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

      dialysis?

  • 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

 

Transplant

 

  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

 

Burn

 

  • 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.

 

Shock HR BP RR UO SVO2
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

 

Complex Care Session 10: hemodynamic monitoring in shock

Session 10: hemodynamic monitoring in shock

 

MAP: mean arterial pressure (average of systolic and diastolic BP)

  • We want it above 65 mmHg 

Systolic BP: want this to be above 90 mmHg in most cases for adequate perfusion

 

Pulse pressure

  • SBP -DBP: greater than 40 is vasodilation. Less than 40 is vasoconstriction.
    • In septic shock there is vasodilation
    • In cardiogenic shock there will be vasoconstriction.

 

CVP – central venous pressure. Venous central line that measures end vena cava pressure.

ABP – 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.

 

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

 

Shock:

Shock HR BP RR UO SVO2
Cardiogenic up down (Low PP)  Up w/ crackles down down
Hypovolemic up down (Low PP)  Up then D down down
Neurogenic down down (high PP) dysfunction dysfunction Normal to high
Anaphylactic up down (high PP) up incontinence Normal to high
Septic up down (high PP) up Down (none) Down, increased late
obstructive up down (Low PP) up down Normal to down

 

Cardiogenic shock: pump issue

  • Decreased stroke volume, decreased stroke volume
  • Causes MI, arrhythmias,
  • s/s: tachypnea, crackles, anxiety,

Hypovolemia: decreased fluid volume

  • absolute hypovolemia: hemorrhage, DI, Diuretics
  • Relative hypovolemia: fluid moving out of the vasculature into extra vasculature. Burns and liver failure.
  • Increased HR, CO, RR
  • Decreased: SV, CVP, PAP (pulmonary arterial pressure)
  • The body can compensate for about a 15% volume deficit

 

Distributive: poor distribution of circulating blood.

  • Neurogenic shock:
    • T6 or above trauma
    • Hypotension, bradycardia, vasodilation relative hypovolemia,
  • Anaphylactic reaction
    • Profound vasodilation, capillary permeability, edema, leading to bronchospasm
    • Angioedema(facial swelling), hives

obstructive:  physical blockage to flow.

  • Cardiac tamponade
  • Pulmonary embolism

 

Complex Care Session 9: Burns

Session 9: Burn

 

Prevention of burn injuries is the top priority

Most common is to get burned by a flame, and next highest is scalding

 

  • Burns are often measured by percentage of total body size
  • Most common complications associated with burns are: in adults, Cellulitis uti and pneumonia, and in older patients tend to get wound infection and pneumonia.
  • Only give antibiotics if there is a high risk of infection, or signs of infection.
  • Depths of burns
    • Superficial, partial thickness, 1st degree: still have hair that is anchored,
      • Caused by, sun, and minor heats
      • Treat with: aloe vera, NSAIDS, no alcohol, benadryl.
    • Deep partial thickness, second degree: loose sweat glands, and hair follicles, has blisters
      • Takes 10-21 days to heal
      • May need skin grafts
      • Need to wait 24 hours to see how deep the burn really is
      • Deroof blisters that are greater than 2 cm
    • Full thickness 3rd and 4th degree: down to the fat layer.
  • Inhalation injury – priority is maintaining the airway.
  • Steven johnson’s – less than 10% of of total body
    • Not very bloody, sloughing off of skin
  • Tens – Affects greater than 30% of total body surface area.
    • Very bloody, Sloughing off of skin.
  • Amniotic graft tissue can be used for grafting over the eyes. This tissue is taken from donated placenta.
  • 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.
  • Phases of burns
    • Emergent first 48 hours
    • Acute – weeks to months
    • Rehabilitation phase – over two years
  • Fluid resuscitation in burns
    • 2ml of LR*TBSA*KG
    • Need 30-50ml/hr of urine output
  • Greater than 20% burn we will gown and glove to prevent infection of the patient.
  • Compartment syndrome – swelling of a compartment and the pressure will need a escharotomy or fasciotomy to relieve pressure.
    • 5 p’s for compartment syndrome: Pulseless, paresthesias, pallor, PAIN, paralysis.
  • Graft types
    • Autograft – patient own skin
    • Allograft – cadaver skin
    • Xenograft – pigskin
    • CEA – cultured epithelial cells
  • Sheet graft – one continuous piece of skin
  • Mesh graft – take the sheet and poke holes in the skin then stretch it out.
  • Meds used:
    • Increased need for pain meds due to the hypermetabolic state.
    • Antianxiety: benzodiazepines,
    • Beta blocker
    • Anabolic steroid – oxandrolone, growth hormone
      • Used for months to promote tissue growth.

Complex Care Session 8: Endocarditis, Pericarditis, and valvular diseases.

Session 8: Infective endocarditis, pericarditis, and valvular diseases.

 

Valvular diseases:

  • 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
  • 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.
    • The aortic valve has two “os” (openings to the coronary arteries) that feed the coronary arteries.
  • Aortic Valve Regurgitation: Floppy valve causing backflow from the Aorta to the LV.
    • Diastolic murmur
  • Treatment: Lower BP and increase CO
    • Meds: vasodilation(nitro), positive inotropes (digoxin), Diuretics, Anticoagulation, antiarrhythmics, beta blockers,

 

  • 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,
    • 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 right side of the heart. If originating on the left side of the heart pulmonary issues are a risk factor.
    • 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,
    • Risk factors: Cardiac conditions, artificial heart valve, IV drug abuse, Bacteremia, Intravascular devices,

 

  • 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.)  
      • This is caused by cardiac tamponade, the fluid that builds up in the pericardium causes pressure changes that decrease the stroke volume of the left ventricle. The right ventricle presses the septum towards the left ventricle causing decreased stroke volume.

 

Test 2 Study Guide Complex Care

  1.   What measurements are used for ECG interpretation? Do you know the normal measurements ?  How do these measurements correlate with what is going on in the heart?
  • The waveform is made up of peaks and valleys that are designated as the letters P through U. Each letter corresponds to a specific part of the Waveform.
  • P wave – Atrial depolarization, rounded and shorter than the QRS complex
  • PR interval – Measurement from the beginning of the p wave to the beginning of the QRS
    • Normal is 0.12-0.2 seconds
    • This is the time is takes for the impulse to travel from the SA node through the AV node and into the ventricles.
  • QRS – ventricular depol, less than or equal to 0.12 seconds
  • ST segment – end of V Depol to the beginning of V Repol
    • Elevation correlates with myocardial infarction
    • Depression correlates with ischemia
  • T – ventricular repolarization
  • QT interval – total duration of depol and repol
  1.   What do these measurements mean to you as a nurse caring for a patient with dysrhythmias?
  • The normal measurements indicate the normal amount of time that it should take for an electrical impulse to do its specific task. Such as Atrial or ventricular depolarization. If the time the impulse takes is increased there may be decreased CO, or increased work of the heart and lungs.
  1.   What are the nursing responsibilities for a patient with a specific dysrhythmia (you will be responsible for only the dysrhythmias we discussed in class).
    • Be able to Identify the rhythm and dysrhythmia
    • See if the patient is tolerating the rhythm ie. Has pulses, awake, oriented, vital signs and breathing normally.
    • When to defibrillate a patient
    • When to use Electro Synchronized cardioversion on a patient.
      • There need to be R peaks in a QRS complex.
      • The shock is automatically delivered on an R peak.
      • There needs to be a pulse
    • what to do with a specific rhythm
      • Sinus Brady that is not tolerated: All Trained Dogs Eat: Atropine, Transcutaneous pacing, Dopamine, Epinephrine
      • Sinus Tach: Beta blockers to reduce rate, If the rate if still uncontrolled Adenosine can be given FAST 4 second push. Adenosine will stop the heart and hopefully restart in a better rhythm.
      • Atrial flutter – saw tooth
        • One ectopic foci that is discharging an impulse at 250-400 times per minute
        • F waves no P waves
        • Saw tooth f waves
        • Need to be on anticoagulants to prevent clots forming in the turbulence of the atria.
        • Controlled is a HR less than 100 uncontrolled is over 100

 

  • Unstable will need Synchronized Electrocardioversion, beta blockers, Vagal maneuver

 

      • Atrial Fibrillation
        • Multiple ectopic foci that are discharging at 250-40 times per minute
        • Most common clinically significant dysrhythmia

 

  • Most common cause of an ischemic stroke.

 

        • Need to be on anticoagulants to prevent clots forming in the turbulence of the atria.
        • Controlled is a HR less than 100 uncontrolled is over 100

 

  • Unstable will need Synchronized Electrocardioversion, beta blockers, Vagal maneuver

 

    • Heart blocks
      • 1st degree
        • Consistent Long PR interval over 0.20
        • Do not treat usually do to lack of signs and symptoms
      • Second degree type one, or wenckebach, or Mobitz 1
        • AV node conduction issue
        • Progressively increasing PR interval until a QRS is missed and the arrhythmia start over
        • Usually asymptomatic
      • Second degree type II, or Mobitz II
        • Normal PR interval with a dropped QRS every so often
        • Monitor for a third degree heart block
      • Third degree heart block
        • No communication between the atria and ventricles
        • Need a pacemaker, from the cath lab
    • Ventricular dysrhythmias
      • PVC – Premature ventricular contraction
        • Can be normal and untreated
        • Bigeminy – on pvc for one normal
        • Trigeminy – two PVC for every normal PQRST
        • Causes – hypoxia
        • Amiodarone is the drug of choice
      • V Tach –
        • Can cardiovert
        • Can easily turn into V fib
        • Pulseless we will defibrillate
        • Large sharp “QRS” complexes one immediately after another with no breaks
      • V Fib
        • Defibrillate to hope the SA node takes over
        • Smooth rapid continuous electrical activity with no breaks
        • Cannot cardiovert
        • AICD is an internal defibrillation device
      • PEA
        • Pulseless electrical activity
        • Give fluids and epi
      • Asystole
        • Straight line on the ECG

 

  1.   How do you know if a patient is hemodynamically compromised with a cardiac dysrhythmia?  Would you know what to do ?
  • Blood pressure changes, Heart rate changes, LOC decrease, pulselessness, reporting symptoms of chest pain or classic MI symptoms.
  • Yes, treat the problem if the patient is showing symptoms, and sometimes even if there are not.
  1.   How does defibrillation differ from cardioversion?  What is the nurse’s role in each?
  • Synchronized cardioversion – synchronized shock on the R wave
    • Need an R wave
    • Can convert them out of A flutter, fib, or V Tachycardia with a pulse.
    • May keep them in sinus for 3-6 months
    • Amiodarone Is used to prolong the time in sinus
    • May throw a clot that was in the atrium once the rhythm converts back to sinus.
    • Get a transesophageal echocardiogram to look for clots.
  • Defibrillation
    • An electric shock that is delivered and does not have to be synchronized
    • Rhythms to shock: Pulseless V Tach, V Fib
  • Cannot shock or cardiovert: PEA, Asystole

 

  1.   When is the use of an ICD warranted?  What is the patient education associated with ICD?
  • Implantable Cardioverter-defibrillator
  • when it senses a specific arrhythmia the device charges and delivers a shock.
  • A patient that can have an ICD is someone that has survived VT/VF, or at high risk for VT/VF after a surgery and cannot tolerate the medication or ablation.
  1.   Be able to identify the ECG dysrhythmias we discussed in class by their defining characteristics.  Identify treatment of specific dysrhythmias.
  2.   Pacemakers:
  • Review the patient and family teaching guidelines
  • What are the nursing interventions after a pacemaker is inserted?
  • What are the indications for a pacemaker (permanent and temporary)?

 

Endocrine

 

  1. What S/S are involved in DKA?  HHS?  What is the pathophysiology behind these S/S?
    • DKA
      • Ketones in the urine and blood
      • More common in DM1 but possible in DM2
      • s/s dry mucous membranes, tachycardia, hypotension, Kussmaul respirations, glucose over 250, dehydrated Altered LOC.
      • HypoKAlemia, HypoNatremia,
      • The cells cannot take in glucose so they must metabolize fats, which causes a waste product of Ketone acid.
      • Give Insulin and monitor electrolytes and replace any that are out of normal, Give bicarb
    • HHNS
      • No Ketones present
      • Common in DM2 or infections
      • s/s: NO ketones production, GLU > 600, Dehydration, hypotension, serum osmolarity >320 mOsm/L

 

  • FIRST THING TO GIVE: FLUIDS!!!!!, then insulin

 

    • Not giving BiCarb
  1. How does DKA differ from HHS?
  • DKA – production of ketones, blood sugar levels > 250, Usually DMI, pH<7.3, CO2 and HCO3 low, osmolality <320
  • HHNS – no ketones, blood sugar > 600, usually DMII, pH>7.3, CO2 and HCO3 levels normal, osmolality >320
  1. How is DKA treated?  HHS?  What are potential complications of DKA and HHS?
  • DKA – give Fluids, insulin, potassium(electrolytes), then bicarb if needed
  • HHNS give Fluids while keeping electrolytes in balance, then insulin.
  1. Differentiate between SIADH and DI.
  • SIADH is too much ADH
  • DI is not enough ADH

How do S/S of SIADH and DI differ in terms of serum osmolarity, serum and urine sodium, and urine osmolarity.  

  • SIADH: high urine osm, Urine sodium, and low serum osm
  • DI: low urine osm, Urine sodium, and high serum osm

What is the pathophysiology behind these differences? Describe the treatment for SIADH and DI.  What are potential complications of SIADH and DI?

  • complications for SIADH are: low serum electrolytes and overhydration
  • complications for DI are: High serum electrolytes and dehydration
  1. The most common cause of Cushing Syndrome is increased levels of _______.  What are the clinical manifestations of increased cortisol levels?  What pt teaching needs to occur around Cushing Syndrome related to exogenous glucocorticoid therapy?
  • ACTH levels are high and the hormone is produced in the pituitary.
  • At risk for everything associated with glucocorticoids
  • Buffalo hump, mustache, hair loss, thin arms, large abdomen, Moon face, weight gain, insomnia, thin skin.
  • Alternate s/s: depression, changes in appetite, Fatigue, decreased concentration and libido.
  1. What are the potential complications of glucocorticoid therapy?  
  • Immunosuppression, cannot stop the medication abruptly.

 

Oncology

General understanding of cancer, risk factors, basic treatment concepts, studies to determine hematologic malignancies, metastasizes, basic function/purpose of chemotherapy and bone marrow transplant, radiation therapy indications and concerns for patient care/side effects, general knowledge related to categories or types of hematologic cancers

 

Risk factors for cancer

 

    • leukemia, acute and chronic – Proliferation of leukemia cells in the bone marrow the eventually move into blood circulation. The cells that are produced takeaway from the body’s ability to make blood cells so levels are decreased of RBC and platelets. WBC are decreased in the beginning, then can be increased in later stages of the disease when the Leukemia cells are moving from the bone into blood circulation (Healthy mature WBCs will always be decreased). This causes the signs and symptoms of fatigue, immune suppression, and clotting issues.
      • Acute Lymphoblastic leukemia ALL

 

  • Most common form of childhood leukemia

 

        • Increased incidence with age
        • HSCT for recurrence
        • Aplastic anemia.
        • Effects more immature blood cells and grows fast
      • Acute Myeloid Leukemia AML
        • bleeding and infections are an initial sign
        • bruising and fatigue
        • Splenomegaly
      • Chronic Lymphocytic Leukemia CLL

 

  • most common leukemia in adults
  • Lymphadenopathy is a hallmark (enlargement of one or multiple lymph nodes)

 

        • 10% have B symptoms (Fever, Night sweats, >10% weight loss in 6 months.)
        • treatment is deferred in early stages
        • doesn’t often show symptoms at diagnosis
        • Effects more mature blood cells and slow progression to s/s (years)
      • Chronic Myeloid leukemia
        • stable for many years without treatment

 

  • Philadelphia chromosome in 90% of patients

 

      • Splenomegaly
  • lymphoma, Hodgkin’s and non Hodgkin’s lymphoma characteristics
    • Hodgkin’s Lymphoma
      • Reed-Sternberg cells are in the biopsied lymph nodes
      • Pertussis is common
      • Lymph Node enlargement is the the first presenting symptom
      • Epstein Barr virus is is associated with this
      • Radiation treatment is a part of the high cure rate.
    • Non Hodgkin’s
      • Chromosomal translocation can often correlate with the cause of this
      • CHOP Chemo is used
      • Autoimmune diseases are a risk factor for this
      • No Reed-Sternberg cells
  • Multiple myeloma
    • Cancer of plasma Cells
    • Proliferation of Plasma cells affecting the bone marrow and destroy bone
    • Increased production of a random Ig (antibody) also called monoclonal production
    • Treatable but not often curable.
    • First s/s is BONE PAIN, Pathologic fractures are common
    • Diagnosis with Monoclonal antibody production, X-ray, increased bone marrow plasma cells, Beta 2-microglobulin and albumin
    • Tired, thirsty, fatigue, pallor, dull low back pain, GI issues, common in the elderly
    • Signs and symptoms – Babs the CRAB: HyperCalcemia, Renal failure, Anemia thrombocytopenia, and Bone pain
    • Hypercalcemia is due to high bone turnover causing pathological fractures
    • Renal failure is due to Monoclonal production of Ig
    • Anemia is due to the resources going to make cancerous plasma cells instead of regular RBCs and thrombocytes.
    • Bone pain is due to increased bone turnover
  • what are the main nursing concerns in administration of chemo; complications and nursing care concerns related to decreases in WBC, platelets, H/H
    • PPE
    • WBC – risk for infection
    • Platelets – risk for bleeds
    • H/H – risk for anemia
  • what are the concerns with radiation (internal and external)
    • topical and deep burns
    • adjacent body features and organs that can have side effects of radiation.
  • how are cell counts influenced by cancer and cancer therapy
  • cell counts can decrease if there is a leukemia, myeloma, myeloid cancer taking up the resources to make healthy cells
  • in cancer therapy there can be a decreased number of natural healthy cells and then the low levels will be replaced with healthy stem cells.
  • Chemo induced anemia
  • concepts of targeted therapy, stem cells, and bone marrow transplants; graft vs host disease
    • targeted therapies are biologic therapies
    • BMT is done after chemo kills the cancerous cells then they are replaced through a central line into the bloodstream
  • side effects and symptom management strategies
    • fatigue, pallor, anemias of all types, pain, thirst
    • Manage the symptoms and treat the cause of the disease.

Session 5: Endocrine

Session 5: Endocrine

 

Diabetic Ketoacidosis

  • More common in DM1 but possible in DM2
  • s/s dry mucous membranes, tachycardia, hypotension, Kussmaul respirations, glucose over 250, dehydrated Altered LOC.
  • HypoKAlemia, HypoNatremia,
  • The cells cannot take in glucose so they must metabolize fats, which causes a waste product of Ketone acid.
  • Give Insulin and monitor electrolytes and replace any that are out of normal, Give bicarb

 

HHNS – Hyperosmolar Hyperglycemic nonketotic Syndrome

    • Common in DM2
    • s/s: NO ketones production, GLU > 600,

 

  • FIRST THING TO GIVE: FLUIDS!!!!!, then insulin

 

  • Not giving BiCarb

 

SIADH – Retaining water, not urinating

  • Too much ADH
  • Low electrolytes
  • Do not replace Na too quick due to cerebral swelling.
  • 8-12 MeQ per day Na replacement.
  • These people may need to be on a fluid restriction, with no free water.
  • Demeclocycline – reduces the action of ADH

DI – always urinating

  • Not enough ADH
  • Dehydration
  • Tachycardia, hypotension, thirsty, dehydration…
  • DDAVP – reduces the urine output
    • This will not work with nephrogenic DI because the issue is with the nephron not ADH.

 

Cushing’s disease

  • Increased production of the “stress” hormone ACTH from the pituitary tumor
    • This is usually caused by a pituitary tumor
  • At risk for everything associated with glucocorticoids
  • Buffalo hump, mustache, hair loss, thin arms, large abdomen, Moon face, weight gain, insomnia, thin skin.
  • Alternate s/s: depression, changes in appetite, Fatigue, decreased concentration and libido.
  • These people will need to be on exogenous corticosteroids to counteract the glucocorticoid ACTH
    • Do not abruptly stop the medication.

Session 4: ECG

Session 4: ECG Electrocardiogram

 

Properties of cardiac tissue

  • Automaticity – tissue that can initiate an impulse without an outside force acting on it.
  • Contractility – the ability to respond to an impulse through a mechanical force
  • Conductivity – transmit an impulse
  • Excitability – the ability to be stimulated by the electric impulse.

 

  • Polarized is the resting state of the heart
    • Na out and K in the cell
  • Depolarized is the working of contraction phase of the heart
    • Na inside and K moves outside
    • If depolarization does not happen in a synchronized way then the chamber will not be able to contract effectively
  • Repolarization – the recovery phase moving from depolarization to polarized
  • Absolute refractory phase – the muscle cannot be depolarized under any physiologic stimuli. This occurs after the start of depolarization, during repolarization.
    • From the beginning of the QRS to the peak of the T
  • Relative refractory phase – after the absolute refractory phase where the muscle will respond to strong stimulus.
    • A vulnerable phase during the t wave, where we do not want to shock.
  • Nodes
    • SA node –  located in the right atrium and automatically fires 60-100 times per minute.
    • AV node – on the right side of the heart between the right atria and the right ventricle, this can fire at 40-60 beats per minute if needed,
    • Bundle of His – central heart in between all of the chambers.
    • Right and left bundle branches –  in between the ventricles
    • Purkinje fibers – in the bottom sides of the heart. This can fire at 15-40  

Getting an ECG

  • Electrodes are placed on the chest and the electrical activity reflects the activity in the heart.
  • The electrodes are placed at specific locations.
  • Common forms of ECGs are 3, 5, and 12 lead. The more leads the better “picture” of the heart we can get.

Interpreting the graph

  • Horizontal lines represent voltage (up and down)
  • Vertical lines represent time (left to right)
  • One small box represents 0.04 second from left to right, and 0.1mV up and down
  • One large box represents 0.2 seconds from left to right, and 0.5mV up and down
    • One large box is 5×5 small boxes.

Waveform

  • The waveform is made up of peaks and valleys that are designated as the letters P through U. Each letter corresponds to a specific part of the Waveform.
  • P wave – Atrial depolarization, rounded and shorter than the QRS complex
  • PR interval – Measurement from the beginning of the p wave to the beginning of the QRS
    • Normal is 0.12-0.2 seconds
    • This is the time is takes for the impulse to travel from the SA node through the AV node and into the ventricles.
  • QRS – ventricular depol, less than or equal to 0.12 seconds
  • ST segment – end of V Depol to the beginning of V Repol
    • Elevation correlates with myocardial infarction
    • Depression correlates with ischemia
  • T – ventricular repolarization
  • QT interval – total duration of depol and repol

ECG interpretation

  1. Determine regularity
    1. Regular? Regularly irregular? Irregularly irregular?
  2. Calculate the heart rate
    1. Count the R waves on a 6 second strip and multiply by ten
    2. Do the atrial and ventricular waves match?
  3. Assess the P waves
    1. Are they present?
    2. Are the a consistent shape
    3. Is the ratio of P:QRS 1:1?
  4. Measure the PR interval
    1. Is is consistent? Is it normal?
    2. Can it be measured?
  5. Measure the QRS
    1. Do the complexes look the same?
    2. Is the measurement normal?

Rhythms

  • sinus tach – BPM over 100
    • Beta blockers will reduce rate
    • Adenosine given in a FAST 4 second push will slow or stop the heart to restart in a better rhythm
  • Sinus Brady – normal rhythm less than 60 bps
    • All Trained Dogs Eat
    • Atropine
    • Transcutaneous pulsing
    • Dopamine
    • Epinephrine
  • Atrial dysrhythmias
      • Likely to form a clot in the atrial these people need to be on anticoagulants for life.
      • AV node controls the  number of impulses that pass and then depolarize the ventricles. Needs a good AV node to control rate.
      • Controlled is a HR less than 100 uncontrolled is over 100
      • Unstable will need Synchronized Electrocardioversion, beta blockers, Vagal maneuver
      • Decreased CO and increased chance for clots.
    • Atrial flutter – saw tooth
      • One ectopic foci that is discharging an impulse at 250-400 times per minute
      • F waves no P waves
    • Atrial Fibrillation
      • Multiple ectopic foci that are discharging at 250-40 times per minute
      • Most common clinically significant dysrhythmia
      • Most common cause of a ischemic stroke.
  • Synchronized cardioversion – synchronized shock on the R wave
    • Need an R wave
    • Can convert them out of A flutter or fib
    • May keep them in sinus for 3-6 months
    • Amiodarone Is used to prolong the time in sinus
    • May throw a clot that was in the atrium once the rhythm converts back to sinus.
    • Get a transesophageal echocardiogram to look for clots.
  • Heart blocks
    • 1st degree
      • Consistent Long PR interval over 0.20
      • Do not treat usually do to lack of signs and symptoms
    • Second degree type one, or wenckebach, or Mobitz 1
      • AV node conduction issue
      • Progressively increasing PR interval until a QRS is missed and the arrhythmia start over
      • Usually asymptomatic
    • Second degree type II, or Mobitz II
      • Normal PR interval with a dropped QRS every so often
      • Monitor for a third degree heart block
    • Third degree heart block
      • No communication between the atria and ventricles
      • Need a pacemaker, from the cathlab
  • Ventricular dysrhythmias
    • PVC – Premature ventricular contraction
      • Can be normal and untreated
      • Bigeminy – on pvc for one normal
      • Trigeminy – two PVC for every normal PQRST
      • Causes – hypoxia
      • Amiodarone is the drug of choice
    • V Tach –
      • Can cardiovert
      • Can easily turn into V fib
      • Pulseless we will defibrillate
      • Large sharp “QRS” complexes one immediately after another with no breaks
    • V Fib
      • Defibrillate to hope the SA node takes over
      • Smooth rapid continuous electrical activity with no breaks
      • Cannot cardiovert
      • AICD is an internal defibrillation device
  • PEA
    • Pulseless electrical activity
    • Give fluids and epi
  • Asystole
    • Straight line on the ECG