Questions to Prepare for OSCE 1. Describe the pathophysiologic changes in DKA. a. Why do blood glucose levels increase? - Without insulin, the amount of glucose entering the cells is reduced, so then the liver increases glucose production The patient lacks insulin which is required to breakdown sugar for energy. This results in an increase in glucose levels. b. What are commonly seen blood glucose levels? - Blood glucose levels may vary from 16.6 to 44.4 mmol/L. Some may have lower, and others may have values of 55.5mmol/L c. What fluid and electrolyte disturbances commonly occur? -Water, sodium, potassium, and chloride d. What causes the fluid and electrolyte disturbances? -In an attempt to rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes. Patients with DKA may lose up to 6.5 litres of water and up o 400 to 500 mmol/L each of sodium, potassium, and chloride. Due to the lack of insulin, cells are not receiving an adequate fuel source to produce energy. Even though the blood is loaded with glucose, the cells go into a starvation mode. This triggers the release of glucagon and other counter-regulatory hormones that promote the breakdown of triglycerides into free fatty acids and initiate gluconeogenesis to produce more glucose for the starving cells. This further elevates the blood glucose level as the body begins to metabolize protein and fat to produce a source of energy. Due to the insulin deficiency and release of large amounts of glucagon, free fatty acids circulate in abundance in the blood and are metabolized into acetoacetic acid and B-hydroxybutric acid — both of which are strong organic acids and are referred to as ketones. As acetoacetic acid is metabolized it produces acetone, which begins to accumulate in the blood. Small amounts of acetone are released in respiration and produce the characteristic “fruity breath” odor. In normal metabolism, ketones would be used as fuel in the peripheral tissue; however, due to the starvation state of the cells, the ketones are not used. An increase in ketone production and a decrease in peripheral cell use lead to metabolic acidosis – also called ketoacidosis. This is reflected in a decreasing pH value typically less than 7.40. The patient will also begin to eliminate large amounts of ketones through excretion in the urine. Typically, when the blood glucose level reaches approximately 225 mg/dL a significant amount of glucose spills over into the urine. A glucose molecule produces an osmotic effect by drawing water across a semipermeable membrane. As an excessive amount of glucose enters the renal tubules, it draws a large amount of water that ends up producing a significant amount of urine. This is known as osmotic diuresis and leads to volume depletion and dehydration in the patient. Large amounts of ketones also collect in the urine. Because ketones are strong organic acids, they must be buffered in order to be excreted. Sodium is typically used as the buffer. As we have been instructed, where sodium goes, water follows. Thus, the sodium used to buffer the ketones also draws a large amount of water into the renal tubules, which produces excessive urine and leads to further volume depletion and dehydration. The loss of large amounts of fluid also leads to the excretion of other electrolytes, such as potassium, calcium, magnesium and phosphorous. This produces electrolyte imbalance and disturbances. e. What acid-base disturbances are commonly seen? -Excessive ketone bodies f. Why do the acid-base disturbances occur? –The insulin deficiency or deficit causes the breakdown of fat (lipolysis) into free fatty acids and glycerol. The free fatty acids are converted into ketone bodies by the liver. Insulin would normally prevent this from happening. 2. Describe the medical management of a patient in DKA. a. How is fluid status monitored in the acute stage of DKA? -Monitoring fluid volume status involves frequent measurements of vital signs, lung assessment, and monitoring intake and output. Frequent measurements of VS including BP, HR, lung assessment and ins and outs Patients with marked intravascular volume depletion may have a drop in systolic blood pressure of 20mm Hg + upon standing Volume depletion may also lead to a weak, rapid pulse b. How is hypovolemia corrected? How rapidly is fluid volume replaced? Why? –Patients may need up to 6 to 10 liters of IV fluid to replace fluid losses causes by polyuria, hyperventilation, diarrhea, and vomiting. - Initially, 0.9% sodium chloride (NS) solution is administered at a rapid rate, usually 0.5 to 1 Lper hour for 2 to 3 hours. -0.45% NS is sln of choice for continued rehydration if BP stable and sodium levels not low -Moderate to high rates (200-500 mL/hr) continue for several hours to stabalize volume (continue to monitor ins/outs) -When blood glucose level reaches 16.6 mmol/L or less, IV fluid may be changed to D5W to prevent decline in glucose level c. How are blood glucose levels monitored? How often? –Monitor glucose levels every hour Self monitoring of blood glucose- various method available, most common involve obtaining a drop of blood from the fingertip, applying blood to a special reagent strip, and allow the blood to stay on the strip for a specific amount of time (identified by manufacturer), and meter gives read out of blood glucose value Used mostly for those with unstable diabetes, tendency for severe ketosis, hypoglycemia without warning, or use of sliding scale. For those who have insulin it is recommended that glucs are taken 2 to 4 times daily (usually before meals, and at bedtime) Pt. who take insulin before meals, should test their glucs 3x a day before meals Pt. who do not receive insulin should check their glucs 2-3x a week including 2 hours after a meal Whenever hypoglycemia or hyperglycemia is suspected Increase in frequency if changes in medication, activity, diet, stress, and illness. d. How are elevated blood glucose levels corrected? – Given insulin drip e. How quickly is blood glucose corrected? Why? – Insulin is usually infused intravenously at a slow, continuous rate (eg, 5 units per hour). It also depends on the type of insulin: Time Agent Onset Peak Duration Indications Course RapidActing Analogue Humalog, NovoRapi d 10-15 min 60-70 min 4-5 h Rapid reduction of glucose level, prevent nocturnal hypoglyce mia Fast-Acting Humalog R, Novalin ½-1 h 2-4 h 5-8 h Intermediate -Acting Humulin L &N 1-3 h 5-8 h Up to 18 h LongActing Humulin U 3-4 h 8-15 h 22-26 h 90 min Continuous (no peak) 24 h Administer ed 20-30 min before meal, may be taken along or with long acting Usually taken after food Used primarily to control fasting glucose level Used for basal dose Extended Lantus Long-Acting Analogue 3. What electrolytes are monitored in the acute stage of DKA? Why? – The major electrolyte of concern is potassium. It is vital to avoid dysrhythmias. a. How are electrolyte imbalances corrected? How rapidly is this accomplished? Why? – Up to 40 mmok/L per hour may be needed for several hours. Because extracellular potassium levels drop during DKA treatment, potassium must be infused even if the plasma potassium level is normal. May need 6-10 liters of IV fluid to replace fluid loss caused by polyuria, hyperventilation, diarrhea, and vomiting 0.9% NaCl is administered at rapid rate, usually 0.5 to 1 liter per hour for 2- 3 hours 0.45 NaCl can be used for pt with hypertension and hyperatremia After the first few hours, half- normal saline solution (0.45%) is the choice for continued rehydration, if the blood pressure is stable and the Na+ is not low When the blood glucs reach 16.6 mmol/L or less the IV solution should be changed to dextrose 5% in water to prevent a precipitous decline in blood glucose level Frequently take vitals, lung assessment, monitor I & O Plasma expander may be used to correct severe hypotension Monitor signs of fluid overload especially important for older adults, renal impaired pt. and those at risk for heart failure Major concern in K+ (that’s why he is on telemetry) Insulin is usually infused intravenously at a slow, continuous rate Hourly blood glucs done IV fluid solution with higher concentration of glucose such as NS (D5NS) are administered when blood gluc reach 13.8 to 16.6 mmol/L to avoid too rapid a drop in blood gluc levels 100 units of regular insulin are mixed in 500 mL 0.9% NS, then 1 unit of insulin equal 5 mL. 5 units per hour would equal 25mL per hour Even if blood glucose levels are dropping to normal the insulin drip must not be stopped; rather the rate, or concentration of the dextrose infusions should be increased b. How are acid-base disturbances monitored? How often? – Frequent (every 2-4 hours initially) electrocardiograms and la measurements of potassium are necessary during the first 8 hours of treatment. c. How are acid-base disturbances corrected? How quickly is this accomplished? Why? – IV insulin drip. It must be continued for 12 to 24 hours until the serum bicarbonate level improves (to at least 15 to 18 mmol/L) and until the patient can eat. Treat the underlying cause. Depending on what type of imbalance is occurring, the treatment is different. For our scenario, DKA, it would most likely be: Metabolic Acidosis (pH <7.35; bicarbonate <22mEq/L). This condition is related to an overproduction of ketone bodies, which occurs when the body has used up its glucose supplies and draws on its fat stores for energy converting fatty acids to ketone bodies. To correct: Address symptoms and underlying cause Respiratory therapy is usually the first line of therapy including mechanical ventilation For patient’s with diabetes expect to administer rapid-acting insulin to reverse DKA and drive potassium back into the cell Monitor serum potassium levels as well as other electrolyte imbalances and correct Expect to administer sodium bicarbonate intravenously Replace other fluids IV as needed Dialysis may be needed in patients with renal failure or a toxic reaction to a drug Antibiotic to treat infection Antidiarrheal for diarrhea induced bicarbonate loss Other imbalances: Respiratory Acidosis with a pulmonary cause: Bronchodilator to open constricted airways Supplemental oxygen PRN Drug therapy to treat hyperkalemia Antibiotic therapy to treat infection Chest physiotherapy to remove secretions from the lungs Respiratory Alkolosis Treat underlying disorder Remove causative agent (if one) Take steps to reduce fever and eliminate source of sepsis If hypoxemia: oxygen therapy If anxiety: sedative or anxiolytic Metabolic Alkalosis IV administration of ammonium chloride Discontinuation of thiazide diuretics and NG suctioning Administration of an antiemetic Addition of Diamox to inhibit calcium and increase renal excretion of bicarbonate 4. Describe the nursing management of a patient in DKA – Focuses on monitorning fluid and electrolyte status as well as blood glucose levels; administering fluids, insulin, and other medications; and preventing other complications such as fluid overload. Urine output is monitored to ensure adequate renal function before potassium is administered to prevent hyperkalemia. Vital signs, arterial blood gases, and other clinical findings are recorded on a flow sheet. The nurse documents the patients lab values and the frequent changes in fluids and medications that are prescribed and monitor the patients responses. Fluid can be assessed by: assessing mucous membranes- they should look smooth and moist, if dehydrated they should look dry and the lips looks parched and cracked Assess for edema- edema should not be present. Edema- skin looks puffy and tight, if it leaves a dent-pitting edema- which can mask the normal skin colour Mobility and turgor- Pinch the leg fold of skin under the clavicle. Mobility is decreased when edema is present, and poor turgor is evident in severe dehydration Monitor vitals Monitor ins and outs- during a 24hr period it is important to asses for fluid and electrolyte balance. Output every hours should be 30cc, and within 8 hours 240cc b. What are the complications of fluid replacement and how are they prevented? – By monitoring intake and output c. How are blood glucose levels assessed? How often? – Hourly blood glucose levels must be measured. d. What are the complications of lowering blood glucose levels and how are they prevented? – Insulin will be given to lower blood sugar and to prevent further ketone formation. Once blood glucose levels have fallen to 13.8 to 16.6 mmol/L, additional glucose may be given to allow continued insulin administration without the development of hypoglycemia Possible hypoglycaemia, coma, or seizure Intense therapy must be used with caution, with constant monitoring e. How are electrolyte disturbances assessed? How often? – Frequent (every 24 hours initially) electrocardiograms and la measurements of potassium are necessary during the first 8 hours of treatment. f. What are the complications of electrolyte replacement and how are they prevented? – The patients serum potassium level may drop quickly due to rehydration and insulin treatment, potassium replacement must begin once the potassium levels drop to normal. Dysrhythmias- cautious but timely potassium replacement is vital to avoid these Potassium should be given during DKA treatment g. How are acid-base disturbances assessed? How often? Through plasma pH (arterial blood) normal range 7.37 – 7.43 h. What are the complications of acid-base correction and how are they prevented? To correct for metabolic acidosis, IV insulin is given, however, this may drop glucose levels too low and result in hypoglycemia often more dangerous than hyperglycemia. In this case dextrose 5% in 1/2 NS. Another complication would be speed shock where fluids are given back into the body too quickly. The patient will show facial flushing, irregular pulse, headache, decreased BP, LOC and cardiac arrest may also occur. Fluid overload is another complication that may occur. To prevent: • check the order, make sure it is complete and accurate • monitor daily weights to document fluid loss or retention • measure I&O carefully and at scheduled intervals • carefully monitor infusion especially those that include medications • keep in mind the patient’s size, age, and history to prevent fluid overload • note the pH of a solution i. Define anion gap, serum osmolality and venous CO2. Anion gap: A measurement of the interval between the sum of "routinely measured" cations minus the sum of the "routinely measured" anions in the blood. The anion gap = (Na+ + K+) - (Cl- + HCO3-) where Na- is sodium, K+ is potassium, Cl- is chloride, and HCO3- is bicarbonate. The anion gap can be normal, high, or low. A high anion gap indicated metabolic acidosis, the increased acidity of the blood due to metabolic processes. A low anion gap is relatively rare but may occur from the presence of abnormal positively charged proteins, as in multiple myeloma. Serum Osmolality: a measure of the number of dissolved particles per unit of water solution, the fewer the particles of solute in proportion to the number of units of water (solvent), the less concentrated the solution. A low serum osmolality would be indicative of a higher than usual amount of water in relation to the amount of particles dissolved in it. It would be expected, then, that a low serum osmolality would accompany overhydration, or edema, and an increased serum osmolality would be present in a state of fluid volume deficit. Measurement of the serum osmolality gives information about the hydration he cells because of the osmotic equilibrium that is constantly being maintained on either side of the cell membrane (homeostasis). Water moves freely back and forth across the membrane in response to the osmotic pressure being exerted by the molecules of solute in the intracellular and extracellular fluids. Serum osmolality reflects the status of hydration of the intracellular as well as the extracellular compartments and thus describes total body hydration. Venous CO2 – amount of carbon dioxide in the blood? Chronic Heart Failure 1. When assessing a pt with symptoms of heart failure, how does the nurse differentiate between right and left sided failure? Left-sided failure- “backward failure” -dyspnea, cough, pulmonary crackles and lower than normal oxygen saturation levels. An extra heart sound, S3, may be detected on auscultation. -Dyspnea, or SOB may be precipitated by minimal to moderate activity, dyspnea may also occur at rest. -Orthopnea, difficulty in breathing when lying flat. -Cough is usually dry and non productive- dry hacking cough. The cough may become moist. Large quantities of frothy sputum, which is sometimes pink or blood tinged, may be produced. This usually indicated severe pulmonary congestion (pulmonary edema). -Adventitious breath sounds may be heard in various lobes of the lungs. Usually crackles that do not clear with coughing are heard in the early phase of left ventricular failure. As it worsens, crackles may be heard throughout the lung field. - Blood flow to the kidneys decreases, causing decreased perfusion and reduced urine output (oliguria). - Sodium and fluid retention increases. -dizziness, lightheadedness, confusion, restlessness, and anxiety are due to decreased 02, -peripheral blood vessels constrict, so the skin appears pale or ashen and feels cool and clammy Right-sided failure -congestion of the peripheral tissues predominates. -increase in venous pressure leads to jugular vein distention -edema of the lower extremities, hepatomegaly, distended jugular veins, ascites (accumulation of fluid in the peritoneal cavity), weakness, anorexia and nausea, and paradoxically, weight gain due to fluid retention. -edema usually affects the feet and ankles, worsening when patient stands or dangles legs. Swelling decreasing when pt elevated legs. -hepatomegaly and tenderness in right upper quadrant because of enlargement. This can also increase pressure on the diaphragm, causing respiratory distress. -anorexia and nausea or abdominal pain. 2. What are the compensatory mechanisms the overloaded heart resorts to when attempting to maintain normal cardiac output? Remember that CO= HR x Stroke Volume Systolic HF (alteration in ventricular contraction) decreases amt. of blood ejected from ventricle - causes SNS responses and neurohormonal responses that lead to increased workload and further damage to heart Decreased contractibility causes increased end-diastolic blood volume in ventricles therefore increasing the size of the ventricle. Increased size leads to increased workload. This is also called the “Vicious cycle of HF” (p. 797) To compensate for increased workload: Ventricular hypertrophy to help with contractability –but does not increase capillary supply (so can lead to myocardial ischemia) Diastolic HF (alteration in ventricular filling) develops due to an increased workload on heart To compensate: Increased number and size of myocardial cells WHICH Cause resistance to ventricular filling WHICH Increase ventricular filling pressures WHICH Cause low CO (cardiac output) WHICH Cause neurohormonal responses 3. What drug therapies are commonly used for a person who has an exacerbation of chronic heart failure? How do these medications work? - ACE inhibitors- major role in management of HF, may be the first medication prescribed for mild failure. They have been found to relieve the S&S of HF and decrease mortality and morbidity. ACE promotes vasodilatation and dieresis by decreasing after load and preload. This helps to decrease the workload of the heart. ACE stimulates the kidneys to excrete sodium and fluid, while keeping potassium. This reduces left ventricular filling pressure and decreasing pulmonary congestion. - Angiotensin II Receptor Blockers (ARBs)- usually prescribed when patients can’t tolerate ACEs. ARBs block the effects of angiotension II at the angiotension II receptor. They lower blood pressure and lower systemic vascular resistance. - Beta-blockers- When used with an ACE, they have been found to reduce mortality and morbidity. However, beta blockers may produce side effects such as exacerbation of HF, which are most common in the initial few weeks of treatment. The most frequent side effects are dizziness, hypotension, and bradycardia. To minimize effects, stagger beta blockers and ACEs. Any type of beta blocker is contraindicated in patients with severe or uncontrolled asthma because it can cause bronchiole constriction. - - - - Diuretics- increase rate of urine production and remove excess extracellular fluid from the body. Three most common are: Thiazide- inhibit sodium and chloride reabsorption mainly in the early distal tubules. They also increase potassium and bicarbonate excretion Loop- inhibit sodium and chloride reabsorption mainly in the ascending loop of Henle. Potassium sparing- inhibits sodium reabsorbtion in the late distal tubule and collecting duct. Digitalis- most commonly prescribed for is digoxin. The medication increases the force of myocardial contraction and slows conduction through the AV node. It also enhances dieresis, which removes fluid and relieves edema. It is effective in decreasing the symptoms of systolic HF and in increasing the patient’s ability to perform activities of daily living. Calcium Channel Blocker- Contraindicated in pt. with systolic dysfunction although they may be used in pt. with diastolic dysfunction. Cause vasodilation, reducing systemic vascular resistance. Improve symptoms in pt’s with nonischemic cadiomyopathy Other Medications- Anticoagulants, especially if the patient has a Hx of an embolic event or atrial fibrillation. Antianginal medications. NSAIDs should be AVOIDED! As they increase systematic vascular resistance and decrease renal perfusion, especially in the elderly. Use of decongestants should be avoided 4. What are other therapeutic interventions would be anticipated for a person who has an exacerbation of chronic heart failure? -provide general counseling and education about sodium restriction, monitor daily weights and other signs of fluid retention, encourage regular exercise, and recommending avoidance of excessive fluid intake, alcohol, and smoking. -Mechanical devices (ventricular devices and counterpulsation) may provide respite for the heart in acute failure. -Supplemental oxygen-by mask or cannula relieve hypoxia and dyspnea and improve oxygen-carbon dioxide exchange. For hypoxemia, partial breather masks with a flow rate of 8-10L/min can be used to deliver oxygen concentrations of 40%-70%. A non-breathing mask can achieve even higher oxygen concentrations. -If supplemental oxygen does not raise the arterial oxygen tension (PaO2) above 60mm Hg, the client may need intubation and ventilator management. Intubation also provides a route for removing secretions from the bronchi. -If severe bronchospasm or bronchoconstriction occurs, bronchodilators are given. ****the heart rhythm is monitored because some bronchodilators may lead to dysrhythmias -Position the client in a high Fowlers position or chair to reduce pulmonary venous congestion and to relieve dyspnea. The legs remain in a dependent position as much as possible. Even if legs are edematous they should not be elevated. Elevating legs increases venous return rapidly. -Reduce fluid retention. Controlling sodium and water retention improves cardiac performance. Sodium restriction should be in place. Potassium supplements and adequate dietary potassium are important. -Reduce stress and risk of injury. This means reducing physical and emotional stress. Rest is also important. 5. What are the nursing responsibilities related to the administration of digoxin? What are the signs and symptoms of digitalis toxicity? Digoxin: increases the force of myocardial contraction; slows cardiac conduction through the AV node and therefore slows the ventricular rate in instances of supraventricular dysrhythmias; increases cardiac output by enhancing the force of ventricular contraction; promotes dieresis by increasing cardiac output. Therapeutic level is usually 0.5 to 2.0 ng/ml -Take vitals before administering drug -Before administration it is standard to assess apical heart rate for 1 MINUTE and make sure heart rate is above 60 beats per min. Note rate, rhythm, and quality. - Withhold medication and notify physician if apical pulse falls below ordered parameters - dray blood samples for determining plasma digoxin levels at least 6 hours after daily dose and preferably just prior to next scheduled dose. -Monitor doe drug toxicity. Digoxin Toxicity - fatigue, depression, malaise, anorexia, nausea, and vomiting (early effects of digitalis toxicity). -change in hear rhythm: new onset of regular rhythm or new onset of irregular rhythm. -ECG changes indicating SA or AV block; new onset of irregular rhythm indicating ventricular dysrthythmias; and atrial tachycardia with block, junction tachycardia, and ventricular tachycardia. 6. Outline and prioritize a long term care plan for someone with an exacerbation of chronic heart failure. Goals for the patient with chronic congestive heart failure include: decreased peripheral edema, decreased shortness of breath, increased exercise tolerance, decreased drug regimen, and no complications related to CHF. -promoting activity tolerance- prolonged bed rest should be avoided because of effects such as, pressure ulcers, phlebothrombosis, and pulmonary embolism. A total of 30 minutes of physical activity 3-5 times a week should be encouraged. Alternate periods of activity and rest. Increase activities, such as walking, gradually, as long as they don’t cause fatigue or shortness of breath. -managing fluid volume- oral diuretics should be taken in the early morning so it does not interfere with nighttime rest. Teach patient about low-sodium diet by reading food labels, and avoiding high sodium foods such as canned, processed, and convenience foods. Teach patient about different positions and how to assume those positions to shift fluid away from the heart. Increase number of pillows, head of bed elevated, or pt. may sit in a chair. Lower arms are supported by pillows to eliminate fatigue caused by constant pull of their weight on the shoulder muscles. Frequent change in position to avoid pressure, and the use of compression stockings, and leg exercises can help to prevent skin injury. -controlling anxiety- HF patients have difficulty maintaining adequate oxygenation, they are likely to be restless and anxious and fell overwhelmed by breathlessness. Symptoms intensify at night. O2 may be administered during an event to decrease the work of breathing and increase comfort. -relaxation techniques to help relax patient. -inform that lack of sleep can effect anxiety -drug therapy- Take each drug as prescribed. Make a daily chart to ensure drugs have been taken. Take pulse daily before taking medication and know the parameters your health care provider wants your heart rate. Learn how to take your own BP at specific pre-determined times and know the parameters that are acceptable for you as provided by your doctor. Know the signs and symptoms of orthostatic hypotension and know how to prevent them. Know the signs and symptoms of internal bleeding such as: bleeding gums, increased bruises, blood in the urine or stool, and what to do if on anticoagulants. Know how often to have blood monitored if on warfarin (usually weekly once at an acceptable level) and know where you INR should be (2-3)