------------------- ---------- **TABULAR NOTES ( Insert Tab \> Table )** **INFO** **INFO** **Diagnostic Finding** **Description** **Serum Potassium Level** **Crucial to the diagnosis of hyperkalemia** **ECG Changes** **Peaked, narrow T waves, ST-segment depression, shortened QT interval, etc.** **ABG Analysis** **May reveal metabolic or respiratory acidosis** ------------------------------------------- -------------------------------------------------------------------------------- ---------- - **Medical Management: \"CIGS B\"** - **C** - Calcium Gluconate (IV): Antagonizes hyperkalemia effects on the heart. - **I** - Insulin (Regular): Causes a temporary shift of potassium into cells. - **G** - Glucose (Hypertonic Dextrose Solution): Also shifts potassium into cells. - **S** - Sodium Bicarbonate: Alkalinizes plasma to help shift potassium into cells. - **B** - Beta-2 Agonists: Decrease potassium levels but may cause side effects. - **Nursing Management: \"I\'M VIBRANT\"** - **I** - Identify patients at risk: Closely monitor those at risk for potassium excess. - **M** - Monitor I&O: Keep track of intake and output. - **V** - Vital signs: Measure vital signs, especially apical pulse. - **B** - Be alert for muscle weakness: Observe for signs of muscle weakness and arrhythmias. - **R** - Recognize the presence of tingling or numbness. - **A** - Assess GI symptoms: Watch for nausea and intestinal cramping. - **N** - Note laboratory values: Monitor serum potassium, BUN, serum creatinine, serum glucose, and ABG values. - **T** - Take action: Implement appropriate interventions based on findings. -- ------------------------ **Calcium Imbalances** -- ------------------------ - **Calcium** is a major component of bones and teeth - Plays a crucial role in transmitting nerve impulses - Regulating muscle contraction and relaxation - Blood coagulation - **Normal Calcium Levels:** - Total serum calcium: **8.8 to 10.4 mg/dL** (2.2 to 2.6 mmol/L) - Ionized serum calcium: **4.5 to 5.1 mg/dL** (1.1 to 1.3 mmol/L) - **Forms of Calcium in Plasma:** - Ionized (physiologically active) - Bound (to serum proteins, primarily albumin) - Complex (combined with nonprotein anions: phosphate, citrate, and carbonate) - **Calcium Absorption and Excretion** - **Absorption:** Calcium is absorbed from foods through the gastrointestinal (GI) tract, but this requires: - Normal gastric acidity - Vitamin D - **Excretion**: - Primarily excreted through feces. - The remainder is excreted through the urine. - **Hormonal Control of Calcium Levels** - Calcium regulation in the blood is primarily controlled by two hormones: - **Parathyroid Hormone (PTH)**: Secreted by the parathyroid glands in response to low calcium levels. - **Calcitonin**: Secreted by the thyroid gland when calcium levels are too high. - **Mechanism of Action of PTH (Parathyroid Hormone)** - When ionized serum calcium levels decrease in the bloodstream: - PTH is released from the parathyroid glands. - PTH increases calcium levels by: - **Increasing calcium absorption in the GI tract**: This enhances calcium uptake from food. - **Increasing calcium reabsorption in the kidneys**: Less calcium is lost through urine. - **Stimulating bone resorption**: Calcium is released from bones into the bloodstream. - As calcium levels rise, the parathyroid glands **reduce PTH secretion** to maintain balance. - **Mechanism of Action of Calcitonin** - When calcium levels increase excessively in the bloodstream: - The **thyroid gland releases calcitonin**. - Calcitonin **lowers serum calcium** by: - **Inhibiting bone resorption**: Prevents the release of calcium from bones. - **Reducing calcium reabsorption in the kidneys**: This allows more calcium to be excreted in the urine. -- ------------------------------------ **Calcium Deficit (Hypocalcemia)** -- ------------------------------------ - Condition where the serum calcium level falls **below 8.8 mg/dL.** - A person can have low calcium in their bones (e.g., osteoporosis) but still present with a normal serum calcium level. - Indicates that hypocalcemia is not always directly reflective of the body's overall calcium stores, as calcium may be depleted from bones without immediately lowering serum calcium. - **Risk factors:** - Older adults and individuals with disabilities - Immobility - **Causes:** - **Hypoparathyroidism (both primary and surgical)** is a major cause of hypocalcemia. - Massive Administration of Citrated Blood - During **massive hemorrhage and shock**, citrated blood is used, which can bind to **ionized calcium**, removing it temporarily from circulation. - Pancreatitis - **Excess glucagon** from the inflamed pancreas increases **calcitonin secretion**, which lowers calcium levels. - Acute Kidney Injury (AKI) - Often have **elevated serum phosphate** levels (**hyperphosphatemia**) that can cause **reciprocal drop** in serum calcium. - **Predisposing factors:** - Inadequate vitamin D intake - Magnesium deficiency - Medullary thyroid carcinoma - Low serum albumin - Alkalosis - Alcohol abuse - Medications (Antacids, Antibiotics, Chemotherapy Agents, Corticosteroids, Diuretics, and Caffeine) - **Clinical Manifestations: \"TENTC BO\"** - **T**: Tetany (Muscle cramps, spasms, and weakness) - **E**: ECG changes (Prolonged QT, Torsades de pointes) - **N**: Neurological symptoms (Seizures, Mental changes) - **T:** **Trousseau sign** (Twitching of facial muscles upon tapping the facial nerve). - **C**: **Chvostek sign** (Carpal spasm elicited by inflating a blood pressure cuff). - **B**: Breathing difficulties (Dyspnea, Laryngospasm) - **O**: Osteoporosis  - **Diagnostic Evaluation** - **Serum Calcium & Albumin Assessment:** - Normal Serum Albumin: **4 g/dL** - For every decrease of 1 g/dL albumin: Serum calcium is underestimated by **0.8 mg/dL.** - **Corrected Serum Calcium Formula:** - Corrected Calcium=Reported Calcium+\[0.8×(4 - Serum Albumin)\] - **pH Effect on Calcium** - **Alkalosis**: Increases calcium binding to proteins, decreasing ionized calcium → Symptoms of hypocalcemia. - **Acidosis:** Less calcium binds to proteins, increasing ionized calcium. - **Medical Management: "CALCIUM"** - **C**hoose gluconate (less irritant) - **A**void NaCl and phosphate solutions - **L**ook for digitalis toxicity (during Ca therapy) - **C**ontrol IV infusion rate - **I**nfuse slowly (risk of cardiac arrest) - **U**se D5W for dilution - **M**onitor BP & IV site (WOF: risk of extravasation) - **Nutritional Therapy: "VIT-CALM"** - **V**itamin D aids absorption - **I**ntake 1000-1500 mg/day - **T**ake calcium in divided doses - **C**hoose leafy greens & dairy (Milk, leafy greens, canned salmon/sardines, oysters) - **A**void high alcohol & caffeine (increase calcium excretion) - **L**ook out for smoking effects (increase calcium excretion) - **M**onitor phosphorus in chronic kidney disease patients - **Nursing Management: "SAFE-CAL"** - **S**eizure precautions - **A**irway monitoring (laryngospasm) - **F**ocus on calcium diet - **E**ducating patients on supplements - **C**aution with laxatives & phosphorus (decrease calcium absorption) -- ------------------------------------ **Calcium Excess (Hypercalcemia)** -- ------------------------------------ - Serum calcium **\> 10.4 mg/dL (2.6 mmol/L).** - **Causes**: - Malignancies (breast, lung, renal, multiple myeloma) - Vitamin intoxication (A & D) - Hyperthyroidism (increased PTH → increased calcium release) - Diuretics (thiazide) - **Pathophysiology:** - **Calcium-Phosphorus Relationship:** High calcium can lead to calcifications if calcium × phosphorus \> 70 mg/dL. - **Neuromuscular Effects:** Hypercalcemia reduces neuromuscular excitability - **Clinical Manifestations: "CLAMPS"** - **C**onfusion - **L**ethargy - **A**bdominal cramps - **M**uscle weakness - **P**olyuria - **S**evere thirst - **Diagnostic Evaluation:** - Serum calcium **\> 10.4 mg/dL (2.6 mmol/L).** - **ECG changes:** arrhythmias, shortened QT interval, possible heart blocks. - **PTH Test:** Increased in hyperparathyroidism, suppressed in malignancy. - **Medical Management:** - **Goals:** Decrease serum calcium, treat underlying cause. - **Pharmacologic Therapy:** - **Hydration:** IV fluids (0.9% NaCl) to dilute and promote calcium excretion. - **Calcitonin:** Reduces serum calcium levels, especially in cardiac/renal patients. - **Bisphosphonates:** (pamidronate, ibandronate) inhibit osteoclasts. - **Mithramycin:** Lowers serum calcium but has significant side effects. - **Nursing Management:** - Monitor at-risk patients. - Encourage mobility and hydration (2.8 to 3.8 L daily). - Dietary fiber for constipation. - Assess for digitalis toxicity if on digitalis medications. - Monitor ECG for arrhythmias. -- -------------------------- **Magnesium Imbalances** -- -------------------------- - Abundant intracellular cation. - Activates many intracellular enzyme systems. - Involved in carbohydrate and protein metabolism. - Normal Serum Magnesium Levels: **1.8 to 2.6 mg/dL** (0.74 to 1.07 mmol/L) - **Distribution of Magnesium**: - One-third bound to protein (e.g., albumin). - Two-thirds as free cations (active component: Mg++). - **Neuromuscular Function**: - Influences excitability of muscle cells: - **Excess Mg**: Decreases muscle excitability. - **Deficit Mg:** Increases neuromuscular irritability and contractility. - Acts at the myoneural junction by inhibiting acetylcholine release. - Increases stimulus threshold in nerve fibers. - **Effects on the Cardiovascular System**: - Produces vasodilation. - Decreases peripheral resistance. - **Magnesium Storage**: - Most stored in bone; blood magnesium is either bound to protein or free as Mg++ ions. -- ---------------------------------------- **Magnesium Deficit (Hypomagnesemia)** -- ---------------------------------------- - Below-normal serum magnesium concentration; often associated with hypokalemia and hypocalcemia. - Less than **1.8 mg/dL** (0.74 mmol/L) - **Causes**: "**GAMMA"** - **G**I losses - **A**lcohol withdrawal - **M**alabsorption - **M**edications - **A**bnormal conditions (e.g., DKA) - **Clinical Manifestations:** - **Neuromuscular:** Muscle weakness, Chvostek's sign, Trousseau's sign. - **Psychological:** Apathy, confusion, agitation, hallucinations. - **Cardiac:** ECG changes (prolonged QRS, ST segment depression), arrhythmias (torsades de pointes). - **Diagnostic Evaluation:** - **Serum magnesium:** less than 1.8 mg/dL. - Urine magnesium levels post-loading dose to identify depletion causes. - **Advanced techniques:** NMR spectroscopy and ion-selective electrodes for ionized magnesium. - **Medical Management:** - **Dietary Sources:** - Green leafy vegetables, nuts, legumes, bananas, whole grains. - **Oral Supplements:** Magnesium oxide or gluconate (can cause diarrhea). - **IV Magnesium:** Necessary for parenteral nutrition or severe hypomagnesemia. - **Nursing Management:** - **Monitoring:** - **Vital signs:** Check for changes in cardiac rhythm, hypotension. - **Urine output:** Monitor for less than 100 mL in 4 hours. - Patients on digitalis should be closely observed for toxicity. - **Education**: Teach patients about magnesium-rich foods. -- ---------------------------------------- **Magnesium Excess (Hypermagnesemia)** -- ---------------------------------------- - Serum magnesium level higher than **2.6 mg/dL** (1.07 mmol/L). - **Causes**: - Kidney injury (most common) - Untreated DKA (diabetic ketoacidosis) - Excess magnesium (e.g., in pregnancy or hypomagnesemia treatment) - Adrenocortical insufficiency (e.g., Addison\'s disease) - Medications: Magnesium-based antacids/laxatives, opioids, anticholinergics - Lithium intoxication - Soft tissue injury (trauma, shock, sepsis, burns) - **Pathophysiology:** - Elevated magnesium levels lead to: - CNS depression - Neuromuscular junction depression - **Serious consequences**: Coma, heart block, cardiac arrest when levels exceed **10 mEq/L** (5 mmol/L). - **Clinical Manifestations: "HARD CUES"** - **H**ypotension - **A**rrhythmias (bradycardia, heart block) - **R**espiratory depression - **D**ecreased DTRs - **C**onfusion (altered LOC) - **U**nable to respond (weakness) - **E**CG changes (prolonged intervals) - **S**hallow respirations - **Diagnostic Evaluation:** - **Serum Magnesium:** \> 2.6 mg/dL (1.07 mmol/L) - Increased Potassium and Calcium - **ECG changes:** PR interval, T waves, QRS, QT interval prolongation, AV block. - **Medical Management:** - Avoid magnesium in patients with kidney injury. - Discontinue all magnesium in severe cases. - Emergency treatments: - IV calcium (antagonist) - Ventilatory support if needed - Hemodialysis with magnesium-free dialysate - **Nursing Management: "VITALS"** - **V**ital signs monitoring: BP, RR - **I**nformation on medications - Avoid magnesium-containing medications with kidney issues - Consult primary providers for OTC supplements - **T**est for DTRs (deep tendon reflexes) - Neuromuscular status muscles strength - **A**rrhythmias awareness - **L**iquid intake/output monitoring - **S**afety precautions (patient education) -- --------------------------- **Phosphorus Imbalances** -- --------------------------- - Critical for all body tissues. - Abundant in developed countries\' diets. - Normal Serum Phosphorus Levels: **2.7 to 4.5 mg/dL** (0.87 to 1.45 mmol/L) in adults. - **Essential for:** - Muscle and RBC function - Formation of ATP and 2,3-diphosphoglycerate (facilitates oxygen release from hemoglobin) - Maintenance of acid-base balance - Nervous system function - Intermediary metabolism of carbohydrates, proteins, and fats - **Major structural component of:** - Bones and teeth - Cell membranes (phospholipids) - Nucleotides and nucleic acids (DNA and RNA) - **Distribution:** - 85% in bones and teeth - 14% in soft tissues - \ - **Homeostasis Regulation:** - Absorption: GI tract - Excretion: Kidneys - Bone Interaction: Shifts into/out of bones - **Hormonal Regulation:** - **Parathyroid Hormone (PTH):** Increases phosphate reabsorption in kidneys; shifts phosphate from bone to plasma. - **Vitamin D:** Aids in phosphate homeostasis. -- ------------------------------------------- **Phosphorus Deficit (Hypophosphatemia)** -- ------------------------------------------- - A condition characterized by serum phosphorus levels below **2.7 mg/dL (0.87 mmol/L).** - **Causes:** - Inadequate intake - Excess excretion (renal phosphate wasting) - Shift from extracellular to intracellular spaces - Decreased intestinal absorption - **Pathophysiology:** - **Commonly occurs in:** - GI malabsorption disorders (e.g., Crohn\'s disease) - Eating disorders (anorexia, bulimia) - Vitamin D deficiency (reduces absorption) - Antacid use (high in calcium, magnesium, aluminum) - **Key conditions**: - Severe malnutrition - Alcoholism - Hyperparathyroidism - **Clinical Manifestations:** - Muscle weakness and pain - Bone pain - Altered mental status - Seizures - Heart failure - **Diagnostic Evaluation:** - **Serum Phosphorus:** Less than 2.7 mg/dL (0.87 mmol/L) - **Considerations:** - Insulin/glucose administration may lower phosphorus - Elevated PTH may indicate renal phosphate wasting - 24-hour urine collection for phosphorus if renal issues are suspected - **Medical Management:** - **Goals**: - Prevention of hypophosphatemia - Treat underlying cause - Mild cases: Oral phosphate supplements (dairy, meats, beans) - Severe cases: Aggressive IV phosphorus correction if levels \ - **Nursing Management:** - Monitor at-risk patients (e.g., those on parenteral nutrition) - Gradually introduce calories to avoid rapid shifts - Encourage phosphorus-rich foods (milk, organ meats, beans) - Monitor serum calcium and phosphate levels during IV therapy -- ------------------------------------------- **Phosphorus Excess (Hyperphosphatemia)** -- ------------------------------------------- - Serum phosphorus level \ **4.5 mg/dL** (1.45 mmol/L). - **Causes:** - Kidney injury (most common) -- reduced phosphate excretion. - Increased intake of phosphorus. - Shift from intracellular to extracellular space. - **Other conditions:** - Excessive vitamin D, - Hypoparathyroidism, - Chemotherapy, - Total parenteral nutrition (TPN). - **Pathophysiology:** - Kidney dysfunction (renal function ↓ 40-50%) → phosphate retention. - Hypoparathyroidism → kidneys fail to inhibit phosphate reabsorption. - Risk of soft tissue calcification (e.g., organs, joints, arteries). - **Clinical Manifestations:** - Tetany (muscle cramping) due to low calcium (hypocalcemia). - Soft tissue calcifications in patients with reduced glomerular filtration rate (GFR). - Hypocalcemia → neuromuscular irritability (muscle spasms). - **Long-term effects:** - Pruritus (itching), - Decreased urine output, - Vision impairment, - Palpitations. - **Diagnostic Evaluation:** - **Serum phosphorus** \ 4.5 mg/dL (1.45 mmol/L). - **Low serum calcium** (due to reciprocal relationship). - **X-rays**: Skeletal changes, abnormal bone development. - **PTH levels decreased** in hypoparathyroidism. - **BUN and creatinine:** Assess renal function. - **Medical Management:** - Reduce phosphate intake (low-phosphate diet). - **Phosphate binders with meals:** - Calcium carbonate/citrate (monitor for hypercalcemia), - Sevelamer (calcium-free binder), - Lanthanum or Sucroferric oxyhydroxide. - **Diuresis:** Forced saline diuresis with loop diuretics (if normal renal function). - **Hemodialysis**: Lowers phosphorus in severe cases. - **Nursing Management:** - Monitor for signs of hypocalcemia (e.g., muscle cramping). - Educate patients on low-phosphorus diet: - Avoid foods like **cheese, nuts, meats, whole grains, sardines, dairy**. - Monitor urine output during diuresis. - Educate about avoiding phosphate-containing laxatives/enemas. - Monitor calcium levels when administering phosphate binders. -- ------------------------- **Chloride Imbalances** -- ------------------------- - **Major anion of ECF:** Maintains water and acid--base balance. - **Key electrolyte:** Works with sodium to maintain osmotic pressure. - **Involved in:** Gastric acid (HCl), pancreatic juices, sweat, bile, and saliva production. - Normal serum chloride: **97--107 mEq/L** (97--107 mmol/L); intracellular level is 4 mEq/L. - **Chloride balance:** Dependent on dietary intake, kidney excretion, and reabsorption. - **Chloride Regulation:** - **Direct link to sodium:** Changes in serum chloride mirror sodium levels. - **Aldosterone:** Increases sodium reabsorption, enhancing chloride reabsorption. - **Chloride shift:** Movement of chloride into RBCs in exchange for bicarbonate (inverse relationship). - **Chloride's Role in the Body:** - **Cerebrospinal fluid:** Sodium and chloride attract water to form fluid. - **Acid--base balance:** Assists in buffering oxygen and CO₂ exchange in RBCs. - **Dietary source:** Primarily from table salt. -- -------------------------------------- **Chloride Deficit (Hypochloremia)** -- -------------------------------------- - **Serum chloride level \< 97 mEq/L.** - **Causes:** - GI losses (tube drainage, gastric suction, vomiting, diarrhea) - Chloride-deficient IV fluids - Low sodium, DKA, respiratory acidosis, blood transfusions, diuretics - SIADH, burns, sweating, fever - Medications: Aldosterone, ACTH, corticosteroids, bicarbonates, diuretics, laxatives - **Clinical Manifestations: \"TWITCH\"** - Associated with hyponatremia, hypokalemia, metabolic alkalosis. - **T**etany - **W**eaknesses - **I**rregular heartbeat (arrhythmias) - **T**witching - **C**ramps - **H**yper DTRs - **Diagnostic Evaluation: \"CUPS\"** - **C**hloride levels low - **U**rine chloride decreases - **P**otassium/Sodium loss - **S**erum bicarbonate increase (metabolic alkalosis) - **Medical Management: \"SALT\"** - **S**aline IV (Chloride replacement) - **A**mmonium chloride (for alkalosis) - Contraindicated: Liver/renal impairment. - **L**ower diuretics/Restricted - **T**reatment of underlying cause - **Nursing Management:** - **Monitor:** - I&O, ABG, serum electrolytes - LOC, muscle strength/movement, vital signs, respiratory status - **Educate on high chloride foods:** - Tomato juice, bananas, dates, eggs, cheese, milk, salty broth, canned veggies, processed meats - Avoid excess water intake without electrolytes (e.g., bottled water). -- -------------------------------------- **Chloride Excess (Hyperchloremia)** -- -------------------------------------- - **Serum chloride \> 107 mEq/L (107 mmol/L)**. - Often accompanied by **hypernatremia**, **bicarbonate loss**, and **metabolic acidosis**. - **Pathophysiology:** - **Usually caused by iatrogenic (medical treatment) factors like:** - Excessive chloride administration (e.g., 0.9% saline, 0.45% saline, or Lactated Ringer\'s). - Bicarbonate loss (via kidneys or GI tract) increases chloride ions. - **Acidosis** develops as chloride accumulates and bicarbonate decreases. - **Causes:** - Head trauma - Excess adrenocortical hormone production - Increased perspiration - Decreased glomerular filtration - **Clinical Manifestations: \"TWIRL\"** - **T**achypnea - **W**eaknesses - **I**mpaired cognition - **R**apid breathing (deep) - **L**ethargy/Low cardiac output - **Diagnostic Evaluation: \"CHOPS\"** - Chloride **\> 108 mEq/L** - Hypernatremia **\> 145 mEq/L** - Urine chloride increased - **PH \< 7.35** (acidosis) - Serum bicarbonate **\< 22 mEq/L** - **Medical Management:** - Correct the underlying cause. - **Hypotonic IV solutions** to restore fluid and electrolyte balance. - **Lactated Ringer\'s** to convert lactate to bicarbonate (correct acidosis). - **IV sodium bicarbonate** increases bicarbonate and promotes renal chloride excretion. - **Diuretics** to eliminate chloride. - Restrict sodium, chloride, and fluids. - **Nursing Management:** - Monitor vital signs, ABG values, and I&O. - Document changes in respiratory, neurologic, and cardiac status. - Educate on proper diet and hydration to manage hyperchloremia. -- ------------------------------- **🌊 Acid--Base Disturbances** -- ------------------------------- - **pH** is an indicator of H+ concentration in blood. - Normal pH range: **7.35--7.45** - **\7.45**: Alkalosis - **Key Systems for Acid--Base Balance** - **Buffer Systems** - **Bicarbonate--Carbonic Acid System:** - Normal ratio: 20 HCO3⁻ (Bicarbonate) to 1 H2CO3 (Carbonic acid) **\[20:1\]** - If ratio changes, pH imbalance occurs. - **CO2 + H2O → H2CO3 → H+ + HCO3⁻** - **Kidneys** - Regulate bicarbonate (HCO3⁻) in ECF. - Acidosis: Kidneys excrete H+ and conserve HCO3⁻. - Alkalosis: Kidneys retain H+ and excrete HCO3⁻. - Slow response: Takes hours to days. - **Lungs** - Control CO2 (and thus carbonic acid) by adjusting ventilation. - High CO2 (PaCO2 \> 45 mmHg): Stimulates respiration. - **Acidosis**: Increased breathing rate → Eliminates CO2 (reducing acid load). - **Alkalosis**: Decreased breathing rate → Retains CO2 (increasing acid load). - **Arterial Blood Gas (ABG) Normal Values** - pH: **7.35--7.45** - PaCO2: **35--45 mmHg** - **\45:** Respiratory Acidosis - HCO3⁻: **22--26 mEq/L** - **\26:** Metabolic Alkalosis - PaO2: **\>80 mmHg** (Oxygenation) - Oxygen saturation (SaO2): **\>94%** - **Respiratory and Metabolic Responses:** - **Metabolic Acidosis:** - Lungs compensate by **increasing respiratory rate** (eliminates CO2). - **Metabolic Alkalosis**: - Lungs compensate by **decreasing respiratory rate** (retains CO2). - **Respiratory Acidosis** (hypoventilation): - **CO2 retention** → Increased H+ → Acidosis. - **Respiratory Alkalosis** (hyperventilation): - **CO2 loss** → Decreased H+ → Alkalosis. - **\"ROME\"**: - **Respiratory Opposite** (pH ⬆, CO2 ⬇ = Alkalosis; pH ⬇, CO2 ⬆ = Acidosis) - **Metabolic Equal** (pH ⬆, HCO3 ⬆ = Alkalosis; pH ⬇, HCO3 ⬇ = Acidosis). -- ------------------------ **Metabolic Acidosis** -- ------------------------ - A clinical disturbance characterized by low pH and decreased bicarbonate concentration - **Forms**: - High Anion Gap Metabolic Acidosis (HAGMA) - Normal Anion Gap Metabolic Acidosis (NAGMA) - **Anion Gap Calculation:** - **Formula:** Anion Gap=Na+−(Cl−+HCO3−​) - **Normal Values**: - Without Potassium: **8-12 mEq/L** - With Potassium: **12-16 mEq/L** - **Interpretation**: - Normal Anion Gap (NAGMA): **8-12 mEq/L** - High Anion Gap (HAGMA): **\> 16 mEq/L** - **Pathophysiology:** - **Normal Anion Gap Metabolic Acidosis:** - Causes: Direct loss of bicarbonate (e.g., diarrhea, renal insufficiency, diuretics). - **High Anion Gap Metabolic Acidosis**: - Causes: Accumulation of acids (e.g., lactic acidosis, renal failure, DKA). - **Clinical Manifestations: \"HANDS\"** - **H**eadache - **A**rrhythmias - **N**ausea/Vomiting - **D**rowsiness - **S**kin cold and clammy - **Diagnostic Evaluation:** - **ABG Values:** - Low bicarbonate: **\< 22 mEq/L** - Low pH: **\< 7.35** - **Potassium Levels:** Elevated initially (due to H⁺ shift), then may cause hypokalemia after correction. - **Medical Management: \"CAMP\"** - **C**orrect the cause - **A**dminister bicarbonate (if indicated) - Avoiding excessive chloride intake - **M**onitor potassium levels - **P**rovide supportive care (dialysis if needed -- ------------------------- **Metabolic Alkalosis** -- ------------------------- - A clinical disturbance characterized by high pH and increased bicarbonate concentration - **Causes:** - **Loss of H⁺ ions:** - Severe vomiting or gastric suction (loss of HCl) - Pyloric stenosis - **Gain of bicarbonate**: - Excessive alkali ingestion (e.g., antacids, sodium bicarbonate) - **Diuretic therapy** (promotes potassium loss): - Thiazides - Furosemide - **Hormonal disorders**: - Hyperaldosteronism - Cushing\'s syndrome - **Pathophysiology:** - **Loss of H⁺ ions lead to:** - Decreased H⁺ in blood → alkalosis - Decreased free Ca²⁺ (hypocalcemia) → neuromuscular symptoms (tingling, dizziness, tetany) - **Clinical Manifestations:** - **Symptoms of hypocalcemia:** - Tingling of fingers and toes - Dizziness - Tetany (muscle cramps) - **ECG changes**: - Prominent U wave - Ventricular rhythm disturbances (e.g., PVCs) - **Diagnostic Evaluation:** - **Arterial Blood Gases (ABGs):** - pH **\> 7.45** - HCO₃⁻ **\> 26 mEq/L** - **Increased PaCO₂** (due to respiratory compensation) - **Urine chloride levels**: - **\< 25 mEq/L**: vomiting or diuretic therapy - **\> 40 mEq/L:** mineralocorticoid excess or alkali loading - **Medical Management:** - **Restore normal fluid volume:** Administer normal saline - **Replace potassium**: Potassium chloride (KCl) - **Reduce gastric HCl production**: Proton pump inhibitors (e.g., omeprazole) - **Enhance bicarbonate excretion**: Carbonic anhydrase inhibitors (e.g., acetazolamide) -- -------------------------- **Respiratory Acidosis** -- -------------------------- - Clinical disorder with **pH:** \< 7.35 and **PaCO2:** \> 45 mm Hg - **Pathophysiology:** - Inadequate CO2 excretion due to: - Inadequate ventilation - Elevated plasma CO2 → Increased carbonic acid - **Acute Causes: "PASTE"** - **P**ulmonary edema - **A**spiration (foreign object) - **S**edative overdose - **T**ension pneumothorax - **E**xacerbation of COPD - **Chronic Causes:** - Diseases like COPD, sleep apnea, obesity hypoventilation - **Clinical Manifestations:** - **Acute Symptoms: "COFFEE"** - **C**onfusion - **O**ut of breath (tachypnea) - **F**ibrillation (ventricular) - **F**ast pulse and blood pressure - **E**levated PaCO2 (\>60 mm Hg) - **E**levated intracranial pressure - **Chronic Symptoms:** - Asymptomatic unless there is a rapid increase in PaCO2 - **Diagnostic Evaluation:** - **ABG Findings:** - pH: **\< 7.35** - PaCO2: **\> 45 mm Hg** - Bicarbonate: Variable; may normalize with compensation - **Other Diagnostics:** - Serum electrolyte levels - Chest X-ray - Drug screen if overdose suspected - **Medical Management:** - **Goals:** Improve ventilation and treat underlying causes - **Pharmacological Treatments: "BAT"** - **B**ronchodilators (reduce spasm) - **A**ntibiotics (for infections) - **T**hrombolytics/anticoagulants (for pulmonary emboli) - **Supportive Treatments:** - Hydration: 2-3 L/day - Nebulizer treatments for mucus clearance - Low-concentration oxygen supplementation - **Mechanical Ventilation:** Caution to avoid rapid CO2 loss leading to alkalosis -- --------------------------- **Respiratory Alkalosis** -- --------------------------- - A condition characterized by: Arterial pH **\> 7.45** and PaCO2 **\< 35 mm Hg** - **Pathophysiology:** - **Cause:** Hyperventilation → Excessive loss of CO2 → Decreased plasma carbonic acid. - **Chronic:** Chronic hypocapnia → Decreased H+ ions → Alkalosis. - **Causes:** - Anxiety (panic disorder) - Hypoxemia - Salicylate intoxication - Gram-negative sepsis - Inappropriate ventilator settings - **Clinical Manifestations:** - Cerebral Effects: Lightheadedness, inability to concentrate (vasoconstriction). - Neurological Effects: Numbness and tingling (decreased calcium ionization), tinnitus. - Cardiac Effects: - Tachycardia - Arrhythmias (ventricular and atrial) - **Diagnostic Evaluation:** - **ABGs:** - **Acute:** pH \> 7.45, PaCO2 \< 35 mm Hg, normal bicarbonate. - **Chronic:** pH \> 7.45, low bicarbonate (compensation). - **Electrolytes:** - Decreased potassium (due to H+ exchange). - Decreased calcium (carpopedal spasms, tetany). - Decreased phosphate (increased cellular uptake). - **Toxicology Screen:** Rule out salicylate intoxication. - **Medical Management: "A SMART"** - **A**nxiety management - **S**low breathing - **M**edications (Antianxiety agents) - **A**ddress cause (treat underlying cause) - **R**ebreather (CO2 rebreather mask (paper bag) - **T**reatment -- -------------------------------- **Mixed Acid--Base Disorders** -- -------------------------------- - Simultaneous occurrence of two or more independent acid-base disorders. - Normal pH with changes in PaCO2 and plasma HCO3− suggests mixed disorder. - **Example**: Metabolic acidosis (e.g., lactic acid accumulation) + respiratory acidosis (e.g., hypoventilation) → excessive acid accumulation. - **Compensation Mechanisms:** - **Pulmonary & Renal Compensation:** Systems work together to normalize pH. - **Single Acid-Base Disorder:** The non-affected system compensates for maintaining the bicarbonate to carbonic acid ratio (20:1). - **Lung Compensation**: - **Metabolic disturbances**: - Hypoventilation → CO2 accumulation - Hyperventilation → CO2 loss - **Kidney Compensation:** - **Respiratory disturbances**: - Alter bicarbonate reabsorption and H+ secretion. - **Compensation Examples**: - **Respiratory Acidosis**: - Excrete excess H+ in urine, conserve HCO3−. - **Respiratory Alkalosis**: - Increase bicarbonate excretion, retain H+. - **Metabolic Acidosis**: - Increase ventilation, retain bicarbonate. - **Metabolic Alkalosis**: - Decrease ventilation to conserve CO2. - **Blood Gas Analysis (ABG)** - **Purpose:** Identify acid-base disturbance and compensation degree. - **Sample Type:** Arterial blood sample preferred; mixed venous sample if unavailable. - **Parameters Evaluated:** - Alveolar ventilation - Oxygenation - Acid-base balance - Serum electrolytes (Na, K, Cl) - Evaluate health history, physical examination, previous blood gas results, and serum electrolytes to avoid interpretation errors. - Treatment of the underlying condition usually corrects acid-base disorders. -- ----------------------------------- **Arterial Blood Gas Assessment** -- ----------------------------------- - **Key Normal Values:** - pH: **7.35--7.45** - PaCO2: **35--45 mm Hg** - HCO3−: **22--26 mEq/L** - **Steps for Evaluation:** 1. **Assess pH:** - **Normal pH (7.4):** May indicate normal gases or compensated imbalance. - **pH \> 7.45:** Alkalosis - **pH \< 7.35:** Acidosis 2. **Determine Primary Cause:** - **For alkalosis:** - **PaCO2 \< 35 mm Hg:** Respiratory alkalosis (hyperventilation) - **HCO3− \> 26 mEq/L:** Metabolic alkalosis (excess bicarbonate) - **For** **acidosis:** - **PaCO2 \> 45 mm Hg:** Respiratory acidosis (hypoventilation) - **HCO3− \< 22mEq/L:** Metabolic acidosis (bicarbonate loss or acid gain) 3. **Check for Compensation:** - If the non-primary value moves in the same direction as the primary: - Compensation is occurring. - Example of values: - **Acute Respiratory Acidosis**: - pH: 7.2, PaCO2: 60 mm Hg, HCO3−: 24 mEq/L (no compensation) - **Chronic Respiratory Acidosis:** - pH: 7.4, PaCO2: 60 mm Hg, HCO3−: 37 mEq/L (compensation) 4. **Identify Simultaneous Disturbances:** - **If pH does not explain one of the changes:** - PaCO2 ↑ and HCO3− ↓: Respiratory acidosis + Metabolic acidosis - PaCO2 ↓ and HCO3− ↑: Respiratory alkalosis + Metabolic alkalosis 5. **Calculate Anion Gap (if metabolic acidosis is present):** - AG = Na⁺ − (Cl⁻ + HCO3⁻) - Normal AG: 10--14 mmol/L 6. **Evaluate Clinical Signs and Symptoms:** - Confirm if compatible with the acid-base analysis. -- ----------------- **Burn Injury** -- ----------------- - Burn injuries can lead to pain, high costs, disfigurement, and long-term disability. - They involve complex, multisystem pathophysiology, challenging health systems despite advances in treatment. - Significant improvements in care for severe burns include: - Critical-care management - Fluid resuscitation - Nutrition - Surgical debridement - Wound coverage - Antimicrobial therapies - **Education** is vital in preventing burn injuries: - Keep matches and lighters away from children. - Never leave children unattended near fire or in bathrooms. - Install and maintain smoke and CO detectors. - Conduct home exit fire drills. - Set water heater temperatures below 48.9°C (120°F). - Warn against smoking in bed or while using oxygen. - Avoid using flammable liquids for fires. - Educate on the dangers of hot car engines and overhead wires. - Keep hot appliances out of reach children. - Store flammable liquids safely. - Ensure awareness of loose clothing when cooking. - Have a working fire extinguisher and know how to use it. - **Factors influencing burn severity:** - **Patient age:** Young children and older adults face higher morbidity and mortality**.** - Burn depth and surface area burned. - Inhalation injuries and comorbid conditions**.** - **Location of injury** (e.g., face, hands, perineum). - **Burn Depth Classification** - **First-degree burns:** Superficial, painful, and erythematous; intact epidermis (e.g., sunburn). - **Second-degree burns:** Partial thickness; involves the entire epidermis and part of the dermis, causing blisters; healing takes 2-3 weeks. - **Third-degree burns:** Full thickness; des