Metabolic Acidosis Study Guide (Cortisol) | NUR MISC | Rasmussen College

Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: • increased aci d production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) • decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) • loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: • HCO3: decreased 22 • Blood pH: decreased 7.35 • CO2: 35 or normal (may be normal but if it is decreased this is the body’s way of trying to compensate). **Remember the respiratory system is causing hyperventilation. The respiratory system tries to increase the pH from its acidotic states through tachypnea with Kussmaul’s breathing. The goal is to “blow off” the CO2 which is acidic to help alleviate the already acidotic conditions in the body. Memorize these normal values for ABGs: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Metabolic Acidosis High anion gap & Normal anion gap problems: What is an anion gap? Simplified this is where the doctor look at various lab results from a patient’s lab work (such as electrolytes (chloride, bicarbonate, sodium) and calculates them to see the difference between the anions and cations. If there is a gap (14 mEq/L from normal (normal is: 10-14 mEq/L) there is high anion gap metabolic acidosis going on. In other words the anion gap tells us what type of acidosis we have going on which is important so it can be treated appropriately. High Anion Acidosis is conditions that cause the body to produce too much acid or NOT enough bicarb (DKA, Aspirin toxicity, renal failure, high-fat diet, low carb diet, malnutrition) Normal Anion acidosis is loss of the bicarbonate from the body. Examples: diarrhea via GI fluids, ostomies or fistula drainage (ileostomies or pancreatic fistula)…which are rich in alkalotic fluids, however when lost it causes acidosis, or drugs ingestion: Diamox (diuretic)…. carbonic anhydrase inhibitor which reduces reabsorption of bicarb. Combine all of this to form the Mnemonic “Acidotic” Aspirin toxicity: (high anion gap) which increases the acid in the body and this also causes respiratory alkalosis (hyperventilation) Carbohydrates not metabolized (high anion gap): when there isn’t enough oxygen to break down carbs the pyruvic acids (that supplies the cells with energy) starts to turn into lactic acid and when you get acid building up you get acidosis Insufficiency of kidneys (high anion gap): kidneys are failing to filter out metabolic waste products, acids increase, and bicarb cannot keep up so it depletes Diarrhea (normal anion gap): profuse diarrhea leads to loss bicarbonate, DKA (diabetic ketoacidosis) body is breaking down ketones and is not metabolizing glucose correctly which leads to high blood glucose levels and breakdown of acids in the blood Ostomy drainage (excessive) ileostomies, Ureteroenterostomies (normal anion gap)… ostomies are an opening of an organ to allow drainage…depending on where the ostomy is these fluids are rich in bicarb and if loss directly at this spot (instead of travelling through the body to form into stool (which doesn’t lose much bicarb)…it can deplete the bicarb fast. fisTula (pancreatic fistula) (normal anion gap) fistula : a fistula is a passage between an hollow organ and body surface or between two organs….same concept with the ostomy…losing fluids where you shouldn’t be and they are not being absorbed by the body…you are wasting the bicarb Intake of high-fat diet: eating too much fat leads to the building-up of waste product which in turn leads to buildup of ketones and acids Carbonic anhydrase inhibitors (Diamox): diuretic which reduces the reabsorption of bicarb Signs & Symptoms of Metabolic Acidosis • ****Kussmaul’s respiration (body’s way of trying to compensate by exhaling the excessive CO2…in hopes of increasing bicarb and blood pH) • Confused, weak, low blood pressure, cardiac changes (if hyperkalemic …can happen EXCEPT with diarrhea or with Diamox usage which causes hypokalemia), n & v Nursing Interventions for Metabolic Acidosis Vary depending on the causes of acidosis: • Watch respiratory system and ABGs closely…if too bad may need intubation • Assess other electrolyte levels (esp. potassium because during active acidosis it will be high…however when it resolves there is an extracellular to intracellular shift of K+ back into the cell which will causes hypokalemia) • Watch neuro status, safety, and place in seizure precaution • Dialysis may be needed if they patient is experiencing acidosis (high anion gap issue ex: renal failure) • Diabetic ketoacidosis: administer prescribed insulin to help glucose go back into cell which will help the body start regulating how it metabolizes glucose…hence not more ketones (acids) Respiratory Acidosis What’s involved:…let’s look at normal breathing: 1. Oxygen enters through the mouth or nose 2. down through the Pharynx 3. into the Larynx (the throat) 4. then into the Trachea 5. and the Bronchus (right and left) which branches into the bronchioles and ends in alveoli sac *The alveolar sacs are where gas exchange takes place (oxygen and carbon dioxide diffuse across the membrane). The oxygen enters into your blood stream and CARBON DIOXIDE CO2 is exhaled through your nose or mouth. The diaphragm also plays a role in allowing lungs into inflate and deflate. Note: if there is any problem with the patient breathing rate (too slow), alveolar sacs (damaged), or diaphragm (weak) the patient can experience respiratory acidosis. *Main cause of respiratory acidosis is bradypnea (slow respiratory rate 12 bpm which causes CO2 to build-up in the lungs) When this happens the following lab values are affected: • Blood pH decreases (7.35) • Carbon dioxide levels increase (45) • **To compensate for this the Kidneys start to conserve bicarbonate (HCO3) to hopefully increase the blood’s pH back to normal…..so HCO3 becomes 26. REMEMBER (memorize) these lab values: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Respiratory Acidosis Remember “DEPRESS” Breathing (anything that causes you to breathe slowly, blocks the airway, or causes the diaphragm not to work properly will cause respiratory acidosis) Drugs (opioids (fentanyl, morphine), sedation (versed), ….causes respiratory depression “hypoventilation….retain carbon dioxide….increase PaCO2 and decreased pH” ) & Diseases of the neuromuscular system…Myasthenia gravis, Guillain–Barré syndrome (weakness of voluntary muscles affects the diaphragm….can’t expelled the carbon dioxide) Edema (pulmonary) extra fluid in the lung causes impaired gas exchange Pneumonia…excessive mucous production affect gas exchange…the alveoli are majorly affected because they are filled with pus and fluid Respiratory center of brain damaged (brain injury, stroke) Emboli (blocks the pulmonary artery or branch of the lungs causes carbon dioxide to increase) Spasms of bronchial tubes (asthma) bronchioles constrict and you have decreased gas exchange Sac elasticity of alveolar sac are damaged and this restricts air flow in and out of the lungs and this increases carbon dioxide (Emphysema & COPD) Signs and Symptoms of Respiratory Acidosis • Major neuro changes: Confused, very drowsy, and reports a headache • respiration rate less than 12 • low blood pressure Nursing Interventions for Respiratory Acidosis • Administer oxygen • encourage coughing and deep breathing • suction (pneumonia) • may need respiratory treatment (asthma) • hold respiratory depression drugs (know the category of drugs used opiods, sedatives etc) • ****Watch potassium levels that are 5.1…remember in hyperkalemia video we talked about how respiratory acidosis caused increase potassium ….can cause dysrhythmias) • administer antibiotics for infection • may need endotracheal intubation if CO2 rise above 50 mmhg or respiratory distress is present Metabolic Alkalosis Metabolic alkalosis in simple terms: a metabolic problem caused by the excessive loss of acids (H+) or increased amount of bicarb (HCO3) produced in the body that leads to an alkalotic state in the body. Disease processes and drugs can cause metabolic alkalosis. When metabolic alkalosis happens in the body other systems try to compensate by hopefully fixing the blood’s pH and bicarb level. One system that does this is the respiratory system by stimulating the respiratory system to hypoventilate (decrease respirations) which will retain PCO2 (carbon dioxide) so it will decrease the pH back to normal, hence you will start to see bradypnea in your patient. If a patient is experiencing metabolic alkalosis they will present with the following labs: • HCO3: increases 26 • Blood pH: increases 7.45 • CO2: 45 or normal (may be normal but if increased this is the body’s way of trying to compensate. Remember the respiratory system tries to decrease the pH from its alkalotic state by causing hypoventilation ( bradypnea). The respiratory system hopes that if the CO2 increase enough it will cause the pH to decrease and the kidneys will start to excrete the bicarb which will hopefully decrease the overall HCO3. Remember what normal values are: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Metabolic Alkalosis Remember: “Alkali” (**these are the most common causes) **Aldosterone production excessive (hyperaldosteronism) activates renin-angiotensin- aldosterone system : the adrenal cortex is releasing too much aldosterone which causes the renal tubule in the kidneys to keep sodium which wastes hydrogen ions (ex: potassium) and this causes you to keep bicarb (HCO3) Loop **diuretics (Lasix) or thiazide therapy: causes the kidneys to waste hydrogen ions and chloride through the urine (ALSO LOSING K+) which in turn increases the bicarb alKali ingestion of food (baking soda, milk, antacids) increases bicarb level in the blood Anticoagulant “citrate” (used as a storage agent in blood and during continuous forms of renal replacement therapy) Caused from a massive transfusion of whole blood (patient needs several bags of blood) and the body metabolizes the citrate used in the blood as bicarb which increases the HCO3 level in the body. Also, patients who undergo continuous forms of renal replacement therapy (CRRT) (an alternative therapy for patients who can’t undergo hemodialysis) are affected by the citrate used in the therapy. Loss of fluids (**vomiting and **GI suctioning) hence this fluids are rich in K+ and when you lose them you are losing hydrogen ions and this causes the body to increase the bicarb level, Low potassium levels cause reabsorption of HCO3- Increased sodium bicarb administration (trying to correct metabolic acidosis) Signs and Symptoms of Metabolic alkalosis • Bradypnea (hypoventilation) 12 bpm o Many symptoms due to low potassium (dysrhythmia), tetany, tremors, muscle weakness/cramping, tired, irritable, vomiting, Depression ST, flat or inverted T wave and prominent u-wave) Nursing Interventions for Metabolic Alkalosis • Based on the cause: vomiting (give antiemetic ex: Zofran, Phenergan), stop diuretics • Doctor may order Diamox (Carbonic anhydrase inhibitors): a diuretic which reduces the reabsorption of bicarb • Watch ABGs and signs of respiratory distress • Monitor potassium and chloride levels (wasted in this condition) Respiratory Alkalosis What’s involved:…let’s look at normal breathing: 1. Oxygen enters through the mouth or nose 2. down through the Pharynx 3. into the Larynx (the throat) 4. then into the Trachea 5. and the Bronchus (right and left) which branches into the bronchioles and ends in alveoli sac *The alveolar sacs are where gas exchange takes place (oxygen and carbon dioxide diffuse across the membrane). The oxygen enters into your blood stream and CARBON DIOXIDE CO2 is exhaled through your nose or mouth. The diaphragm also plays a role in allowing lungs into inflate and deflate. Note: if there is any problem with the patient breathing rate (too fast), alveolar sacs (damaged), hyperventilation, or a brain injury that affects the respiratory center a patient is at risk for respiratory alkalosis *Main cause of respiratory alkalosis is tachypnea (fast respiratory rate 20 bpm which causes CO2 to decrease in the lungs) When this happens the following lab values are affected: • Blood pH increases (7.45) • Carbon dioxide levels increase (35) • **To compensate for this the Kidneys start to excrete bicarbonate (HCO3) to hopefully decrease the blood’s pH back to normal…..so HCO3 becomes 22. REMEMBER (memorize) these lab values: • pH 7.35-7.45 • PaCO2 35-45 • HCO3 22-26 Causes of Respiratory Alkalosis Remember: TACHYPNEA (fast breathing leads to “hyperventilation” which leads to respiratory alkalosis) Temperature increase (fever) due to increased metabolic needs of the body which causes the respiratory center (medulla and pons) to try to compensate by making the respiratory rate increased…hence exhaling too much carbon dioxide (CO2) Aspirin toxicity: too much aspirin in the body leads to hyperventilation due to the stimulation of the respiratory center and fever Controlled ventilation (excessive usage)…mechanical ventilation****hyperventilates the patient with too much oxygen and depletes carbon dioxide Hyperventilation (excessive respirations) expelling too much carbon dioxide hYsteria (anxiety) leads to rapid breathing and expelling of carbon dioxide Pain…rapid breathing (blowing off too much carbon dioxide), Pregnancy (especially in 3rdtrimester due to changes of the respiratory tract), Pneumonia Neurological injuries from a head injury or stroke (affects the respiration system of the brain which is located in the medulla and pons) Embolism or Edema in the lungs Asthma due to hyperventilation (however, asthma can cause respiratory acidosis as well due to bronchospasms which is causing the alveoli to not properly deflate) Signs and Symptoms of Respiratory Alkalosis • ***Classic Assessment Sign is fast respiratory rate (normal for adult is 12- 20) TACHYPNEA(20 bpm) • Neuro changes: Tired, lethargy, fast heart rate • **Tetany, dysrhythmias, muscle cramps, positive Chvostek’s sign due to hypocalcemia and hypokalemia Nursing Interventions for Respiratory Alkalosis • Teach patient breathing techniques to slow down breathing, holding breath…”rebreathing into a paper bag or re-breather mask • Watch potassium levels (hypokalemia..remember hyperkalemia in respiratory acidosis & hypocalcemia) and for signs and symptoms of low calcium and potassium levels. • **Closely watch patients on mechanical ventilation to ensure breaths are not hyperventilating the patient Hyponatremia Hypo: “under/beneath” Natr: Prefix for Sodium Emia: blood Meaning of Hyponatremia: low sodium in the blood Normal sodium levels: 135 to 145 mEq/L (135 = hyponatremia) Role of sodium in the body: An important electrolyte that helps regulate water inside and outside of the cell. Remember that water and sodium loves each other and where ever sodium goes so does water. Learn about Hypertonic, Hypotonic, & Isotonic Solutions. For example, in hyponatremia sodium outside of the cell is very low and this causes water to move inside the cell. In turn, the cell will swell and you will start to see problems in the body, especially with brain cells (confusion). Sodium also play a role in muscle, nerves, and organ function. Types of Hyponatremia Euvolemic Hyponatremia is where the water in the body increases but the sodium stays the same. The causes include: SIADH (Syndrome of inappropriate antidiuretic hormone secretion) which is due to the increased amount of secretion of antidiuretic hormone. This hormone retains water in the body which dilutes sodium. Other causes: diabetes insipidus, adrenal insufficiency, Addison’s disease etc. Hypovolemic Hyponatremia is where the patient has lost a lot of fluid and sodium. Causes: vomiting, diarrhea, NG suction, diuretic therapy, burns, sweating Hypervolemic Hyponatremia is where the body has increased in fluid and sodium. However, sodium decreases due to dilution and because total body water and sodium are regulated independently in the body. Causes: congestive heart failure, kidney failure, IV infusion of saline, liver failure etc. Causes of Hyponatremia Remember “NO Na+” Na+ excretion increased with renal problems, NG suction (GI system rich in sodium), vomiting, diuretics, sweating, diarrhea, decreased secretion of aldosterone (diabetes insipidus) (wasting sodium) Overload of fluid with congestive heart failure, hypotonic fluids infusions, renal failure (dilutes sodium) Na+ intake low through low salt diets or nothing by mouth Antidiuretic hormone over secreted **SIADH (syndrome of inappropriate antidiuretic hormone secretion…remembers retains water in the body and this dilutes sodium) Signs & Symptoms of Hyponatremia Remember “SALT LOSS” Seizures & Stupor Abdominal cramping, attitude changes (confusion) Lethargic Tendon reflexes diminished, trouble concentrating (confused) Loss of urine & appetite Orthostatic hypotension, overactive bowel sounds Shallow respirations (happens late due to skeletal muscle weakness) Spasms of muscles Nursing Interventions for Hyponatremia • Watch cardiac, respiratory, neuro, renal, and GI status • Hypovolemic Hyponatremia: give IV sodium chloride infusion to restore sodium and fluids (3% Saline hypertonic solution….harsh on the veins…given in ICU usually through central line very slowly…must watch for fluid overload) • Hypervolemic Hyponatremia: Restrict fluid intake and in some cases administer diuretics to excretion the extra water rather than sodium to help concentrate the sodium. If the patient has renal impairment they may need dialysis. • Caused by SIADH or antidiuretic hormone problems: fluid restriction or treated with an antidiuretic hormone antagonists called Declomycin which is part of the tetracycline family (don’t give with food especially dairy or antacids…bind to cations and this affect absorption). • If patient takes Lithium remember to monitor drug levels because lithium excretion will be diminished and this can cause lithium toxicity. • Instruct to increase oral sodium intake and some physicians may prescribe sodium tablets. Food rich in sodium include: bacon, butter canned food, cheese, hot dogs, lunch meat, processed food, table salt Hypokalemia Hypo= low Kal= root word for potassium….. don’t get it confused with cal= calcium Emia=blood Meaning of hypokalemia: Low Potassium in the Blood Normal Potassium Level 3.5-5.1 (2.5 or less is very dangerous) Most of the body’s potassium is found in the intracellular part of the cell compared to the extracellular which is where sodium is mainly found. Blood tests measure potassium levels via the outside of the cell (extracellular fluid). Remember potassium is responsible for nerve impulse conduction and muscle contraction. Causes of Hypokalemia “Your Body is trying to DITCH potassium” Drugs (laxatives, diuretics, corticosteroids) Inadequate consumption of Potassium (NPO, anorexia) Too much water intake (dilutes the potassium) Cushing’s Syndrome (during this condition the adrenal glands produce excessive amounts of cortisol (if cortisol levels are excessive enough, they will start to affect the action of the Na+/K+ pump which will have properties like aldosterone and cause the body to retain sodium/water but waste potassium)…hence hypokalemia Heavy Fluid Loss (NG suction, vomiting, diarrhea, wound drainage, sweating) (Other causes: when the potassium moves from the extracellular to the intracellular with alkalosis or hyperinsulinism (this is where too much insulin in the blood and the patient will have symptoms of hypoglycemia) Signs & Symptoms of Hypokalemia Try to remember everything is going to be SLOW and LOW. Don’t forget potassium plays a role in muscle and nerve conduction so muscle systems are going to be messed up and effect the heart, GI, renal, and the breathing muscles for the lungs. • Weak pulses (irregular and thread) • Orthostatic Hypotension • Depression ST, flat or inverted T wave and prominent u-wave • Shallow respirations with diminished breath sounds….due to weakness of accessory muscle movement to breath) • Confusion, weak • Flaccid paralysis • Decrease deep tendon reflexes • Decreased bowel sounds Easy way to Remember 7 L’s 1. Lethargy (confusion) 2. Low, shallow respirations (due to decreased ability to use accessory muscles for breathing) 3. Lethal cardiac dysrhythmias 4. Lots of urine 5. Leg cramps 6. Limp muscles 7. Low BP & Heart Nursing Interventions for Hypokalemia Watch heart rhythm (place on cardiac monitor…most are already on telemetry), respiratory status, neuro, GI, urinary output and renal status (BUN and creatinine levels) Watch other electrolytes like Magnesium (will also decrease…hard to get K+ to increase if Mag is low), watch glucose, sodium, and calcium all go hand-in-hand and play a role in cell transport Administer oral Supplements for potassium with doctor’s order: usually for levels 2.5- 3.5…give with food can cause GI upset IV Potassium for levels less 2.5 (NEVER EVER GIVE POTASSIUM via IV push or by IM or subq routes) -Give according to the bag instruction don’t increase the rate…has to be given slow… patients given more than 10-20 meq/hr should be on a cardiac monitor and monitored for EKG changes -Cause phlebitis or infiltrations Don’t give LASIX, demadex , or thiazides (waste more Potassium) or Digoxin (cause digoxin toxicity) if Potassium level low…notify md for further orders) Physician will switch patient to a potassium sparing diuretic Spironolactone (Aldactone), Dyazide, Maxide, Triamterene Instruct patient to eat Potassium rich foods Remember POTASSIUM to help you remember the foods • Potatoes, pork • Oranges • Tomatoes • Avocados • Strawberries, • Spinach • fIsh • mUshrooms • Musk melons: cantaloupe Also included are: (carrots, raisins, bananas) Addison’s Disease vs Cushing’s Major Players in these endocrine disorders: • Adrenal Cortex • Steroid Hormones o Corticosteroids (specifically Aldosterone (mineralocorticoid) & Cortisol (glucocorticoid) Role of Adrenal Cortex: releases steroid hormones and sex hormones Role of Aldosterone: regulates blood pressure through renin-angiotensin-aldosterone system, helps retain sodium and secretes potassium (balances sodium and potassium levels). Role of Cortisol: “STRESS Hormone” helps the body deal with stress such as illness or injury, increases blood glucose though glucose metabolism, break downs fats, proteins, and carbs, regulates electrolytes. Lecture on Cushing’s vs Addison’s Disease Cushing’s (Syndrome & Disease) Cushing’s: hyper-secretion of CORTISOL (watch video for clever ways to remember this) Cushing’s Syndrome vs Cushing’s Disease Cushing’s Syndrome: caused by an outside cause or medical treatment such as glucocorticoid therapy Cushing’s Disease: caused from an inside source due to the pituitary gland producing too much ACTH (Adrenocorticotropic hormone) which causes the adrenal cortex to release too much cortisol. Signs & Symptoms of Cushing’s Remember the mnemonic: “STRESSED” (remember there is too much of the STRESS hormone CORTISOL) Skin fragile Truncal obesity with small arms Rounded face (appears like moon), Reproductive issues amennorhea and ED in male(due to adrenal cortex’s role in secreting sex hormones) Ecchymosis, Elevated blood pressure Striae on the extremities and abdomen (Purplish) Sugar extremely high (hyperglycemia) Excessive body hair especially in women…and Hirsutism (women starting to have male characteristics), Electrolytes imbalance: hypokalemia Dorsocervical fat pad (Buffalo hump), Depression Causes of Cushing’s • Glucocorticoid drug therapy ex: Prednisone • Body causing it: due to tumors and cancer on the *pituitary glands or adrenal cortex, or genetic predisposition Nursing Management for Cushing’s Syndrome • Prep patient for Hypophysectomy to remove the pituitary tumor • Prep patient for Adrenalectomy: o If this is done educate pt about cortisol replacement therapy after surgery • Risk for infection and skin breakdown • Monitor electrolytes blood sugar, potassium, sodium, and calcium levels Addison’s Disease Addison’s: Hyposecretion of Aldosterone & Cortisol (watch the video for a clever way on how to remember this and not get it confused with Cushing’s) Signs & Symptoms of Addison’s Disease Remember the phrase: “Low STEROID Hormones” (remember you have low production of aldosterone & cortisol which are STEROID hormones) Sodium & Sugar low (due to low levels of cortisol which is responsible for retention sodium and increases blood glucose), Salt cravings Tired and muscle weakness Electrolyte imbalance of high Potassium and high Calcium Reproductive changes…irregular menstrual cycle and ED in men lOw blood pressure (at risk for vascular collapse)….aldosterone plays a role in regulating BP Increased pigmentation of the skin (hyperpigmentation of the skin) Diarrhea and nausea, Depression Causes of Addison’s Disease • Autoimmune due to the adrenal cortex becoming damaged due to the body attacking itself: o Tuberculosis/infections o Cancer o Hemorrhaging of the adrenal cortex due to a trauma Nursing Management of Addison’s Disease • Watching glucose and K+ level • Administer medications to replace the low hormone levels of cortisol and aldosterone • For replacing cortisol: o ex: Prednisone, Hydrocortisone ▪ Education: Patient needs to report if they are having stress such as illness, surgery, or extra stress in life ( will need to increase dosage), take medication exactly as prescribed….don’t stop abruptly without consulting with MD. • For replacing aldosterone: • ex: Fludrocortisone aka Florinef ▪ Education: consume enough salt..may need extra salt • Wearing a medical alert bracelet • Eat diet high in proteins and carbs, and make sure to consume enough sodium • Avoid illnesses, stress, strenuous exercise Watch for Addisonian Crisis This develops when Addison’s Disease isn’t treated. In addisonian crisis, the patient has extremely LOW CORTISOL levels (life threatening). Remember the 5 S’s 1. Sudden pain in stomach, back, and legs 2. Syncope (going unconscious) 3. Shock 4. Super low blood pressure 5. Severe vomiting, diarrhea and headache • NEED IV Cortisol STAT: o Solu-Cortef and IV fluids (D5NS to keep blood sugar and sodium levels good and fluid status) • Watch for risk for infection, neuro status (confusion, agitation), electrolyte levels (sodium and potassium, glucose) Heart Failure Definition: the heart is too weak to pump efficiently so it can’t provide proper cardiac output to maintain the body’s metabolic needs. • Results on the body: organs and tissues will suffer from the decreased blood flow, pressure in the heart increases which over works the ventricles, body can become congested with fluids (enter into congestive heart failure) that can cause life-threatening complications. Note: the left ventricle is the largest of all four chambers which allows for maximum pumping power. Causes of Heart Failure: Mainly due to the heart muscle (specifically the ventricles) becoming damaged or too stiff. Remember the mnemonic: Failure Faulty heart valves: AV and SL valve problems (due to congenital issues or infection (endocarditis) that causes blood to back flow (regurgitation) or stenosis (narrowing of the valves that increases pressure of blood flow through the valves). This causes the heart to work harder and become weak over time. Arrhythmias: atrial fibrillation or tachycardia Infarction (myocardial)…coronary artery disease: part of the heart muscle dies due to a blockage in the coronary arteries…muscle become ischemic and can die (main cause of left ventricular systolic dysfunction) Lineage (congenital)…family history Uncontrolled Hypertension: overtime this can lead to stiffening of the heart walls because with untreated HTN the heart has to work harder and this causes the ventricles to become stiff. Recreational Drug Use (cocaine) or alcohol abuse Envaders (instead of Invaders): viruses or infections that attack the heart muscle Types of Heart Failures: Left & Right Side Heart Failure (can have both at the same time as well) Left-Sided Heart failure: the left side of the heart cannot pump blood out of the heart efficiently so blood starts to back-up in the lungs. • Most common type of heart failure. • Left-sided heart failure is likely to lead to right-sided heart failure. The left ventricle becomes too weak and doesn’t squeeze blood out properly….the heart failure can be either SYSTOLIC OR DIASTOLIC. • Systolic: “Left ventricular systolic dysfunction” remember systolic is the contraction or “squeezing” phase of the heart. In systolic dysfunction, there is an issue with the left ventricle being able to eject blood properly out of the ventricle and the organs can’t get all that rich-oxygenated blood it just received from the lungs. Patients will have a low ejection fraction. o What is ejection fraction? Ejection fraction is a calculation used to determine the severity of heart failure on the left side. A normal EF is 50% or greater meaning that more than half of the blood that fills inside the ventricles is being pumped out. An EF can be measured with an echocardiogram, heart cath, nuclear stress test. An EF of 40% or less is a diagnosis for heart failure. • Diastolic: “left ventricular diastolic dysfunction” remember diastole is the filling or resting phase of the heart. In diastolic dysfunction, the ventricle is too stiff to allow for normal filling of blood. Since there isn’t an issue with contraction but filling the ejection fraction is usually normal. Left-sided heart failure will present with PULMONARY Signs and Symptoms. Right-Sided Heart Failure: the right side of the heart cannot pump the “used” blood it received from the body efficiently so it can’t get the blood back to the lungs to get replenished with oxygen. The causes the blood to back up peripherally (legs, hands, feet, abdomen). • Right-sided heart failure causes congestion of blood in the heart and this increases the pressure in the inferior vena cava (which normally brings “used” blood back to the heart for re-oxygenation). This built-up pressure causes the hepatic veins to become very congested with blood which leads to hepatomegaly and swelling peripherally. o Right-sided heart failure is usually caused from left-sided heart failure because of the increased fluid pressure backing up from the left side to the right. This causes the right side of the heart to become overworked. o Other causes: pulmonary heart disease “cor pulmonale” as a complication from pulmonary hypertension or COPD. Right-sided heart failure presents with PERPHIERAL SIGNS AND SYMPTOMS. Signs and Symptoms of Heart Failure Know the difference between the signs and symptoms of left vs. right sided heart failure. Left-sided heart failure: Remember the mnemonic DROWNING (these patients are literally drowning in their own fluid from the heart’s failure to pump efficiently) Difficulty breathing Rales (crackles) Orthopnea (cannot tolerate lying down…must sit-up to breath, especially while sleeping) Weakness (extremely tired and fatigued due to shortness of breath and heart can’t compensate for increased activity) Nocturnal Paroxysmal dyspnea (awaking during sleep with extreme dyspnea) Increased heart rate (due to fluid overload and the heart is trying to get the blood to organs but it can’t because of muscle failure) Nagging cough (can be frothy or blood-tinged sputum from fluid overload in the lungs… very bad sign) Gaining weight from the body retaining fluid…2 to 3 lb in a day or 5 lbs in a week Right-Sided Heart Failure: Remember the mnemonic SWELLING (fluid is backing up in the right side of the heart which causes fluid to back-up in the hepatic veins and peripheral veins) Swelling of legs, hands, liver, abdomen Weight gain Edema (pitting) Large neck veins (jugular venous distention) Lethargic (weak and very tired) Irregular heart rate (atrial fibrillation) Nocturia (frequent urination at night) lying down elevates the legs and allows the extra fluid to enter into the vascular system which allows the kidneys to eliminate the extra fluid. Girth of abdomen increased (from swelling of the liver and building up fluid in the abdomen)…can’t breathe well and this causes nausea and anorexia. Tests used to Diagnose Heart Failure: • BNP (b-type natriuretic peptide) blood test: a biomarker released by the ventricles when there is excessive pressure in the heart due to heart failure. o 100 pg/mL no failure o 100-300 pg/mL present o 300 pg/mL mild o 600 pg/mL moderate o 900 pg/mL severe ▪ Source ClevelandC • Chest x-ray • Echocardiogram • Heart cath • Nuclear stress test Heart failure can be acute or chronic and can be triggered/exacerbated with: • High salt intake or fluid (watch fluids) • Infection • Uncontrolled atrial fibrillation • Renal failure Nursing Interventions for Heart Failure Role: Assessing, monitoring, intervening, and educating Assessing: • Assess patient for worsening symptoms (right-sided failure…peripheral swelling vs left-sided failure…pulmonary edema) • Patient responsiveness to medication treatment: o watch heart rate (Digoxin) o respiratory status o blood pressure (vasodilators cause hypotension) o diuretics (strict intake and output, daily weights, monitor electrolyte levels, especially K+) Monitoring: • Fluid status (may be ordered a Foley catheter, if on diuretics) • Cardiac diet (low in salt and fats) • Fluid restriction (no more than 2 L per day) • Lab values: watching BNP, kidney function BUN & creatinine, troponins levels, electrolytes (especially potassium…if on Lasix: waste potassium and low potassium increases risk of digoxin toxicity) • Edema in leg: Keep legs elevated and patient in high Fowler’s to help with breathing • Safety (at risk for falls due to fluid status changes, swelling in legs and feet, and orthostatic hypotension) Educating: • Early signs and symptoms heart failure exacerbation o Shortness of breath o Weight gain o Orthopnea • Low salt (allowed 2-3 G sodium per day) and fluid restriction (no more than 2 L per day) • Vaccination to prevent illness, such as annual flu and to be up-to-date with pneumonia vaccine • Exercise aerobic (as tolerated) • Daily weights (watch for no more than 2-3 lb per day and 5 lbs per week) • Compliance with medications • Smoking cessation • Limiting alcohol Administering medications: Know the drug categories a patient will be taking with heart failure and what drugs are included in that category, the pharmacodynamics, and side effects: To remember the groups of drugs use this mnemonic: Always Administer Drugs Before A Ventricle Dies! Ace Inhibitors (angiotensin-converting-enzyme inhibitors): • first line of treatment for heart failure with beta blockers • end in “pril” Lisinopril, Ramipril, Enalapril, Captopril • works by allowing more blood to get to the heart muscle which allows it to work easier. Also, blocks the conversion of Angiotensin I or Angiotensin II (this causes vasodilation, lowers blood pressure, allows kidneys to secrete sodium because it decreases aldosterone) • side effects: dry, nagging cough and can increase potassium (inhibiting angiotensin II which decreases aldosterone in the body which causes the body to retain more potassium and excrete sodium) ARBs (Angiotensin II receptor blockers): • end in “sartan” like Losartan, Valsartan • used in place of ACE inhibitors if patient can’t tolerate them • blocks angiotensin II receptors which causes vasodilation. This lowers blood pressure and helps the kidneys to excrete sodium and water (due to the affects that blocking angiotensin II has on the kidneys…decreases aldosterone). • side effects: increases potassium levels….NO dry nagging cough Diuretics: • used along with ACE inhibitors or ARBs to decrease water and sodium retention which will decrease edema in the body and lungs. This allows the heart to pump easier. • Patients will urinate a lot! • Loop diuretics (most common) like Lasix or Furosemide (watch potassium level because they will waste potassium) • Potassium-sparing diuretics like “Aldactone” (can cause hyperkalemia, especially if taking with ACE or ARBs) Beta Blockers: • blocks norepinephrine and epinephrine effects on the heart muscle • given in stable heart failure with ACE inhibitors • end in “lol” like Metoprolol, Carvedilol and Bisoprolol • not for acute heart failure because the negative inotropic effect on the heart. The negative inotropic effect causes decrease myocardial contractility (slows heart) and decreases cardiac work load. • used in stable heart failure in people with ventricular systolic dysfunction (there is a contraction problem with the left ventricle) and to treat diastolic heart failure (remember there is a problem with the heart filling in diastolic dysfunction). It will help the heart rest so the stiff ventricle can fill properly and the volume of blood pumped out increases. • side effects: check pulse (bradycardia), no grape juice; mask hypoglycemic signs in diabetics, respiratory issues in asthmatics and patients with COPD Anticoagulants: • not used in all patients with heart failure • Typically, used in patients with heart failure who are in a-fib because they are at risk for blood clot formation or certain scenarios of left ventricular systolic heart failure when there is a low ejection fraction of 35%. Vasodilators: • (arterial dilator) Hydralazine…prescribed with a nitrate like Isordil (venous dilator) • sometimes used in place of an ACE or ARB, if patient can’t tolerate them • this causes vasodilation in the arteries and veins to help decrease the amount of blood and fluid going back which helps decrease the work load on the heart • side effects: low blood pressure, orthostatic hypotension Digoxin: • Positive inotropic effect that increases the heart’s ability to contract stronger and it has a negative chronotropic action that causes the heart to beat slower • So, the heart slows down and contracts stronger which allows the heart to pump more blood. • treatment for patients with left ventricular systolic dysfunction (however, not usually the first line of treatment due to side effects and toxicity risks)…used alongside ACE/beta blockers, and diuretics • toxicity issues: monitor patient potassium level (hypokalemia 3.5 mEq/L) because hypokalemia increases digoxin toxicity • S & S of toxicity: nausea, vomiting, visual changes yellowish green halos • normal Digoxin range 0.5 to 2 ng/mL • not for patients with a second or third degree heart block • check apical pulse before giving….60 bpm • antidote: Digibind Hyperphosphatemia Hyper: “excessive” Phosphat: prefix for phosphate Emia: blood Meaning of Hyperphosphatemia: High levels of phosphate in the blood Normal Phosphate levels: 2.7 to 4.5 mg/dL (4.5 is hyperphosphatemia) Role of phosphate in the body: helps build bones and teeth and nerve/muscle function. Stored mainly in the bones. The kidneys and parathyroid play a role in the regulation of calcium and phosphate. **Calcium and phosphate influence each other in opposite way. For example, when calcium levels increase in turn phosphate levels decrease (vice versa). Vitamin D plays an important role in phosphate absorption. Causes of Hyperphosphatemia (**main cause is Renal Failure) Remember “PhosHi” (there is a drug called Phoslo (calcium acetate) which is prescribed for patients in end stage renal failure (ESRF) to help keep phosphate levels low. Phoslo is a phosphate binder and it prevents the GI system from absorbing phosphate. Phospho-soda overuse: phosphate containing laxatives or enemas (Sodium Phosphate/Fleets Enema) ….do not administer to patients with renal failure Hypoparathyroidism due to under secretion of parathyroid hormone. The parathyroid plays a role in maintaining calcium and phosphate levels and it normally inhibits reabsorption of phosphate by the kidneys. In hypoparathyroidism, there is under secretion of PTH which causes phosphate to become over absorbed by the kidneys. Overuse of Vitamin D (remember Vitamin D helps with phosphate absorption. Too much vitamin-d would cause too much phosphate to be absorbed) Syndrome of Tumor Lysis is a metabolic problem that mainly occurs with treatment of cancer with chemotherapy. It causes the electrolytes to imbalance due to the cell dying and releasing intracellular contents into the blood, hence too much phosphate is released into the blood rHabdomyolysis is rapid necrosis of the muscles and this leads to myoglobin being released into the bloodstream which affects the kidneys and causes renal failure. In renal failure, you start to have phosphate excretion decreased. Insufficiency of Kidneys (end renal failure) causes phosphate to not be excreted Signs & Symptoms of Hyperphosphatemia Will have many of the same symptoms as hypocalcemia because remember phosphate and calcium function oppositely. Remember CRAMPS (same mnemonic used for hypocalcemia) Confusion Reflexes hyperactive Anorexia Muscle spasms in calves or feet, tetany, seizures Positive Trousseau’s Signs, Pruritis Signs of Chvostek Nursing Interventions of Hyperphosphatemia • **Administer phosphate-binding drugs (PhosLo) which works on the GI system and causes phosphorus to be excreted through the stool.*** NCLEX: Give with a meals or right after eating meal • Avoid using phosphate medication such as laxatives and enema • Restrict foods high is phosphate ***eat, poultry, fish, dairy, nuts, sodas, oatmeal • Prepare patient for dialysis if patient in renal failure Hypophosphatemia Hypo: “below” Phosphat: prefix for phosphate Emia: blood Meaning of Hypophosphatemia: Low levels of phosphate in the blood Normal Phosphate levels: 2.7 to 4.5 mg/dL (2.7 is hypophosphatemia) Role of phosphate in the body: helps build bones/teeth and nerve/muscle function. Stored mainly in the bones. The kidneys and parathyroid play a role in the regulation of calcium and phosphate. **Calcium and phosphate influence each other in opposite way. For example, when calcium levels increase in turn phosphate levels decrease (vice versa). Vitamin D plays an important role in phosphate absorption. Causes of Hypophosphatemia Remember phrase: Low “Phosphate” Pharmacy: drugs such as aluminum hydroxide-based or magnesium based antacids cause malabsorption in the GI system, so no phosphate is absorbed through the GI track and the lack of vitamin d (which plays a role in phosphate absorption). Hyperparathyroidism: due to over secretion of parathyroid hormone (parathyroid plays a role in maintaining calcium and phosphate levels and it normally inhibits re-absorption of phosphate by the kidneys). However, in hyperparathyroidism there is an over secretion of PTH which causes phosphate to NOT be reabsorbed at all. Oncogenic osteomalacia: kidneys start to waste phosphate which leads to low phosphate levels and softening of the bones (this puts the patient at risk for bone fractures). Syndrome of Refeeding (aka Refeeding Syndrome): causes electrolytes and fluid problems due to malnutrition or starvation. **Watch patients who are on TPN (total parenteral nutrition). This happens when food is reintroduced after the body being in starvation mode (hence the body went into survival mode and is depleted of almost everything). When the nutrition is introduced, the body releases insulin due to the increased blood sugar from the food which causes the body to rapidly use the already low stores of phosphate, magnesium, and potassium to help with synthesizing. This depletes phosphate levels. Pulmonary issues such as respiratory alkalosis (under alkalotic conditions phosphate moves out of the blood into the cell which causes phosphate blood levels to decrease) Hyperglycemia leads to symptoms of glycosuria, polyuria, ketoacidosis which causes the kidneys to waste phosphate Alcoholism: alcohol affects the body’s ability to absorb phosphate and many alcoholics are already malnourished (hence already have low phosphate level to begin with) Thermal Burns due to the shifting of phosphate intracellularly Electrolyte imbalances: hypercalcemia, hypomagnesemia, hypokalemia also cause phosphate levels to decrease Signs & Symptoms of Hypophosphatemia Remember the word: “BROKEN” These patients are at risk for broken bones and the systems of the body are breaking down (respiratory, muscles, neuro, immune etc.) Breathing problems due to muscle weakness Rhabdomyolysis which is caused by an electrolyte disorder. This happens which there is rapid necrosis of the skeletal muscles which leads to renal failure. **These patients will have tea-colored looking urine due to myoglobin in the urine and will have muscle weakness/pain. The renal failure occurs because when the muscle dies, myoglobin is released into the blood which is very toxic to the kidneys. Reflexes (deep tendon) decreased Osteomalacia (softening of the bones) fractures and decreased bone density (alteration in bone shape), cardiac Output decreased Kills immune system with immune suppression and decreases platelet aggregation (which leads to increased bleeding) Extreme weakness, Ecchymoses from decreased platelets Neuro status changes (irritability, confusion, seizures) Nursing Interventions for Hypophosphatemia **Administer oral phosphorus with Vitamin-D supplement (remember vitamin-d helps with absorbing phosphate) If patient is receiving TPN watch for patient complaints of muscle pain or weakness (may be due to rhabdomyolysis or refeeding syndrome) Ensure patient safety due to risk of bone fractures Encourage foods high is phosphate but low in calcium: **Foods high in phosphate are fish, organ meats, nuts, pork, beef, chicken, whole grains If phosphate levels less than 1mg/dL, the doctor may order IV phosphorous which affects calcium levels causing hypocalcemia or increase phosphate levels (Hyperphosphatemia). ***Also, assess renal status (BUN/creatintine normal) before administering phosphorous because if the kidneys are failing the patient won’t be able to clear phosphate). Place on cardiac monitor and watch for EKG changes. Hypermagnesemia NCLEX Review Notes Are you studying hypermagnesemia and need to know some mnemonics on how to remember the causes, signs & symptoms, nursing interventions? This article will give you some clever mnemonics on how to remember hypermagnesemia for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate hypomagnesemia from hypermagnesemia. Don’t forget to take the hypomagnesemia & hypermagnesemia quiz. In this article you will learn: Normal Magnesium Level Causes of Hypermagnesemia Signs & Symptoms of Hypermagnesemia Nursing Interventions for Hypermagnesemia Teaching Tutorial on Hypermagnesemia Hypermagnesemia Hyper: “excessive” Magnes: prefix for magnesium Emia: blood Meaning of Hypermagnesemia: High levels of magnesium in the blood Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (2.6 hypermagnesemia) Magnesium plays a role in: major cell functions like transferring and storing energy, regulation of parathyroid hormone PTH (which also plays a role in calcium levels). In hypermagnesemia, the release of calcium is inhibited and that is why you will see hypocalcemia if you have a high magnesium level. Magnesium also plays a role in the metabolism of carbs, lipids, and proteins, and blood pressure regulation. Magnesium is absorbed in the small intestine and excreted via the kidneys (any issues with these systems can cause magnesium level issues). Causes of Hypermagnesemia Remember “MAG” Hypermagnesemia is less common than hypomagnesemia. It typically happens when you are trying to correct hypomagnesemia with magnesium sulfate IV infusion. However, other causes can include: Magnesium containing antacids and laxatives***(Mylanta, Maalox) Addison’s disease (adrenal insufficiency) Glomerular filtration insufficiency (30mL/min) renal failure. This is because the kidneys are keeping too much magnesium. Signs & Symptoms Hypermagnesemia Remember: Every system of the body is “Lethargic” (opposite of hypomagnesemia where the body systems are experiencing hyper-excitability) Note: You will typically only see symptoms in severe cases of hypermagnesemia (mild cases patient will be asymptomatic) Lethargy (profound) EKG changes with prolonged PR & QT interval and widened QRS complex Tendon reflexes absent/grossly diminished Hypotension Arrhythmias (bradycardia, heart blocks) Respiratory arrest GI issues (nausea, vomiting) Impaired breathing (due to skeletal weakness) Cardiac arrest Nursing Interventions for Hypermagnesemia • Monitor cardiac, respiratory, neuro system, renal status. Put patient on cardiac monitor (watch for EKG changes) • Ensure safety due to lethargic/drowsiness • Prevention: 1. Avoid giving Magnesium containing antacids/laxative to patients with renal failure 2. Assess for hypermagnesemia during IV infusions of magnesium sulfate for hypomagnesemia (sign and symptom would be diminished/absent deep tendon reflexes) 3. Withhold foods high in magnesium, such as: Remember: “Always Get Plenty Of Foods Containing Large Numbers of Magnesium” • Avocado • Green leafy vegetables • Peanut Butter, potatoes, pork • Oatmeal • Fish (canned white tuna/mackerel) • Cauliflower, chocolate (dark) • Legumes • Nuts • Oranges • Milk • Administer diuretics that waste magnesium (if patient is not in renal failure) such as Loop and Thiazide diuretics • Patient in renal failure patient prep for dialysis • IV calcium may be order to reverse side effects of Magnesium (watch IV for infiltration…prefer central line) Hypomagnesemia Hypo: “under” Magnes: prefix for magnesium Emia: blood Meaning of Hypomagnesemia: Low levels of magnesium in the blood Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (1.6 hypomagnesemia) Magnesium plays a role in: major cell functions like transferring and storing energy, regulation of parathyroid hormone PTH (which also plays a role in calcium levels). In hypomagnesemia, the release of calcium is inhibited and that is why you will see hypocalcemia if you have low magnesium level. Magnesium also plays a role in the metabolism of carbs, lipids, and proteins, and blood pressure regulation. Magnesium is absorbed in the small intestine and excreted via the kidneys (any issues with these systems can cause magnesium level issues). Causes of Hypomagnesemia Remember “Low Mag” Limited intake Mg+ (starvation) Other electrolyte issues cause low mag levels (hypOkalemia, hypOcalcemia) Wasting Magnesium kidneys (loop and thiazide diuretics & cyclosporine…stimulates the kidneys to waste Mag) Malabsorption issues (Crohn’s, Celiac, proton-pump inhibitors drugs “Prilosec, Nexium, Protonix”…drug family ending in “prazole” Omeprazole, diarrhea/vomiting) Alcohol (due to poor dietary intake, alcohol stimulates the kidneys to excreted mag, acute pancreatitis) Glycemic issues (Diabetic Ketoacidosis, insulin administration) Signs & Symptoms of Hypomagnesemia Remember “Twitching” because the body is experiencing neuromuscular excitability. This is the OPPOSITE in hypermagnesemia where everything system of the body is lethargic. Trouesseau’s (positive due to hypocalcemia) Weak respirations Irritability Torsades de pointes (abnormal heart rhythm that leads to sudden cardiac death…seen in alcoholism) Tetany (seizures) Cardiac changes (moderate loss: Tall T-waves and depressed ST segments*** severe loss: prolonged PR & QT interval (prolong of QT interval increases patient’s risk for Torsades de pointes) with widening QRS complex, flattened t-waves, Chvostek’s sign (positive which goes along with hypocalcemia) Hypertension, hyperreflexia Involuntary movements Nausea GI issues (decreased bowel sounds and mobility) Nursing Interventions for Hypomagnesemia • Monitor cardiac, GI, respiratory, neuro status. Place on a cardiac monitor (watching for any EKG changes prolonging of PR interval and widening QRS complex) • May administer potassium supplements due to hypokalemia (hard to get magnesium level up if potassium level is down) • Administering calcium supplements (oral calcium supplements w/ Vitamin-D or 10% Calcium Gluconate) • Administer Magnesium Sulfate IV route. Monitor Mg+ level closely because patient can become magnesium toxic (***Watch for depressed or loss of deep tendon reflexes) • Place patient in seizure precautions • Oral forms of Magnesium may cause diarrhea which can increase magnesium loss so watch out for this • Watch other electrolyte levels like calcium and potassium • Encourage foods rich in Magnesium: “Always Get Plenty Of Foods Containing Large Numbers of Magnesium” • Avocado • Green leafy vegetables • Peanut Butter, potatoes, pork • Oatmeal • Fish (canned white tuna/mackerel) • Cauliflower, chocolate (dark) • Legumes • Nuts • Oranges • Milk Hypernatremia Hyper: “excessive” Natr: Prefix for Sodium Emia: blood Meaning of Hypernatremia: excessive sodium in the bloodisotonic, hypotonic, and hypertonic tonicity. Normal sodium levels: 135 to 145 mEq/L (145 sodium is hypernatremic) Hypernatremia is a water problem rather than a sodium problem. This is because when the body collects sodium it causes a lot of water retention and this is what causes the patient problems. Role of sodium in the body: It’s an important electrolyte that helps regulate the amount of water inside and outside of the cell (water and sodium loves each other). Where ever sodium goes, so does water. Watch my video on hypotonic, hypertonic, and isotonic tonicity. For example, in hypernatremia there is a lot of sodium outside the cell and this attracts the water from inside the cell which will cause water to move outside the cell and dehydrate the cell. Sodium also plays a role in muscle, nerves, and organ function. Causes of Hypernatremia Remember the phrase “HIGH SALT” Hypercortisolism (Cushing’s Syndrome), hyperventilation Increased intake of sodium (oral or IV route) GI feeding (tube) without adequate water supplements Hypertonic solutions Sodium excretion decreased (body keeping too much sodium) and corticosteroids Aldosterone overproduction (Hyperaldosteronism) Loss of fluids (dehydrated) infection (fever), sweating, diarrhea, and diabetes insipidus Thirst impairment Signs & Symptoms of Hypernatremia Remember: “No FRIED foods for you!” (too much salt) Fever, flushed skin Restless, really agitated Increased fluid retention Edema, extremely confused Decreased urine output, dry mouth/skin Nursing Interventions for Hypernatremia • Restrict sodium intake! Know foods high in salt such as bacon, butter, canned food, cheese, hot dogs, lunch meat, processed food, and table salt. • Keep patient safe because they will be confused and agitated. • Doctor may order to give isotonic or hypotonic solutions such as 0.45% NS (which is hypotonic and most commonly used). Give hypotonic fluids slowly because brain tissue is at risk due to the shifting of fluids back into the cell (remember the cell is dehydrated with hypernatremia) and the patient is at risk for cerebral edema. In other words, the cell can lyse if fluids are administered too quickly. • Educate patient and family about sign and symptoms of high sodium level and proper foods to eat. Hyponatremia Hypo: “under/beneath” Natr: Prefix for Sodium Emia: blood Meaning of Hyponatremia: low sodium in the blood Normal sodium levels: 135 to 145 mEq/L (135 = hyponatremia) Role of sodium in the body: An important electrolyte that helps regulate water inside and outside of the cell. Remember that water and sodium loves each other and where ever sodium goes so does water. Learn about Hypertonic, Hypotonic, & Isotonic Solutions. For example, in hyponatremia sodium outside of the cell is very low and this causes water to move inside the cell. In turn, the cell will swell and you will start to see problems in the body, especially with brain cells (confusion). Sodium also play a role in muscle, nerves, and organ function. Types of Hyponatremia Euvolemic Hyponatremia is where the water in the body increases but the sodium stays the same. The causes include: SIADH (Syndrome of inappropriate antidiuretic hormone secretion) which is due to the increased amount of secretion of antidiuretic hormone. This hormone retains water in the body which dilutes sodium. Other causes: diabetes insipidus, adrenal insufficiency, Addison’s disease etc. Hypovolemic Hyponatremia is where the patient has lost a lot of fluid and sodium. Causes: vomiting, diarrhea, NG suction, diuretic therapy, burns, sweating Hypervolemic Hyponatremia is where the body has increased in fluid and sodium. However, sodium decreases due to dilution and because total body water and sodium are regulated independently in the body. Causes: congestive heart failure, kidney failure, IV infusion of saline, liver failure etc. Causes of Hyponatremia Remember “NO Na+” Na+ excretion increased with renal problems, NG suction (GI system rich in sodium), vomiting, diuretics, sweating, diarrhea, decreased secretion of aldosterone (diabetes insipidus) (wasting sodium) Overload of fluid with congestive heart failure, hypotonic fluids infusions, renal failure (dilutes sodium) Na+ intake low through low salt diets or nothing by mouth Antidiuretic hormone over secreted **SIADH (syndrome of inappropriate antidiuretic hormone secretion…remembers retains water in the body and this dilutes sodium) Signs & Symptoms of Hyponatremia Remember “SALT LOSS” Seizures & Stupor Abdominal cramping, attitude changes (confusion) Lethargic Tendon reflexes diminished, trouble concentrating (confused) Loss of urine & appetite Orthostatic hypotension, overactive bowel sounds Shallow respirations (happens late due to skeletal muscle weakness) Spasms of muscles Nursing Interventions for Hyponatremia • Watch cardiac, respiratory, neuro, renal, and GI status • Hypovolemic Hyponatremia: give IV sodium chloride infusion to restore sodium and fluids (3% Saline hypertonic solution….harsh on the veins…given in ICU usually through central line very slowly…must watch for fluid overload) • Hypervolemic Hyponatremia: Restrict fluid intake and in some cases administer diuretics to excretion the extra water rather than sodium to help concentrate the sodium. If the patient has renal impairment they may need dialysis. • Caused by SIADH or antidiuretic hormone problems: fluid restriction or treated with an antidiuretic hormone antagonists called Declomycin which is part of the tetracycline family (don’t give with food especially dairy or antacids…bind to cations and this affect absorption). • If patient takes Lithium remember to monitor drug levels because lithium excretion will be diminished and this can cause lithium toxicity. • Instruct to increase oral sodium intake and some physicians may prescribe sodium tablets. Food rich in sodium include: bacon, butter canned food, cheese, hot dogs, lunch meat, processed food, table salt Hypercalcemia Hyper: excessive Calc: prefix for calcium Emia: blood Meaning of Hypercalcemia: excessive calcium in the blood Normal calcium levels in the blood: 8.6 to 10.0 mg/dL (10.0 is hypercalcemia) Calcium plays a huge role in bone and teeth health along with muscle/nerve function, cell, and blood clotting. Calcium is absorbed in the GI system and stored in the bones and then excreted by the kidneys. Vitamin D helps play a role calcium absorption. Causes of Hypercalcemia Remember “High Cal” Hyperparathyroidism (high parathyroid hormone causes too much calcium to be released into the blood) Increased intake of calcium (excessive use of oral calcium or Vitamin D supplements) Glucocorticoids usage (suppresses calcium absorption which leaves more calcium in the blood) Hyperthyroidism Calcium excretion decreased with Thiazide* diuretics & renal failure, cancer of the bones Adrenal insufficiency (Addison’s Disease) Lithium usage (affects the parathyroid and causes phosphate to decrease and calcium to increase) Signs & Symptoms of Hypercalcemia “The body is too WEAK” Weakness of muscles (profound) EKG changes shortened QT interval (most common) and prolonged PR interval Absent reflexes, absent minded (disorientated), abdominal distention from constipation Kidney Stone formation Nursing Interventions for Hypercalcemia Mild cases of Hypercalcemia • Keep patient hydrated (decrease chance of renal stone formation) • Keep patient safe from falls or injury • Monitor cardiac, GI, renal, neuro status • Assess for complaints of flank or abdominal pain & strain urine to look for stone formation • Decrease calcium rich foods and intake of calcium-preserving drugs like thiazides, supplements, Vitamin D To help you remember foods high in calcium remember the phrase: “Young Sally’s calcium serum continues to randomly mess-up” Yogurt Sardines Cheese Spinach Collard greens Tofu Rhubarb Milk Moderate cases of Hypercalcemia Administer calcium reabsorption inhibitors: Calcitonin, Bisphosphonates, prostaglandin synthesis inhibitors (ASA, NSAIDS) Severe cases of Hypercalcemia Prepare patient for dialysis Hypocalcemia Hypo: low Calc: pre-fix is calcium Emia: blood Meaning of hypocalcemia: Low calcium in the blood Normal calcium level: 8.6 mg/dL to 10.0 (8.6 mg/dL) Role of Calcium: plays a huge role in bone and teeth health along with muscle/nerve function, cell, and blood clotting. Calcium is absorbed in the GI system and stored in the bones and then excreted by the kidneys. Vitamin D helps play a role in calcium absorption. In addition, phosphorus and calcium affect each other in the opposite way. For instance, if phosphorus levels are high in the blood, calcium will decrease and vice versa. They are always doing the opposite (remember this because it is important for the causes of hypocalcemia. Causes of Hypocalcemia Remember “Low Calcium” Low parathyroid hormone due. This is due to the destruction or removal parathyroid gland (any surgeries of the neck ex: thyroidectomy you want to check the calcium level) Professors love to ask this on an exam. Oral intake inadequate (alcoholism, bulimia etc.) Wound drainage (especially GI System because this is where calcium is absorbed) Celiac’s & Crohn’s Disease cause malabsorption of calcium in the GI track Acute Pancreatitis Low Vitamin D levels (allows for calcium to be reabsorbed) Chronic kidney issues (excessive excretion of calcium by the kidneys) Increased phosphorus levels in the blood (phosphorus and calcium do the opposite of each other) Using medications such as magnesium supplements, laxatives, loop diuretics, calcium binder drugs Mobility issues Signs & Symptoms of Hypocalcemia Remember “CRAMPS” Confusion Reflexes hyperactive Arrhythmias (prolonged QT interval and ST interval) Note: definitely remember prolonged QT interval…another major test question Muscle spasms in calves or feet, tetany, seizures Positive Trousseau’s! You will see this before Chvostek’s sign or before tetany. This sign may be positive before other manifestations of hypocalcemia such as hyperactive reflexes. (KNOW How to elicit a positive Trousseau’s. You do this by using a blood pressure cuff and place it around the upper arm and inflate it to a pressure greater than the systolic blood pressure and hold it in place for 3 minutes. If it is positive the hand of the arm where the blood pressure is being taken will start to contract involuntarily (see the teaching tutorial on a demonstration). Signs of Chvostek’s (nerve hyperexcitability of the facial nerves. To elicit this response you would tap at the angle of the jaw via the masseter muscle and the facial muscles on the same side of the face will contract momentarily (the lips or nose will twitch). Nursing Interventions for Hypocalcemia • Safety (prevent falls because patient is at risk for bone fractures, seizures precautions, and watch for laryngeal spasms)