Final Complex Care Study guide

Care of the Patient with Renal Compromise


  1. How does AKI differ from chronic renal failure?
    • Shorter time period
    • more severe changes in hemodynamics and electrolytes
  2. Review prerenal causes, intrarenal causes and postrenal causes.  Which is the most common cause of AKI?  Know examples of each.
    • Most common causes of AKI: Hypovolemia, Hypotension, Nephrotoxic drugs.
    • Pre: impaired perfusion to kidneys, hypovolemia, hypotension
    • Intra: Acute tubular necrosis, Nephrotoxic drugs, Glomerulonephritis
    • Post: Rare, Kidney stone blockage, BPH blockage, Neurogenic bladder.
  3. Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI – what are some common causes of ATN?
    • Poor perfusion through hypoxia or low blood flow, and nephrotoxic drugs.
  4. What are the three phases of AKI’s clinical course? What do you monitor in each phase of AKI?
    • Oliguria: Low urine output, Increased Potassium and creatinine, increased Ca, low to normal Na,
      • Monitor: fluid and electrolyte balance, High K and Cr
    • Diuretic: High urine output, Decreased Potassium, lowering creatinine, Dehydration
      • Monitor: Fluid and Electrolyte balance
    • Recovery: Normalizing Urine output, normalizing Potassium and creatinine,
      • Monitor: Fluid and Electrolyte balance,
  5. Generally, how long does the oliguric phase last?
    • 10-14 days and starts in 1-7 days
  6. What are the diagnostics used to diagnose AKI?
    • Urine output decrease, High Creatinine
  7. What are the priorities of care of the whole healthcare team for the AKI patient?
    • Normalizing the Potassium levels, replacing fluids.
  8. What are the nurse’s priorities for the AKI patient?
  • Fluid and electrolyte balance
  1. What are the types of dialysis? What are the advantages and risks with each type of


  • HD: need a fistula for long term access, Central line for short term fast access. Blood is filtered through a filter in a machine outside the body. this takes hours at a hospital setting about three times a week.
  • PD: dialysate put into the peritoneum, absorbs waste products and excess electrolytes then is drained. This takes a few hours, multiple times a day.
  • CRRT: continuously connected to a machine that filters the blood.
  1. What are the contraindications for peritoneal dialysis?
    • Peritonitis, abdominal cellulitis, maybe abdominal hernia or adhesions
    • Patient causing infection a certain number of times per hospital policy.
  2. How is continuous renal replacement therapy (CRRT) different from hemodialysis?
    • CRRT: Slow continuous replacement of blood replacing the need for kidneys
    • HD: about three times a week, pt needs to tolerate faster fluid shifts,
  3. When is CRRT contraindicated?
    • The need for emergent hemodynamic stabilization such as high potassium and pericarditis




  1. General concepts of when patients become eligible for organ donation
  • Neurologic death/Brain death, with viable organs.
  1. Organ donation process
  • Patient needs to be perfusing organs, needs to be a donor or family needs to be ok with it.
  1. Role of immunosuppressive agents with organ transplant
  • Suppresses the immune system so that the host does not reject/attack the organ.
  1. Management of the transplanted organ to include HLA matching
  • HLA matching looks at the donor tissue and the host blood to see if the antigens from the donor will be recognized by the host as self instead of non self.


Valvular Heart Disease

  1. Describe the pathophysiologic changes associated with mitral valve stenosis, regurgitation.
  • Mitral Valve stenosis: valve leaflets fuse together and cause a decrease in the blood flow across the valve. Most commonly caused by rheumatic heart disease.
    • Diastolic murmur, loud S1, exertional dyspnea, palpitations, and fatigue.   
  • Mitral Valve regurgitation: incomplete closure of the valve leaflets causing blood to flow backward from the left ventricle to the left atrium. caused by Rheumatic heart disease, endocarditis, cardiomyopathy, and issues with the chordae tendinea
    • s/s: systolic murmur, pulmonary edema, cardiogenic shock
  1. Describe the pathophysiologic changes associated with aortic valve stenosis, regurgitation.
  • Aortic Valve Stenosis: Stenotic valve between the aorta and the Left Ventricle.
    • Systolic murmur, Soft S1,S2, and impressive S4
    • s/s: Angina, Syncope, dyspnea on exertion.
  • Aortic Valve Regurgitation: Floppy valve causing backflow from the Aorta to the LV.
    • Diastolic murmur
  1. Describe the signs/symptoms associated with valvular heart disease. A diastolic murmur is heard with which valvular heart disease?  A systolic murmur is heard with which valvular heart disease? What is the patho associated with each type of murmur?
  • Diastolic murmur in Aortic Regurgitation.
    • During LV diastole blood flows back through the incompetent aortic valve causing a Diastolic murmur.
  • Systolic murmur in Aortic Stenosis
    • During LV Systole the small opening in the stenotic valve causes turbulent blood flow causing the murmur to occur.
  • Diastolic Murmur in Mitral Stenosis
    • During atrial contraction and LV relaxation the small irregular opening in the stenotic mitral valve between the two chambers creates turbulent blood flow creating the murmur.
  • Systolic murmur in Mitral Regurgitation
    • During LV systole blood flows normally out of the aortic valve, but some also goes out of the incompetent mitral valve back into the atrium. This causes turbulent blood flow during Systole.
  1. Describe the assessment, diagnostics and treatment of valvular heart disease.
  • Assess for murmurs, syncope, angina, dyspnea, and any other s/s mentioned above.
  • diagnostic: Chest XR, CBC, ECG, transesophageal echo, cardiac Cath
    • These tests look for the size of vessels and heart chambers, as well as arrhythmias, and pressure changes in the heart.
  • Treatment:
    • Meds: vasodilation(nitro), positive inotropes (digoxin), Diuretics, Anticoagulation, antiarrhythmics, beta blockers,
  1. How does a mechanical valve differ from a biologic valve in terms of anticoagulation therapy?
  • Mechanical valve will need anticoagulation therapy as long as the valve is in use.
    • Risk for hemorrhage with the anticoag therapy.
  • Biologic valve will not need anticoagulation therapy.
  1. “All roads lead to heart failure”.  How is this true for valvular heart disease?  How does this translate into your bedside assessment of the patient with valvular heart disease?
  • Increased work of the heart in all valvular issues causes hypertrophy and decreasing CO. This leads to a backup of blood into the pulmonary vasculature and left sided.
  • Assess for progression of the disease by looking at the patient’s effort doing tasks over time.


Endocarditis, pericarditis, tamponade

  1. What are the pathologic changes associated with endocarditis?  Depending on what valve is involved, what S/S would you see?
  • Endocarditis: Infection of the endocardium usually the heart valves.
    • Strep viridans and staph aureus are the most common types.
    • Effects Left heart 90% of the time, and usually the mitral valve.
    • s/s: new murmur or change in existing murmur, Fever,
    • Right valves are effected at the lower percentage and are correlated with IV drug use.
    • Subacute: Slow and long course, patient usually has a pre-existing heart valve issue.
    • Acute: faster progression of the illness, may not have a pre-existing heart valve issue,
  1. What are the potential complications of  endocarditis?  Would you be able to recognize these complications clinically?  
  • Embolization of a portion of the vegetation: Thrombotic stroke from a vegetation embolus of the bacteria, micro emboli in Kidneys extremities and spleen if the infection is originating on the left side of the heart. If originating on the right side of the heart pulmonary issues are a risk factor.
  • decrease cardiac output due to the infection affecting the valves.
  1. What questions are especially important to ask in taking a history of the patient with   endocarditis?  What are the clinical manifestations of endocarditis?
  • Risk factors: Cardiac conditions, artificial heart valve, IV drug abuse, Bacteremia, Intravascular devices,
  1. What is the treatment of endocarditis?
  • antibiotic therapy
  • prophylactic therapy if the patient is a high risk and has a:
    • GI/GU infection, Dental procedures, and respiratory, tonsil, or adenoid incisions.
  • antimicrobial treatment continued until the patient’s blood cultures come back negative, are afebrile, and have no s/s of endocarditis or heart failure.
  1. What are the physiologic changes that occur with tamponade?  How do these correlate with physical S/S?  Would you be able to tell if your patient was experiencing tamponade?  How?  How is tamponade treated?
  • The pericardium gets inflamed and fluid gets in between the pericardium and the heart decreasing the heart’s ability to fully relax causing a decrease in CO.
  • there will be an narrowing of blood pressure, tachycardia, tachypnea, pulsus paradoxus, and muffled heart tones.
  • Treat with a pericardiocentesis to remove the fluid.
  1. What are the physical S/S of pericarditis?  What are some nursing intervention for the patient with pericarditis?  
  • Pericarditis: inflammation of the pericardium, the sac surrounding the heart.
    • Normal fluid around heart is 15-30ml
    • Increased chest pain with inspiration
    • due to: infection, uremia, acute MI, Trauma, Dissecting AA, Auto immune, Rheumatic diseases, and some medications.
    • s/s:ST elevation on all leads, Echocardiogram to see thickness of pericardial tissue, chest x-ray will show large cardiac shadow, Pericardial tamponade,
    • Pulsus paradoxus – an exaggerated decrease in Blood pressure upon inspiration, greater than 10 mmhg. (you need an arterial line to monitor this.)  
  1. What are the complications associated with pericarditis?
  • Tamponade
  • Pericardial effusion




  • Describe causes of burns and types of injuries it causes.


    • most common cause is flame, then scalding injury.  
  • What are the general principles of burn care?  Know priorities for care in the emergent, acute, and rehabilitation phases.  
    • Phases of burns
      • Emergent first 48 hours
      • Acute – weeks to months
      • Rehabilitation phase – over two years


  • What are the systemic effects of burns?  What type of shock happens with burn patients?  How would the nurse recognize these effects?  What treatment would the nurse anticipate?


    • Electrical injuries – internal burning,visible burns on an entry point and exit point.
      • Deep muscle and nerve injury
      • Difficult to assess the extent of the injury
      • Patient can have rhabdomyolysis and compartment syndrome (five P’s are the s/s for compartment syndrome.)
  • Chemical burns
    • Irrigate the burn to get the chemical out
  • Tar burns
    • Cool the tar then we use oil to get the hard tar off.
  • Frostbite
    • Can regain vasculature to fingers and toes with tPA if treated under 24 hours from injury.


  • What are the special considerations for electrical, chemical, and inhalation burn injuries?


  • How do you assess and what are potential consequences of burns and fluid resuscitation?
    • Fluid resuscitation in burns
      • 2 ml of LR*TBSA*KG
      • Need 30-50 ml/hr of urine output
  • What are risk factors for inhalation injury? Complications? Nursing priorities and concerns?
    • Airway management!
    • inflammation/incompetence of the airway.
  • What are nutritional, pain, and functional concerns for burn patients?
    • Increased nutritional specifically protein due to hypermetabolism
    • Pain needs to be treated on a patient by patient basis and needs to by IV during debridement to control the pain.
    • Bolus or PO pain before debridement
    • Physical therapy is needed to prevent contractures.


Emergency Department Care and Bioterrorism

  • When is a tetanus injection given in the ED?
  • Give when the patient has had less than three doses, unknown doses, 6-10 years since last dose and have a moderate or major trauma, or more than 10 years since last dose.


Emergency severity index 1-5 one being the most severe.

  • 1: Immediate life saving intervention: obvious threat the body or organ
    • MI (cardiac arrest), overdose, severe respiratory distress, intubated trauma patient.
  • 2: High risk: stability of vital functions threatened. likely threat to bod but not always obvious. seen within ten minutes. continuous monitoring, multiple diagnostic studies,
    • chest pain from ischemia, nonresponsive trauma,
  • 3: Two or more resource: stable patient, life or organ threat is unlikely but possible. need to be seen by physician within one hour. medium to high resourses. Hanging fluids will get you here.
    • abdominal pain or gynecological issues (unless severe), hip fracture in older patient.
  • 4: One resource: stable patient with no threat to life or organs. one diagnostic study like x-ray or intervention like sutures, lab studies,
    • lacerations, or closed extremity trauma.
  • 5: stable patient with no life of organ threat. examination only
    • colds, minor burns and wounds, prescription refill.

color system

  • Black: no resps with open airway, no pulses
  • Red: resp > 30(45 for peds),  no radial pulse, altered mental status, cap refill greater than 2
    • control bleeding and open airway before moving on.
  • Yellow: have pulse, can follow commands,
  • Green:  minor injury, walking wounded.

Shock States

  • Underlying pathologic problem with all shock states, knowledge of the various shock states and how you identify, assess, intervene, and anticipated treatment options, to include priority interventions and knowledge of SvO2/ScvO2.  
  • Shock: a decrease in adequate tissue perfusion from low blood pressure.
    • types: Cardiogenic (heart problem), Hypovolemic(low intravascular fluid volume), Distributive (maldistribution of circulating blood), Obstructive (physical blockage to flow)
  • Changes in venous O2 or Arterial O2 (SvO2 vs ScvO2)
  • Increased O2 delivery from: increased SaO2, Increased HGB, Increased cardiac output
  • Decreased O2 consumption: decreased need(hypothermia), access(vasoconstriction), and capability(tissue death)
  • Decreased O2 delivery: decreased O2 sat, decreased HGB, decreased CO
  • Increased


  • Review categories of vasoactive, vasodilator, and inotropic agents.
  • Vasoactive: Epinephrine, Dopamine, phenylephrine.
  • Vasodilator: Nitroglycerin (to decrease after load in cardiogenic shock)
  • Inotropic: Digoxin
  • Principles surrounding the purpose, insertion considerations, use, and monitoring principles of Arterial Lines and Central Venous Catheter lines; no questions on pulmonary artery catheter lines.
  • Arterial Lines:
    • Arterial blood pressure. Catheter inserted into the radial or femoral arteries usually. The tubing is pressurized to overcome the arterial blood pressure. To get an accurate reading the fixture that measures the pressure must be level with the patient.
    • Can draw ABGs more frequently if the patient has an arterial line.
  • Central venous catheter lines:  central venous pressure. Venous central line that measures end vena cava pressure. can also measure venous labs to compare blood gases to arterial gases.
  • What is shock?
  • Shock: a decrease in adequate tissue perfusion from low blood pressure.
  • How do you know what type of shock a patient has? what are the priority interventions for the different shock states?
  • Look at the patient’s vital signs, and history to see if there are risk factors present of a specific type of shock.
  • What do ScvO2 numbers mean?
  • Indicator of global tissue hypoxia, 70-80% indicates stable oxygen balance
  • High SvO2/ScvO2 from increased oxygen delivery (increased SaO2, Hgb, CO) and decreased oxygen consumption (decreased metabolism – hypothermia, access – vasoconstriction)
  • Low SvO2/ScvO2: tissue extracting oxygen faster than can be delivered
  • What are the different categories of drugs? concerns? names of some of these drugs in the categories?
  • Vasopressors – Norepinephrine, Dopamine, Vasopressin
    • Water retention and increased systemic vascular resistance via vasoconstriction, make sure fluid resuscitation has occurred first
      • Increased afterload
      • Watch for MI/heart failure, esp. for cardiogenic shock
    • Administer slowly while monitoring MAP
  • Inotropic agents – Epinephrine, Dopamine, Dobutamine
    • Increases contractility, but also myocardial demand, of heart
  • Vasodilators: indicated for cardiogenic shock to decrease afterload
  • What are the phases of shock states and how do you assess the patient?
  • Compensatory: generally little/no clinical s/sx
    • SNS activated to compensate for initial drop in BP/CO
  • Progressive: compensatory mechanisms and systems begin to fail
    • Massive SNS input causes vasoconstriction
    • Decreased BP, increased HR/RR
  • Irreversible: increased waste products from MODS, cessation of cellular mitochondrial function
  • What is MODS?
  • Multi-Organ Dysfunction Syndrome
    • Failure of 2 or more organs
    • Need to support or bypass the dysfunctional organs
    • Treat or prevent new infections
    • poor prognosis when this stage is reached.


Cardiogenic up down Up w/ crackles down down
Hypovolemic up down Up then D down down
Neurogenic down down dysfunction dysfunction Normal to high
Anaphylactic up down up incontinence Normal to high
Septic up down up Down (none) Down, increased late
obstructive up down up down Normal to down



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