Week Two Fluids and Electrolytes PPT.pdf

Fluids & Electrolytes, Acids & Bases Learning Objectives 1. Identify the fluid compartments of the body 2. Discuss the pathophysiology of altered fluid and electrolyte balances 3. Discuss common electrolyte imbalances of illness and disease 4. Identify clinical manifestations of electroly...

Fluids & Electrolytes, Acids & Bases Learning Objectives 1. Identify the fluid compartments of the body 2. Discuss the pathophysiology of altered fluid and electrolyte balances 3. Discuss common electrolyte imbalances of illness and disease 4. Identify clinical manifestations of electrolyte imbalances 5. Know normal electrolyte and acid/base values 6. Differentiate between acidosis and alkalosis (both respiratory & metabolic) 7. Interpret acid base values Distribution of Body Fluids Total Body Water (TBW): the sum of fluids in all body compartments Body fluids are distributed into 2 compartments: - Intracellular fluid (ICF), all fluid within cells (~2/3rds TBW) - Extracellular fluid (ECF), all fluid outside the cells (~1/3rd TBW) - Interstitial Fluid (the space between cells and outside blood vessels) - Intravascular Fluid (blood plasma) - Lymph, synovial, intestinal, cerebrospinal fluid, sweat, urine, pleural, peritoneal, pericardial, and intraocular fluids Plasma= intravascular fluid PEDIATRIC CONSIDERATIONS At birth, TBW represents 75-80% of body weight Infants are susceptible to significant changes in body fluid due to high metabolic rate & greater body surface area *Dehydration can happen quickly through vomiting or diarrhea* What are signs & symptoms of dehydration in newborns? GERIATRIC CONSIDERATIONS As a person ages, there is a decreased percent in TBW This is due to: - Decreased free fat mass and decreased muscle mass - Renal decline (reduced ability to regulate sodium & water balance) - Diminished thirst perception - Loss of cognition It is important to monitor and maintain hydration status for geriatric people, especially those with loss of cognition. How do we do this in hospital? How does water move between fluid compartments? Plasma & Interstitial Fluid a. OSMOTIC PRESSURE: chemical force pulling water inward b. HYDROSTATIC PRESSURE: mechanical force pushing water outward As plasma flows from the arterial to venous end of capillaries, 4 forces determine fluid movement across the endothelium of the blood vessel. These forces acting together are known as Starling forces Starling Forces 1. Capillary Hydrostatic Pressure (Blood Pressure) a. Outward movement of water from capillary to interstitial space 2. Capillary (plasma) Oncotic Pressure a. Osmotically attracts water from interstitial space back into the capillary 3. Interstitial Hydrostatic Pressure a. Outward movement of water from the interstitial space into the capillary 4. Interstitial Oncotic Pressure a. Osmotically attracts water from the capillary into the interstitial space https://www.youtube.com/watch?v=rPWf43lYcBU&ab_channel=PhysioFlip Fluid Movement Between Plasma and Interstitial Space How does water move between fluid compartments? OSMOSIS: water moves freely by diffusion through lipid bilayer membrane and through aquaporins (water channel proteins). Edema: accumulation of fluid in interstitial space Pathophysiology of Edema - Capillary hydrostatic pressure increases! - venous obstruction (thrombophlebitis, hepatic obstruction, tight clothing around extremities, prolonged standing) - salt & water retention (heart failure, renal failure, and cirrhosis of the liver) - Lymph obstruction Clinical Manifestations - Localized= limited to site of trauma (ex. sprained finger) - Generalized= uniform distribution of fluid in interstitial spaces - Edema is associated with weight gain, swelling, limited joint movement - Pitting edema (+1, +2, +3) can describe severity of edema  Evaluation & Treatment of Edema Evaluating Pitting Edema - +1, +2, +3, +4 Focus on the underlying cause! Symptom management includes - Compression stockings - Elevating edematous limbs - Avoiding prolonged standing - Restricting salt intake - Taking diuretics  Electrolytes & Hormones & Water Balance Antidiuretic Hormone (ADH): regulates water balance by increasing reabsorption into the plasma Sodium (Na+): primary ECF cation, regulates osmotic forces, plays a role in neuromuscular conduction & acid-base balance Chloride (Cl-): primary ECF anion, provides electroneutrality Aldosterone: mediates hormonal regulation of sodium (and potassium) balance Renin: hormone released by the kidneys when circulating blood volume or BP decrease, Na+ decrease, or K+ levels increase →stimulates formation of angiotensin I Angiotensin I: created by renin, triggers release of angiotensin-converting enzyme (ACE) from the pulmonary vessels to convert into angiotensin II Angiotensin II: stimulates the secretion of aldosterone & ADH, causes vasoconstriction Antidiuretic Hormone (ADH) System Thirst perception: - Osmolality receptors - Volume receptors - Baroreceptors Alterations in Sodium, Chloride & Water Balance 1. ISOTONIC a. Changes in TBW occur with proportional changes in electrolytes 2. HYPERTONIC a. Osmolality of ECF if elevated above normal, usually because of an increased concentration of ECF sodium or a deficit of ECF water 3. HYPOTONIC a. Osmolality of ECF is less than normal Isotonic Alterations TBW Fluid Loss DEHYDRATION HYPOVOLEMIA Causes Causes - Excessive diaphoresis - Hemorrhage, severe wound drainage - Inadequate fluid intake Signs & Symptoms Signs & Symptoms - Rapid heart rate - Weight loss - Flattened neck veins - Dryness of mucous membranes - Normal or decreased BP - Decreased urine output TBW Fluid Excess HYPERVOLEMIA Causes= too much IV fluid, hypersecretion of aldosterone Signs & Symptoms= weight gain, increased BP, distended neck veins, potentially leads to pulmonary edema and heart failure Sodium (Na+) Normal Range: 135-145 mmol/L - Regulates water balance - Maintains neuromuscular irritability for conduction of nerve impulses - Balance is mediated by aldosterone; end product of RAAS Chloride (Cl-) Normal Range: 98-106 mmol/L - Chloride follows sodium - Similar function to sodium in the body Hypertonic Alterations HYPERNATREMIA - Na+ >145 mmol/L - Causes: excess sodium intake, kidney failure - Signs and Symptoms - Thirst, weight gain, bounding pulse, and increased BP - *affects CNS*, muscle twitching, hyperreflexia, confusion, coma, convulsions - Treatment: oral fluids or isotonic salt-free IV solutions (D5W) HYPERCHLOREMIA *Chloride follows Sodium* - Cl- >106 mmol/L - There are no specific symptoms or treatment for chloride excess Hypotonic Alterations Sodium deficit or water excess… leads to intracellular overhydration & cell swelling HYPONATREMIA - Na 5.0 mmol/L Caused by - Increased intake, shift of K+ from ICF into ECF, decreased renal excretion, insulin deficiency or cellular trauma S/S: increased neuromuscular irritability (restlessness, cramping and diarrhea), or in severe cases decreased resting membrane potential (muscle weakness, loss of muscle tone, and paralysis) Treatment: treat contributing causes & correct K+ excess - Administer calcium gluconate, glucose/insulin, dialysis, kayexalate (sodium polystyrene) Hypokalemia K+ 1.5 mmol/L Causes: - Acute or chronic kidney failure - Treatment of metastatic tumours with chemotherapy that releases large amounts of PO43+ into serum - Long-term use of laxatives or enemas containing phosphates - Hypoparathyroidism S/S: - Symptoms primarily related to low serum Ca++ levels (caused by high PO43+ levels) similar to the results of hypocalcemia - When prolonged, calcification of soft tissues in lungs, kidneys, joints Magnesium (Mg++) Normal Range: 0.75 - 0.95 mmol/L - Increases neuromuscular excitability - Cofactor in enzymatic reactions Hypomagnesemia Mg < 0.75 mmol/L Causes: - Malnutrition & malabsorption syndromes - Alcoholism - Urinary losses (renal tubular dysfunction, loop diuretics) S/S: - Behavioural changes, Irritability - Increased reflexes, Muscle cramps, Ataxia, Tetany - Nystagmus - Convulsions - Tachycardia - Hypotension Hypermagnesemia Mg > 0.95 mmol/L Causes: - Usually renal insufficiency or failure - Excessive intake of magnesium-containing antacids - Adrenal insufficiency S/S: - Skeletal smooth muscle contraction - Excess nerve function - Loss of deep tendon reflexes - Nausea and vomiting - Muscle weakness - Hypotension - Bradycardia - Respiratory distress REVIEW QUESTIONS 1. Which is the initial treatment for hypernatremia? a. Restriction of fluids b. Administration of a diuretic c. Isotonic 0.9% NS fluid d. Isotonic salt-free fluid (5% Dextrose in water) REVIEW QUESTIONS 2. What organs and glands are part of the Renin-Angiotensin-Aldosterone System? REVIEW QUESTIONS 3. What are the fluid compartments of the body? Acid - Base Balance Carefully regulated to maintain a normal pH *LEVELS TO KNOW* pH: 7.35-7.45 PCO2: 35-45 mmHg (partial pressure of carbon dioxide) HCO3: 22-26 mEq/L (bicarbonate) pH pH (7.35 - 7.45) - If the H+ are high in number, the pH is low (acidic) - If the H+ are low in number, the pH is high (alkaline) - Obtained by arterial blood gas (ABG) sampline - Bones, lungs, and kidneys are the major organs involved of acid-base balance  – Buffering Systems (Bicarbonate (HCO3 )) - A buffer is a chemical that can bind excessive H+ or OH– without a significant change in pH. - Renal Buffering: secretion of H+ in urine & reabsorption of bicarbonate Acid-Base Imbalances What is the range for normal arterial blood pH? Acidosis - Systemic increase in H+ concentration or decrease in bicarbonate (base) Alkalosis - Systemic decrease in H+ concentration or increase in bicarbonate What is happening in the body to cause these imbalances? ROME method to interpret ABG’s (arterial blood gas) 4 Categories of Acid-Base Imbalances Respiratory acidosis—elevation of PaCO2 as a result of ventilation depression Respiratory alkalosis—depression of PaCO2 as a result of alveolar hyperventilation Metabolic acidosis—depression of HCO3– or an increase in noncarbonic acids Metabolic alkalosis—elevation of HCO3– usually caused by an excessive loss of metabolic acids Respiratory Acidosis (PaCO2 >45mmHg, pH < 7.35) OCCURS WHEN: - HYPOventilation, resulting in excess of CO2 in your blood - Common causes: depression of the respiratory centre, paralysis of the respiratory muscles, disorders of the chest wall, and disorders of the lung parenchyma A decrease in ventilation combined with the normal metabolic production of CO2 results in an increase in the concentration of carbonic acid. RENAL COMPENSATION occurs by elimination of hydrogen ion (acidic), and retention of bicarbonate (basic). Restoration of adequate ventilation is necessary. S/S: headache, blurred vision, restlessness (breathlessness), lethargy Respiratory Alkalosis (PaCO2 7.45) OCCURS WHEN: - HYPERventilation (deep, rapid respirations) causing reduction in CO2 - Common causes: hypoxemia, hypermetabolic states (fever, anemia), and cirrhosis, and sepsis RENAL COMPENSATION occurs by decreasing H+ excretion and bicarbonate reabsorption S/S: dizziness, confusion, tingling of the extremities Metabolic Acidosis (HCO3 26 mmol/L, pH > 7.45) OCCURS WHEN: - There is a large loss of metabolic acids - Common causes: vomiting, diuretic use, hypovolemia RESPIRATORY COMPENSATION includes shallow respirations; retaining CO2 S/S: weakness, muscle cramps, confusion, hyperactive reflexes Effective treatment is dependant on the underlying condition. Arterial Blood Gas Analysis (ROME Method) Example ABG RESULT pH 7.46 PaCO2 50 mmHg HCO3 35 mmol/L Chief complaint is severe fatigue and dehydrations secondary to a 4 day hx of vomiting VS: 39 degrees Celsius, pulse 116, respirations deep 24/min, BP 98/60 mm Hg Are we more basic or more acidic? How are our PaCO2 & HCO3 levels? What is our patient experiencing? How is their body compensating?