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
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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)
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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.
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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
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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:
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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
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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
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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.
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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.
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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)