ccrn review

1. CCRN Review Pulmonary – Part 1
2. NOW AVAILABLE: CCRN Exam Review: Cardiovascular, Pt. 1 – MED-ED
3. Multisystem CCRN Review Video
4. CCRN Neurology Review – FULL
5. CCRN Renal Review – FULL
6. CCRN Gastrointestinal Review Video – FULL
7. CCRN Cardiovascular Part One

CCRN Review Pulmonary – Part 1

welcome to another lifelong nursing,video this one focuses on pulmonary CCRN,review on Brent and lets get started,so for the pulmonary test of all areas,in the CCR in exam there is acute lung,injury acute pulmonary embolism acute,respiratory failure acute respiratory,infections air leak syndromes aspiration,asthma and status asthmaticus COPD,failure to in from the ventilator,pulmonary fibrosis pulmonary,hypertension and thoracic surgery and,trauma just for your information the,pulmonary portion includes 17% of the,80% of the clinical judgment portion of,the CCRN exam under normal circumstances,our lungs ventilate and profuse to,provide our body with oxygenated blood,and to get rid of the co2 within our,system so for the ventilation portion,the air moves in and the air moves out,and in a smallest portion of the lung,behavioral or sac this is where gas,exchange occurs the gas exchange is the,perfusion portion of the ventilation and,perfusion that the lungs do the,ventilation is just when air moves in,and air moves out via the pulmonary,artery deoxygenated blood comes through,the lungs and then goes through the,small capillaries to allow diffusion to,allow oxygen and co2 to exchange out of,cellular level once this happens,oxygenated blood continues via the,pulmonary vein into the left atrium into,the left ventricle and in the body,perfusion is the transport of gases,through the body for example the AVR sac,which is perfused with blood circulation,continuing continuing on with anatomy,and assessment the primary muscle of,ventilation is the diaphragm the right,lung has three lobes and the left lung,has two lobes so how do we know that the,patient is ventilating properly this,clinical indication of patient,evaluation is the paco2 on the arterial,blood gas which the normal is 35 to 45,theres a thing called dead space,ventilation where theres no gas,exchange these are the areas of the,pulmonary system for example the nose,the mouth the trachea and the bronchi,remember the only place where gas is,exchanged is the AVL or sex unless,theres altered circulation around that,AVL or sac leading to no gas exchange,and for that Ill show you an example so,again heres the normal perfusion and,ventilation of a pillar sack and once we,have the altered circulation such as a,blood clot thats gonna interrupt the,blood flow to the particular set of,capillaries that passes through these,AVL or sacs,so once the blood flow is interrupted,were not gonna have any more perfusion,of these AVL or sex which does not allow,co2 and oxygen to exchange at a cellular,level this AVL or sac is now considered,dead space ventilation like the trachea,and bronchi well theres no gas exchange,also theres gonna be no forward flow of,blood related to that clot so in,continuation with the pulmonary embolism,some of the signs can be to get near,refractory hypoxemia dyspnea pleuritic,chest pain and some of the causes can be,from air blood fat or amniotic fluid,which puts more strain on the right,ventricle as it tries to pump the same,amount of blood through less of a,circulatory system related to the clock,this leads to right ventricular heart,failure some treatment for the pulmonary,embolism is remembering our ABCs airway,breathing and circulation we want to,intubate the patient if necessary and,administer 100 percent oxygen we want to,give thrombolytics if theres no,contraindication and we can also do it,and electa me we could place the IVC,filter which will not help the current,pulmonary embolism but will help reduce,the ones that could happen in the future,and we also want to have pain management,patient with increased pain uses up a,lot of oxygen requirements and therefore,we want to manage their pain and,decrease their anxiety so moving on to,the oxyhemoglobin disassociation curve,this indicates how your body will,typically react to when it goes through,certain situations such as increase in,pH or decrease in pH so a shift to the,left indicates an increase in pH thats,going to be more on the alcoholic side,so when you have metabolic alkalosis or,respiratory alkalosis that means that,your body is going to have a less,affinity for Co tu just because theres,a shift to the left does not mean your,temperature is gonna go down these are,just indicators this is just an,indicator for say for example if your,temperature goes down as youre,hypothermic that means your bodys gonna,have a less affinity for action again,making you more cyanotic and more than,likely increasing your pH so shift to,the right indicates a lower pH,for example metabolic acidosis or,respiratory acidosis if youre in,respiratory acidosis your PA co2 is,going to be elevated your temperature,necessarily doesnt have to be elevated,but if youre at a hypothermic state,such as increased temperature then often,your pH will be acidic also when theres,just shift to the right on this curve,this is going to cause your hemoglobin,to release oxygen more readily so just,sum it up this is not a graph youre,looking at on a bedside monitor this is,just an association to what happens when,your body becomes more acidic or less,acidic or hyperthermic versus,hypothermic youre gonna have these,indicators on the left here – what is,going to generally happen within your,body so you need to be thinking about,that and how thats going to relate to,what youre doing for the patient this,slide is just a 7-up what I just said in,the previous slide so youre gonna be,more hypothermic foolish shift to the,left you could also have low levels of,to 3 DB G which plays a role and how,much the affinity is for that oxygen on,your hemoglobin molecule and then of,course the rest is what I summed up I do,want to point out some of the causes of,decreased in 2 3 D P G is multiple prvc,transfusions hypothyroidism in -,phosphate emia so when you have a,decreased to 3 DPG you may become more,alkalotic,for example multiple P RBC transfusions,and a shift to the right again making,you more acidic from fever high levels,of – 3 D P G and again respiratory or,metabolic acidosis some of the causes of,increased to 3 D PG is anemia chronic,hypoxemia and hyperthyroidism so again,this d PG plays a large role in how much,the,hemoglobin molecule has an affinity for,oxygen moving on to carbon monoxide,poisoning this is essentially the one of,the easy questions on the test and Ive,provided an example for you a 50 year,old woman who lives at home with her,husband was upstairs in her home while,her husband went to the store all of a,sudden she heard the fire alarm ringing,throughout the house she attempted to go,downstairs to investigate however the,fire was already spread through most of,the downstairs risking her life she,escaped her home but not before inhaling,a lot of smoke and suffering carbon,monoxide poisoning outside the,firefighters who are already on scene,setting up and the woman began to,immediately feel short of breath,dizziness and she faints at a cellular,level,why does she experience these symptoms,the chemical identifier for carbon,monoxide is co not co2 so we have to,think about this this is gonna be very,similar to the co2 which actually,covered monoxide is a cellular level has,a stronger affinity to these hemoglobin,molecules or vice-versa the hemoglobin,molecule has a stronger affinity for the,co the carbon monoxide which will not,allow carrying co2 nor oxygen and that,means the more co2 thats inhaled the,less co2 and the less o 2 that can be,exchanged and utilized in those AVL or,sacs,so the treatment for carbon monoxide,poisoning is 100% oxygen administration,hyperbaric oxygen if possible and to,continue o to administration until a,carboxyhemoglobin level is less than 10%,and this is because when youve put,somebody on the saturation monitor the,o2 saturation monitor its gonna read a,normal level and thats because its,reading that carbon monoxide on that,hemoglobin rather than oxygen so you,dont want to necessarily go by the,oxygen level on the o2 set you want to,administer

NOW AVAILABLE: CCRN Exam Review: Cardiovascular, Pt. 1 – MED-ED

welcome to Meadows presentation of the,CCRN review my name is kami Christie and,Im the speaker for all these modules,for the review now we are going over to,the module cardiovascular and what weve,done is divided into Part one and Part,two so at least you get a break now the,most wonderful thing about taping is,that you can turn me on and turn me off,whatever time you want and come back to,it and you still have all the,information so if you start to get tired,or overwhelmed just click off go on it,and do something come back because you,need to remember pick your strengths and,weaknesses and then study do the S word,study your weaknesses before you take,the exam so ready lets get started with,the first part of cardiac the purpose of,the heart remember it is a pump and the,main purpose of this heart is to pump,blood you know hemoglobin to the cell,now the heart does have some endocrine,property a + BB + P cmp but there are no,questions like that on the exam all you,have to really concentrate is on the,right heart and the left heart the,structure and function the right,ventricle is actually a very thin the,ventricle the septum really doesnt do,anything for right ventricular,contraction the right ventricle you eat,about says bellows action it just goes,like this but you have to remember its,very low pressure and the job of the,right ventricle and right atrium just to,get capture all the venous blood from,the head and neck from the SVC and all,the rest of the blood from the body from,the IVC that then comes to the right,atrium the right atrium pumps to the,right ventricle and in normal people,that normal low pressure right ventricle,pumps this venous blood through the,pulmonary vault normal people low,pressure and fills the left ventricle so,thats perfect it just pumps this venous,but the key is that its low pressure,because it should be pumping against,pulmonary vascular resistance which is,low pressure but what happens to your,patient when they have an icky,isolated white ventricular infarction or,white ventricular failure and this,usually happens very acutely well that,patient had pulmonary edema and the,answer is no when the right heart fails,remember this is the right heart it,fails so it dilates and its not pumping,well so its not pumping blood to the,pulmonary artery or to the lungs so what,happens it dilates the pressure gets,high then the pressure gets higher on,the right atrium and now you will begin,to see tachycardia always tachycardia,jvd right away and then later on because,the IVC gets filled to get liver a,little bit of liver congestion may be a,sadies and peripheral edema but that,doesnt happen right away so what you,see in a cute white ventricular failure,is tachycardia jvd but the lungs are,clear they may had dropped their blood,pressure because the right hearts not,filling the left so always remember that,now heres what I really want you to,remember when somebody has isolated,right ventricular failure the treatment,is volume you got to give this patient,fluid and youll say Ill come to a,bedside soon okay once you give two,liters of fluid in 30 minutes and go,cami the patient jvd youre gonna put,the patient in pulmonary edema and Im,gonna give you the cami look and say,slap yourself you cant get pulmonary,edema from here theres a couple of,concepts here that are very important,and which most nurses dont appreciate,because when was the last time you had a,patient with isolated right ventricular,failure you probably havent probably,havent its not common most of your,patients have by ventricular failure,both ventricles are failing and in those,patients we do not give volume we,diurese them so lets go back to this,white ventricle its failing,but remember Franken Starling the,frank-starling law the more you stretch,the myofibrils the better the heart,contracts well the white heart has a,great potential to stretch and then,contract better so the answer on this,test and any test you ever take that,talks about acute right ventricular,failure the treatment as well,keep it full so it will contract there,good the left ventricle is a little bit,different because the left ventricle now,is pumping against the aortic pressure,much higher pressure so the right,ventricle left ventricle sorry the left,ventricle is thicker and the septum,becomes very important and left,ventricular function the right heart,does this the left heart does this so,that whole septum contracts to get blood,out the aorta pressure and the left,ventricle is much higher so if the,patient has a left ventricular failure,from a STEMI for whatever reason the,left ventricle dilates pressure gets,very high the left atrium dilates,pressure gets high and thats,transmitted right to the pulmonary veins,they stretch get high pressure they leak,the capillaries fail and now the patient,has pulmonary edema,in that patient you would stop giving,fluid and give diuresis so right and,left ventricular failure are very,different so lets talk about this just,for another second because there are,some real good pearls of practice here,mr. Smith is you know 75 years old but,he has smoked cigarettes since he was 20,and he smokes two packs a day so huge,history of smoking,he has COPD so what has happened to his,pulmonary pressures when you have,emphysema the pressures go up so what,has happened to his right heart his,right heart has gotten thicker and,stiffer pumping over all these years,over higher and high pressure so he has,cor pulmonale so his right-sided,pressures are very high,now he gets pneumonia community-acquired,pneumonia comes your er and he has a,pneumonia with sepsis because he has a,dysregulated system and hes hypotensive,and hypoxic and so what do we do for,sepsis right what do you do we identify,the sepsis we get the chest x-ray we get,the blood cultures we get everything we,start the antibiotics we give fluid we,give fluid but remember in the early,sepsis protocol I said put in a central,line measure the CVP make sure its 8 to,12 s 8 to 12 there theyre tanked up,well mr. Smith when you put that CVP in,him hes,have a CVP of 18 and thats his normal,CVP because remember it has cor,pulmonale if youre right hard as,dilated your right atrium is dilated and,the pressure goes up but thats 18 CVP,has nothing to do and it does not,reflect the left ventricle so if,everybody comes in with a normal heart,and lungs then their CVP is reflective,of their left side but if they have lung,problems emphysema asthma they have COPD,theyre hypoxic they have pneumonia that,CVP may only be telling you about,right-sided failure not the left side so,thats an important thing to remember in,anybody who has sepsis whats the,treatment fluid so even if a CVP was 18,he still needs fluid for sepsis so right,and left ventricular function and,structure then the coronary arteries are,very important you know you have your,aortic valve and the aortic root right,above the valve right above the valve is,where the osmiums or openings of the,coronary arteries are the right coronary,and 90% of people feeds the whole right,atrium the entire right ventricle right,II and the top of the septum the very,top one-third of a septum and in ninety,percent of all people that right,coronary artery wraps around behind the,heart behind the heart and feeds the,inferior wall of the left ventricle AHA,thats important so if youve got a,patient that came to you with inferior,wall STEMI its the right coronary,artery now thats just anatomy and there,arent too many Anatomy questions on the,exam but what they might ask you is you,are admitting a patient with a right you,know an inferior wall STEMI what,dysrhythmia might you anticipate theres,a lot of questions about anticipation or,what do you think is going to happen,next so in an inferior wall of mine you,know whats the right coronary the right,coronary feeds the SA node the AV node,in the bundle so the most common,to amuse or bradycardia and first degree,heart block you have to remember that,the left

More: fifa 22 review

Multisystem CCRN Review Video

welcome to another lifelong nursing,video in this video we focus on the,multi system concepts for the CCRN,examination lets get started so the,multi system CCR in testable areas,include multi organ dysfunction syndrome,distributive shock multi-system trauma,sepsis and septic shock inhalation and,ingestion of toxic substances effects,iya toxin and drug exposures so well,first start with trauma when you are,answering trauma related questions you,want to make sure you first know the,first-line assessments and second know,the second-line assessments and well go,over those in this video,this can be the difference between life,and death thinking quickly and acting,quickly are vitally important but,knowing what to do is just as important,if not more important so the first-line,assessments of the trauma is a b c d e,as airway how stable is this patients,airway is it patent does this patient,need intubation do you need to lift up,on the patients chin to provide breaths,B is breathing how deep or shallow is,the patient breathing is the patient,breathing at all during trauma,emergencies provide 100% oxygen and,ventilation,C stands for circulation what is the,circulatory status is it severe bleeding,pale looking patient have you assess the,patients blood pressure provide at,least two large-bore IVs with fluids,opened provide at least two large-bore,IVs with fluids opened typically,isotonic fluids,continuing with the first-line,assessment d stands for disability what,is the patients neurological status can,they move their extremities what,extremities do not move perform a quick,level of consciousness motor and people,assessment remember that the Glasgow,Coma score is only part of the neuro,exam and not all of the nearer exam East,stands for environmental and exposure,where is the patient as a as the patient,in water or snow out in the hot weather,think of their safety and provide warm,or cool changes to the patient to the,best of your ability such as a blanket,for the cold patient,continuing on after the first line,assessment and interventions you perform,on the patient which are the most,important you should immediately move to,the second line assessment the second,line assessment which is more letters F,G H I and the second line assessment F,stands for full set of vitals such as an,ECG monitor pulse oximeter blood,pressure temperature and Ive ordered a,urinary catheter yogic studies a gastric,tube in sebacean and obtaining labs and,things like that G stands for give so,you want to give comfort measures pain,management reassurance hand-holding etc,H stands for history try to obtain what,happened,any recent medications and last dose,taken any allergies etc I inspect fully,inspect every nook and cranny of the,patient to the best of your ability you,want to remember to protect the,patients neck and airway and spine if,it has not been cleared by the doctor or,nurse practitioner while youre doing,this look be sure to look at the back of,the head and the entire posterior of the,patient you do not want to miss anything,on a trauma patient this will delay a,complete care so now that weve got the,basics of trauma were gonna do a little,introduction to shock this will be,primarily what we need to focus on in,this video,contrary to the belief that shock refers,to the patients hypotension and low,blood pressure shock actually means that,the cells are becoming diseased due to,two things one a deficient in oxygen,demand which is not enough oxygen for,the body often due to inadequate,perfusion or the cells of the body,youre not able to utilize that oxygen,they do have or do receive there are,three basic phases of shock now listen,to this phases of shock not types of,shock so well get into the types of,shock a little later so the three basic,phases of shock and how fast the patient,progresses through these three phases,depends on many things such as how,strong the bodys response is to the,shock so the three phases include,compensatory which is the early phase of,shock to progressive,and three refractory so this is the late,stage of shock so the first phase of,shock compensatory while the,compensatory phase of shock which is the,early stage the body responds by,activating the sympathetic nervous,system and the,renin-angiotensin-aldosterone system the,next two slides will show each,respectively so under the sympathetic,nervous system activation this is,activated by a decrease in cardiac,output or an increase in oxygenation,once the sympathetic system is,stimulated by above measures,vasoconstriction begins with the vessels,of the body this increases and maintains,the blood pressure which increases both,the contractility of the heart and the,heart rate the,renin-angiotensin-aldosterone system is,also activated by the same measures of,the sympathetic nervous response so this,is a decrease in cardiac output or an,increase in oxygenation so once,activated both responses are,simultaneously ongoing so on the top we,have the renin secretion which converts,to angiotensin one then converts stay,annuitants into causing vasoconstriction,at the same time aldosterone is being,released and sodium and water are being,retained in the kidneys the extra sodium,and water increases the vascular volume,which helps maintain the blood pressure,so you have two mechanisms,vasoconstriction and another maintaining,sodium and water which will both help,maintain blood pressure this only,continues for a certain amount of time,and if left untreated the body will,continue to deteriorate being able to,compensate less and less through these,methods so what are the signs and,symptoms of the first shock phase,restlessness anxiety tachycardia,- Kip Nia which can lead to respiratory,alkalosis a normal PA o2 so on your,blood gas your normal oxygenation on,your blood gas is going to be normal,oliguria,due to the hypotension pale-skinned,again due to decreased cardiac output,and the patient may be more thirsty,remember in the first phase there is no,significant change in blood pressure,related to the compensatory systems so,moving on if the first stage of,Jacque isnt treated early were gonna,move into the second phase of shock this,is the progressive phase which is when,the compensatory systems begin to start,failing so youre gonna see worsening,tachycardia metabolic acidosis a,decreased pao2 you on your blood gas,cool clammy and mottled skin this is,where youre gonna see a change of level,of consciousness my complain of nausea,and hypotension begins this is also,going to be the reason why you have a,change in level of consciousness and,also for the acidosis so the mechanisms,that keep the blood pressure maintained,is failing which is the angiotensin,aldosterone system and the sympathetic,nervous system responds so these are,going to be leading to a lower blood,pressure this is also called a,sympathetic withdrawal so in the third,phase of shock this is when the body,does not respond to interventions that,you were giving the patient may survive,the shock but die from organ failure,youre gonna have in this phase severe,systemic hypoperfusion which leads to,multi-system organ dysfunction otherwise,known as Maudes neurological signs it,can have encephalopathy possibly a,stroke big eyes heart failure and,ischemia for the lungs youre gonna have,a cute respiratory distress syndrome,ours the liver can also begin to fail,kidneys so youre gonna have acute,tubular necrosis and start going into an,urea hematological signs or di c which,is both the bleeding and clotting,disorder so now that weve been through,the phases of shock were gonna go,through the specific types of shock so,each type of shock hypovolemic septic,and a phylactery cardiogenic neurogenic,obstructive theyre all going to have,those three phases of shock the,compensatory the progressive and the,refractory so its important for you to,recognize the early stages of shock and,begin treatment immediately so that you,hopefully reduce the risk of leading a,patient into ref

More: thursday boot company review

CCRN Neurology Review – FULL

[Music],welcome to the CCRN neurology review on,Brent lets get started the neurology,section on the CCR in tests contain a,lot of testable areas such as an,aneurysm spring death congenital,neurological abnormalities and sent a,lot of the so-and-so,all the way down to strict starting off,with an anime review theres two things,that you need to know on the CCR and,test the trans central shelf the foramen,magnum music to your openings in the,skull you need to really understand what,those openings are there for and what,happens when the brain turns through one,on the other or both the first is the,trans tutoral notch which is a small it,is located here this is the upper,opening in the skull and its typically,smaller the second one is a foramen,magnum and its much larger than the,transgender Lamont,this is where the brain connects to the,spinal cord one of the testable areas on,the CCRN test is the cranial nerves you,dont need to memorize these,however they are and will be implemented,into the questions its important to,note that all cranial nerves with the,exception of one and two originate from,the brainstem cranial nerve one and two,originate from above the brainstem the,ones in red are the ones most tested on,cranial nerve number one the old,factories are smell this is most often,associated with the basilar skull,fracture,cranial nerve number two the optic nerve,is associated with sniped not people,reaction so remember that theyve got a,question on people reaction they are not,talking about the cranial nerve number,to you theyre talking about cranial,nerve number three the oculomotor nerve,which is the pupillary function /,reaction cranial nerve number eight is,best to react ocular its intact and is,tested by the davos eyes test and the,cold calorics assessments well get to,that further along into the video the,brains blood supply and neuroanatomy is,important to understand they have a,basic concept out that way when there is,blockage or bleeding youll know what,area of the brain that leads to the,basil for cable artery supplies the,lower areas of the brain and the brain,stem,well the bilateral carotid arteries,supply typically the upper areas of the,brain while the left internal carotid is,dominant for most of people this is the,view of the brain supply the picture on,the left shows the basal vertebral,artery and shares that it supplies most,of the brainstem and lower areas of the,brain the brains anatomic locations will,not be knowledge-based for example they,will not ask you the frontal lobe is,responsible for what Darren asked you if,you know someone strokes out in this,area of the brain how would they,presented that sort of thing so the,frontal lobe is the long-term memory,abstract thought and personality the,temporal lobe hearing and cavitations,sense and smell occipital is vision,visual recognition and reading,comprehension the parietal lobe object,recognitions by size weight shape and,body part awareness and the cerebellum,is coordination balance and gait so,theres many components for the,neurological assessment starting with,the most one we often think of is the,level of consciousness just note for the,CCR in a change in level of,consciousness is always the first sign,of a narrow problem with the exception,and only one exception of an epidural,hematoma that can cause the people our,changes before a level of consciousness,change now which one was the people Airy,change which cranial nerves screamin or,three not number two so this is the unde,Californian thats the only exception,all other exceptions include or all,other examples include the level of,consciousness being the first assessment,that we we notice of change so that is,the only exception all other areas are,going to demonstrate the level of,consciousness change first so your,second Amendment is arouse ability do,the open their eyes with your walk in,the room do you have to wake them up by,voice by shaking or pain thats the,Glasgow Coma Scale and well go over,that further the video next is the,orientation time person place again,thats the classic coma scale and well,go over that,the reticular activating system is,important to understand its actually a,network of neurons connecting the brain,stem to the cortex so its two parts,theyre lower in the higher both need to,be intact for consciousness to be,achieved theres one of the others,damaged youre gonna have a lower level,of consciousness the other component is,their speech and language again thats,part of the Glasgow Coma Scale the,Brocas area in the left hemisphere is,responsible for speech this can,demonstrate expressive or receptive,aphasia if damaged and if you dont,remember expressive is the ability to,speak or demonstrates an ability to,express someones thoughts or feelings,appropriately and receptive aphasia is,the opposite they might be able to speak,or tell you what they need however when,you speak back to them they probably not,going to understand you or get a,distorted sense of what youre trying to,ask them memory is the other components,a short-term memory typically becomes,abnormal before long-term memory,attention span and thought content and,judgment also can be affected this is,why people can remember their family,members and where they lived and not,remember you walking in the room and,given them their medications earlier,that morning personality can also be a,first sign of a problem especially in,brain tumors the patients personality,certainly can change a person may become,more aggressive or sexually nice you,know thatd be nice for all of them to,be exceptionally nice that can be,certainly a problem neurologically,crossing of the motor fibers occurs in,the medulla and motor problems are,contralateral to the problem so if this,means this is essentially why theres a,deficit on the right side of the body if,there is a left-sided brain deficit,strength and movement are also,indicators of motor function again this,is part of your neuro assessment one of,the assessments you can do is to ask the,patient to close their eyes and hold out,both arms with their palms up and hold,for 15 seconds you assess this having,weakness,if one of those arms drift down and,within the 15 seconds also if the,patient has abnormal flexion or,distinction decorticate Orcas aribert,flaccidity indicates the medulla,dysfunction sensory function includes,assessing the deficits generally the,same size of motor deficits so one,person is flaccid on the left side,typically they can they typically can at,the same time lose sensory function as,well on that side however not always,people area assessment this is one of,the ones we look at for a good neuro,exam,people are responses such as cranial,nerve number 3 ocular motor so the,sympathetic effect on the pupils is,dilate and the parasympathetic effect on,the pupils is to constrict so if you,have a person with a stroke on the left,side of their brain their left people,will typically dilate,changes occur on the side of the injury,which is its a lateral dont forget,that you can have injury on both sides,at the same time so that would be,bilateral reflexes are an important part,of your assessment and therell be a,fair amount of questions on the,narrowest section of the CCR in your pin,ski reflex is back again its not only,in the newborn assessments but its also,an abnormal assessments for your narrow,so positive and adults is abnormal,thats when thats when you start the,bottom of their foot towards the toes,and the toes flare upward that is,positive normal as no response or the,absence of the flare brainstem reflexes,are also assessed if all of our reflexes,are absent and brain death suspected now,just because they have no brainstem,reflexes does not mean it can be legally,called brain-dead its important to,understand that for the test theres a,process you have to go through part of,these brainstem reflexes are the cough,gag and corneal reflex in the akio,cephalic reflex is which is where were,testing the dolls

CCRN Renal Review – FULL

welcome to another video on CCRN review,this one is for the renal system Im,Brent and lets get started so the CCR,in renal testable areas include acute,renal failure chronic renal failure,hemodialysis life-threatening,electrolyte imbalances and everything in,between so Ill start off with renal,anatomy the functional unit of the,kidney is called the nephron which has,both a vascular and a tubular system,each kidney has approximately 1 million,nephrons of which play an important role,in the fluid balance and electrolyte,balance within the body the vascular,system in the nephron contains an artery,an afferent arteriole a capillary system,which is called the glomerulus and an,afferent arteriole and a vein the,afferent arteriole brings the blood to,the glomerulus and the efferent,arteriole is the blood going away from,the glomerulus so thats the filtered,blood essentially so the efferent,arteriole is the pre filtered blood the,efferent arteriole is the filtered blood,the tubular anatomy of the nephron,contains the Bowmans capsule a proximal,tubule the loop of Henle a distal tubule,and the collecting ducts most of the,absorption and/or excretion happens,within the proximal tubule,so the nephron must maintain a pressure,gradient which is going to optimize the,blood flow and this gradient can change,based on the cardiac output the types of,drugs the patients are on and the,conditions the patients are in such as,sepsis and or states of infection so a,condition which impedes this pressure,gradient will cause compensatory,mechanisms implemented so lets say in a,state of severe infection sepsis when,you have hypotension in the late stages,of sepsis theyre efferent arterial the,arteriole bringing blood to the,glomerulus will dilate which will,increase blood flow to the glomerular,capillaries at the same time the,efferent arteriole will constrict,decreasing flow from the glomerular,capillaries so what this does is,increases the pressure and essentially,will allow the glomerulus to be perfused,approp,really and to be able to do its job,thats the basics of the renal Anatomy,for the CCR rim theres other anatomy,involved however this is not as,essential other than just understanding,the concepts of how the kidney functions,as far as the nephron and what will,affect that nephron from from,functioning appropriately so important,lab values we have blood urea nitrogen,the BU n please do not call it the bun,the normal values of the BU n is ten to,twenty three milligrams per deciliter,this is gonna vary on the laboratory,that your hospital uses but just know,generally ten to twenty three this is,useful for measuring the level of serum,nitrogen if the liver forms as a waste,product from metabolism this is not as,useful for indicating the renal function,such as the serum creatinine the,elevated bu n level is called uremia and,the patient is in a uremic state so this,condition the conditions that cause the,elevation of a BU n is dehydration and,shock so essentially it will be a,concentration of nitrogen in the blood,moving on to you the creatinine so,creatinine is the waste product of,skeletal muscle metabolism and this is a,better indication of renal function than,the BU n the normal level for males is,zero point eight to one point four,milligrams per deciliter and this is,because generally males typically have,more mass and the females the normal,level of creatinine is zero point six to,one point one milligrams per deciliter,so the best indicator for monitoring the,renal function otherwise known as the,glomerular filtration rate is obtaining,a 24-hour urine creatinine clearance the,24-hour urine needs to be placed on ice,for the entire time until it gets to you,the lab so what is the GFR the GFR is,the volume of plasma filtered through,the glomerular capillaries into the,Bowmans capsule per minute so the,normal GFR is approximately 125 MLS per,minute and is inversely related to a,serum creatinine so this means that as,it creates serum creatinine Rises your,GFR is going to be lower,normal urine volume is approximately a,thousand milliliters per day thats,going to vary widely on how much input,the patient is getting however on amber,about a thousand a day which 99% of the,filtrates,being reabsorbed from the urine so large,molecules in the urine indicate,glomerular damage as only small,filtrates,are filtered not allowing large,molecules to pass,so the Gamaliel ER membrane is a very,tight-knit membrane when you have large,molecules in the urine that means that,these this membrane is damaged,essentially so some other important lab,values are obtained at urinalysis,your in electrolytes urine cultures can,also be beneficial when the patients in,the state of proteinuria,were saying that there is protein in,the urine so this is important for,detecting early diabetic neuropathy,which is gonna say that damage is being,done to the kidney to the go modular,membrane from diabetes normal abi-maria,is less than 20 milligrams per day of,albumin in the urine microalbuminuria is,approximately 30 to 300 milligrams a day,of albumin or protein so thats thats,quite a lot proteinuria its considered,greater than 300 milligrams per day of,albumin excreted protein this is the,same level that is used to be one of the,markers for eclampsia for pregnant,ladies so important to understand that,serum albumin if low maybe may decrease,oncotic pressure so if youre theres,been a lot of albumin excreted in the,kidneys youre naturally your serum,albumin is gonna be a little bit lower,especially if this patient has other,comorbidities and malnutrition what,happens when you have a decrease in,oncotic pressure that means that,essentially the vascular system within,the body is going to be losing a lot of,oncotic pressure this can make a patient,edematous just remember for the test an,edema this patient can be intravascular,dehydrated so just remember that just,because they look like theyre in a,state of fluid overload they may not,actually be vascular wise other,important lab values include specific,gravity the normal again this is going,to vary depending on your laboratory but,for the test approximately one point,zero one zero to one point zero to zero,is going to be your normal specific,gravity some will have it one point zero,zero five,one point zero three zero just be,understand that 10 to 20 is roughly the,normal range serum creatinine kinase is,another important level to look at not,necessarily for renal function but to,understand why this patient may be going,into renal failure the creatinine kinase,can indicate rhabdomyolysis which often,causes acute renal failure this is,caused from a bunch of breaks down from,muscle damage or trauma or metabolism,this can happen for varying amounts of,reasons from myocardial infarction for,significantly prolonged immobilization,so if youve heard about the elderly,gentleman or the elderly woman thats,fell and laid there for 12 hours and,ends up in acute renal failure because,of these CK levels are extremely,elevated like 27,000 so just be,understand that the CKD does not,indicate renal failure the youre only,going to measure this to see why they,are in renal failure if thats one of,the causes because some of the,treatments can be slightly different so,another important lab values to get,again is to evaluate or what state of,kidney failure this patients n is the,arterial blood gases that means there,could be a decrease in the reabsorption,of sodium and water in this sort of,acidosis so some of the clinical,assessments helpful is an ultrasound,which could be helpful for understanding,a kidney size kidney stones extreme,urinary retention and other useful,information for the kidney as as far as,the kidney is concerned bladder,distension can also indicate an outlet,obstruction such as prostate or cancer,or tumor or strictures or something like,mine origin a bladder from a,neurological disease or diabetes flank,pain can indicate a possible urinary,tract infection you have sever

CCRN Gastrointestinal Review Video – FULL

welcome to another CCRN review video,this one focuses on the GI review and,lets get started the GI portion of the,CCRN test has a few testable categories,ranging from acute GI bleed to,pancreatitis starting with some,gastrointestinal structures we have the,mouth esophagus stomach small intestine,large intestine the pancreas the gall,bladder and the liver and spleen just,some abdominal anatomy overview within,the right upper quadrant we have the,liver the right kidney the right adrenal,gland the duodenum and the head of the,pancreas within the right lower quadrant,we have the appendix cecum the right,ureter the right ovary and fallopian,tube for the females and the right,spermatic cord for the males within the,left upper quadrant we have the spleen,stomach the left kidney and adrenal,gland and the body of the pancreas and,within the left lower quadrant we have,the sigmoid colon the left ureter the,left ovary and fallopian tube and the,left spermatic cord starting with,abdominal trauma there are some common,clinical signs,starting with cur sign this is referred,pain to the left shoulder,due to diaphragmatic irritation which is,common in a ruptured spleen also with a,splenic injury that can be ecchymosis or,or bruising with on the left upper,quadrant the next sign is greater nurse,sign this is bruising within the flank,coming in retroperitoneal bleeding the,next sign is Cullens sign and this is,ecchymosis or bruising around the,umbilicus just very common and intra,pair to no bleeding and also pancreatic,issues such as hemorrhagic pancreatitis,also when you hear bowel sounds in the,chest you can consider diaphragm rupture,when you see free air on the abdominal,x-ray typically think of GI perforation,when you get positive blood from a,peritoneal lavage,you can think intra-abdominal bleeding,moving on to the next slide so one of,the things that can develop that,convenient emergency is in the abdominal,compartment syndrome common causes of,acs is,such as a gunshot wound emergent,abdominal surgery and massive fluid,resuscitation anytime you have increased,intra-abdominal pressure this can result,in a reduced cardiac output increased,the systemic vascular resistance,decreases perfusion to the kidneys and,reduced venous return due to the,pressure being greater than that of the,capillaries within the abdomen which,causes ischemia and subsequent,infarction of the organs its important,to note that this can occur without,abdominal distension what do we call,increase the pressures within the,abdominal cavity intra-abdominal,hypertension this develops when theres,an empty abdominal pressure an ia P of,greater than 12 millimeters of mercury,the normal abdominal perfusion pressure,is measured by taking your mean arterial,pressure and subtracting the,intra-abdominal pressure to get your,abdominal perfusion pressure a PPS of,greater than 60 and have an increased,risk of survival for the patient a PP s,of 50 or less can have an increased risk,of mortality so the less perfusion,pressure in the abdominal cavity the,higher the risk of mortality abdominal,compartment syndrome begins at a,sustained AAP of 20 millimeters of,mercury and this is associated with new,organ dysfunction or failure so how do,we measure the pressures within the,abdomen well were going to assess the,patient and the pressures by measuring,the bladder pressure the normal bladder,pressure is 0 to 5 millimeters of,mercury we measured the bladder pressure,because its closely related to the,intraperitoneal pressure when measuring,the bladder pressure we want to keep the,transducer at the level of the symphysis,pubis again its important to note that,an ia P greater than 12 which is,intra-abdominal hypertension can begin,with physiological compromise to the,patient and a decompression laparotomy,should be considered with an eye AP of,greater than 20 greater than 20 ia P can,be fatal again this is when youre,getting up into the abdominal,compartment syndrome so how do you,prevent abdominal compartment syndrome,or at least reducing your,intra-abdominal pressures so you want to,maintain the head of bed 20 degrees or,less,while sometimes placing the patient in,reverse Trendelenburg you want to manage,their pain in any agitation you want to,loosen all constrictive clothing you,want to prevent fluid overload and,subsequent hypervolemia or any over,hydration you can also place an NG tube,to low intermittent suction to help,decompress the abdomen and also you can,assess for impaction and treat the,patient while optimizing the stool,management,its moving on to bowel infarction this,is when you have a reduced blood flow to,the mesenteric vessels or arteries with,prolonged ischemia which causes edema of,the intestinal walls leading to necrosis,and subsequent perforation common causes,a balun function include,arteriosclerosis surgery thrombus,hypercoagulable intra-abdominal,infection and the use of vasopressors,some of the things to look for with a,balun function presentation is abdominal,distension and vomiting severe abdominal,pain and cramping hypoactive or absent,bowel sounds fever tachycardia and,hypotension,when youre treating bowel and function,you want to start with the emergency,things first such as your airway your,breathing in your circulation things,that will also help balance oxygen,treatment or at least the management of,is gastric decompression be an NG tube,placing the patient NPO,and administer an IV fluids when you,have a bowel infarction surgery is going,to be required to have a bowel resection,which removes the necrotic tissue you,also want to monitor the patient for,sepsis and treat the patients pain,moving on to bowel obstruction there are,three common types of bowel obstruction,you have your paralytic ileus and small,bowel obstruction and a large bowel,obstruction your paralytic ileus is,common from abdominal surgery,hypokalemia peritonitis intestinal,distension opioid use and sepsis,typically the paralytic ileus is usually,transient and is typically less severe,than a small bowel obstruction moving on,to the small bowel obstructions these,are common from adhesions within the,abdominal cavity a hernia volvulus and a,neoplasm and it could be partial or,complete can be described as simple or,strangulated moving on to the large,bowel obstruction this is commonly from,neoplasms diverticulitis strictures,fecal impaction and barium impaction,some of the things to be concerned about,during the bowel obstruction,presentation is when theyre vomiting,and how much abdominal distension they,have so in the small bowel obstruction,you have your vomiting early and you,also have a small amount of abdominal,distension this is because the,obstruction is more proximal which,leaves less bowel for the GI contents to,back up and assess you have your,vomiting early hypokalemia could also be,present and typically the pain is sharp,and episodic you also are going to have,more commonly high-pitched bowel sounds,and the KUB is going to show dilated,loops of gas filled bowel,moving on to the large bowel youre,gonna have vomiting late youre also,gonna have a larger amount of abdominal,distension this is because the blockage,is more distal than the small bowel,leave a more gut to distend youre also,gonna see a change in bowel habits prior,to in the large bowel obstruction or,during and youre gonna end up,auscultate alope itched bowel sounds,instead of high-pitched bowel sounds and,the KB again is going to show dilated,loops of gas billed bowel,so same with your bowel infarction,treatment – your bowel obstruction,treatment thats going to begin with,your ABCs placing the patient NPO and,administering IV fluids there is one,exception during a bowel obstruction if,its very proximal you can end up using,the interval feedings through like a J,tube if that J tube is distal to the,obstruction you can still use the rest,of the bowel thats not obstructed you,want to place your patient with an NG,tube to low in a minute suction to help,d

CCRN Cardiovascular Part One

[Music],hello and welcome to the cardiovascular,content on the CCRN review this is David,Woodruff and I want to talk to you a,little bit about a cardiovascular system,when you take a look at your handout you,see that there are a few concepts that,are listed there like the cardiac cycle,a arctic pressure and coronary artery,perfusion pressure so these are a few,things that we probably need to be,thinking about when we start to answer,those questions in addition take a look,at this picture here and consider the,placement of the heart within the,thoracic cavity when we think about most,pictures of the thoracic cavity they,give us this impression that the lungs,are in this place over here the heart is,sitting here in the mediastinum by,itself and then we have other stuff,going on in the abdomen but all of these,components are touching each other,therefore your patient who has a lung,disease and has air trapping the lungs,are getting it bigger and theyre going,to start to press on the heart which is,going to decrease our cardiac output so,our patients who have COPD in many cases,also have heart failure in addition,those patients who have abdominal,conditions maybe some liver failure or,some other abdominal condition can also,end up having some problems with their,lungs and their heart too because of the,lack of compliance of the diaphragm in,the abdomen so just consider all of,those things together when youre,looking at your patient with a heart,problem and youre thinking how can I,improve cardiac output in this patient,well Ive got to be thinking about all,of those components around the heart -,that may be impeding the patients,ability to be able to have a good,cardiac output as some background,information we do need to know just real,basic stuff about the vasculature of the,heart theyre not going to ask,for very specific arteries that are,feeding the heart but we do need to know,the right coronary artery the left,coronary artery including the circumflex,and they left anterior descending so we,need to know those vessels when they may,ask you questions on the exam so they,may ask you a question about a patient,who has a right-sided MI our patient,whos having a I inferior wall mi and,you need to be able to understand which,one of these vessels is feeding that,area in addition we also need to be,looking at some of the components that,make up our cardiac output so when were,talking about optimizing somebodys,heart condition or optimizing their,cardiac output and improving their,overall outcome theres a lot of,different components we need to look at,its not just as easy as hey lets give,the patient some positive inotropes in,order to be able to increase cardiac,output theres other components that are,involved in the process so we may not,get the outcome we want because were,not considering all of those different,components when were taking a look at,cardiac output so lets take a look from,the bottom up we start out with our,preload our contractility and our after,load so these are the components that we,normally think about as being part of,our cardiac output as being part of,hemodynamics is preload contractility,and afterload those are components that,affect stroke volume,in addition heart rate also affects,cardiac output so we need to consider,those pieces that we normally think,about as being part of hemodynamics and,we also need to consider the heart rate,because stroke volume times heart rate,equals cardiac output do you remember,hearing that somewhere that equation of,stroke volume times heart rate equals,cardiac output in fact it does and the,components of stroke volume are preload,contractility and afterload so again our,patient is having a low cardiac output,state we need to be looking at all of,those components here at the bottom,heart rate preload contractility and,afterload optimize those things if were,going to get an adequate cardiac output,now cardiac output is just part of the,equation your patient can have a,horrible cardiac output and still be,very functional right so theres other,components that are involved to our SVR,systemic vascular resistance our spo2,the amount of oxygen circulating in the,blood and our hemoglobin level how are,we gonna bind oxygen to hemoglobin if we,dont have any hemoglobin so we need to,have an adequate hemoglobin level in the,body and order to be able to get oxygen,to the tissues so our goal when were,treating a patient who has a cardiac,disease is not just hey lets optimize,cardiac output but we need to optimize,oxygen delivery to the tissues so that,our patient can have an optimum outcome,which involves cardiac output but it,also involves blood pressure spo2,and the hemoglobin level were gonna,come back and look at these components,again when we talk about how we treat,patients who have cardiac conditions so,heres another one of our tips avoid,multitasking multitasking requires you,to switch from one activity to another,you know we often think of somebody,whos a multitasker as somebody who is,able to keep many things in the front of,their mind at the same time well the,brain can only work with one activity at,a time so whats really happening is,were doing this switch tasking thing so,when youre studying if youre also,talking to your kids or doing some other,activity at the same time and you think,hey Im just multitasking here Im,trying to memorize these things or Im,studying this thing and Im also making,lunches or watching the news or whatever,the case may be if youre doing the,multitasking thing youre not going to,be as effective as if you stop and do,one thing at a time now this is one of,the pieces were going to come back to,this again,but this is one of the tips that we,really want to work on here studying for,the CCRN break down your study time into,small pieces,frequent small pieces during the day so,that you are repeating some of the same,stuff over and over again so that it,kind of sinks in but youre also doing,it in little pieces often that way you,can really concentrate for a period of,time and then move on to something else,people will often tell me well Im gonna,take the whole day Saturday to study and,at what point in time do you think the,studying becomes less effective right,its not gonna be effective for that,whole eight hours your brains gonna,start to wander youre not youre gonna,start to become mentally fatigued and,youre not going to be taking in as much,as you were when you start it so break,it up break it up into small chunks our,next cardiac condition is acute coronary,syndromes so when our patient has,decreased cardiac output to the heart,itself for whatever reason maybe theres,a blockage of blood flow or maybe the,patient has got decreased cardiac output,as a result of some other condition the,patient can end up having an acute,coronary syndrome now we used to call,this angina unstable angina myocardial,infarction etc now we just kind of lump,them all together into acute coronary,syndromes because this thing is on a,continuum so you see the picture down,there at the bottom we have athletic or,OSIS and were moving from stable angina,where we have a little bit of an,obstruction of a vessel and the patient,may have some chest pain when they,exercise its the unstable engine and,now the patient is having chest pain at,rest,so if you think about this in terms of,whats happening at the tissue level we,have ischemia and then we start to get,into injury when we have unstable angina,now an ST segment elevation MI and then,finally we move into necrosis,we have ischemia injury necrosis moving,across that picture at the bottom across,that a thorough attic picture at the,bottom as we move from stable angina to,unstable at an instan STEMI and then,stem is the presentation will be in,most cases at least we assume in most,cases will be chest pain now when we,talk about these symptoms that a patient,is going to have when they come in to,the hospital with an MI thats what,were talking about were talking