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 rationals but not as much detail as the individual System videos I would greatly appreciated if you liked my video and subscribed to my channel and as always let me know if you have any questions all right let's get into it question number one your patient's initial EKG 4 days ago showed ST segment elevation in leads V1 through V4 he underwent PC I today he develops an S3 heart sound crackles in the bases and extreme dpia 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 sepal rupture is it a decreased cardiac output and decreased svo2 B decreased cardiac output and increased svo2 2 C increased cardiac output and increased svo2 or D increased cardiac output and decreased s spo2 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 anteros sepal infection you are at a high risk for ventricular sepal 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 septile 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 sepal rupture there is a hole in between the right to the left ventricles and I say this casually however a ventricular septile 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 sbo2 rating well the oxygen saturation is going to increase right because now you have all of this 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 back flow 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 oky does moving on question number two your patient has developed abdominal distension 48 hours after abdominal aortic aneurysm repair his intraabdominal pressure is measured to assess for abdominal hypertens tension which of the following statements is inaccurate regarding intraabdominal pressure monitoring a decompression laparotomy should be considered when pressure exceeds 20 mm of mercury B the transducer should be leveled to the phlebostatic axis C the bladder pressure closely reflects intraperitonial pressure or D physiologic compromise begins at a pressure of 12 to 15 mm of mercury we're looking for the inaccurate Choice here and that is going to be B the transducer should not be leveled to the phlebostatic AIS 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 esema and infarction can occur which can lead to serious complications some causes of abdominal hypertension include massive fluid resuscitation or overresuscitation trauma major abdominal surgeries or in critically ill patients in 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 intraabdominal pressures are greater than 20 this is an emergency and decompressive surgery via laparotomy will be indicated you certainly want to keep an eye on these patients intraabdominal pressures and optimize the patient 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 tacac cardia topia dpia and crackles a loud holosystolic 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 mitro stenosis B mitro regurgitation C aortic stenosis or D aortic regurgitation and the answer is is B mitro regurgitation you have to know that prominent V waves are associated with mitro 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 could describe what kind of cardiac emergency you have a loud holosystolic murmur audible at the Apex you have pulmonary edema respiratory compromise mitro 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 therosis of the liver a prolong PT decreased albumin and increased Billy Rubin B increased alt decreased transferin and decreased PTT C elevated CA decreased as and hyponatremia or D decreased Billy Rubin decreased LDH and hypernia the answer is a a prolonged PTT decreased albumin and increased Billy Rubin 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 patic 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 a alt will also be elevated and our PTINR and PT will be elevated because remember the liver is supposed to synthesize plasma proteins and make Co ulation factors however when the liver isn't working properly it can't make the prothombin fibrinogen and other clotting factors the liver also can't properly release Billy ruin in the form of bile when it's injured so that leads to a backup of Billy ruin 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 aites 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 eoh use question number five a 55-year-old patient has a headache nucal rigidity photophobia and positive KCK 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 menial 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 menitis menitis irritates that meningi with menial irritation you will see these two signs flag as positive so again in subb arachnoid Hemorrhage and in menitis keric 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 brinsky sign is positive when you move the patient's chin to his or her chest and the patient 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 P2 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 PAC 2 that is now normal B increased bilateral wheezing on oscilation c a bicarb that is now elevated above normal or D A bicarb that is now decreased below normal the answer is a a pac2 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 that carbon dioxide because you're starting to breathe slower so in status as maticus patients normalization of carbon dioxide or hypercapnea 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 in citus is it a a serum o molality 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 mqu per liter the answer here is d a serum sodium of 165 mives 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 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's 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 a DH 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 1 diabetic in dka a hypoglycemia hypokalemia acidosis and an elevated serum osmolality B hypoglycemia hyperemia acidosis and an elevated serum osmolality C hyperglycemia hypernia alkalosis and a decreased serum osmolality or D hypoglycemia hyponatremia acidosis and a decreased serum osmolality the answer is B you'll see hyperglycemia hyper calmia acidosis and an elevated serum osmo in dka diabetic keto acidosis or dka results in metabolic acidosis and Ketone production you're going to have polyurea polydipsia and polyphasia as well as hyper calmia in the serum an acidosis causes potassium to rise due to the trans cellular 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 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 hypo magnesia 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 thren time and increased fibrin degradation products or fdps B increased platelets increased fibrinogen normal PT PT normal throon time and increased fibrin degradation products C increased platelets decreased fibrinogen prolonged PT PT prolonged thrombin time and decreased fdps or D decreased platelets increased fibrinogen normal PT PT normal thrombin time and increased fdps the answer is a decreased platelets decreased fibrinogen prolonged PT PT thrombin time and an increase in fdp or fibrin degradation products so let's talk about diic 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 obstetric emergency can all lead to diic 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 ecosis as far as Labs go these are a must know you are going to see a decreased platelet count a decreased iogen 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 test that indicate the presence of DIC you will also have an increased PT PT and INR due to consumption of these clotting factors lastly the D dier will be elevated because dher is a nonspecific test that tells us that 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 following laboratory findings would be expected in a patient with acute pancreatitis is it a decreased serum Amalise elevated serum calcium and elevated serum glucose B elevated serum Amala decreased serum calcium and decreased total protein C elevated total protein decreased serum calcium and decreased PT or elevated alkaline phosphatase elevated Billy Rubin and decreased serum glucose the answer is B you're going to see elevated serum Amal 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 amas 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 true so sign and the shastic 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 a 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 mqu per liter blood Ura nitrogen of 40 mg per deciliter and a creatinin of 1.2 mg per deciliter your analysis reveals no protein Uria 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 pre-renal injury we have a urine specific gravity of 1.035 that is greater than our normal of 1.010 or 10 10 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 which is the important part of differentiating between prerenal and intrarenal injury so in a pre-renal injury our renal tubules are still working in an intrarenal injury there is structural damage and when the bu is elevated you want to look at that bu to creatinin ratio here it's about 40 because we divide 40 by 1.2 so I don't know I round 1.2 down to one 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 anyway your bu to creatin ratio is about 40 which is high and that would be in the preal category to sum up prerenal vers intrarenal here are all of the different characteristics that you should be aware of so The Bu to creatinin ratio is going to be different between the two with pre- reinal 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 on to 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 prerenal and intrarenal failure question number 14 which of the following is associated with chest pain confusion and petii 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 petii although they could cause either chest pain or confusion so the petii 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 AR DS you will see refractory hypoxemia and decreased lung compliance AR RDS will absolutely be on the CCRN so make sure that you master this concept an ARS is a massive inflammatory response which results from some kind of precipitating aventor injury some examples are sepsis trauma pneumonia there are many many more and this massive inflammatory response leads to damage to both type 2 Alvar 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 alvioli 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 one lecture to really go into detail here question number 16 a 76-year-old man with endstage 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 anti-depressant 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 patients request if at all possible but you want to make sure that it is safe question number 17 a patient has a s staken 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 S SP 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 feal 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 vers 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 torsade St poan shortly after arrival which of the following is the most likely cause of this Rhythm dist disturbance is it a oxycodone B madine C fluoxitine or D amitryptiline the answer is D amitryptiline amitryptiline is one of the tricyclic anti-depressants that can cause QT prolongation that can lead to torsades can you think of any other medication that lead to torsades because of their QT prolongation we've definitely talked about this a few times but other medications like amiodarone halol procainamide or tricylic anti-depressants like amitryptiline 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 ined 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 RP or the r atrial pressure but we also have our PA op 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 pore 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 and 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 all right 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 comprehens ensive 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