CCRN/PCCN Practice Questions & Case Studies

 Which of the following would be a consequence of acidemia?

A.  Decreased fibrillation threshhold, CNS depression, decreased responsiveness to catecholamines, & increased oxygen unloading to the tissues

B.  Increased fibrillation threshhold, CNS excitation, decreased responsiveness to catecholamines, & increased oxygen unloading to the tissues

C. Decreased fibrillation threshhold, CNS excitation, increased responsiveness to catecholamines, & increased oxygen unloading to the tissues

D.  Increased fibrillation threshhold, CNS depression, decreased responsiveness to catecholamines, & increased oxygen unloading to the tissues

Rationale:  The answer is: A.  In the presence of acidemia, the heart is more likely to fibrillate.  The CNS is depressed so the patient becomes more somnolent.  The cardiovascular system also does not respond normally to catecholamines.  That's why we see that when the pH is low (<7.2) our catecholamines (e.g. Norepinephrine) do not work as well.  Finally, in acidemia, the oxyhemoglobin dissociation curve is shifted to the right which causes hemoglobin to unload oxygen to the tissues more readily.

You are caring for a 32 yo male s/p MVC with subarachnoid hemorrhage.  On day four, you note a decline in his neurologic status.  The most likely complication causing this is?

A.  Cerebral vasospasm

B.  Rebleed

C.  Cerebral edema

D.  Hydrocephalus

Rationale:  The most likely complication is cerebral vasospasm (option A).  This patient is at highest risk for the development of cerebral vasospasm within 4-10 days of the subarachnoid hemorrhage (SAH) with peak incidence at 6-8 days. In this case study, the nurse notices the change on day four.  The highest risk for rebleeding is within the first 24 hours.  Acute hydrocephalus is most likely to develop within 24-72 hours.  Cerebral edema is most likely to develop within the first 24-48 hours.

 The critical care nurse is analyzing the labs of a patient that has been on heparin for the past 5 days.  It is noted that the platelet count has dropped from 158,000 to 88,000.  What is the appropriate action?

A.  Continue to monitor

B.  Stop heparin immediately

C.  Reduce dosage of heparin

D.  Anticipate a switch to warfarin

Rationale:  An abrupt drop in a patients platelet count when on heparin suggests heparin induced thrombocytopenia which is a severe immune reaction to heparin that causes the platelet count to drop and [possibly] a hypercoagulable state.  The heparin should be stopped immediately and another IV anticoagulant chosen.  Argatroban or bivalirudin are suitable substitutes.

A patient with a history of renal disease presents with ventricular arrhythmias, ECG changes, weakness with ascending paralysis and hyperreflexia, diarrhea, and increasing confusion.  The most likely electrolyte disturbance is:

A.  Hypokalemia

B.  Hyperkalemia

C.  Hypercalcemia

D.  Hypocalcemia 

Rationale:  Patients with renal disease commonly present with hyperkalemia.  All of the clinical manifestations in this question 'fit' this electrolyte disturbance.   Patients with hypokalemia will present with weakness, lethargy, nausea and vomiting, paresthesias, PVCs, flattened T-waves, muscle cramps with hyporeflexia, hypotension and tetany.  Patients with hypocalcemia presents with tetany, tingling, seizures, altered mental status, and ventricular tachycardia.  Hypercalcemia can be seen in patients that present with increasing muscle weakness, hypotonicity, constipation, anorexia, nausea and vomiting, and bradycardia.

A patient presents with retrosternal chest pain, diaphoresis, hypotension, and tachycardia.  There is ST-elevaton in Leads V1-V6, I and avL.  Which of the following arrhythmias is/are indicative of this extensive infarct?

I.  Junctional 

II. Vtach/Vfib

III. Left bundle branch block

VI. Atrial fibrillation

A.  II & III

B.  I, II & III

C.  II, III & IV

D.  All of the above

Rationale:  This patient is having an anterior-lateral MI.  Ventricular tachycardia and ventricular fibrillation, of course, are very indicative of the extent of the infarction.  Because this infarct is most likely a result of left main disease, blood flow is blocked from going down the left anterior descending (LAD) and the left circumflex coronary arteries.  Keep in mind that the LAD supplies the bundle of his as well as the right and left bundle branches.  Left bundle branch block in the face of acute anterior or acute anterior/lateral MI is reflective of an extensive infarct and most likely to result in a poor outcome.

The nurse would anticipate administering ketorolac for which of the following disorders?

A.  Endocarditis

B.  Myocarditis

C. Pericarditis

D. Angina

Rationale:  Ketorolac is given to reduce inflammation in pericarditis.  Myocarditis treatment includes: ACEIs for heart failure, treating the underlying cause (e.g. antivirals, antibiotics), ECMO, IV IG, VAD, or transplant.  Treatment for endocarditis includes:  antibiotics and supportive/preventive care.  Treatment for angina is nitrates.

  Patient Information

• Name: DT
• Age: 68
• Sex: Male
• Medical History: COPD, hypertension, Type 2 diabetes
• Social History: Smoker (40 pack-years), lives alone
• Medications: Lisinopril, metformin, salbutamol (PRN inhaler)

DT presented to the emergency department with worsening shortness of breath, increased sputum production, and confusion. His family states that he’s been ill for 3 days and has not been using his inhalers properly.

• Vital Signs:
  • BP: 146/92 mmHg
  • HR: 112 bpm
  • RR: 30 breaths/min
  • SpO₂: 82% on room air
  • Temp: 38.3°C (100.9°F)
• Physical Exam:
  • Use of accessory muscles
  • Diffuse wheezing and coarse crackles
  • Lethargy, responds slowly to questions
• Intervention:  O₂ was started at 2L/min via nasal cannula; ABG drawn

• pH: 7.28
• PaCO₂: 68 mmHg
• PaO₂: 58 mmHg
• HCO₃⁻: 28 mEq/L
• SaO₂: 86%

1. What is the primary acid-base disorder?  The primary disorder is a Respiratory Acidosis
2. Is there evidence of compensation?  In the presence of compensation, we would anticipate seeing an elevation of the bicarbonate level.  In this example, the bicarbonate is barely elevated (if you are using 22-26 mEq as your normal).  Based on the COPD history (and chronic smoking), you would expect this patient to be a long-term pCO2 retainer.  So, in this case, the bicarb of 28 clearly represents the fact that there is inadequate compensation for this respiratory acidosis.  You would expect it to climb.  You must also question whether this patient is developing an underlying metabolic acidosis (in addition to the respiratory acidosis) due to the barely elevated bicarbonate level.  This would be particularly true in a situation in the patient is a chronic PaCO2 retainer (because they should have a bicarb level typically in the 30s range).  Tissue hypoxia could be the cause for a developing metabolic acidosis.
3. What type of respiratory failure is present?  This is Type II respiratory failure which means that it is both Hypoxemic as well as Hypercapnic Respiratory Failure.
4. What could be causing this ABG profile in the context of his history?  One of the most common causes of an acute exacerbation of COPD is a respiratory infection.  Sometimes it's due to improper inhaler use. 
5. What immediate nursing interventions are needed?  (1) Careful titration of FiO2 to maintain a target SpO2 of 88-92% (2) Monitoring mental status (particularly CNS depression), RR, HR, SpO2 & ABGs (3) Prepare for the use of BiPAP  (4) Bronchodilators, corticosteroids, and antibiotics

 A patient is admitted with severe peripheral arterial disease.  The nurse would expect to see all of the following assessment findings except:

A.  Lower extremities pale with shiney skin and hair loss

B.  Rubor noted when the lower extremities are dependent and pallor when elevated

C. Necrotic ulcerations on the great toe(s) & heel(s)

D. Hemosiderin deposits in feet, ankles & lower legs

Answer: D  Options A-C would be found in a patient with severe areterial disease.  Hemosiderin deposits occur in venous disease due to venous stasis.  Hemosiderin is a yellowish brown, iron-containing pigment formed when ferritin is broken down.

While evaluating the morning rhythm strip, the nurse notes that the atrial rate is 300/min and the ventricular rate is 75/min and regular.  The most likely rhythm that correlates with these findings is:

A.  Atrial Fibrillation

B.  Atrial Tachycardia

C. 4:1 Atrial Flutter

D. 2:1 Atrial Flutter

Answer: C  The atrial rate in this question is 300/min.  In atrial fibrillation, we are unable to discern the atrial rate so that cannot be the answer.  The atrial rate in Atrial Tachycardia is 150-250/min ... so that is not the answer.  With an atrial rate of 300 and a ventricular rate of 75/minute, there must be a consistent conduction pattern of 4:1.  Just think 300 divided by 75 is 4. Thus, C is the answer.

 Ischemic changes on a 12-Lead ECG would be indicated by the following changes:

A.  Deep Q-waves

B.  ST-segment elevation

C.  Flattening or inversion of T-waves

D.  Elevated symmetrical T-waves

Answer: C Ischemia effects the repolarization phase and is manifested as a change in T-wave.  In most cases, the T-wave will flatten or become inverted.  However, the focus must be on the word 'change'.  That is why it is important to compare an ECG taken in the presence of chest pain with a baseline (or painfree) tracing.  If a patient has a T-wave that is normally inverted and it changes to an upward deflection DURING CHEST PAIN, this too represents a T-wave 'change' and, thus, ischemia.  It is termed 'pseudonormalization' (false normalization).  Another finding noted in ischemia is ST-depression which is not one of the options.  Q-waves represent tissue necrosis (infarct...not ischemia).  ST-elevation indicated acute myocardial injury.

Identify the TRUE statement regarding adrenergic receptors and commonly used critical care infusions:

A. Dexmedetomidine can cause bradycardia and hypotension due to its alpha-2 antagonist properties

B. Phenylephrine is an alpha-1 agonist producing vasoconstriction

C. Dobutamine is a beta-adrenergic receptor antagonist 

D. High dose dopamine can result in pronounced vasoconstriction due to its beta-adrenergic properties

Answer: B The only True statement is that Phenylephrine is an alpha-1 agonist producing vasoconstriction.  Dexmedetomidine (option A) definitely can cause bradycardia and hypotension ... but it does so because it is an alpha-2 AGONIST.  Dobutamine (option C) is a beta-adrenergic receptor AGONIST not antagonist.  High dose dopamine (option D) causes pronounced vasoconstriction due to it's ALPHA adrenergic affect.

 Which of the following is TRUE regarding the S4 heart sound?

A. It can be heard in children

B. It can never be heard in A-fib

C. It is best heard with the diaphragm

D. It is a systolic extra sound  

Answer:  B  Remember that the S4 is known as the 'atrial gallop' sound.  It occurs as the atria contract duing the end of ventricular diastole due to ventricular non compliance.  We know it as 'atrial kick'.  Since the atria are fibrillating .... rather than contracting, you would never hear an S4 with atrial fib.  S4 is always pathologic so it is not a sound that should be heard in children (although S3 can be).  It is best heard with the bell of the stethoscope.  It is a diastolic extra sound.

A 66-year-old male presents with retrosternal chest pressure, diaphoresis, and shortness of breath.  Cardiac biomarkers are pending.  A 12-lead ECG is completed and shows ST segment depression and T-wave inversion.  It is crucial for the critical care nurse to suspect:

A. ST-elevation MI

B. Cardiac ischemia

C. Non ST-elevation MI

D. Coronary vasospasm

Answer:  C  This patient presents with ST segment depression and T-wave inversion.  This may indicate a Non ST Elevation MI.  Biomarkers will be valuable here in helping us to determine whether this is true or not.  This type of MI involves the inner surface of the heart . . . that is why it was once called a 'subendocardial MI'.  ST elevation (option A) indicates a 'transmural' infarct which involves all layers of the heart.  It is sometimes called a 'through and through' MI.  Coronary vasospasm (option D) would produce ST segment elevation.

A patient is admitted with an acute MI & cardiogenic shock. He is taken to the cath lab and found to have multivessel disease which requires bypass surgery. Which of the following conditions would prevent the insertion of an intra aortic balloon pump to support cardiac function?

A. Papillary muscle rupture

B. Incompetent aortic valve

C. Left ventricular failure

D. Refractory unstable angina

Answer:  B  Intra-aortic balloon insertion would be contraindicated in the face of aortic insufficiency because balloon inflation would worsen the aortic regurgitation.   In all of the remaining answers IABP insertion would take the workload off the left ventricle and decrease afterload, increase coronary artery perfusion, and decrease myocardial oxygen consumption. 

 A patient is admitted to the ICU with hypotension, tachycardia and fever.  The abdomen is distended and firm.  Bowel sounds are absent.  Which of the following labs would NOT support a diagnosis of bowel obstruction?

A. Increased white blood cell count

B. Decreased BUN

C. Decreased bicarbonate

D. Increased hematocrit

Answer:  B  The BUN would increase ... not decrease in a bowel obstruction due to dehydration.  Leukocytosis (an elevated WBC) would be present due to toxic proliferation of bacteria across the damaged membrane of the bowel.  The hematocrit would be increased due to dehydration and a hemoconcentration effect.  The bicarbonate would decrease due to a developing metabolic acidosis. 

A patient in the ICU with a diagnosis of cardiogenic shock post myocardial infarction develops new onset of a holosystolic murmus and a giant V-wave in the PAOP tracing.  Cardiac output/index drop and the heart rate increases to 160/minute.  The most likely  cause of this event is:

A.  Acute ventricular septal rupture

B.  Sustained ventricular tachycardia

C.  Acute mitral insufficiency

D.  Ruptured left ventricle

Answer: C Acute mitral insufficiency.  While acute ventricular septal rupture will cause a holosystolic murmur and a drop in cardiac output/index, it would not cause an elevated v-wave in the PAOP tracing. In the case of ventricular septal rupture, we would look for a 'step-up' in oxygenation between the right atrium and the pulmonary artery. Sustained ventricular tachycardia would not result in the new onset of a holosystolic murmur or a giant v-wave although it would cause a drop in cardiac output/index.  A ruptured left ventricle would not cause a holosystolic murnur or a giant v-wave although it would cause a drop in CO/CI.  The patient would develope signs/symptoms of cardiac tamponade.