ATI Adult Health Final Study Guide, Exams of Community Health

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ATI Adult Health Final Study Guide  Introduction: o Patient education in critical care is ongoing and frequently reinforced  Use layman terms and stop/explain what you’re doing to family/patient  Patient can be scared when transitioning to independence = help the know this is a good thing o Purpose of the Code of Ethics  Prevention of malpractice or maltreatment of patient  Protects patients and possible healthcare providers  Autonomy = independence  Beneficience = do good  Nonmaleficence = do no harm  Justice = be fair  Fidelity – be failthful, truth o Palliative care – see below o Advanced directives – see below Test 1  Chapter 1: Critical Care Nursing Practice o Contemporary Critical Care  Critical care uses a multidisciplinary team  Includes nurses, physicians, clergy, OT, PT, etc.  Each have in depth knowledge  Wide range of discipline = should take advantage of lots of specialties. Diabetes specialties, heart doctor, respiratory, etc.  High risk patients  Specialized units  There is now a continuum of care with critical care  Critical care goes to progressive care o In between medical/surgical floor and critical care  There are units that are specialized and based on the pts. (age, etc._ o Neonatal (nicu), pediatric (picu), adult, (icu), geriatric etc. o Not every hospital will have all these designation areas, if a hospital doesn’t have picu, and have a child who is really sick they will transfer them to another hospital.  Medical vs. surgical problems o Medical icu from what’s coming in vs. surgical icu which deals with pts. in critical care after surgery  Special pt. populations o Cardiac, pulmonary, neurologic etc. o Critical care nursing roles  Expanded role nursing positions  Case managers  Patient educators – diabetes nurse, hand hygiene etc.  Cardiac rehabilitation specialties  Office nurses  Infection control specialists  Advanced practice nurse (APNs)  Clinical nurse specialists (CNS) – in charge of leadership type stuff  Nurse practitioner (NP) or acute care nurse practitioner (ACNP) - like a doctor, orders tests, labs, meds  Certified registered nurse anesthetist (CRNA)  Animals – provide positive pt. outcomes with orientation, mobility, communication, and moods o Nursing’s unique role in health care  Both independent and dependent nursing roles  Interdependence with all health care professionals  We must be the eyes and ears for the provider o Is what they are hearing from the pt. what’s actually going on. o Explain, intervene, create best plan of action o We need to be professional o Clarify orders  We must be exceptional at communication skills  Facilitate communication between health workers, family, patiet  Need to communicate with lots of different people in different ways  Assertive in communication o Critical care nursing practice  Research  Studies link between clinical judgement and interventions  Identifies two major categories of thought and action o Nursing thought/action  Clinical grasp  Clinical inquiry  Problem identification  Problem solving  Clinical forethought – preventing problems in the future o Clinical practice  Diagnosing/managing functions  Managing a crisis  Providing comfort measures  Caring for families  Prevent hazards  Facing death and end of life care  Communicating/negotiating  Monitoring/managing quality of care  Clinical leadership o Interprofessional Collaborative practice  Increases quality of care and services  Contains or decreases costs  Core competencies for interprofessional collaborative practice  Assess competencies relevance  Develop plan of action  This involves a collaboration between disciplines (doctors, dieticians, therapy, speech  Decrease costs, increase care, better results  Improve communication/accuracy  Different departments are experts on different things o Pharmacist – meds, dietician etc. o Care management methods  Care management  Enables, supports, and coordinates care  Seen in many settings  Pt. focused, continuum driven, and team approach is goal driven  Care manager o Facilitate care services as a pt. moves through places  Case management  Oversees care and organizes services  Collaboration  Case management tools  Clinical algorithm o Disease population management  Manage the populations’ health over a lifetime  Diabetes, heart failure, etc. o This is a stepwise decision making flowchart  Helps to guide clinicians through the decision making process  Identify treatments  Ex  Practice guideline  Plan for diabetes, first try lifestyle management, then oral diabetics, then insulin o Resources to help form algorithms o Created by expert panels and professional organizations  Protocol o Directive, useful tool for research studies o Direct plan of action o Don’t vary o If you see a high potassium, don’t give potassium, o Rigid guidelines to follow based on what’s going on with the pt. o Do not vary from protocol  Order set o Preprinted orders from the provider  Nurses play a unique role in addressing the needs of patients and families in a busy and complex environment  Remember the family is going through a lot. They have to take home the person and figure out how to take care of them in the ICU afterwards. This was not the plan and now life is just a little crazy. They have a lot of stress  They don’t have the same knowledge as you do. Don’t take your knowledge for granted. Just because you feel like you don’t know a lot doesn’t make it true.  Need to explain what is going on with the pt., if you don’t tell them then they assume things = BAD o Ex: you’re waking up the pt. every hour because you are mean not because you care.  Make sure to be the pt. advocate = how can we get them more sleep, privacy, etc. o Critical care environment  The ICU is designed for efficient lifesaving interventions.  Lots of equipment, noise, lights, no privacy, lots of people, not a great relaxing environment.  Patients and families have little advanced preparation for the environment and it will probably cause stress and anxiety.  There is CPR, no modesty, loss of privacy, multiple caregivers, sensory deprivation, can’t see what is going on.  Lots of things are challenging  Things that cause stress  Loss of privacy o Multiple caregivers o Multiple people in and out of the room o Gown  Lack of physical contact o Always clinical checking, but not actually caring touching  Emotional and physical pain  Increased perceptual disturbances  Treatment o Make sure to address the family and pt. o Stress will affect how they sleep, breath, oxygen, blood pressure, heart rate, and ability to heal/recover o Make sure you give them a peaceful environment if possible  Visitors = visitors actually help to calm and soothe the pt. even if it is not convenient for you  Photos  Soothing music  Low lighting  Lots of talking  Patient’s recall about critical care o The pts. have zero control over their situation o Example  Difficult communication  Pain  Thirst  Difficulty swallowing  Anxiety  Lack of control  Depression  Fear  Lack of family  Dread  Discomfort  Difficulty sleeping  Loneliness  Thoughts of dying  Physical restraint  Loss of autonomy  Can’t do anything for themselves. Make sure you are thinking about how they are doing. o Helping them  Make sure to address their stress.  Explain why things are happening and always tell them what is happening.  Explain why they can’t have water, let them know what is going on.  Provide listening to them, physical touch and being there when their family cannot be. o Top stressors  Pain  Important that you treat pain  They can’t move/breathe appropriately when they are in pain  Inability to sleep  Pain cause problems, lights, visitors, VS  Financial problems o Functional decline o Decrease quality of life o May have prolonged stay, less understanding, more negative outcomes, don’t cope o It is harder for them to adjust o Increase mortality  Family needs  Receiving assurance  Remaining near the patient  Receiving information  Being comfortable  Having support available  What can you do? o Communication o Facilitate visitation o Encourage family involvement in pt. care  Need to understand the family can be helpful and how good they are for the pt.  Make sure to give them information on the pt.  Inform the fam of what is going on  Family is a good constant o In 1979 research found fams. Need to be near the pt. to reassure them the pt.  VALUE o Value what the family tells you o Acknowledge family emotions  End of life care o Listen to family members o Understand the pt. as a person o Elicit questions from family members o End of life language  Allow natural death  Important to be ready spiritually, but also know the wishes of the family during death and what the pt. wants  Change the language to make it sound more pleasant o Allow natural death rather than DNR  DNR feels like they are killing them because they are making the decision not to revive them  You need to have a counseling moment where you tell them what’s going on. Just because its DNR doesn’t mean you are killing them  DNR – what you are not doing for momma rather than what you are allowing her to do  Withholding of nonbeneficial treatment o Palliative care – until there is a cure or death  Improve quality of life  Helping feel okay while dying o End of life experiences in critical care  Approaching death: improving end of life care  Need to do better at improving death  Want to understand pt. preferences  Palliative care o How do hospitals benefit – pt. satisfaction, decrease in cost, more comfort  Advanced directives  Important to understand what they are  This tells you what a patient wants when they die o Tube feedings, life sustaining treatment, DNR  Need to direct this beforehand  Physician orders for life sustaining treatment  POLST  Depends on what state you are in on if they are going to listen to the orders or not  Advance care planning  Ethical legal issues  Pt. self determination act o Pt. can decide what they want and cannot be influenced  If they have a DNR = need to have an order from the doctor  DNR = no cardiac resuscitation, does not mean let them die o Remember that the patient has the right to refuse treatment when they are in their right mind, and are not at risk for other people. Not thinking clearly or under drugs or unconscious means you look at the next of kin  Comfort care  Not doing anything to prolong your life  Keeping you comfortable during death  Example o Pain meds o s/sx management o Zofran for nausea o Oxygen o Probably no insulin, antibiotics  Ways to donate  Post cardiac death o Will see ahead of time they likely won’t survive off the ventilator o Health company will know the organs they can donate  Will have lots of testing to see what they wanna do  If they are a viable candidate then they will talk to the family o Pt will go to the ER, extubate the pt. with the family there, wait for the pt. to pass and let family cope o Wait a certain time then have family leave and the surgeons begin removing organs  Brain death o Pt. is determined brain dead o Can keep pt. on a ventilator because they are already dead and they can remove the organs o Better organs  We never want to miss an opportunity to donate  When a patient is getting close to death = call the IDN (integrated delivery network) and let them know o Family care o Makes the process go faster, test everyone o Hard to keep body alive when the brain is dead o Then do surgery  Family presence  It is appropriate for the family to be there when you revive the pt.  Allows the family to see everything nurses are doing to save the family members lives  They can see what happens during a code and how many people are involved  Comfort cards  Supplies, food, coloring books, etc. to help the family if they don’t want to leave the hospital  Spiritual comfort  Assess and allow spiritual care to occur  Stress  After death  Take your time and care for the pt. and family after death  After the family has had some time make sure you ask them to step out o Clean the body, glasses on, etc. o Clean the room, get rid of extra stuff o Allow time for the family to say goodbye uninterrupted o Give privacy  Self care o Adjust, make sure you use hospital resources, time off, communicate o The stress response  Non specific systemic response to stress (internal or external)  May me modified in specific situations o General adaption syndrome  Triad/syndrome of manifestations that represent a nonspecific response to noxious stimuli  Three stages  Stage 1 = Alarm stage o CNS is aroused and defenses are mobilized o Initiates hypothalamus in the SNS  Stage 2 = resistance/adaptation o Adaption to the stress o Mobilization of defenses starts the fight or flight response o Begins with action of cortisol/epi/norepi  Stage 3 = Exhaustion o Continued stress causes exhaustion o There is a breakdown of compensatory mechanisms o If stress response continues and you cannot adapt there is impairment in the body, brain and kidneys o When we don’t have CO we need and compensation fails then you may lead to organ failure o Stress  Stress is experienced when demands exceed coping abilities  Some people have more or less stress and they handle it differently  We perceive stress differently and cope in different ways  Will have different disturbances in cognition, emotion, and behavior  Will affect well-being and homeostasis  Stressors will elicit reactions  Reactive response = physiological response from psychologic stressors  Anticipatory response = develops in anticipation of a disturbance/stress  Conditional response = learn certain stimuli stimulate stress because they signal danger (Pavlov’s dogs)  Stress can cause a weakened immune  Diabetes, HF, COA, o Physiological Response to Stress  Stress causes CNS activation  The CNS activates  CNS stimulation – more alert and have greater muscle tone d/t more oxygen  Vasodilation to skeletal muscle – more oxygen to your muscles so you can move faster and have better function  Increased lipolysis – increases the amount of free fatty acids, breakdown fat stores, to increase cholesterol  Decrease loss of cholesterol  Decrease glucose uptake in the muscles (anaerobic activity), decrease insulin release from the pancreas, promotion of glucose production (glyconeogenesis, glycogenolysis) = increase blood sugar  Posterior pituitary is stimulated  Causes release of Corticotropin release hormone (CRH)  CRH release Antidurietic hormone (ADH) o ADH is released from the posterior pituitary d/t CRH o Causes you to hold onto water  Water reabsorption in the kidneys  Increased blood volume  Increased blood pressure  Electrolytes might get out of wack  Anterior pituitary  Stimulates release of ACTH (andrenocorticotropin hormone)  ACTH stimulates release of cortisol and aldosterone from the adrenal cortex  Cortisol – steroid that can help increase healing by suppressing the immune system o Suppress immune system o Increase glucose o Increase water (Cushing’s syndrome) o In detail:  Protein catabolism and gluconeogenesis – causes an increase in blood sugar, because more glucose from non carb source. Break down proteins as well. Decrease in healing because all the glucose. (think about diabetes and poor healing). Also don’t have proteins to heal either. = increase risk of pressure ulcers  Stabilize the cardiovascular system – they basically enhance catecholamine action. Increased BP, increased pulse, preload, cardiac output, etc.  Decreased allergic reaction  Decreased inflammatory response – suppress the immune response, decreased white blood cells, may not have normal signs of infection (red, heat, fever, etc) = atrophy of lymphoid tissue, decreased lymphocytes, decreased antibody production = could actually increase risk of infection  Aldosterone too. o Aldosterone holds onto sodium which causes you to hold onto water  Increase in water causes an increase in blood volume, which causes a greater blood pressure, which causes a better preload, which means greater output o An increase in sodium causes a decrease in potassium  Make sure to watch for hypokalemia  Spironolactone – hold onto potassium diuretic  Why do we want an increase in volume of water? o Preload = preload is the volume in the ventricle. It is how much the ventricle can fill up during diastole  Starlings law = the more a ventricle fills the more contraction it will have (greater stretch, greater contraction, like a rubber band)  The volume in the vascular space affects preload  The more venous return you have, the more is returned to the heart, the more it fills, the more it stretches, the more it contracts o Also remember  Insulin goes into the cell and potassium will follow  May cause hypokalemia  Monitor labs o You will transition from continuous insulin to intermittent coverage as the pt. recovers  Maintain tight control ----- less than 180  The glucose levels will be affected by how they are getting their nutrition, TPN, THA, PO, etc. ----  Check glucose every 4 hours, possibly every six o Remember that insulin is a high risk medication  Have several RNs check the medication amount, sign off.  Hypoglycemia management o Have a risk for hypoglycemia with continuous insulin o Need to know the protocol for this. o If blood glucose is below the hypoglycemia border (70 or below)  d/c the infusion  give glucose – depends on pt. status, oral, alert, oriented, not  can they take by mouth or through IV?  Amount of glucose depends on protocol o Make sure to monitor every 15 minutes until it is above 70  Then check every 30 minutes, then an hour  Nursing management o Monitor blood glucose d/t hyperglycemia effects of vasopressors  Vasopressors – epi/norepi which can increase glucose  Vasopressin, epinephrine, norepinephrine, dopamine o Administer prescribed corticosteroids (d/t cortisol being insufficient) o Monitor blood glucose, insulin, and avoid adverse effects o Provide nutrition  Need this esp. protein  Protein helps with osmotic pressure  Osmotic pressure helps to prevent edema by pulling water into the solutes o Educate the family and pt.  More time teaching family  Family is helping take care of pt. and will need to know how to take care of them at home  Monitor for skin ulcers, etc.  Remember for review o HR, BP, and sugar will be elevated at risk for pressure ulcers – blood isnt’ going to gut, stress o Keep blood glucose around 180?  Insulin management o Significant effects of the stress response  Body effects  Increased BP/HR  Bronchodilation and ventilation  Increase blood sugar  Arousal of CNS  Decreased inflammatory and immune responses  Increased serum cholesterol  These changes are good for  Increasing oxygen  Increase circulation  Increase cell metabolism  Stress plays a significant role in the development of diseases or the exacerbation of disease  Disease include  Hypertension, diabetes, coronary artery disease, etc.  Adverse heart effects o Ischemia may develop with stress in pts. with coronary artery disease because systemic vascular resistance (afterload) will increase o The heart will be working harder so then it will need more oxygen o May have left ventricle dysfunction  LV is working hard but can’t pump like it should. So the blood will start backing up into the lungs  See heart failure – pulmonary edema, crackles, rales, dyspnea, etc.  Could lead to right sided heart failure  JVD, edema, abdominal distention, enlarged organs, higher pressure on veins  Other effects of prolonged stress o Acute renal failure – vasoconstriction cause decreased blood flow to the vital organs and could cause organ failure o Stress ulcers d/t increased secretions o Infection o Impeded healing o Cancer  The amount of resistance the ventricle must overcome to eject blood o Right heart – must overcome resistance from the pulmonary vascular bed (PVR) o Left heart – must overcome resistance exerted from aorta and systemic vascular beds (SVR) kidney failure increases afterload.  Vasodilated – decrease afterload, vasoconstricted = increase afterload  Things that increase pressure o Hypertension, atherosclerosis, obesity, o Things to know increase afterload = hypertension, kidney failure (if kidney isn’t filtering water out, then increased volume, incrased volume means more pressure)  Contractility  The ability of the muscle fibers to contract and eject blood into the pulmonary or systemic vasculature  Starlings law – the more blood in the heart (the more it stretches) the more the heart is going to contract  Ejection fraction o The amount of blood pushed out with each contraction (beat) of the heart in percentage form o Normal = 50- 55%  If its lower then you have poor function  Less than 35 is bad o Equation  Amount of blood pumped out of ventricle/total amount of blood in ventricle = Ejection fraction  Normal = 55%, greater than 55% is best  Starling’s law = bigger stretch = bigger the snap o If you have a decreased preload you can still have a normal ejection fraction  Diastolic heart failure  Stroke volume – volume of blood pumped out with each beat of the heart o Average is 60-70 ml  Cardiac output o Stroke volume X heart rate = volume/minute o 4-6 L is average o Three invasive tools for measuring hemodynamic pressures  Intrarterial catheter (A line, arterial line)  Line placed into an artery  Usually radial or femoral  o Prefer radial over femoral. The femoral is dirty and has a higher risk of infection  Allows continuous monitoring of blood pressure  Central venous pressure (CVP line)  Not as invasive  Measures pressure on the right side of the heart  2-5 is normal  Superior vena cava  High pressure indicates fluid excess o JVD, peripheral edema, and enlarged organs  Pulmonary artery line (PA line)  Goes into the heart to get to the pulmonary artery  Wedge pressure,  Can give us cardiac output, stroke volume, and mixed venous oxygen saturation  Left side of the heart  Located in the pulmonary artery  5—12 is normal  Will indirectly measure left atrium pressure  The higher pressure in the left ventricle the greater the risk of cardiac dysfunction o Bedside hemodynamic monitoring  There are four components of hemodynamic monitoring  The invasive catheter o Always assess if we really need this information or not, is it worth the risk of infection and blood clots o Use of monitoring is decreasing  High pressure tubing with flush solution o Usually filled with saline 500 ml  We used to use heparin but now we avoid it because of heparin induced thrombocytopenia  Pressure tubing allows us to keep line open and prevent arterial blood from backing up  Transducer “brains” of system o Fluid filled interface between catheter tip and monitor (blood/fluid interface) o Computer chip that converts pressure signals to waveforms and pressure values o Zeroing the transducer o Cardiovascular assessment and monitoring  Intra- arterial blood pressure monitoring  Indications = continuous blood pressure monitoring – located in the artery, blood pressure in real time o Indicated for any major medical or surgical condition that could compromise cardiac output, tissue perfusion, or fluid status o It is the continuous blood pressure reading for a pt. o Allows to monitor systole, diastole, and mean arterial pressure  Tells us how well the organs are being perfused o Labile BP o Too many ABGs o Many medications o DO NOT GIVE MEDICATIONS THROUGH AN ART LINE o Make sure to test patency of ulnar and radial artierals o Allows for constant3 BP monitoring  Location o Radial or femoral – prefer radial because less of an infection risk  If you do a radial line you need to perform an allen test – distal pulse  Assess ulnar blood flow to the hand to make sure the hand is going to get blood flow if the radial artery is blocked  Perform allen test with arterial blood blood gas  If pt. is unconscious with allen test  Put pulse ox on the finger and measure to see if you are getting oxygen again  Nursing management o Infection  Risk for infection with the arterial catheter as well as central venous cath  Need to maintain sterile technique with changing lines or dressing  Monitor for s/sx of infection o Perfusion pressure  Need to monitor the mean arterial pressure (MAP)  MAP = diastolic pressure X 2 + systolic pressure /3  Reason is because we are in diastole twice as long as we are in systole  In order to maintain MAP, systolic pressure drops, so there would be an increase in diastole o If decreasing there should be some vasoconstriction to cause some better perfusion  Normal 60-70 mm Hg  Should be at least 60, but really you want it around 65  60 means coronary arteries are being perfused  Kidneys and brain need higher than that o Pulse pressure = difference between systolic and diastolic  Difference between systole and diastole is pulse pressure  Normal is 40 (think 120-80)  If decreasing, there should be some vasoconstriction to cause some better perfusion o Cuff blood pressure  If the artery line isn’t working use a cuff to find the pressure  If they are normotensive it should read fine, if they have a low BP might not read accurately  Nursing management of Arterial Line o Monitor peripheral perfusion and document assessment of tissue distal to the arterial line  Risk of blow flow being affected so you need to identify this.  6 P’s  Pain, pallor, paresthesia, paralysis, poquilothermia, pulse, pressure  Document and check pulses after it is removed  Do this because risk of blood flow being affected o Complications of Arterial line  Blood loss  Opening to an artery means lots of blood loss if released because high pressure  Emboli  Always a risk with catheters.  Identify clots  If you can’t draw blood a clot might be why o Also know that if you have collateral circulation, this is better, old is better cause better collateral circulation  A younger more acute case won’t have as long to form collateral circulation o Removing arterial lines  Assess for sutures – remove these if needed  Apply direct pressure to site when removing  Or if pt. is to be receiving large amounts of fluid they may want a CVP because you will have multiple lumens and wont’ have to worry about interactions, also can draw blood out of one to save the pt. from multiple arterial sticks  Insertion  The catheter itself comes in different forms. (double, single quad)  Sites for insertion (same as with pulmonary arterial line) o Subclavian  Least risk of infection  Highest patient comfort  Difficult to access  Higher risk for pneumo. – closest to the lungs  Good for CVP for more than four days o Intra jugular vein  Most frequently used  Easy to canalize  High blood flow  Decreased risk of pneumothorax  Disadvantages  Discomfort  Hard to get an occlusive dressing in area  Contamination from secretions  If its in place for more than 4 days, = high risk of infection use the subclavian instead o Femoral vein  Only if thoracic veins are not accessible  High risk of infection  Very sweaty, can’t get dressing  Easiest to access o Thoracic veins always have risk of pneumo.  Complications of CVP  Air embolus o Not common, but always want to decrease risk o Precautions  Always use screw connections  Avoid long loops  Closed tops on stop cops – does not allow air to come through  Have pt. take deep breathe with removal  Thrombus formation in CVP o High risk, very common o Clots can form from catheter to vessel wall o Monitor for risk (in Aline and PICC)  Measure arm circumference (2 cm above catheter insertion line)  Monitor for swelling, redness, and pain in the extremity  If you cannot draw back with the catheter it might be because an embolus is there o With CVP  Look for blue hand decrease peripheral blood flow o Follow hospital protocol – probably a thrombolytic  Infection o Depends on how long the catheter is in place, the longer it’s there the higher the risk o Part of monitoring means monitoring for infection at the insertion site o Look systemically too  Fever, redness, swelling, etc.  Systemic – may not see site, and WBC  WBC 4-10,000 o If there are s/sx of infection  Remove line  Antibiotics possibly  New catheter at a different location o Routine dressing changes  First dressing change = 24 hours after placement  Going to be soiled fast after insertion d/t blood  After that every couple days or when it is soiled  Nursing management  Central venous pressure – volume assessment o The CVP monitors the right side of the heart o Color blue ?? o Determines the lowest pressure in the vena cava o The volume is usually 2-5 mm Hg  If this is high it can indicate fluid excess = you will see peripheral edema, JVD, and organ enlargement  This makes sense –high pressure means the system is starting to back up, it would back up from the right atrium into the body  When it is removed o Nurses remove the catheter o Typically no complications o The pulmonary artery catheter can calculate the systemic vascular resistance o Know that some pharmacological treatments can affect SVR  Vasodilators – decrease resistance  Vasoconstriction – increase resistance o In a person with a healthy heart, the body can work against an increased SVR when we are stressed to meet the needed cardiac output, but this can be a struggle in someone who has a bad heart or is dying.  Contractility o Factors that affect contractility  Preload – starlings law, more volume in, the greater the stretch, the better the contraction  Right = cvp  Left = wedge  SVR – how much ventricles have to push against  Myocardial oxygenation – how much oxygen is the heart getting to let it pump like it needs to  Electrolyte balance  Inotropic ends  + inotropic meds – increase contractility  - inotropic meds = decrease  Amount of functional myocardiac muscle available o PA cath can measure preload, SVR, and CO o Commonly used intravenous meds for the +inotropic effect  Dopamine  Dobutamine  Melrinnin  After insertion o Suture in place to the skin o There will be a plastic sheath as it comes out of the skin to maintain sterility o Sterile occlusive dressing over the insertion site o Tape the cath. To the person so it doesn’t move around and is secure  Don’t tape over plastic sheath o When it is in place  Verify position with x ray o Make sure there is no s/sx of a pneumothorax  Nurse management  Patient position o Remember that the pt. position affects the reading from the PA catheter  Lateral/supine, etc and respiration variations o HOB  You can be flat up to 60 degrees  Make sure the cath. Is zeroed and leveled appropriately – each position has a different leveling point  Phlebostatic axis  If pt. is moved make sure you wait 5 minutes to stabilizes before your get readings o Respiratory ventilation  Get the readings at the end of expiation  This is the most stable point in the resp. cycle  Remember pulsus paradoxus  During expiratory there is a decreased pressure so it is the most normal o Mechanical ventilation  PEEP = positive end expiratory pressure  This is what keeps the alveoli open  Most people have a peep of about 5.  However, you may need an increased PEEP with someone on a mechanical vent. An increased PEEP increases the intrathoracic pressure, and this can effect your overall cardiac output. o Need ot notice an overall trend with measurements because a mechanical vent might effect normal numbers o Avoid complications  Infection  Monitor site of insertion for redness, fever, increased WBC etc.  Remove if needed  Increased risk of ventricle dysrhythmias  The cath. Can irritate the ventricle because it is going through (tickling) the heart  Heart doesn’t like this and might have dysrhythmias  Make sure to monitor  Endocarditis/infections/inflammation of the heart  Will see a change in labs  Normal WBC = 4,000-10,000  Arterial waveform pulse contour  Use arterial wave form to find CO  Esophageal Doppler cardiac output  This is done under sedation  Partial carbon dioxide rebreathing cardiac output  Additional probe on the vent. Tube  Looks at the CO2 rebreathing  Only used for pts. on a mechanical vent.  Continuous monitoring of venous oxygen saturation o Types of SVO2 caths.  PA  Triple lumen o Indications – when you want to know if you sent out enough oxygen or if you are using enough oxygen  This is fairly new  Usually quick preocedure  Important for ICU pt. who is at risk of developing imbalances between oxygen supply and demand  Fiberoptics tip is at the end of the catheter o What is this?  SVO2/SCVO2 – mixed venous oxygen saturation  SCVO2 = blood returning from superior vena cava (on a triple lumen -CVP)  SVO2 = blood entering the pulmonary artery (PA)  Normal is 60-80  SAO2 – overall oxygen saturation  VO2 – cellular oxygen consumption o Continuous monitoring is nice because it is sensitive and identifies early changes in the pt.  This is a measurement of the consumed oxygen. It is done in the vena cava before you get into the lungs to reoxygenate the blood  Balance between the venous oxygenation and the arterial oxygenation because of supply and demand  Normal o Normal Arterial O2 and high venous O2 = demand is low  You aren’t using o Normal arterial o2, and low venous O2 = high demand  Helps to determine the demand in the body of oxygen o Low arterial and high veonous = loooooow demand  Supply of oxygen o Respirations o Gas exchanges o Hemoglobin on the RBC o RBC count know the normal o Hematocrit o HR o Perfusion o CO o SV  Hemoglobin is the transport mechanism for oxygen transport  Id there is a decline in hemoglobin we will have a decline in oxygenation  If there is red blood cell loss, you will have changed effects on transportation etc.  If the heart is having a hard time meeting demands the heart is going to work harder  Increased need of oxygen (or decreased transport) will be compensated by increasing the HR to maintain the oxygen supply  Another mechanism of maintence is th use the oxygen reservoirs of the venous blood return o Could see a change in the SVO2 because of increased oxygen consumption o Indicated for crtically ill pts. with potential to develop imbalances of oxygen supply and metabolic tissue demands o  Cardiovascular Alterations o Cardiovascular disease  Public education  Need to teach them  Understand the pathophys of CVD  Disease processes  One of the leading causes of mortality in the US o d/t our lifestyle  Cardiac disorders seen in critical care o Coronary Artery disease  gender – males  men at younger age  women at older age  family history  Prevention if there is a family hx.  d/t genetics  increase age  45 years and older  abnormal cholesterol – hyperlipidemia  diabetes  sleep apnea  race  pathophysiology  development of atherosclerosis o fat deposits of cholesterol and lipids within the wall of the artery  plaque is on the wall and inflammation  high levels of LDL leads to inflammation and injury and moves onto the wall  HDL helps to remove LDL, good.  chronic inflamation o leads to inflammation and injury of the endothelium o endothelium is altered and becomes more reactive to platelets, firbrolynic factors, and leukocytes o leads to further complications of blood flow within the arteries. o Leads to narrowing of the arteries, eventually occlusion, or obstruction  As plaque develops they can break apart and cause a thrombosis in other areas o Something that helps  Poor circulation over a long period of time can help form collateral circulation  Acute is worse than chronic  If we can control cholesterol then the atherosclerosis will decrease  There can be plaque regression  Acute coronary syndrome  Angina o Types of angina  Stable angina  Precipitating event  Partial obstruction of the artery  There is an increased demand of the hearts need for oxygen, and the partial blockage prevents good oxygenation. So their heart starts to heart and is a warning that you are not getting enough oxygen o Lack of oxygen to the heart o Caused by increased demands (mowing law, stairs, etc). o Consistent, pattern,  Unstable angina  Pain does not go away when you stop the increased demand or take a nitro  There is not pattern o Worse chest pain o Requires immediate medical intervention  It continues  It is not consistent, does not go away with nitro  Care for unstable angina o Take a nitro o IF YOU ARE STILL HAVING PAIN AFTER THE FIRST NITRO CALL 911 after 5 minutes o Keep taking nitro every 5 minutes until EMTs come. Try to relax  Variant angina = prinzmental  Spasms of the coronary artery – come and go o Vasoconstriction of coronary arteries o May or may not have atherosclerosis  Happens at the same time of the day  Can happen at rest  Different than blockage of the heart  Silent ischemia  At risk = diabetes, open heart surgery  Don’t have pain because they can’t have chest pain, nerve o Symptoms damange  Can still see EKG damage but don’t have the same pain  Classic = chest, neck, arms, back, most commonly is pressure behind the sternum, radiate to left arm, back, shoulder, neck  Women are weird  Before beginning PCI then we are giving dual antiplatelet therapy with admission (combination of aspirin with another antiplatet)  Glycoprotein 2B3A inhibitor = antiplatelet o Abciximab (reopro), eptifibatide (integrilin)  Balverorootin = direct thrombin inhibitor  Clopitogril – loading dose, antiplatelet (Plavix)  Nursing management  Recognize MI  Relieve chest pain o Control angina o Watching over and monitoring o MONA  Maintain calm environment o Prevent pt. from being fearful and anxious o Be ready for acute situation  Education o Don’t strain – no Valsalva maneuver  No bearing down because it will increase intrathoracic pressure, decrease venous return, and that would decrease preload, etc, o Don’t stress out the pt. o Make sure to explain everything you are doing, EKG, and why you are going to cath. Lab o Teach pt. when they are stable  Teach risk factors  s/sx of angina  when to call physician  medications o Myocardial Infarction  Describes irreversible myocardial necrosis  d/t decrease/obstruction of blood flow through coronary arteries  often describe as acute MI  3 types o Plaque rupture o New coronary artery thrombosis o Coronary artery spasm o Goal – save/reperfuse heart tissue  Myocardial tissue is most likely to survive if it is treated within 2 hours of onset of s/sx  Processs o Nitro doesn’t work o EMS is called for chest pain o 12 lead EKG  Stemi or nstemi o Which hospital  Can they go to PCI? o PCI  90 –120 minutes  Or transfer within 120 minutes o Fibrinolytic therapy within 30 minutes o MONA  Morphine = pain and vasodilation  Oxygen  Nitro -= make sure to watch BP because it casuses vasodilation and will decrease preload  Aspirin  Chew it up and swallow to increase absorption  Pathophysiology  Three levels of injury o Ischemia – most outer area of damage to cardiac muscle  Interventions targeted towards saving viable muscles o Injury – potential viable o Infarction – dead muscle in the myocardial, not viable  T wave inversion is a sign of ischemia  ECG readings o A = Normal ECG reading o B = ischemia  T wave inversion o C = ischemia and current injury  T wave inversion and ST elevation o D = three levels of MI  Infarction = Q wave prolongation  Injury = ST elevation  Ischemia = T wave inversion o Identify MI based on location of the heart and layers of the heart  Layers  Epicardium – outer  Myocardium – middle  Endocardium – inner  Damage to the heart muscles, SA node, AV node, and perking fibers will cause a loss in normal heart contractions  See changes to MI cell sensitivity  Tachycardia – heart beating too fast, over 100  Bradycardai- heart too losw, under 60  Heart block  Specific portions of the conduction system are destroyed  Ventricular defirbrilatoin  Lethal  Seen within first 4 hours after pain  Premature ventriclular contraction  Ventricles contract early o Rupture  Rupture of heart strings and arteries outside the heart o Tamponade  Liquid fills pericardium and heart cannot expand correctly  Extra pressure on the heart so the heart quivers and can’t pump o Heart failure  Loss of Myocardial tissue means it can’t pump at all  Can have o Valve disease o Aneurysm of ventricle  Can have thnning of tissue sin ventricle over time after MI  Don’t havea normal recoil and instead blood bulges in the pockets o Dressler’s syndrome = pericarditis  Inflammation o Embolism  Blood clot could be due to blood sitting and pooling in the heart when it doesn’t contract right o Recurrence/mitral regurgitation  Valves may not fully close and you can’t move blood forward  Complications of MI  Heart failure o Pumping power of the heart has been diminished due to damage to the heart o Can be subtle or severe  Initially s/sx could be subtle but could get worse over time as it progresses o Right heart failure = edema, dependent edema, enlarged organs, JVD, systemic peripheral edema, organ edema, JVD - hepatomegaly o Left heart failure – pulmonary congestion, pulmonary edema, dyspnea, crackles, pink frothy sputum, crackles, SOB, dyspnea, pulmonary edema, decreased perfusion, pallor  Cardiogenic shock o Condition in which your heart suddently cant’t pump enough blood to meet your body’s need, not a lack of volume, heart just can’t pump like it should o There is a disconnect between oxygen supply and the body  When oxygen supply to tissues is inadequate to left ventricular failure  Avoided with quick treatment o Leads to death o Want to maximize oxygen, and reduce demand  Give coreg (beta blocker) - lebetolol  Relaxes the heart and makes it chill out and slow down – doesn’t use as much oxygen  Give beta blockers  Vasodilators - open up blood vessels so the heart is pumping against as much resistant  Treatment of MI o Diuretic – help with edema, get rid of fluids, less volume to go thorugh, lower blood pressure o Beta blockers – lower blood pressure, decrease workload by decreasing afterload, vasodilation o Oxygen – more oxygen to heart and body o Riase head of bed – increase breathing, less pressure on the heart o Reduce stimuli =- don’t stress out the patient o Reduce Valsalva - increases intrathoracic pressure, heart cant pump, oxygen isn’t as full o Stool softener – no straining o Morphine – relax, no pain o Oxygen o Nitrates o Antiplatelets – Plavix, aspirin - prevent clots    Papillary muscle dysfunction o Infarcted area involves/surrounds papillary muscle o Connects to mitral valve  Aspirin o Dysrhythmias prevention  Antidysrthmic  Amiodarone  Beta blockers o Prevention of ventricular remodeling  Give ACE or ARBs  Ventricular remodeling happens after an injury, this is left ventricular hypertrophy idea, want to prevent the heart from getting huge  Help decrease risk of heart failure  Nursing management o Nurse must implement management to help with oxygen o Balance of myocardial oxygen supply and demand  O2 via nasal cannula  How far can they walk, how often should they get up, moving,    o Prevention of complications  Monitor cardiac  Identify s/x of dysrhythmias  Identify s/sx of ischemia  s/sx of bleeding d/t antiplatelet  integilin, fibrinolytics o Depression after MI  Put life at risk, still at risk, affects ADLs  Change in appetite, sleep disturbance, mood changes  Patient education o Risk factor reduction o Manifestations of angina o When to call a physician or emergency services o Medications  Amiodarone – for dysrhythmias  ACE/ARBs with ventricular remodeling o Resumption of physical and sexual activities  Different form person to person  Follow up with doctor  Don’t want to ignore this o Work with cardiac rehabilitation  Cardiac rehab program  Enforce education o Sudden Cardiac death  Description  Higher incidence in men than women  Usually d/t abnormal rhythms o V. Tach to V. fib.  Etiology  Most often have Preexisting ventricular dysfunction o How long they are down changes how much damage happens  Usually from V fib. = ventricular is quivering and isn’t contracting o Need to treat with CPR and defibrillator o  Medical  CPR  Defibrillator  Stabilize o Heart failure  Description and etiology  Things that lead to heart failure: endocarditis, valve stenosis/regurgitation, cardiomyopathy, etc.  Effect the ventricles ability to meet the body’s needed cardiac output  Pathophysiology  Assessment and diagnosis  New York heart association criteria o Classifies heart failure symptoms  Determine underlying structural abnormality o The amount of ventricular remodeling over time  The more the more severe, the more s/sx o Severity of heart failure o s/sx o  Testing o Identifies structural changes o Echocardiogram – imaging to identify structures of heart, size of heart, s/sx of damage, valve damage o Labs  Assessment and diagnosis - not all pts. have the same type.cause of heart failure  Left ventricular failure o Failure on the left side of the heart  Sympathetic nervous systemic o Release of catecholamine’s (epi/norepi)  Increase heart rate, increase vasoconstriction, increase systemic vascular resistance and cardiac preload/contractility  Initially this is sorta helpful  Increases preload/volume to push out  But heart is having to pump out more and against more resistance  Ultimately causes damage  Renin-angiotensin aldosterone system (RAAS) o Causes vasoconstriction o Aldosterone causes retention of sodium – absorption of more water o decrease of potassium o overall  causes fluid retention, fluid overload  the body wants to increase volume, to increase preload, to increase CO  however, this makes the heart work harder  worsens the heart failure  Ventricular hypertrophy o Muscle increases in size to try and push against the SVR o This is causing remodeling o Causes ventricular dilation – leads to a floppy heart that has poor contractility  Ventricular remodeling  Heart failure s/sx  Dilated pupils  Pale/grey/cyanotic skin  Dyspnea – SOB with activity or rest  Orthopnea  Crackles  Wheezes  Decreased blood pressure  Cough, frothy sputum  Nausea/vomting  Ascities  Dependent pitting edema  Falling O2  Confusion  JVD  infarct  fatigue  tachycardia, S3 gallop  enlarged spleen and liver  decreased urine output  weak pulse, cool moist skin  BNP o Indicates HF  BNP – tells the heart hey this compensation isn’t working anymore, stop releasing epi/norepi and sop the RAAS. It’s only tiring us out more o Over 100 = releated to Heart failure, rather than respiratory issues  Pulmonary edema o Initially will probably have a hard time breathing at rest, but the worse pressure will increase fluids leaking into alveoli which affects gas exchange o ABG’s will be effected  Hyperventilation – will pour off CO2 (acid) and will be intitally respiratory alkalosis  Overtime breathing becomes impaired and they will have slow labored breathing and will be in respiroatory acidosis  As they become more serious, decreased ejection fraction (<30%) o Will have dysrhythmias – specifically VT, or VFib.  Ventricle can’t provide CO  Vfib – quivering, no pulse  VT – may or may not have a pulse  AFib – common, atrium is quivering, not a strong contraction  Will be on a blood thinner to prevent clots  Will also be on digoxin to keep HR under control  Beta blockers - look up  Medical management of heart failure  This is progressive disease that isn’t going to get better, just want to slow progression  Relief of symptoms and enhancement of cardiac performance o Want to relieve s/sx o Correct causes of HF o Manage fluid overload o Cardiomyopathy  Description and etiology  Disease of the heart muscle  3 categories o Hypertrophic  Genetic disease  Autosomal dominant trate  Will have a big thick muscled wall around the ventricule which prevents it from filling like it needs to o Dilated  Dilation of both ventricles w/o muscle hypertrophy  Could have several causes including ischemia, MI, genetic, idiopathic, vavle heart dysfunction, bacteria/viral infections, myocarditis,  Reduced ejection fraction o Restrictive  Least common in developed countries  Involves abnormalities of the dystolic function  Ventricle can’t relax/open and fill like it should     Similar s/sx as heart failure and will lead to heartfilue  Nursing management  Will mimic heart failure management  Depends on types  Stable fluid balance  Increase mobility  Pharmacology  Education  Patient education o Hypertensive emergency  Description  Hypertensive emergency - high blood pressure with potentially life threatening s/sx indicative of acute impairment of one or more organ systems in cluding the CNS, heart or kidneys (>180/120)  Hypertensive urgency – high blood pressure (>180/110) with minimal to no s/sx of acute organ damage  Etiology  No prior history o No history of hypertension, but all of the sudden have these and issues with renal failure, aortic dissection and, and leads to hypertension  Noncompliance or inadequate medication therapy o Big issue if pts. are not taking their medications appropriately  Medical management o Hypertensive emergencies  Acute blood pressure elevation greater than 180/120 mm Hg,  May include s/sx of CNs or cardiovascular compromise  Acute kidney failure, or catecholamine excess  Medical management – medications  Nursing management = monitoring s/sx and meds  BP over 180/120  Admitted to ICU  Need to monitor ECG  Continuous arterial line  Goal is to lower blood pressure  Prevent organ damage  Can’t lower it too quickly (more than 20-25% over a few hours)  Common meds  Nitroprusside/nipride = continuous IV drip o Half life is just seconds, so if BP is lowered too fast, then it would reverse really fast o Need to be careful because you can’t let this medication run out o Always have an extra bag on hand o Never let it run dry – don’t let air run in the line because priming takes too much time o Always be checking this bag o Make sure not to put in volume entirely with bag so warning bell before it goes out o This medication is titrated based on the blood pressures = doctor will probably write parameters for you to titrate  Other continuous o Nitroglycerin o Lasix- with extra fluid on board  Other meds o IV push labetolol – beta blocker o Enalopril - Ace o Anticoagulants  Affects thrombin formation  Prevent clot formation  Coumadin, heparin o Firbinolytics  Affect the fibrin and actually break down the clot  Fibrinolytic medications/agents o Streptokinase (SK)  Systemically, not clot specific  Long half life – 20-25 minutes  Issues with bleeding o Tissue plasminogen activator (Tpa_  Altiplase  Short half life 3-4 minutes  Helps with opening up coronary blood artieries by busting clots  Fibrinolytic therapy o Recombinant plasminogen activator (Rpa)  Retiplace  Longer half life  Given as double bolus  Not weight based o Tenecteplase (TNKase)  Fibrin specific  Single bolus  Weight based  Very specific  Slow plasmic clearance o Outcomes  Normal blood flow, no obstruction  Risk of bleeding  May have increased risk of bleeding with combinations of meds  What to watch for? o Change in LOC, unable to arouse, confusion,  Evidence of reperfusion hernation in brain o Pain and reperfusion dysrhythmias  Chest pain goes away  Pt. will have reperfusion dysrhtymias  Short amount of time  Need to monitor ECG  Watch for deterioration  Unlikely you need meds., but be prepared for meds o ST segment  Will return to normal and go to baseline  If not normal in 60 minutes then it was a failure o Cardiac biomarkers  Cardiac enzymes will have dramatic fall with reperfusion o Fiibrinolytics  Will break up clot, but we will need further interventions  PCI/CABAGE  Nursing Management o Candidate identification  Is the pt. able to do this?  12 hours of chest pain, ST elevation, etc. o Patient preparation  Baseline labs  Baseline EKg  PT/INR  Head injuries/recent surgeries  Give IV  Cardiac labs o Assessment  Hemorrhage –watch for s/sx of bleeding  Limit activities that have high risk of bleeding  Look for reperfusion o Bleeding  Patient education o Fibrinolytic therapy  Risk  Why we gave it  Minimizing risk of bleeding o Bleeding  Cerebral hemorrhage – life threatening  Watch LOC and notify physician immediately  Percutaneous Coronary Intervention (PCI)  Indications for catheter interventions (include catheter procedures like stent placement, balloon angioplasty, arthrectomy) o Tell pt. not to strain o Late complications  Restenosis  Dual antiplatelet use  Higher risk –complex lesion, multiple arteries, diabetes, d/c meds.  Late thrombosis o Make sure to keep limb from catheter straight for 4-6 hours (no flexion of the himp) because of increased pressure and bleeding  Nursing management for stent placement  Watch for recurrent angina o During procedure it is normal to have angina o Could recure after procedure with irriation or it might be more serious o If not perfusing = ST elevation = MI bad o If pt. is complaining of angina = indicate MI  Renal perfusion o Risk for kidneys d/t contrast during PCI o Make sure to protect kidneys  Well hydrate pt. before procedure  Hydrate pt. after to flush kidneys out  Increase blood flow o Prior to PCI give sodium bicarbonate to protect kidneys  Vascular site care o At risk for bleeding  Monitor site for bleeding and hematoma  d/t anticoagulants during procedures  VS show s/sx of bleeding o Peripheral ischemia  Site of cath. Should be monitored  Prevent it with HOB at <30 degrees  Keep cannulated limb straight  P’s = nervovascular checks  Pulse, pressure, pallor, paralysis, pain, paresthesia, temperature o Bed rest isn’t as long o Move earlier o Still need neurovascular check o Make sure there is not hematoma  Patient education o Medication regimen  How long to take, follow up etc. o Risk factors  s/sx of obstruction and when to call  angina o refer to cardiac rehabilitation o Percutaneous valve repair  Used for pts. who cannot doo surgery  Hemodynamically unstable  Too many problems  Balloon valvuplasty  For aortic stenosis  Restenosis in 6 to 12 months  Only for too high risk  Transcether aortic valve replacement  Used for severe stenosis  Prosthetic valve in place of bad valve loaded on a stent  No sturues  Complications d/t complex procedure o Vascular complications  Takes a large sheath to get valve right  Femoral artery is used o Regurgitation  Assessment o Hemodynamic stability o Stroke monitoring o Monitor s/sx kidney injury – contrast o Monitor for dysrhythmias o Cardiac Surgery  Coronary artery bypass surgery (CABG)  Bypass an occlusion with a vein or artery o Artery is best - internal mammary artery, radial artery o Common vein – saphenous vein o When harvesting you can use open or endoscopic approach  Valvular surgery  Valve repair o Preferred over replacing because of long term use of anticoagulants  Valve replacement o Prosthetic valves vs. mechanical