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Pccn Review Part 2

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Progressive Critical Care Nurse Certification Review, Part 2 of 2

Progressive Critical Care Nurse Certification Review, Part 2 of 2

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  • 1.
        • “ Education is a progressive discovery of our own ignorance”  Will Durant 
    PCCN REVIEW PART 2 Sherry L. Knowles, RN, CCRN, CRNI
  • 2.
    • TOPICS
    • Renal Alterations
      • Acute Renal Failure
      • Electrolytes
      • IV Fluid Therapy
    • Neurological Alterations
      • AVM’s & Cerebral Aneurysms
      • Intracranial Hemorrhage
      • Stroke
    PCCN REVIEW PART 2
    • Metabolic Alterations
      • DKA & HNNK
      • DI & SIADH
      • DIC
      • Shock States
      • Sepsis
  • 3.
    • OBJECTIVES
    • List the main functions of the kidney.
    • List the common diagnostic tests associated with renal function.
    • List the complications associated with acute renal failure.
    • Describe the common treatments of acute renal failure.
    • List the major signs & symptoms associated with electrolyte disturbances of sodium, potassium magnesium and calcium and phosphorus.
    • Define serum osmolality.
    • List the intracellular & extracellular fluid compartments of the body.
    • Describe the effects of hypotonic, isotonic and hypertonic IV fluids.
    • Describe the different treatments for intravascular depletion verses cellular dehydration.
    • Identify the risk factors and signs & symptoms of brain aneurysms and AVM’s.
    • Explain the current treatments available for brain aneurysms and AVM’s.
    • Describe the different types of intracranial hemorrhage and their associated signs & symptoms.
    PCCN REVIEW PART 2
  • 4.
    • OBJECTIVES
    • List the potential complications of associated with intracranial hemorrhages, brain aneurysms and AVM repairs.
    • List the types of CVA’s, their risk factors and related pathophysiology.
    • Identify the recommended treatments for CVA’s.
    • Differentiate between the signs and symptoms of DKA and HHNK.
    • Describe the treatment of DKA and HHNK.
    • Differentiate between the signs and symptoms of DI and SIADH.
    • Describe the treatment of DI and SIADH.
    • List the signs & symptoms of Disseminated Intravascular Coagulation.
    • Explain the treatments for disseminated intravascular coagulation.
    • Understand the different stages of shock.
    • Differentiate between different types of shock.
    • Identify the different treatments used for the different types of shock.
    • Describe the stages of the sepsis syndrome.
    • Explain the treatment of septic shock.
    PCCN REVIEW
  • 5.
    • Acute Renal Failure
    • Electrolytes
    • IV Fluid Therapy
    Renal Alterations
  • 6.
    • WHAT DO THE KIDNEYS DO?
      • Filter blood
        • Regulates electrolytes
      • Regulate blood pressure
        • Renin-angiotensin system (RAS)
      • Maintain acid/base balance
        • Removes wastes, detoxifies blood
    Acute Renal Failure
  • 7.
    • WHAT ELSE DO THE KIDNEYS DO?
      • Stimulate RBC production
        • Make erythopoietin
      • Make corticosteroids
        • Regulate kidney function
      • Increase calcium absorption
        • Convert Vitamin D to its active form  Calcitriol
    Acute Renal Failure
  • 8. The Kidney
  • 9. The Nephron
  • 10.
    • Glomerulus
      • Network of capillaries
    • Bowman’s capsule
      • Membrane that surrounds the glomerulus
    • Renal Tubules
      • Travel from cortex to medulla and back to cortex
    • Collecting duct
      • Within the medulla
    The Nephron
  • 11. The Kidney
    • The Renal Cortex Contains
      • Bowman's Capsules
      • Glomerulus
      • Proximal Tubules
      • Distal Convoluted Tubules
    • The Renal Medulla Contains
      • The Pyramids
        • Loop of Henle
        • Collecting Duct
        • Blood Vessels
  • 12.
    • Lies within Cortex
    • Controls the activity of the nephron
    • Plays major role in the renin-angiontension-aldosterone system
    The Juxtaglomerular Apparatus
  • 13. Urine Formation
  • 14.
    • DEFINITIONS
      • Sudden interruption of kidney function resulting from obstruction, reduced circulation, or disease of the renal tissue
      • Rapid deterioration of renal function
        • increase of creatinine of >0.5 mg/dl in <72hrs
        • “ azotemia” (accumulation of nitrogenous wastes)
        • elevated BUN and Creatinine levels
        • decreased urine output (usually but not always)
    Acute Renal Failure
  • 15.
    • TERMINOLOGY
      • Anuria: No UOP (or <100mL/24hrs)
      • Oliguria : UOP<400-500 mL/24hrs
      • Azotemia : (Increased BUN, Cr, Urea)
        • May be prerenal, renal, postrenal
        • Does not require any clinical findings
      • Chronic Renal Insufficiency
        • Deterioration over months-years
        • GFR 10-20 mL/min, or 20-50% of normal
      • ESRD: GFR <5% of mL/min
    Acute Renal Failure
  • 16.
    • PERSONS AT RISK
      • Major surgery
      • Major trauma
      • Receiving nephrotoxic medications
      • Hypovolemia > 40 minutes
      • Elderly
    Acute Renal Failure
  • 17.
    • SIGNS & SYMPTOMS
      • Azotemia
      • Hyperkalemia
      • Electrolyte Disturbances
        •  K+  phosphate
        •  Na+  calcium
        •  Cr  BUN
      • Metabolic acidosis
      • Nausea/Vomiting
    • Oliguria - anuria
    • HTN
    • Hypovolemia
    • Pulmonary edema
    • Ascites
    • Metabolic acidosis
    • Asterixis
    • Encephalopathy
    Acute Renal Failure
  • 18.
    • COMPLICATIONS
      • Results in retention of toxins, fluids, and end products of metabolism
      • May be reversible with medical treatment
    Acute Renal Failure
  • 19.
    • DIAGNOSTIC TESTS
      • H&P
      • BUN, creatinine, sodium, potassium, pH, bicarb, Hgb and Hct
      • Urine studies
      • US of kidneys
      • 24 hour urine for protein and creatinine
      • Urine eosinophils
    Acute Renal Failure
  • 20.
    • OTHER DIAGNOSTIC TESTS
      • Albumin, glucose, prealbumin
      • KUB
      • ABD and renal CT/MRI
      • Retrograde pyloegram
      • Renal biopsy
      • Post-void residual or catheterization
    Acute Renal Failure
  • 21.
    • PHASES
      • Onset
        • 1-3 days with  BUN and  creatinine and possible decreased UOP
      • Oliguric
        • UOP < 400/day,  BUN,  Cr,  P04,  K, may last up to 14 days
      • Diuretic
        • UOP  to as much as 4000 mL/day but without waste products, may begin to see improvement at end of this stage
      • Recovery
        • things go back to normal or may remain insufficient and become chronic
    Acute Renal Failure
  • 22.
    • CAUSES
      • Pre-renal (hypoperfusion)
      • Renal (intrinsic)
      • Post-renal (obstructive)
    Acute Renal Failure
  • 23.
    • SPECIFIC CAUSES
      • Prerenal
        • Hypovolemia, shock, blood loss, embolism, pooling of fluid due to ascites or burns, cardiovascular disorders, sepsis
      • Intrarenal
        • ATN, nephrotoxic agents, infections, ischemia acute tubular necrosis, acute nephritis, polycystic kidney disease
      • Postrenal
        • Stones, blood clots, BPH, urethral edema from invasive procedures, renal calculi
    Acute Renal Failure
  • 24. Pre-Renal or Intra-Renal?
  • 25.
      • TREATMENT
        • Make/consider the diagnosis
        • Treat life threatening conditions
        • Identify the cause if possible
          • Hypovolemia
          • Toxic agents (drugs, myoglobin)
          • Obstruction
        • Treat reversible elements
          • Hydrate
          • Remove drug
          • Relieve obstruction
    Acute Renal Failure
  • 26.
    • NURSING CARE
      • Fluid and dietary restrictions
        • Protein, potassium & phosphate restriction
      • Maintain electrolytes
      • D/C or reduce causative agent
      • Adjust medication doses
      • May need dialysis to jump start renal function
      • May need to stimulate production of urine with IV fluids, Dopamine, diuretics, etc.
    Acute Renal Failure
  • 27.
    • DIALYSIS
      • Hemodialysis
      • Peritoneal Dialysis
      • Continuous Renal Replacement Therapy (CRRT)
    Acute Renal Failure
  • 28.
      • TREATMENT
        • Strict I&O
        • Daily weights
        • Watch for heart failure
        • Monitor lab results
        • Watch for hyperkalemia
      • Watch for hyper/hypoglycemia
      • Maintain nutrition
      • Mouth care
      • Monitor skin
      • S & S of Hyperkalemia: Malaise, anorexia, parenthesia, muscle weakness,EKG changes
    Chronic Renal Failure
  • 29. Electrolyte Disturbances Na+ Ca++ Cl- Mg+ K+ PO 4 NH 3 Cu HCO 3 - NaCl
  • 30.
    • Dominant intracellular electrolyte
    • Primary buffer in the cell
    K+ Potassium (K + ) Normal serum K+ level: 3.5-5.5 mEq/L
  • 31.
      • INVOLVED IN
      • Muscle contraction
      • Nerve impulses
      • Cell membrane function
      • Attracting water into the ICF
      • Imbalances interfere with neuromuscular function and may cause cardiac rhythm disturbances
    Potassium (K + )
  • 32.
    • SIGNS & SYMPTOMS
      • Weakness, malaise, lethargy
      • Anorexia
      • Muscle cramps
      • Paresthesias
      • Dysrhythmias
    Hyperkalemia
  • 33.
    • K > 5.5 -6
    • Tall, peaked T’s
    • Wide QRS
    • Prolong PR
    • Diminished P
    • Prolonged QT
    • QRS-T wave merge = “sine wave”
    Hyperkalemia
  • 34.
    • CAUSES
      • Chronic or acute renal failure
      • Burns
      • Crush injuries
      • Excessive use of Potassium salts
    Hyperkalemia
  • 35.
    • TREATMENT
      • Calcium Gluconate (carbonate)
      • Calcium Chloride
      • Sodium Bicarbonate
      • Insulin/glucose
      • Kayexalate
      • Lasix
      • Albuterol
      • Hemodialysis
    Hyperkalemia
  • 36.
    • SIGNS & SYMPTOMS
      • Malaise
      • Skeletal muscle weakness
      • Decreased reflexes
      • Hypotension
      • Vomiting
      • Excessive thirst
      • Cardiac arrhythmias and cardiac arrest
      • Flattened T wave
      • U wave
    Hypokalemia
  • 37. Sine Wave
  • 38.
    • CAUSES
      • Reduced dietary intake
      • Poor absorption by the body
      • Vomiting and/or diarrhea
      • Renal disease
      • Medications (typically diuretics)
    Hypokalemia
  • 39.
    • SIGNS & SYMPTOMS
      • Cold, clammy, pale skin
      • Nervousness
      • Shakiness, lack of coordination, staggering gait
      • Irritability, hostility, and strange behavior
      • Difficulty concentrating
      • Fatigue
      • Excessive hunger
      • Headache
      • Blurred vision and dizziness
      • Abdominal pain or nausea
      • Fainting and unconsciousness
    Hypoglycemia
  • 40.
    • SIGNS & SYMPTOMS
    • Cardiovascular Signs
    • Palpitations
    • Tachycardia
    • Anxiety
      • Irritability
      • Diaphoresis
      • Pale, cool skin
      • Tachypnea
    • Neurological Signs
        • Agitation
        • Confusion
        • Slurred Speech
        • Staggering Gait
        • Paraplegia
        • Seizures
        • Coma
    Acute Hypoglycemia
  • 41.
    • SIGNS & SYMPTOMS
      • Thirst
      • Polyuria
      • Dehydration
      • Nausea, vomiting
      • DKA
      • HNNK
    Hyperglycemia Normal serum Glu level: 70 - 110 mg/dL
  • 42.
    • Dominant extracellur electrolyte
    • Chief determinant of osmolality
    NaCl Sodium (Na + ) Normal serum Na+ level: 135-145 mEq/L
  • 43.
    • SIGNS & SYMPTOMS
      • Deficiency of sodium in the blood
      • Hypotension
      • Tachycardia
      • Muscle weakness
      • Mental Confusion
    Hyponatremia
  • 44.
    • SIGNS & SYMPTOMS
      • Excess sodium in the blood
      • Hypertension
      • Muscle twitching
      • Mental confusion
      • Coma
    Hypernatremia
  • 45.
    • Activates many enzymes
    • 50% is insoluble in bone
    • 45% is intracellular
    • 5% is extracellular
    Mg+ Magnesium (Mg + ) Normal serum Mg+ level: 1.5 - 2.5 mg/dL
  • 46.
    • SIGNS & SYMPTOMS
      • Tremors
      • Positive Chvostek & Trousseau
      • Nystagmus
      • Confusion/Hallucinations
      • Diarrhea
      • Hyperactive deep reflexes
      • Seizures
    Hypomagnesemia
      • Dysrhythmias
      • ECG Changes
        • Flat T wave
        • ST interval depression
        • Prolonged QT interval
          • May lead to Torsade de Pointes
  • 47.
    • CAUSES
      • Alcoholism
      • Malabsorption
      • Starvation
      • Diarrhea
      • Diuresis
    Hypomagnesemia
  • 48.
    • SIGNS & SYMPTOMS
      • Peaked T wave
      • Bradycardia
      • CNS Depression
      • Areflexia
      • Sedation
      • Respiratory paralysis
    Hypermagnesemia
  • 49.
    • CAUSES
      • Not common
      • Occurs with chronic renal insufficiency
      • Treatment is hemodialysis
    Hypermagnesemia
  • 50.
    • ESSENTIAL FOR
      • Neuromuscular transmission
      • Growth and ossification of bones
      • Muscle contraction
    Ca++ Calcium (Ca ++ ) Normal serum Ca++ level: 8 - 11 mg/dL
  • 51.
    • INVOLVED IN
      • Blood clotting
      • Nerve impulse
      • Muscle contraction
    Ca++ Calcium (Ca ++ ) Excreted through urine, feces, and perspiration
  • 52.
    • SIGNS & SYMPTOMS
      • Tetany (cramps/convulsions in wrists and ankles)
      • Weak heart muscle
      • Increased clotting time
      • Prolonged QT interval
        • May lead to Torsade de Pointes
      • Abnormal behavior
      • Chvostek's sign (facial twitching)
      • Paresthesia
    Hypocalcemia
  • 53.
    • CAUSES
      • Renal insufficiency
      • Decreased intake or malabsorption of Calcium
      • Deficiency in or inability to activate Vitamin D
    Hypocalcemia
  • 54.
    • SIGNS & SYMPTOMS
      • Kidney stones
      • Bone pain
      • Hypotonicity of muscles (decreased tone)
      • Altered mental status
      • Cardiac arrhythmias
      • Shortened QT interval
    Hypercalcemia
  • 55.
    • CAUSES
      • Neoplasms (tumors)
      • Excessive administration of Vitamin D
    Hypercalcemia
    • TREATMENT
      • Usually aimed at underlying disease and hydration
      • Severe hypercalcemia may be treated with forced diuresis
  • 56.
    • INVOLVED IN
      • Energy metabolism
      • Genetic coding
      • Cell function
      • Bone formation
    PO 4 Phosphorus (P, PO 4 ) Normal serum PO4 level: 2.5-4.5 mg/dL
  • 57.
    • SIGNS & SYMPTOMS
      • Respiratory difficulty
      • Confusion
      • Irritability
      • Coma
    Hypophosphatemia
  • 58.
    • CAUSES
      • Severe infections
      • Kidney failure
      • Thyroid failure
      • Parathyroid Failure
      • Often associated with hypercalcemia or hypomagnesemia or too much Vitamin D
      • Cell destruction - from chemotherapy, when the tumor cells die at a fast rate
        • Can cause tumor lysis syndrome
    Hypophosphatemia
  • 59.
    • SIGNS & SYMPTOMS
      • Elevated blood phosphate level
      • There are no symptoms of hyperphosphatemia
    Hyperphosphatemia
  • 60.
    • TREATMENT
      • Calcium Carbonate tablets
      • Aluminum hydroxide
        • Can cause aluminum toxicity
    Hyperphosphatemia
  • 61.
    • OSMOLALITY
      • Concentration of a solution
      • The higher the osmolality the greater its pulling power for water
    IV Fluid Therapy Normal serum osmolality is 275 to 295 mOsm/L
  • 62.
    • Sodium = major solute in plasma
      • Estimated serum osmolality = 2 X serum Na
    • Urea (BUN) and glucose are large molecules that  serum osmolality
      • When either or both are elevated, the serum osmolality will be higher than 2 times the sodium level, so the following formula is more accurate:
      • Serum osmolality = 2 X serum Na + BUN + glucose
      • 3 18
    Serum Osmolality
  • 63. Major Mediators of Sodium and Water Balance
    • Angiotensin II
    • Aldosterone
    • Antidiuretic hormone (ADH)
  • 64. Renin-Angiotensin-Aldosterone Angiotensin II  1. Stimulates production of aldosterone 2. Acts directly on arterioles to cause vasoconstriction 3. Stimulates Na + /H + exchange in the proximal tubule Aldosterone  1. Stimulates reabsorption of Na + and excretion of K + in the late distal tubule 2. Stimulates activity of H + ATPase pumps in the late distal tubule
  • 65. Antidiuretic Hormone (ADH)
    • Synthesized in the hypothalamus and stored in the posterior pituitary
    • Released in response to plasma hyperosmolality and decreased circulating volume
    • Actions of ADH
      • Increases the water permeability of the collecting tubule (makes kidneys reabsorb more water)
      • Mildly increases vascular resistance
  • 66.
      • Isotonic – same osmolality as serum
      • Hypotonic – lower osmolality than serum
      • Hypertonic – higher osmolality than serum
    IV Fluid Therapy
  • 67. Effect on Cells
  • 68. IV Solutions D5NS D51/2 NS NS ½ NS D50W D10W D5W Hypotonic in the body D5W Hypertonic Hypertonic Isotonic Hypotonic Hypertonic Hypertonic Isotonic Hypertonic Hypertonic Hypertonic Hypertonic Hypertonic Isotonic Hypertonic PRBC’s Hetastarch Dextran Albumin D5LR LR 3% NaCl
  • 69. IV Solutions Pulls fluid into vascular space Hypertonic Solutions Hydrates extracellular compartment Isotonic Solutions Used for cellular dehydration Not used with head injuries Hypotonic Solutions Hypotonic in the body D5W
  • 70. Daily Fluid Balance Intake: 1-1.5 L Insensible Loss - Lungs 0.3 L - Sweat 0.1 L Urine: 1.0 to 1.5 L
  • 71. Intracellular (2/3) Extracellular (1/3) Solids 40% of Wt H 2 O H 2 O Na
  • 72. Intra-vascular( 1/4) E.C . F . COMPARTMENTS Interstitial (3/4) H 2 O H 2 O Na Na Colloids & RBC’s
  • 73. “ Third Space”
    • Third space refers to collection of fluids (usually isotonic) that is sequestered in potential spaces.
    • This situation is not normal and the fluid is derived from extracellular fluid.
  • 74. Principles of Treatment
    • How much volume?
      • Need to estimate fluid deficit
    • Which fluid?
      • Which fluid compartment is predominantly affected?
      • Must evaluate other acid/base, electrolyte & nutrition needs
  • 75. Fluid Replacement Products
    • Crystalloids – able to pass through semi permeable membranes
      • Isotonic solutions
      • Hypotonic solutions
      • Hypertonic solutions
    • Colloids – do not cross the semi permeable membrane and remain in the intravascular space for several days (pulling fluid out of the intracellular and interstitial space)
      • Albumin
      • Dextran
      • Hetastarch
  • 76. 1 liter 5% Albumin Intravascular=1 liter Total body water ECF
  • 77. 1 Liter 0.9% saline Total body water ECF=1 liter ICF=0 Intravascular =1/4 ECF=250 ml Interstitial=3/4 of ECF=750ml
  • 78. 1 liter 5% Dextrose Total body water ECF=1/3 = 300ml ICF=2/3 = 700ml Intravascular =1/4 of ECF~75ml
  • 79. Ringers Lactate
    • Infusion of Ringer Lactate solution may lead to metabolic alkalosis because of the presence of lactate ions
    • Lactated Ringer’s should be used with great care with patients with hyperkalemia, severe renal failure, and hepatic insufficiency
    • Solutions containing lactate are not for use in the treatment of lactic acidosis
  • 80.
        • BREAK
    PCCN REVIEW PART 1
  • 81.
    • Brain Aneurysms & AVM’s
    • Intracranial Hemorrhage
    • Stroke
    Neurological Alterations
  • 82. The Human Brain
  • 83. Cerebral Spinal Fluid The serum-like fluid that circulates through the ventricles of the brain, the cavity of the spinal cord, and the subarachnoid space
  • 84.
    • Brain Aneurysm
      • An intracranial aneurysm is a weak or thin spot on a blood vessel in the brain that balloons out and fills with blood
    • AV Malformation (AVM)
      • Arteriovenous malformation (AVM) of the brain is a &quot;short circuit“ between the arteries and veins
    Brain Aneurysms & AVM’s
  • 85. Intracranial Aneurysms
    • Usually occur at bifurcations and branches of the large arteries located in the Circle of Willis
    • The most common sites include the:
      • Anterior Communicating artery (30 - 35%)
      • Bifurcation of the Internal Carotid and Posterior Communicating artery (30 - 35%)
      • Bifurcation of Middle cerebral (20%)
      • Basilar artery bifurcation (5%)
      • Remaining posterior circulation arteries (5%)
  • 86. Types of Aneurysms
    • Saccular aneurysm
      • Occurs at bifurcations
    • Fusiform aneurysm
      • Often in basilar artery
    • Dissecting aneurysm
    • Ruptured aneurysm
  • 87. Brain Circulation
  • 88. Arterial Circulation in the Brain
  • 89.
    • RISK FACTORS
      • Smoking
      • Hypertension
      • Coarctation of the aorta
      • Dissections/trauma
      • Intracranial neoplasm
      • Polycystic kidney disease
      • Abnormal vessels or High-flow states (eg, vascular malformations, fistulae)
      • Hypercholesterolemia
      • Connective tissue disorders (eg, Marfan, Ehlers-Danlos)
    Intracranial Aneurysms
  • 90.
    • SIGNS & SYMPTOMS
      • Usually asymptomatic until rupture
        • Cranial Nerve Palsy
        • Dilated Pupils
        • Double Vision
        • Pain Above and Behind Eye
        • Localized Headache
      • Warning signs prior rupture
        • Localized Headache
        • Nausea & Vomiting
        • Stiff Neck
        • Blurred or Double Vision
        • Sensitivity to Light (photophobia)
        • Loss of Sensation
    Intracranial Aneurysms
  • 91. Treatment of Brain Aneurysms
    • Surgery
    • – Craniotomy and clipping
    • Endovascular coiling
  • 92. Aneurysm Post-Op Risks
    • Rebleeding
      • Most frequently within the first 24 hours
      • Up to 20% of patients rebleed within 14 days
      • Main preventative measure is control of blood pressure (preferably beta blockers)
    • Vasospasm
      • Usually occurs before 3 days or after 10 days (post bleed)
      • May require hypervolemic therapy
    • Hydrocephalus
    • Hyponatremia
    • Fluids / Electrolytes
  • 93. Arterio-Venous Malformation
  • 94.
    • The arteries and veins have a direct connection, bypassing the capillary network
    • Presents with ongoing headaches, seizures, hemorrhage, or progressive neurological dysfunction
    Arterio-Venous Malformation
  • 95. Arterio-Venous Malformation
    • SIGNS & SYMPTOMS
      • Seizures
      • Headaches
      • “ Whooshing&quot; Sound (Bruit)
      • Other Signs
        • Subtle behavioral changes
        • Communication or thinking disturbances
        • Loss of coordination and balance
        • Paralysis or weakness in one part of the body
        • Visual disturbances
        • Abnormal sensations
  • 96. Arterio-Venous Malformation
    • COMPLICATIONS
      • Hemorrhage (into surrounding tissue)
      • Ischemia
      • Seizures
      • Brain Cell Death
  • 97. Arterio-Venous Malformation
    • DIAGNOSIS
      • MRI (including MR Angiography) as well as CT Angiography help identify AVM’s
      • Cerebral Angiography is a prerequisite to treatment
        • To identify the precise anatomy and configuration of both the lesion and the feeding and draining vessels
  • 98. Arterio-Venous Malformation
    • TREATMENT
      • Surgery
        • Usually delayed
        • Open ligation and/or resection of the AVM
      • Radiosurgery
      • Embolization
        • Usually as adjunct to surgery
      • Observation
  • 99. Arterio-Venous Malformation
    • RADIOSURGERY
      • Believed to &quot;work&quot; by initiating an &quot;inflammatory&quot; response in the pathological blood vessels ultimately resulting in their progressive narrowing and ultimate closure
      • The risk for hemorrhage is not reduced during this lag time
      • There is the added risk of radiation necrosis of adjacent healthy brain tissue or brain cyst formation
  • 100. Brain Radiosurgery
    • ADVANTAGES
      • Noninvasive
      • Can access all anatomic locations of the brain
    • DISADVANTAGES
      • Can only treat smaller lesions (<3 cm in diameter)
      • Requires 2 or more years to complete
  • 101. AVM Post-Op Risks
    • Perfusion-breakthrough bleeding
    • Endovascular occlusion
  • 102.
      • Sudden onset of “the worst headache of my life”
    Intracranial Hemorrhage
  • 103.
    • Epidural
    • Subdural
    • Subarachnoid
    • Intraparencymal
    • Intraventricular
    • Cerebellar
    Intracranial Hemorrhage
  • 104.
    • ICH is a dynamic, not a static process
    • Hemorrhage volume can increase over time
    • CT scan is the most important diagnostic tool
    • Managing blood pressure is extremely important
    • Must aggressively manage fever and seizures
    • Consider hyperventilation and paralytics in setting of increased ICP and deterioration
    Intracranial Hemorrhage
  • 105. Treatment of ICH
    • KEY CONCEPTS
      • Intracranial Pressure
          • Elevated when ICP >20 mm Hg
      • Cerebral Perfusion Pressure
          • CPP = MAP - ICP
          • Must maintain CPP > 70 mm Hg
          • Example: MAP = 100, ICP = 20
          • CPP = 80 mmHg
  • 106. Subarachnoid Hemorrhage (SAH)
    • DEFINITION
      • When a blood vessel just outside the brain ruptures, the area of the skull surrounding the brain (the subarachnoid space) rapidly fills with blood
  • 107. Subarachnoid Hemorrhage (SAH)
    • SIGNS & SYMPTOMS
      • Sudden, intense headache
      • Neck pain
      • Nausea or vomiting 
      • Neck stiffness
      • Photophobia
    • Sudden onset of “the worst headache of my life”
  • 108. Subarachnoid Hemorrhage (SAH)
    • SAH may be spontaneous or traumatic
    • Spontaneous SAH causes
      • Cerebral aneurysms
      • AV malformations
      • Trauma
    • Uncommon causes
      • Neoplasms, venous angiomas, infections
  • 109.
    • Warning bleeds” are relatively common
    • Sentinel headache 30-50%
    • Early diagnosis prior to rupture will improve outcomes
    • 50% of patients die within 48 hours irrespective of therapy
    Subarachnoid Hemorrhage
  • 110.
    • Often accompanied by a period of unconsciousness (50% never wake up)
    • Common signs include neck stiffness, photophobia, headache
    • 20% have ECG evidence of myocardial ischemia
    Subarachnoid Hemorrhage
  • 111. Complications of SAH
    • Hydrocephalus may develop within the first 24 hours because of obstruction of CSF outflow in the ventricular system by clotted blood
    • Rebleeding of SAH occurs in 20% of patients in the first 2 weeks. Peak incidence of rebleeding occurs the day after SAH and may be from lysis of the aneurysmal clot
    • Vasospasm from arterial smooth muscle contraction (symptomatic in 36% of patients)
  • 112. Re-bleeding After SAH
    • Re-bleeding occurs most frequently within the first 24 hrs
    • Up to 20% of patients rebleed within 14 days
    • The main preventative measure is to control the blood pressure – preferably beta blockers
    • Early clipping of the aneurysm allows hypertensive and hypervolemic therapy to prevent vasospasm
  • 113. Vasospasm After SAH
    • Worst time is day 7 to day 10 (most frequent time for vasospasms)
    • Diagnosed by neurologic exam, transcranial doppler and angiography
    • May use calcium channel blockers
      • Reduces vasospasm, neurological deficit, cerebral infarction and mortality
    • May use some antispasmodics
  • 114. Vasospasm & HHH Therapy
    • Hemodilution
      • Hct 30-35%
    • Hypertension
      • Phenylephrine / Norepinephrine
      • BP titration to CPP/exam
    • Hypervolemia
      • Colloids/crystalloids
  • 115. Other Vasospasm Therapy
    • Angioplasty
      • BP management during procedure
      • Reperfusion issues
      • Timing
    • Papaverine Infusion
      • Side effects
      • Repeated trips
  • 116.
    • Neurologic deficits from cerebral ischemia, peaks at days 4-12
    • Hypothalamic dysfunction causes excessive sympathetic stimulation, which may lead to myocardial ischemia or labile BP
    • Hyponatremia may result from cerebral salt wasting / SIADH
    • Nosocomial pneumonia and other such complications
    • Pulmonary edema neurogenic & non-neurogenic
    Other Complications of SAH
  • 117.
    • Identify and treat the causative lesion
      • Thus preventing re-bleeding
    • Treat hydrocephalus
    • Treating and prevent vasospasm
    Treatment of SAH
  • 118.
    • Maintain systolic BP >130mmHg
      • Use vasopressors if necessary to maintain CPP and reduce ischemic complications from vasospasm
      • Generally avoid vasodilators (except calcium channel blockers)
    Treatment of SAH
  • 119. Stroke
  • 120. Stroke
  • 121.
    • RISK FACTORS
    • TIA
    • CAD
    • High Blood Pressure
    • High Cholesterol
    • Smoking
    • Heart Disease
    • Diabetes
    • Excessive alcohol
    • Family History
    • Age
    • Sex
    • Race
    • Obesity
    Annual risk of stroke: Increases with age Stroke
  • 122.
    • Computed Tomography (CT)
    • Magnetic Resonance Imaging (MRI)
    • Cerebral Angiography: identify responsible vessel
    • Carotid Ultrasound: carotid artery stenosis
    • Echocardiogram: identify blood clot from heart
    • Electrocardiogram (ECG): underlying heart conditions
    • Heart monitors, blood work and more tests!!
    Stroke Tests
  • 123. CT MRI
    • http://www.strokecenter.org/education/ais_ct_tool/ct04/ct04-frames.htm
    http://www.strokecenter.org/education/ais_ct_tool/index.htm
  • 124.
    • Tissue plasminogen activator (tPA) can be given within three hours from the onset of symptoms
    • Heparin
    • Intra-arterial thrombolysis
    • Hemicraniectomy
    • In addition to being used to treat strokes, the following can also be used as preventative measures
      • Anticoagulants/Antiplatelets
      • Carotid Endarterectomy
      • Angioplasty/Stents
    Treatment of Ischemic CVA
  • 125.
    • Surgery is often required to remove pooled blood from the brain and to repair damaged blood vessels
    • Prevention:
      • An obstruction is introduced to prevent rupture and bleeding of aneurysms and AVM’s
      • Surgical Intervention
      • Endovascular Procedures
    Treatment of Hemorrhagic CVA
  • 126.
    • Control high Blood Pressure
    • Lower cholesterol
    • Quit smoking
    • Control diabetes
    • Maintain healthy weight
    • Exercise
    • Manage stress
    • Eat a healthy diet
    Prevention of CVA
  • 127.
        • BREAK
    PCCN REVIEW PART 1
  • 128.
    • DKA & HHNK
    • DI & SIADH
    • DIC
    • Shock States
    • Sepsis
    Metabolic Alterations
  • 129. Diabetic Ketoacidosis
    • What is DKA?
      • Diabetic Ketoacidosis
      • A life-threatening complication seen with Diabetes Mellitus Type 1
  • 130.
    • SIGNS & SYMPTOMS
      • Serum Glucose 300-800
      • Ketoacidosis Present
      • Large Serum And Urine Ketones
      • Fruity Breath
      • Kussmaul Respirations
      • Serum pH < 7.3
      • Dehydration
    Diabetic Ketoacidosis
  • 131. HHNK
    • What is HHNK?
        • Hyperglycemic Hyperosmolar Nonketonic Coma
        • A life threatening complication seen with Diabetes Mellitus Type 2
  • 132.
    • SIGNS & SYMPTOMS
      • Serum Glucose 600-2000
      • Ketoacidosis Not Present
      • Absent Or Slight Serum And Urine Ketones
      • Normal Breath
      • Shallow Respirations
      • Serum pH Normal
      • Severe Dehydration
    HHNK
  • 133. DKA vs HHNK
    • DKA
    • Faster Onset
    • Glucose 300-800
    • Acidosis
    • Fruity Breath
    • Kussmaul Respirations
    • HHNK
    • Slower Onset
    • Glucose 600-2000
    • No Acidosis
    • Normal Breath
    • Shallow Respirations
  • 134. Treatment of DKA & HHNK
    • Reverse Dehydration
            • NS, then ½ NS
    • Restore Glucose Levels
            • D 5 ½ NS When Glu 250
    • Restore Electrolytes
  • 135.
    • What is Diabetes Insipitus?
      • A Condition resulting from too little ADH
    • Why is it called Diabetes Insipitus?
      • The term Diabetes refers to polyuria
    Diabetes Insipitus
  • 136.
    • SIGNS & SYMPTOMS
      • Polyuria
      • Severe Hypovolemia
      • Severe Dehydration
      • Elevated Serum Osmolality
      • Elevated Serum Sodium
      • Shock
    Diabetes Insipitus
  • 137.
    • CAUSES
      • Decreased ADH
      • Neurological Surgery
      • Head Trauma
      • Dilantin or Lithium
    Diabetes Insipitus
  • 138.
    • TREATMENT
      • Fluid Resuscitation
      • ADH Replacement
        • Vasopressin, Pitressin, DDAVP
      • Treat The Cause
    Diabetes Insipitus
  • 139.
    • What is SIADH?
      • Syndrome of Inappropriate ADH
      • Too much ADH
    SIADH
  • 140. SIADH
    • SIGNS & SYMPTOMS
    • Hyponatremia
    • Low Serum Sodium
      • Serum NA < 135
    • Low Serum Osmolality
    • High Urine Osmolality
    • Elevated Specific Gravity
      • Urine specific gravity
      • > 1.030
    • Elevated Urine Osmolality
    • Elevated ADH Level
    • Weight Gain Without Edema
    • Elevated CVP, PAP, PAWP
    • Hypertension
    • Concentrated And  UOP
    • Headache
    • Altered LOC
    • Seizures
  • 141.
    • CAUSES
      • Head Trauma
      • Oat Cell Carcinoma
      • Other Cancers
      • Viral Pneumonia
    SIADH
      • Medications
      • Stress
      • Mechanical Ventilation
  • 142.
    • TREATMENT
      • Monitor Fluid Balance, Monitor I & O
      • Restrict Fluids
      • Replace Na+ loss when necessary
      • May Give 3% (Hypertonic) Saline
      • May Give Dilantin or Lithium
      • May require PA Catheter For Monitoring
      • May Give Diuretics
    SIADH
  • 143. DI vs SIADH
    • DI
    • Too Little ADH
    • Dehydration
    • High Serum Sodium
    • High Serum Osmolality
    • Low Urine Osmolality
    • SIADH
    • Too Much ADH
    • Water Intoxication
    • Low Serum Sodium
    • Low Serum Osmolality
    • High Urine Osmolality
  • 144. DI vs SIADH Treatment
    • DI
    • Lots of Fluids
    • Hold Dilantin
    • Hold Lithium
    • Give ADH
    • SIADH
    • Fluid Restriction
    • May Give Dilantin
    • May Give Lithium
    • 3% Saline
  • 145.
    • What is DIC?
      • Disseminate Intravascular Coagulation
      • A clotting disorder that ultimately causes bleeding
    DIC
  • 146.
    • Caused by over-activation of the clotting pathways
    • Causes widespread fibrin deposits
    • Bleeding and renal failure are most common manifestations
    • Treating the underlying disease is the most important step
    DIC
  • 147. Disseminated Intravascular Coagulation Systemic activation of coagulation Intravascular deposition of fibrin Depletion of platelets and coagulation factors BLEEDING Thrombosis of small and midsize vessels with organ failure
  • 148.
    • SIGNS & SYMPTOMS
      • Bleeding
      • Thrombosis
      • Organ Failure
    DIC
  • 149. DIC
  • 150.
    • CAUSES
      • Massive Tissue Injuries
      • Obstetric Emergencies
      • Septicemia
      • Cancers
      • Vascular Disorders
      • Systemic Disorders
      • Many More Causes
    DIC
  • 151.
    • CLOTTING FACTORS DEPLETED
      • Platelets 
      • Fibrinogen 
      • Protein C 
      • Antithrombin 
    DIC Lab Results
    • CLOTTING TESTS ELEVATED
      • PT 
      • aPTT 
      • Fibrin degradation products (D-dimer) 
  • 152.
    • TREATMENT
      • Treat the Cause
      • Replace Clotting Factors
      • Anticoagulation Therapy (Heparin)
    DIC
  • 153.
    • DEFINITION
      • Inadequate perfusion to body tissues
    Shock
  • 154.
    • COMPENSATORY MECHANISMS
      • Tachycardia
        • Attempts to deliver more blood to the tissues
      • Vasoconstriction
        • Attempts to maintain adequate BP in order to adequately perfuse the body tissues
      • Increased ADH Secretion
        • ADH makes the body hold onto water in an effort to maintain volume and thus enough blood pressure to perfuse the body tissues
    Shock
  • 155.
    • Hypovolemic Shock
      • Inadequate perfusion to the tissues due to insufficient intravascular volume
    • Cardiogenic Shock
      • Inadequate perfusion to the tissues due to heart failure
    • Distributive Shock
      • Inadequate perfusion to the tissues due to blood flow out of the intravascular space causing insufficient intravascular volume
      • Anaphylactic, Septic, and Spinal Shock
    • Obstructive Shock
      • Inadequate perfusion to the tissues due to obstruction of blood flow
    Types of Shock
  • 156.
    • SIGNS & SYMPTOMS
      • Low BP Tachycardia
      • Orthostatic Hypotension Restlessness
      • Confusion Agitation (or listless)
      • Thirst Pallor
      • Cool, Clammy Skin  Resp. Rate
      •  UOP  CO
      •  PAWP  CVP
      •  SVR  Lactate Levels
    Hypovolemic Shock
  • 157.
    • TREATMENT
      • Volume (IVF, Blood)
    Hypovolemic Shock
  • 158.
    • SIGNS & SYMPTOMS
      • Low BP Restlessness
      • Agitation (or listless) Confusion
      • Tachycardia Pallor
      •  UOP  CO
      •  PAWP (low with RVF)  CVP
      •  SVR  Lactate Levels
      • JVD Peripheral Edema
      • Ventricular Gallop (S3) Dyspnea
      • Pulmonary Crackles
    Cardiogenic Shock
  • 159.
    • TREATMENT
      • Bedrest O2
      •  CO Positive Inotropes
      •  Preload & Afterload Diuretics
      •  Vasodilators Positioning
      •  Myocardial Demand IABP
    Cardiogenic Shock
  • 160.
    • SIGNS & SYMPTOMS
      • Low BP Tachycardia
      • Restlessness Confusion
      • Agitation (or listless) Thirst
      • Pallor Warm Feeling
      • Pruritus Hives
      • Angioedema Bronchoconstriction
      • Wheezing Laryngoedema
      • Dyspnea Cool, Clammy Skin
      •  UOP  CO
      •  PAWP  CVP
      •  SVR  Lactate Levels
    Anaphylactic Shock
  • 161.
    • TREATMENT
      • Epinephrine
      • IVF
      • Vasoconstrictors
      • Support/Maintain Airway
    Anaphylactic Shock
  • 162.
    • EARLY STAGE (Hyperdynamic)
      • Normal BP Tachycardia
      • Confusion Agitation (or listless)
      •  Respiratory Rate Temperature
      • Normal Color Normal or  UOP
      • Normal PAWP  CO  SVR
    • LATE STAGE (Hypodynamic)
      • Low BP Tachycardia
      • Orthostatic Hypotension Restlessness
      • Confusion Agitation (or listless)
      • Thirst Pallor
      • Cool, Clammy Skin  UOP
      •  CO  PAWP
      •  CVP  SVR
      •  Lactate Levels
    Septic Shock
  • 163.
    • TREATMENT
      • IVF (150cc/hr or wide open)
      • Treat Cause (Pan culture, antibiotics)
      • Vasoconstrictors in warm phase
      • Treat Temp as needed
    Septic Shock
  • 164.
    • CAUSES
      • Pulmonary Embolus Tamponade
      • Tension Pneumothorax Aortic Aneurysm
    • TREATMENT
      • Treat the Cause
    Obstructive Shock
  • 165.
    • SIRS Sepsis Severe Septic MODS Death
    • Infection Sepsis Shock
    Sepsis Syndrome
  • 166. Sepsis Syndrome
    • Sepsis
      • SIRS’ response with presumed/confirmed infection
    • Severe Sepsis
      • Sepsis associated with organ dysfunction, hypoperfusion (lactic acidosis, oliguria, altered mental status etc.), or hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)
    • Septic Shock
      • Sepsis with perfusion abnormalities and hypotension despite adequate fluid resuscitation
  • 167.  
  • 168. Homeostasis Gets Lost
  • 169.
    • Improve Perfusion
        • Prevent organ dysfunction
    Treatment for Sepsis
    • Treat The Cause
        • Seek primary site of infection
        • Direct therapy to primary cause
    • Stabilize The Patient
        • Fluids (lots of fluids)
        • Vasoconstrictors
  • 170.
        • THE END
        • PART 2
    PCCN REVIEW
  • 171.
        • THANK YOU!
    PCCN REVIEW
  • 172.
        • GOOD LUCK!
    PCCN REVIEW
  • 173.
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            • Balk, R. A. (2000). Severe sepsis and septic shock. Critical Care Clinics; (2)179-92.
            • Block, C., and Manning, H. (2002). Prevention of acute renal failure in the critically ill. American Journal of Respiratory and Critical Care Medicine; (165)320-324.
            • Brenner, B. M., and Rector, F.C. (2000). The kidney (6th ed), Vol I. Philadelphia: W.B. Saunders Company; (1)399-416.
            • Brettler S. (2005). Endovascular coiling for cerebral aneurysms. AACN Clinical Issues; (16)515-525.
            • Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranial aneurysms? Lancet; (366)783-785.
            • Campbell, D. (2003). How acute renal failure puts the breaks on kidney function. Nursing 2003; (33)59-63.
            • Guyton, A. C., and Hall, J. E. (2000). Unit V: The kidneys and body fluids. In A. C. Guyton & J. E. Hall. Textbook of medical physiology (10th ed.). Philadelphia: W.B. Saunders Company; pg. 264-379.
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            • Khurana, V. G., Friedman, J. A., Meyer, F. B. (2004). Chapter 11: Biology of Cerebral Blood Vessels and Blood Flow. In Le Roux, P. D., Winn, H. R., Newell, D. W. (eds). Management of Cerebral Aneurysms, Philadelphia, WB Saunders, pp 139-167, 2003.
            • Marino, P. L. (2006, September). The ICU Book. Lippincott Williams & Wilkins: Philadelphia.
            • Metheny, N. (2000). Fluid and Electrolyte Balance: Nursing Considerations (4th ed.) Philadelphia: Lippincott Williams & Wilkins; (4)158-200.
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    Resources Continued