Hi everyone, Nurse Jenny here from Nurse Life Academy. I figured I would do a comprehensive review that covers all of the potential content that you can see on the CCRN in one video, and there's no way that I can cover every topic, otherwise we would be here for hours, but if you guys like this comprehensive review, let me know and I can do a few parts. I will go into a little bit more detail explaining the answers and rationales, but not as much detail as the individual system videos. I would greatly appreciate it if you liked my video and subscribed to my channel, and as always, let me know if you have any questions. Alright, let's get into it.
Question number one. Your patient's initial EKG four days ago showed ST-segment elevation in leads V1 through V4. He underwent PCI.
Today he develops an S3 heart sound, crackles in the bases, and extreme dyspnea. Your assessment reveals a loud holosystolic murmur at the lower left sternal border. Which of the following hemodynamic parameters would be consistent with a suspected ventricular septal rupture? Is it A, decreased cardiac output and decreased SVO2?
B, decreased cardiac output and increased SVO2? C, increased cardiac output and increased SVO2? Or D, decreased SVO2? Increased cardiac output and decreased SVO2.
And the answer is C, increased cardiac output and an increased SVO2. So this question is nice because it gave us all of the signs and symptoms of a ventricular septal rupture, and then it told us exactly what it was. However, sometimes they only give you the symptoms and you have to figure it out from there.
So this patient had V1 through V4 ST elevation, meaning he had an anterior infarction. And we know that an anterior or anteroceptal infarction, you are at a high risk for ventricular septal rupture. He also had a development of a new systolic murmur at the lower left sternal border.
The lower left sternal border should alert you that this is a possible ventricular septal rupture. So what exactly is a ventricular septal rupture? Well, if you dissect it, it is simply a rupture in the wall of the septum between the ventricles.
If you look at the heart on the right hand side here, I will circle it in black for you. So there is that septal rupture. There is a hole in between the right to the left ventricles. And I say this casually, however, a ventricular septal rupture is an emergency.
And it's an emergency because it disrupts the normal flow of blood because of this huge hole in the septum. So instead of unoxygenated blood flowing through the pulmonary artery and going into the lungs, getting oxygenated, going back into the heart. and then being pumped out to the rest of the body, the oxygenated blood on the left side of the heart gets shunted to the right side of the heart and ends up mixing with that deoxygenated blood, which you see represented as the purple blood here. So what does that mean for our oxygen saturation or our SVO2 rating? Well, the oxygen saturation is going to increase, right?
Because now you have all of this oxygen. oxygenated blood flowing through that right ventricle from the left one, so it's going to increase that SVO2. You also are going to have a falsely elevated cardiac output because of the backflow of blood to the right ventricle. This chart is from my cardiology lecture and it has a lot of important information that would be helpful to know for the CCRN.
Okie dokes. Moving on, question number two. Your patient has developed abdominal distension 48 hours after abdominal aortic aneurysm repair. His intra-abdominal pressure is measured to assess for abdominal hypertension.
Which of the following statements is... inaccurate regarding intra-abdominal pressure monitoring. A. Decompression laparotomy should be considered when pressure exceeds 20 mmHg. B.
The transducer should be leveled to the phlebostatic axis. C. The bladder pressure closely reflects intraperitoneal pressure.
Or D. Physiologic compromise begins at a pressure of 12 to 15 mmHg. We're looking for the inaccurate choice here, and that is going to be B. The transducer should not be leveled to the phlebostatic axis.
The transducer is leveled to either the symphysis pubis or the iliac crest, depending on your hospital policy. So real quick, just to review some important information about abdominal hypertension. If the pressure in the abdominal cavity becomes greater than the pressure in the vessels that perfuse the abdominal organs, ischemia and infarction can occur, which can lead to serious complications.
Some causes of abdominal hypertension include massive fluid resuscitation or over-resuscitation, trauma, major abdominal surgeries, or in critically ill patients. And signs and symptoms of abdominal hypertension usually include abdominal distension. If you have a Foley and can measure a bladder pressure, it will be greater than 12. And there will be decreased urine output as it starts affecting your other organs. There will be respiratory compromised and decreased cardiac output. And the most severe form of abdominal hypertension is called abdominal compartment syndrome.
And this is when intra-abdominal pressures are greater than 12. 20, this is an emergency, and decompressive surgery via laparotomy will be indicated. You certainly want to keep an eye on these patients'intra-abdominal pressures and optimize the patient's position by placing them in reverse Trendelenburg. You don't want to elevate their head of bed, which could further compromise the pressure in their abdomen as well as their respiratory and cardiovascular status. Question number three. A patient is admitted to the critical care unit with tachycardia, tachypnea, dyspnea, and crackles.
A loud halosystolic murmur is audible at the apex. Prominent V-waves are seen on the PAOP waveform. This clinical presentation is indicative of pulmonary edema associated with which of the following? Is it A, mitral stenosis?
B, mitral regurgitation? C, aortic stenosis? or D, aortic regurgitation?
And the answer is B, mitral regurgitation. You have to know that prominent V waves are associated with mitral regurgitation, and that's because of the backflow of blood into the left atrium. And just to go a step further, because that's what I love to do, this assessment is could describe what kind of cardiac emergency.
You have a loud hollow systolic murmur audible at the apex. You have pulmonary edema, respiratory compromise, mitral regurge. All of this sounds like someone with a papillary muscle rupture. So that's just something to keep in mind.
Question number four. Which of the following laboratory profiles would be expected in a patient with a history of alcoholism and cirrhosis of the liver? A.
Prolonged PTT, decreased albumin, and increased bilirubin. B. Increased ALT, decreased transferrin, and decreased PTT.
C. Elevated CEA, decreased AST, and hyponatremia. Or D. Decreased bilirubin, decreased LDH, and hypernatremia. The answer is A, prolonged PTT, decreased albumin, and increased bilirubin. The liver has multiple jobs in the body.
It filters medications and filters toxins, most significantly ammonia or NH3. It also synthesizes plasma proteins, which make albumin and coagulation factors such as prothrombin, fibrinogen, and other clotting factors. And in reviewing hepatic failure labs, our ammonia level is going to be elevated.
The ammonia level tells you how well the liver is filtering, and in liver failure it's not doing a good job, so the ammonia is going to build up and end up being elevated. Liver enzymes AST, ALT will also be elevated, and our PTINR and PTT will be elevated, because remember, the liver is supposed to synthesize plasma proteins and make coagulation factors, However, when the liver isn't working properly, it can't make the prothrombin, fibrinogen, and other clotting factors. The liver also can't properly release bilirubin in the form of bile when it's injured, so that leads to a backup of bilirubin in the body, and that's where you see your jaundice come from.
Of note, scleral jaundice is one of the first places you will see that jaundice visibly. So let's talk about which labs trend down. Hepatic failure will certainly result in low levels of albumin since the liver isn't producing enough plasma proteins, which make albumin, and that's why these patients have such bad third spacing and ascites.
Their body is hypoalbuminemic, so it does not keep fluid in the vessels. Additionally, platelets and fibrinogen will be low due to the lack of clotting factors. and glucose will also be low because the liver plays a role in making glucose.
Please remember that there are different causes between acute and chronic hepatic failure, with acetaminophen being the most common cause of acute hepatic failure, whether it is intentional or it's accidental, and chronic hepatic failure will most likely be due to ETOH use. Question number five. A 55-year-old patient has a headache, nuchal rigidity, photophobia, and positive Koenig and Brudzinski signs.
These are consistent with which of the following? A. Intracranial hemorrhage, B. Subarachnoid hemorrhage, C.
Epidural hemorrhage, or D. Subdural hemorrhage. And the answer here is B.
Subarachnoid hemorrhage. Remember that these signs and symptoms are characteristic of meningeal irritation from either blood or infection. And there is another diagnosis that's not listed here where a patient would have these signs and symptoms.
Can you think of it? It is meningitis. Meningitis irritates that meningi.
With meningeal irritation, you will see these two signs flag as positive. So again, in subarachnoid hemorrhage and in meningitis. Kernic sign is positive if you move the patient's legs up and out, and in doing so, it leads to pain in the neck and the leg. And Brudzinski sign is positive when you move the patient's chin to his or her chest and the patient's legs come up. Question number six.
A 36-year-old woman with a history of asthma is admitted to the ICU. Blood pressure is 110 over 80, heart rate is 110, and respiratory rate is 28 breaths per minute. Her ABG is a pH of 7.48, a PaCO2 of 26, a PaO2 of 59, and a bicarb of 26. Which change would indicate that the patient's ventilation status is worsening? Is it A, a PaCO2 that is now normal, B, increased bilateral wheezing on auscultation, C, a bicarb that is now elevated above normal, or D, a bicarb that is now decreased below normal? The answer is...
A. A PaCO2 that is now normal. Remember, in the early stages of status asthmaticus, the patient will be in respiratory alkalosis because their body is hyperventilating, so they are blowing off a ton of CO2, hence the CO2 being low. But when these patients start tiring out and the body starts giving up, you start retaining the PaCO2 that is now normal.
that carbon dioxide because you're starting to breathe slower. So in status asthmaticus patients, normalization of carbon dioxide or hypercapnia, which is an elevated carbon dioxide level, are both ominous signs. One other thing that I want to mention is that although an increase in bilateral wheezing sounds scary for these patients, wheezing is actually good because it means that they are still moving air. When they stop moving air and you don't hear anything, that becomes really concerning. Refer back to this chart for the causes of respiratory acidosis and alkalosis.
Remember, respiratory acidosis is due to someone hypoventilating or breathing slowly and retaining that CO2, and respiratory alkalosis will be present in hyperventilation, where you are blowing off a ton of carbon dioxide. Make sure to know the difference between early and late respiratory failure and where they fall in the chart. Question number seven. Which of the following findings would be consistent with the occurrence of diabetes insipidus? Is it A, a serum osmolality of 260 milliosmoles per liter, B, a urine output of 15 to 20 milliliters an hour, C, a urine-specific gravity of 1.025, or D, a serum sodium of 165 mQ per liter?
The answer here is D, a serum sodium of 165 mQ per liter. So in DI, we do not have enough ADH. And we know that ADH acts to conserve water in the body and to concentrate urine. But if we don't have have any of it, well, that's just not going to happen. And what is the result?
Water loss. You are going to pee like it is your full-time job. And since you are peeing so much, that urine is going to be super dilute.
And that means that you're going to have a low urine specific gravity because there is going to be a low number of solutes and it will be light. At the same time, since you're peeing out all that water, there isn't going to be much water left in your vessels. And as a result, your serum sodium concentration and your serum osmolality are going to increase. What medication do we give to treat DI? Think about what we are missing.
We are missing ADH. So let's give our body some. The synthetic form of ADH is desmopressin, or DDAVP, and since we've lost a lot of fluid, we do also want to replace the fluid so we don't continue to stay dry and dehydrated. Question number eight.
Which of the following lab results would the nurse expect in a type one diabetic in DKA? A, hyperglycemia, hypokalemia. acidosis, and an elevated serum osmolality.
B, hyperglycemia, hyperkalemia, acidosis, and an elevated serum osmolality. C, hyperglycemia, hypernatremia, alkalosis, and a decreased serum osmolality. Or D, hypoglycemia, hyponatremia, acidosis, and a decreased serum osmolality.
The answer is B. You'll see hyperglycemia, hyperkalemia, acidosis, and an elevated serum osmo in DKA. Diabetic ketoacidosis or DKA results in metabolic acidosis and ketone production.
You're going to have polyuria, polydipsia, and polyphagia as well as hyperkalemia. in the serum. And acidosis causes potassium to rise due to the transcellular shifting, and potassium and pH have an inverse relationship. So every decrease of 0.1 in pH, there will be an increase of 0.6 in the serum potassium.
Question number nine. Magnesium is being administered to a patient. Which of the following would not be an indication that magnesium levels are too high? Is it A. Diminished deep tendon reflexes, B.
Hypotension, C. Tetany, or D. Muscle weakness? The answer is C, tetany.
This question is asking what we would see if a magnesium level is not high. So we know that high levels of magnesium cause smooth muscle relaxation, resulting in what's called the mag drag. So you would see the diminished deep tendon reflexes, you would see hypotension.
tension because of the smooth muscle relaxation, and you would see muscle weakness. Tetany is involuntary muscle contractions of overly stimulated peripheral nerves, and that would occur with hypomagnesemia. I know it seems a little bit counterintuitive, but just remember mag drag. When you've got a lot of mag, everything is slowed down.
Question number 10. Which of the following labs would be consistent with DIC, disseminated intravascular coagulation? A. Decreased platelets, decreased fibrinogen, prolonged PT, prolonged PTT, prolonged thrombin time, and increased fibrin degradation products, or FDPs.
B. Increased platelets. increased fibrinogen, normal PT, PTT, normal thrombin time, and increased fibrin degradation products. C, increased platelets, decreased fibrinogen, prolonged PT, PTT, prolonged thrombin time, and decreased FTPs.
Or D, decreased platelets, increased fibrinogen, normal PT, PTT, normal thrombin time, and increased FTPs. The answer is A, decreased platelets, decreased fibrinogen, prolonged PT, PTT, thrombin time, and an increase in FDP or fibrin degradation products. So let's talk about DIC, which is a state of hypercoagulation that is always secondary to another problem. Usually some kind of big inflammatory response or endothelial damage such as sepsis, trauma, or an obstetrics emergency can all lead to DIC. And in DIC, your body is going haywire because it is making clots because of that endothelial damage, but it's also trying to break down all the clots that it's making.
So at a certain point, you use up all of your clotting factors from making these clots, and then you just start bleeding because you have no clotting factors left. And this is DIC. It is a clotting problem, not a bleeding problem.
Some clinical signs that you will see will be bleeding from multiple sites of the body or ecchymosis. As far as labs go, these are a must know. You are going to see a decreased platelet count, a decreased fibrinogen, and a decreased hematocrit. You're going to see an increase in fibrin split products or fibrin degradation products.
Same thing. Why are we going to see that? Because your body is breaking down these microvascular clots. Fibrin split products or fibrin degradation products are the definitive lab tests that indicate the presence of DIC. You will also have an increased PT, PTT, and INR due to consumption of these clotting factors.
Lastly, the D-dimer will be elevated because D-dimer is a non-specific test that tells us there is clotting somewhere, and there definitely is, but it's not a definitive test for DIC like the fibrin degradation products or split products. Question number 11. Which of the following laboratory findings would be expected in a patient with acute pancreatitis? Is it A, decreased serum amylase, elevated serum calcium, and elevated serum glucose? B, elevated serum amylase, decreased serum calcium, and decreased total protein? C, elevated total protein, decreased serum calcium and decreased PT, or D, elevated alkaline phosphatase, elevated bilirubin, and decreased decreased serum glucose?
The answer is B. You're going to see elevated serum amylase, a decreased serum calcium, and a decreased total protein in a patient with acute pancreatitis. I'm going to point out a couple things here.
As far as our labs go, Our lipase and amylase are two digestive enzymes that are found in the pancreas, so they will absolutely be elevated in the setting of acute pancreatitis. Lipase does stay elevated for longer, so it is a more trustworthy measure between the two. Additionally, we will have a high white blood cell count, high blood glucose due to injury of the pancreatic beta cells, which is where insulin is produced. We will see hypocalcemia, and that's because calcium is used up for autodigestion, and it binds with fatty acids from necrotic fat.
Albumin will also likely be low due to leaky capillaries, and potassium and magnesium will be low due to malabsorption. You'll see two signs associated with the hypocalcemia. That is the trousseau sign and the schwastik sign. And another thing I want to point out, in patients with acute pancreatitis, you want to make sure that you do a good pulmonary assessment. They're going to potentially have pulmonary problems because the pancreas lies right underneath the diaphragm.
So it can irritate that diaphragm and it can cause lung issues, most likely on that left side. So just make sure that these patients have a close lung assessment and to monitor for signs of respiratory distress. Question number 12. A patient with heart failure most likely would have which of the following?
A, an S3. B. A. Murmur C. An S4 or D. A pericardial friction rub The answer is A. A patient with heart failure will most likely have an S3 heart sound.
And an S3 heart sound is present because of the blood backup into the left atrium and into the lungs. So think fluid overload with an S3 heart sound. Question number 13. A patient has a urine-specific gravity of 1.035, a urinary sodium of 5 milliquivs per liter, blood urea nitrogen of 40 milligrams per deciliter, and a creatinine of 1.2 milligrams per deciliter. Urinalysis reveals no proteinuria. These findings indicate which type of acute kidney injury.
Is it A, prerenal, B, intrarenal, C, postrenal, or D, there is no acute kidney injury present. Based on all of this data that we have here, we can say that this is most likely a prerenal injury. We have a urine-specific gravity of 1.035. That is greater than our normal of 1.010 or 1010. So that tells us that this urine is heavy, meaning that it is concentrated. We have a low urine sodium.
It is less than 20. So that means that the renal tubules are able to hold on to sodium and they are still functioning, star, star. Star. which is the important part of differentiating between pre-renal and intra-renal injury. So in a pre-renal injury, our renal tubules are still working.
In an intra-renal injury, there is structural damage. And when the BUN is elevated, you want to look at that BUN to creatinine ratio. Here it's about 40 because we divide 40 by 1.2. So I don't know, I round 1.2 down to 1. It's about 40 or so.
You don't need to be exact. They're not going to ask you crazy calculation questions on the test. But anyways, your BUN to creatinine ratio is about 40, which is high, and that would be in the pre-renal category.
To sum up pre-renal versus intrarenal, here are all of the different characteristics that you should be aware of. So the BUN to creatinine ratio is going to be different between the two with pre-renal injury being higher. Your urine sodium is going to be lower in pre-renal injury because the renal tubules are still able to function. So the renal tubules are going to be holding onto that sodium in the body. So they're not going to be excreting a lot of sodium.
You can look at the rest of the chart on your own, but again, it's important to be able to distinguish between pre-renal and intra-renal failure. Question number 14. Which of the following is associated with chest pain, confusion, and petechiae? Is it A, a dissecting aneurysm, B, a fat embolism, C, a pneumothorax, or D, a myocardial infarction? The answer is B, a fat embolism. All of these symptoms are suggestive of a fat embolism, especially within the first 48 to 72 hours after a long bone fracture.
None of the other answer choices would cause petechiae, although they could cause either chest pain or confusion. So the petechiae should be that indicator that this is a fat embolism. Question number 15. Which of the following are the two clinical hallmarks of acute respiratory distress syndrome or ARDS? Is it an increased lung compliance and pulmonary edema?
B. an increased functional residual capacity and a decreased compliance, C, refractory hypoxemia and decreased lung compliance, or D, refractory hypoxemia and an increased functional residual capacity? And the answer here is C. In ARDS, you will see refractory hypoxemia and decreased lung compliance. ARDS will absolutely be on the CCRN, so make sure that you master this concept.
An ARDS is a massive inflammatory response which results from some kind of precipitating event or injury. Some examples are sepsis, trauma, pneumonia, there are many, many more. And this massive inflammatory response leads to damage to both type 2 alveolar cells and capillary endothelial cells. And this damage to those cells results in increased capillary permeability, aka leaky capillaries, and it also leads to decreased compliance and decreased surfactant, which leads to an increase in surface tension.
So all in all, this damage leads to flooding of the alveoli, massive atelectasis, and refractory hypoxemia. I'll let you guys look at the rest of this on your own, or you can refer to my respiratory part 1 lecture to really go into detail here. Question number 16. A 76-year-old man with end-stage heart failure is admitted. He has no immediate family.
He does have a neighbor who is taking care of his terrier and who visits occasionally. The patient tells the nurse that he knows that he will never leave the hospital and would love to hold his terrier one last time. Which of the following would be the most appropriate action?
A. Gently inform him that pets are not allowed in the critical care unit. B.
Make appropriate arrangements for his neighbor to bring the dog in for a visit. C. Arrange to have a therapy dog visit him.
Or D. Discuss sedative and antidepressant therapy for the patient with the physician. The answer here is B. You want to make appropriate arrangements for his neighbor to bring the dog in for a visit.
So at end of life, we want to make it happen for these patients. You want to try to meet the patient's requests if at all possible, but you want to make sure that it is safe. Question number 17. A patient has a Sengstaken Blakemore tube inserted to control his bleeding esophageal varices. Later that evening, he develops extreme respiratory distress.
Which of the following would be the priority action in this situation? A. Initiate fluid resuscitation.
B. Monitor for overt bleeding. C.
Administer an H2 antagonist. Or D. Cut the SB tube and remove it. The answer is D. You want to cut the esophageal tube and remove it. The most likely reason that this patient all of a sudden is suffering from extreme respiratory distress is because the gastric balloon ruptured and it lodged in the upper airway.
This is why you always want to have scissors at the bedside. Question number 18. Which of the following sign or symptom is most specific to a small bowel obstruction? Is it A.
Abdominal pain, B. Change in bowel habits, C, mucus and blood in the stool, or D, vomiting of fecal material. The answer is D, vomiting of fecal material.
So mucus and blood in the stool is characteristic of inflammatory bowel disease. Abdominal pain and change in bowel habits could occur in small or large bowel obstruction, but the sign and symptom that is most specific to a small bowel obstruction is going to be the vomiting of fecal material. because a small bowel obstruction causes reverse peristalsis and it actually moves the contents of the bowel into the stomach and then you end up vomiting it. Also of note, an early bowel obstruction is going to have hyperactive bowel sounds while a late bowel obstruction causes hypoactive and then it leads to absent bowel sounds.
I have a chart here differentiating the different symptoms of small versus large bowel obstructions. Signs and symptoms are different, but in general, the treatment is going to be the same. Question number 19. A patient is brought to the emergency department with an overdose of prescription drugs.
She develops torsades de poins shortly after arrival. Which of the following is the most likely cause of this rhythm disturbance? Is it A, oxycodone, B, mipyridine, C, fluoxetine, or D, amitriptyline? The answer is D, amitriptyline. Amitriptyline is one of the tricyclic antidepressants that can cause QT prolongation that can lead to torsades.
Can you think of... any other medications that lead to torsades because of their QT prolongation? We've definitely talked about this a few times, but other medications like amiodarone, haldol, procainamide, or tricyclic antidepressants like amitriptyline, and absolutely hypomagnesemia.
Question number 20. A patient is admitted with the family reporting that the patient had consumed many pills of various types. Regardless of the drugs that were actually consumed, the initial management of any overdosage is A. Securing the airway, B. Administering the antidote, C. Preventing further gastrointestinal absorption, or D.
Increasing the excretion of toxins. The answer is A. You want to secure that airway.
Airway is always the first priority, just go back to your ABCs. I know we all love hemodynamic questions so much, so I had to just throw one more in here for you guys. So which of the following best differentiates hypovolemic from cardiogenic shock? Is it A.
an increased systemic vascular resistance, B, a decreased cardiac index, C, a decreased urine output, or D, a decreased pulmonary artery occlusive pressure. There is one difference in the hemodynamics between hypovolemic and cardiogenic shock, and that difference is our preload. So what are the two measurements of preload?
We have our CVP or our RAP or the right atrial pressure, but we also have our PAOP. And those tell us about volume status on either the right side or the left side of the heart. In hypovolemic shock, there is hypovolemia.
There is not enough volume, so our preload is going to be low. But in cardiogenic shock, we have a poor pump, which leads to a backup of fluid. And that leads us to a high preload or a high PAOP, leading to a backup of fluid and a high PAOP.
So the answer here is D. We have a decreased pulmonary artery occlusive pressure in hypovolemic shock, and there is an increased pulmonary artery occlusive pressure in cardiogenic shock. You definitely want to memorize and be able to walk through the hemodynamics of the different shock states. If this is not your strong suit, I'd like to point you in the direction of my hemodynamics and shock video, which goes a lot more in depth on this and really helps you master it. Alright you guys, we have made it to the end.
If you liked my video or found it helpful, please like and subscribe to my channel. I would greatly appreciate it. Let me know if you have any questions.
I would be more than happy to help. And also let me know if you liked this comprehensive review that kind of combined everything. I can make a lot more of them just because there is so much content to cover.
If you are taking your CCRN anytime soon, good luck. You have got this. You need to put in the hard work. and believe in yourself.
Thank you everyone for watching. Nurse Jenny signing off for Nurse Life Academy. Have a good one.