PCCN Review Part 2 (of 2)


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  • Detoxify harmful substances (e.g., free radicals, drugs) Increase the absorption of calcium by producing calcitriol (form of vitamin D) Produce erythropoietin (hormone that stimulates red blood cell production in the bone marrow) Secrete renin (hormone that regulates blood pressure and electrolyte balance)
  • Detoxify harmful substances (e.g., free radicals, drugs) Increase the absorption of calcium by producing calcitriol (form of vitamin D) Produce erythropoietin (hormone that stimulates red blood cell production in the bone marrow) Secrete renin (hormone that regulates blood pressure and electrolyte balance)
  • Kidney - has 3 main sections         1. Renal Cortex - outer region (most of the nephron is located here)         2. Renal Medulla - inner region             a. columns - contains blood vessels             b. pyramids - contain loops of henle and collection ducts 3. Renal Pelvis
  • Network of Tubes Each kidney has approximately 1 million nephrons Most parts of the Nephron are in the renal cortex
  • Proximal Convoluted Tubule Leads away from Bowman’s capsule to the Loop of Henle Removes waste products (ammonia, nicotine) Reabsorbs useful substances (glucose, soduim, chloride, potassium, amino acids, vitamins, water and more) Loop of Henle a U-shaped extension of the proximal convoluted tubule The descending loop is highly permeable to water and impermeable to substances in the urine (e.g., salt, ammonia), The ascending loop is impermeable to water and permeable to other substances Distal Convoluted Tubule Leads away from the Loop of Henle to the collecting tubule substances are directly transferred from the surrounding capillaries into the renal tubule Secretes & collects potassium and bicarbonate (hydrogen ions) Collecting Tubule Concentrates urine in the medulla The channels are controlled by ADH Aldosterone receptors regulate Na uptake and K excretion
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • BUN / Cr ratio normally 12:1-20:1
  • If caused by meds, must stop meds If caused by obstruction, must remove obstruction If caused by blockage of artery, must open artery Dietary restrictions may include : low K+, adequate carbs, also may give TPN Fluids : calculate closley I/O Hyperkalemia is life threatening Lower K+ with Kayexalate, glucose, insulin, NaBicarb, caalcium carbonate
  • Neurological signs due to sympathetic nervous system stimulation
  • Osmolality = the concentration of solute (particles) per kilogram of water, which creates the pulling power of that solution for water Osmolarity – concentration of solute (particles) per liter of solution, which creates the pulling power of that solution for water Because body fluid solvent is water and one liter of water weighs one kilogram, the terms can be used interchangeably in discussing human fluid physiology
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • To begin this discussion, one needs to know what the volume of distribution of water is. Water accounts for 50% of total body weight in females and up to 60% in males. Thus if one administers 1 liter of water to a 70 kg female, it will be diluted 1 in 35 liters (total body water= 0.5 x body weight in females).
  • Total body water is divided in to 2 basic compartments: Intracellular (2/3) and extracellular (1/3). The cell membrane is freely permeable to water but dissolved electrolytes do not share the same permeability. Examples 1. 5% Dextrose in water (D5W) is handled just as free water is (since dextrose is metabolized). 2. Intravenous 0.9% saline (isotonic) does not diffuse through all compartments since the cell membrane is impermeable to sodium. 3. If 1 liter 0.45% saline is administered, ½ behaves as free water and ½ as saline.
  • Extracellular water is further divided into intravascular and extravascular (interstitial) compartments. The distribution of IV fluids may be further restricted by the capillary membrane, thus: 5% albumin is restricted to the intravascular space Isotonic saline can easily cross the capillary membrane and disperse throughout the extravascular (interstitial) space.
  • Since this fluid accumulates under conditions when patients are ill and thereby are not able to take in enough fluids, IV replacement frequently becomes necessary to prevent/treat extracellular volume depletion.
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • 5% Albumin will remain in the intravascular space, at least acutely. It is the most efficient way to treat shock. However, this effect is not permanent and, paradoxically in patients who are hypoalbuminemic (cirrhosis, nephrotic syndrome), albumin eventually enters the interstitial space because the integrity of the capillary barrier is not intact.
  • Isotonic (normal, 0.9%) saline is distributed in extracellular fluid since the cell membrane is not permeable to sodium. Thus, of 1 liter of NS in our hypothetical 70 kg male: 250ml will remain in the intravascular space and the remainder 750ml will exit into the interstitial space. In a patient with shock from fluid depletion, 1 liter of intravascular saline = 4 liters total saline may be required to restore hemodynamics
  • Solutions containing dextrose in water are handled like free water (although dextrose enters cells, it is metabolized). Thus 1 liter of D5W in a 70kg male will diffuse throughout body water 60ml will remain in the intravascular space, 240 will be in interstitial fluid and, 700ml will enter cells Dextrose in water is obviously not an efficient method to treat someone with shock.
  • CSF is produced in the choroid plexus. CSF is absorbed into the blood stream through the arachnoid villi. Protection : the CSF protects the brain from damage by "buffering" the brain. In other words, the CSF acts to cushion a blow to the head and lessen the impact. Buoyancy : because the brain is immersed in fluid, the net weight of the brain is reduced from about 1,400 gm to about 50 gm. Therefore, pressure at the base of the brain is reduced. Excretion of waste products : the one-way flow from the CSF to the blood takes potentially harmful metabolites, drugs and other substances away from the brain. Endocrine medium for the brain : the CSF serves to transport hormones to other areas of the brain. Hormones released into the CSF can be carried to remote sites of the brain where they may act.
  • Pheochromocytoma Cocaine
  • Pheochromocytoma Cocaine
  • AVM = defect of the circulatory system consisting of an abnormal connection between the arterial system (which normally has a higher intravascular pressure) and the lower pressure venous pathways.
  • Normally the connection between arteries and veins is through a network of smaller vessels (capillaries) which slow the blood down and permit the exchange of food, oxygen and nutrients into the tissues.
  • 20% have ECG evidence of myocardial ischemia • ST segment elevation, T wave changes ( Due to high levels of circulating catecholamines)
  • Papaverine is an opium alkaloid with vasodilatory action.
  • Stroke is the third leading cause of death in the United States. Every year 600,000 people will suffer a new or recurrent stroke, and of those, 160,000 will die. That’s one in 20 people that will suffer a stroke or TIA in their lifetime. Types of Ischemic strokes: Thrombotic Stroke Embolic Stroke
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One High BP : weakens and damages blood vessels High cholesterol : increase risks of arthrosclerosis and plaque buildup in arteries.
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One A 60-year-old woman was brought to the Emergency 3 hours after developing left hemiparesis. 1. A CT scan taken after being admitted. 2. An MRI scan performed the next day.
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
  • Metabolizes fats for energy resulting in buildup of fatty acids. Kussmaul = Rapid and deep respirations Polyuria Unconsciousness
  • Similar Symptoms include: Hypotension, LOC Changes, N/V, Polyuria, Thirst, Dry Mouth, Dry Skin, Weakness,
  • Severe Dehydration With HHNK NS X 1 Hours, then ½ NS with DKA NS X 2 Hours, then ½ NS with HHNK Continue NS as needed. Give insulin Watch for dilutional electrolyte lows
  • Decreased ADH Causes Inability To Concentrate Urine, Thereby Losing Water (Polyuria) Severe Hypovolemia
  • Watch for chest pain or abdominal cramps. Watch for for ST depressions.
  • Seizures due to cerebral edema
  • Holding onto water Water Intoxication
  • Activation of intrinsic or extrinsic pathways
  • Fibrin deposition in organs, leading to organ failure
  • Replacement Therapy FFP Platelets Cryoprecipitate Packed Red Blood Cells Anticoagulation Therapy Heparin Antithrombin III Recombinant tissue plasminogen activator Activated protein C
  • Orthostatic Hypotension
  • Orthostatic Hypotension
  • Toxins and bradykinins cause massive vasodilatation, a positive inotropic effect and stimulate the respiratory rate. May cause release of myocardial depressant factor in late phase. May stimulate the clotting cascade. Often leads to ARDS or/and DIC.
  • MODS = Multiple Organ Dysfunction Syndrome
  • Definitions – ACCP/SCCM Consensus Conference Definition Bone et al.1992. Chest 101:1644-1655. Sepsis: a systemic inflammatory response to infection Severe Sepsis: systemic inflammation, coagulation and impaired fibinolysis. Septic Shock: severe sepsis defined as sepsis-induced hypotension (systolic blood pressure < 90mmHg or a reduction of=40mmHg from baseline in the absence of other causes for hypotension) despite adequate fluid resuscitation along with the presence of perfusion abnormalities. Patients receiving inotropic or vasopressor agents may no longer be hypotensive by the time that they manifest hypoperfusion abnormalities or organ dysfunction, yet they would be considered having septic shock.
  • The cumulative effect of the cascades is an unbalanced state, with inflammation dominant over anti-inflammation and coagulation dominant over fibrinolysis. Microvascular thrombosis, hypoperfusion, ischemia, and tissue injury result. Severe sepsis, shock, and multiple organ dysfunction may occur, leading to death.
  • Optimize intravascular volume Consider Xygris (Activated Protein C)
  • PCCN Review Part 2 (of 2)

    1. 1. PCCN REVIEW PART 2 “Education is a progressive discovery of our own ignorance” - Will Durant - Sherry L. Knowles, RN, CCRN, CRNI
    2. 2. PCCN REVIEW PART 2 TOPICS Renal Alterations  Metabolic Alterations – Acute Renal Failure – DKA & HNNK – Electrolytes – DI & SIADH – IV Fluid Therapy – DIC Neurological Alterations – Shock States – AVM’s & Cerebral – Sepsis Aneurysms – Intracranial Hemorrhage – Stroke
    3. 3. PCCN REVIEW PART 2 OBJECTIVES1. List the main functions of the kidney.2. List the common diagnostic tests associated with renal function.3. List the complications associated with acute renal failure.4. Describe the common treatments of acute renal failure.5. List the major signs & symptoms associated with electrolyte disturbances of sodium, potassium magnesium and calcium and phosphorus.6. Define serum osmolality.7. List the intracellular & extracellular fluid compartments of the body.8. Describe the effects of hypotonic, isotonic and hypertonic IV fluids.9. Describe the different treatments for intravascular depletion verses cellular dehydration.10. Identify the risk factors and signs & symptoms of brain aneurysms and AVM’s.11. Explain the current treatments available for brain aneurysms and AVM’s.12. Describe the different types of intracranial hemorrhage and their associated signs & symptoms.
    4. 4. PCCN REVIEW OBJECTIVES13. List the potential complications of associated with intracranial hemorrhages, brain aneurysms and AVM repairs.14. List the types of CVA’s, their risk factors and related pathophysiology.15. Identify the recommended treatments for CVA’s.16. Differentiate between the signs and symptoms of DKA and HHNK.17. Describe the treatment of DKA and HHNK.18. Differentiate between the signs and symptoms of DI and SIADH.19. Describe the treatment of DI and SIADH.20. List the signs & symptoms of Disseminated Intravascular Coagulation.21. Explain the treatments for disseminated intravascular coagulation.22. Understand the different stages of shock.23. Differentiate between different types of shock.24. Identify the different treatments used for the different types of shock.25. Describe the stages of the sepsis syndrome.26. Explain the treatment of septic shock.
    5. 5. Renal Alterations  Acute Renal Failure  Electrolytes  IV Fluid Therapy
    6. 6. Acute Renal Failure WHAT DO THE KIDNEYS DO? – Filter blood  Regulates electrolytes – Regulate blood pressure  Renin-angiotensin system (RAS) – Maintain acid/base balance  Removes wastes, detoxifies blood
    7. 7. Acute Renal Failure 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
    8. 8. The Kidney
    9. 9. The Nephron
    10. 10. The Nephron  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
    11. 11. The Kidney The Renal Cortex Contains – Bowmans Capsules – Glomerulus – Proximal Tubules – Distal Convoluted Tubules The Renal Medulla Contains – The Pyramids  Loop of Henle  Collecting Duct  Blood Vessels
    12. 12. The Juxtaglomerular Apparatus Lies within Cortex Controls the activity of the nephron Plays major role in the renin-angiontension- aldosterone system
    13. 13. Urine Formation
    14. 14. Acute Renal Failure 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)
    15. 15. Acute Renal Failure 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
    16. 16. Acute Renal Failure PERSONS AT RISK – Major surgery – Major trauma – Receiving nephrotoxic medications – Hypovolemia > 40 minutes – Elderly
    17. 17. Acute Renal Failure SIGNS & SYMPTOMS – Azotemia – Oliguria - anuria – Hyperkalemia – HTN – Electrolyte Disturbances – Hypovolemia ⇑ K+ ⇑ phosphate – Pulmonary edema ⇓ Na+ ⇓ calcium – Ascites – Metabolic acidosis ⇑ Cr ⇑ BUN – Asterixis – Metabolic acidosis – Encephalopathy – Nausea/Vomiting
    18. 18. Acute Renal Failure COMPLICATIONS – Results in retention of toxins, fluids, and end products of metabolism – May be reversible with medical treatment
    19. 19. Acute Renal Failure 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
    20. 20. Acute Renal Failure OTHER DIAGNOSTIC TESTS – Albumin, glucose, prealbumin – KUB – ABD and renal CT/MRI – Retrograde pyloegram – Renal biopsy – Post-void residual or catheterization
    21. 21. Acute Renal Failure 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
    22. 22. Acute Renal Failure CAUSES – Pre-renal (hypoperfusion) – Renal (intrinsic) – Post-renal (obstructive)
    23. 23. Acute Renal Failure 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
    24. 24. Pre-Renal or Intra-Renal? Pre-renal Intra-renal BUN/Cr > 20 < 20 UNa (mEq/L) < 20 > 40Specific gravity high lowBUN/CR Ratio > 20:1 10-15:1
    25. 25. Acute Renal Failure 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
    26. 26. Acute Renal Failure 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.
    27. 27. Acute Renal Failure DIALYSIS – Hemodialysis – Peritoneal Dialysis – Continuous Renal Replacement Therapy (CRRT)
    28. 28. Chronic Renal Failure TREATMENT – Strict I&O – Watch for hyper/hypoglycemia – Daily weights – Watch for heart failure – Maintain nutrition – Monitor lab results – Mouth care – Watch for hyperkalemia – Monitor skin – S & S of Hyperkalemia: Malaise, anorexia, parenthesia, muscle weakness,EKG changes
    30. 30. K+ HCO3- PO4 Ca++ Mg+ Cu Na+ Electrolyte Disturbances NaClCl- NH3
    31. 31. Potassium (K+) Dominant intracellular electrolyte Primary buffer in the cell K+ Normal serum K+ level: 3.5-5.5 mEq/L
    32. 32. Potassium (K+) 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
    33. 33. Hyperkalemia SIGNS & SYMPTOMS – Weakness, malaise, lethargy – Anorexia – Muscle cramps – Paresthesias – Dysrhythmias
    34. 34. Hyperkalemia K > 5.5 -6 Tall, peaked T’s Wide QRS Prolong PR Diminished P Prolonged QT QRS-T wave merge = “sine wave”
    35. 35. Hyperkalemia CAUSES – Chronic or acute renal failure – Burns – Crush injuries – Excessive use of Potassium salts
    36. 36. Hyperkalemia TREATMENT – Calcium Gluconate (carbonate) – Calcium Chloride – Sodium Bicarbonate – Insulin/glucose – Kayexalate – Lasix – Albuterol – Hemodialysis
    37. 37. Hypokalemia SIGNS & SYMPTOMS –Malaise –Skeletal muscle weakness –Decreased reflexes –Hypotension –Vomiting –Excessive thirst –Cardiac arrhythmias and cardiac arrest –Flattened T wave –U wave
    38. 38. Sine Wave
    39. 39. Hypokalemia CAUSES – Reduced dietary intake – Poor absorption by the body – Vomiting and/or diarrhea – Renal disease – Medications (typically diuretics)
    40. 40. Hypoglycemia 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
    41. 41. Acute HypoglycemiaSIGNS & SYMPTOMSCardiovascular Signs Neurological Signs Palpitations Agitation Tachycardia Confusion Slurred Speech Anxiety Staggering Gait Irritability Paraplegia Diaphoresis Seizures Pale, cool skin Coma Tachypnea
    42. 42. Hyperglycemia SIGNS & SYMPTOMS – Thirst – Polyuria – Dehydration – Nausea, vomiting – DKA – HNNK Normal serum Glu level: 70 - 110 mg/dL
    43. 43. Sodium (Na+) Dominant extracellur electrolyte Chief determinant of osmolality NaCl Normal serum Na+ level: 135-145 mEq/L
    44. 44. Hyponatremia SIGNS & SYMPTOMS – Deficiency of sodium in the blood – Hypotension – Tachycardia – Muscle weakness – Mental Confusion
    45. 45. Hypernatremia SIGNS & SYMPTOMS – Excess sodium in the blood – Hypertension – Muscle twitching – Mental confusion – Coma
    46. 46. Magnesium (Mg+) Activates many enzymes 50% is insoluble in bone Mg+ 45% is intracellular 5% is extracellular Normal serum Mg+ level: 1.5 - 2.5 mg/dL
    47. 47. Hypomagnesemia SIGNS & SYMPTOMS – Tremors – Positive Chvostek & Trousseau – Nystagmus – Dysrhythmias – Confusion/Hallucinations– ECG Changes – Diarrhea  Flat T wave – Hyperactive deep reflexes  ST interval depression – Seizures  Prolonged QT interval – May lead to Torsade de Pointes
    48. 48. Hypomagnesemia CAUSES –Alcoholism –Malabsorption –Starvation –Diarrhea –Diuresis
    49. 49. Hypermagnesemia SIGNS & SYMPTOMS – Peaked T wave – Bradycardia – CNS Depression – Areflexia – Sedation – Respiratory paralysis
    50. 50. Hypermagnesemia CAUSES – Not common – Occurs with chronic renal insufficiency – Treatment is hemodialysis
    51. 51. Calcium (Ca++)– ESSENTIAL FOR – Neuromuscular transmission – Growth and ossification of bones – Muscle contraction Ca++ Normal serum Ca++ level: 8 - 11 mg/dL
    52. 52. Calcium (Ca++)– INVOLVED IN – Blood clotting – Nerve impulse – Muscle contraction Excreted through urine, feces, and perspiration Ca++
    53. 53. Hypocalcemia 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 – Chvosteks sign (facial twitching) – Paresthesia
    54. 54. Hypocalcemia CAUSES – Renal insufficiency – Decreased intake or malabsorption of Calcium – Deficiency in or inability to activate Vitamin D
    55. 55. Hypercalcemia SIGNS & SYMPTOMS – Kidney stones – Bone pain – Hypotonicity of muscles (decreased tone) – Altered mental status – Cardiac arrhythmias – Shortened QT interval
    56. 56. Hypercalcemia CAUSES – Neoplasms (tumors) – Excessive administration of Vitamin D TREATMENT – Usually aimed at underlying disease and hydration – Severe hypercalcemia may be treated with forced diuresis
    57. 57. Phosphorus (P, PO4) INVOLVED IN –Energy metabolism PO4 –Genetic coding –Cell function –Bone formation Normal serum PO4 level: 2.5-4.5 mg/dL
    58. 58. Hypophosphatemia SIGNS & SYMPTOMS – Respiratory difficulty – Confusion – Irritability – Coma
    59. 59. Hypophosphatemia 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
    60. 60. Hyperphosphatemia SIGNS & SYMPTOMS – Elevated blood phosphate level – There are no symptoms of hyperphosphatemia
    61. 61. Hyperphosphatemia TREATMENT – Calcium Carbonate tablets – Aluminum hydroxide  Can cause aluminum toxicity
    62. 62. IV Fluid Therapy OSMOLALITY – Concentration of a solution – The higher the osmolality the greater its pulling power for water Normal serum osmolality is 275 to 295 mOsm/L
    63. 63. Serum Osmolality 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
    64. 64. Major Mediators ofSodium and Water Balance  Angiotensin II  Aldosterone  Antidiuretic hormone (ADH)
    65. 65. Renin-Angiotensin-AldosteroneAngiotensin II  1. Stimulates production of aldosterone 2. Acts directly on arterioles to cause vasoconstriction 3. Stimulates Na+/H+ exchange in the proximal tubuleAldosterone  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
    66. 66. 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
    67. 67. IV Fluid TherapyIsotonic – same osmolality as serumHypotonic – lower osmolality than serumHypertonic – higher osmolality than serum
    68. 68. Effect on Cells
    69. 69. IV SolutionsD5W Isotonic 3% NaCl HypertonicD10W Hypertonic LR IsotonicD50W Hypertonic D5LR Hypertonic½ NS Hypotonic Albumin HypertonicNS Isotonic Dextran HypertonicD51/2 NS Hypertonic Hetastarch HypertonicD5NS Hypertonic PRBC’s HypertonicD5W Hypotonic in the body
    70. 70. IV Solutions D5W Hypotonic in the body Hypotonic Used for cellular dehydration Solutions Not used with head injuries Isotonic Hydrates extracellular compartment Solutions Hypertonic Pulls fluid into vascular space Solutions
    71. 71. Daily Fluid Balance Intake: 1-1.5 LInsensible Loss - Lungs 0.3 L - Sweat 0.1 L Urine: 1.0 to 1.5 L
    72. 72. Solids 40% of WtIntracellular Extracellular (2/3) (1/3) H2O H2O Na
    73. 73. E.C.F. COMPARTMENTSInterstitial (3/4) Intra- vascular (1/4) H2O H2O Na Na Colloids & RBC’s
    74. 74. “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.
    75. 75. 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
    76. 76. 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
    77. 77. 1 liter 5% Albumin Total body water ECFIntravascular=1 liter
    78. 78. 1 Liter 0.9% saline Total body waterECF=1 liter ICF=0 Interstitial=3/4 of ECF=750mlIntravascular=1/4 ECF=250 ml
    79. 79. 1 liter 5% Dextrose Total body water ECF=1/3 = 300ml ICF=2/3 = 700mlIntravascular=1/4 of ECF~75ml
    80. 80. 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
    82. 82. Neurological Alterations Brain Aneurysms & AVM’s Intracranial Hemorrhage Stroke
    83. 83. The Human Brain
    84. 84. Cerebral Spinal FluidThe serum-like fluid that circulates through the ventricles of thebrain, the cavity of the spinal cord, and the subarachnoid space
    85. 85. Brain Aneurysms & AVM’s 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 "short circuit“ between the arteries and veins
    86. 86. 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%)
    87. 87. Types of Aneurysms Saccular aneurysm – Occurs at bifurcations Fusiform aneurysm – Often in basilar artery Dissecting aneurysm Ruptured aneurysm
    88. 88. Brain Circulation
    89. 89. Arterial Circulation in the Brain
    90. 90. Intracranial Aneurysms 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)
    91. 91. Intracranial Aneurysms 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
    92. 92. Treatment of Brain Aneurysms Surgery – Craniotomy and clipping Endovascular coiling
    93. 93. 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
    94. 94. Arterio-Venous Malformation
    95. 95. Arterio-Venous Malformation The arteries and veins have a direct connection, bypassing the capillary network Presents with ongoing headaches, seizures, hemorrhage, or progressive neurological dysfunction
    96. 96. Arterio-Venous Malformation SIGNS & SYMPTOMS – Seizures – Headaches – “Whooshing" 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
    97. 97. Arterio-Venous Malformation COMPLICATIONS – Hemorrhage (into surrounding tissue) – Ischemia – Seizures – Brain Cell Death
    98. 98. 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
    99. 99. Arterio-Venous Malformation TREATMENT – Surgery  Usually delayed  Open ligation and/or resection of the AVM – Radiosurgery – Embolization  Usually as adjunct to surgery – Observation
    100. 100. Arterio-Venous Malformation RADIOSURGERY – Believed to "work" by initiating an "inflammatory" 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
    101. 101. 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
    102. 102. AVM Post-Op Risks  Perfusion-breakthrough bleeding  Endovascular occlusion
    103. 103. Intracranial HemorrhageSudden onset of “the worst headache of my life”
    104. 104. Intracranial Hemorrhage  Epidural  Subdural  Subarachnoid  Intraparencymal  Intraventricular  Cerebellar
    105. 105. Intracranial Hemorrhage 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
    106. 106. Treatment of ICH KEY CONCEPTS 1) Intracranial Pressure – Elevated when ICP >20 mm Hg 2) Cerebral Perfusion Pressure – CPP = MAP - ICP – Must maintain CPP > 70 mm Hg – Example: MAP = 100, ICP = 20 CPP = 80 mmHg
    107. 107. 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
    108. 108. 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”
    109. 109. Subarachnoid Hemorrhage (SAH) SAH may be spontaneous or traumatic Spontaneous SAH causes –Cerebral aneurysms –AV malformations –Trauma Uncommon causes –Neoplasms, venous angiomas, infections
    110. 110. Subarachnoid Hemorrhage 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
    111. 111. Subarachnoid Hemorrhage 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
    112. 112. 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)
    113. 113. 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
    114. 114. 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
    115. 115. Vasospasm & HHH Therapy Hemodilution –Hct 30-35% Hypertension –Phenylephrine / Norepinephrine –BP titration to CPP/exam Hypervolemia –Colloids/crystalloids
    116. 116. Other Vasospasm Therapy Angioplasty –BP management during procedure –Reperfusion issues –Timing Papaverine Infusion –Side effects –Repeated trips
    117. 117. Other Complications of SAH 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
    118. 118. Treatment of SAH1) Identify and treat the causative lesion – Thus preventing re-bleeding1) Treat hydrocephalus2) Treating and prevent vasospasm
    119. 119. Treatment of SAH Maintain systolic BP >130mmHg – Use vasopressors if necessary to maintain CPP and reduce ischemic complications from vasospasm – Generally avoid vasodilators (except calcium channel blockers)
    120. 120. PCCN REVIEW PART 1 BREAK
    121. 121. Stroke
    122. 122. Stroke
    123. 123. Stroke RISK FACTORS TIA  Excessive alcohol CAD  Family History High Blood Pressure  Age High Cholesterol  Sex Smoking  Race Heart Disease  Obesity Diabetes Annual risk of stroke: Increases with age
    124. 124. Stroke Tests 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!!
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    126. 126. Treatment of Ischemic CVA 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
    127. 127. Treatment of Hemorrhagic CVA 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
    128. 128. Prevention of CVA  Control high Blood Pressure  Lower cholesterol  Quit smoking  Control diabetes  Maintain healthy weight  Exercise  Manage stress  Eat a healthy diet
    129. 129. PCCN REVIEW PART 1 BREAK
    130. 130. Metabolic Alterations  DKA & HHNK  DI & SIADH  DIC  Shock States  Sepsis
    131. 131. Diabetic Ketoacidosis What is DKA? – Diabetic Ketoacidosis – A life-threatening complication seen with Diabetes Mellitus Type 1
    132. 132. Diabetic Ketoacidosis  SIGNS & SYMPTOMS – Serum Glucose 300-800 – Ketoacidosis Present – Large Serum And Urine Ketones – Fruity Breath – Kussmaul Respirations – Serum pH < 7.3 – Dehydration
    133. 133. HHNK What is HHNK? – Hyperglycemic Hyperosmolar Nonketonic Coma – A life threatening complication seen with Diabetes Mellitus Type 2
    134. 134. HHNK 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
    135. 135. DKA vs HHNK DKA HHNK Faster Onset  Slower Onset Glucose 300-800  Glucose 600-2000 Acidosis  No Acidosis Fruity Breath  Normal Breath Kussmaul Respirations  Shallow Respirations
    136. 136. Treatment of DKA & HHNK  Reverse Dehydration NS, then ½ NS  Restore Glucose Levels D5 ½ NS When Glu 250  Restore Electrolytes
    137. 137. Diabetes Insipitus What is Diabetes Insipitus? – A Condition resulting from too little ADH Why is it called Diabetes Insipitus? – The term Diabetes refers to polyuria
    138. 138. Diabetes Insipitus SIGNS & SYMPTOMS – Polyuria – Severe Hypovolemia – Severe Dehydration – Elevated Serum Osmolality – Elevated Serum Sodium – Shock
    139. 139. Diabetes Insipitus  CAUSES – Decreased ADH – Neurological Surgery – Head Trauma – Dilantin or Lithium
    140. 140. Diabetes Insipitus  TREATMENT – Fluid Resuscitation – ADH Replacement  Vasopressin, Pitressin, DDAVP – Treat The Cause
    141. 141. SIADH What is SIADH? – Syndrome of Inappropriate ADH – Too much ADH
    142. 142. SIADH SIGNS & SYMPTOMS– Hyponatremia – Elevated ADH Level– Low Serum Sodium – Weight Gain Without Edema  Serum NA < 135 – Elevated CVP, PAP, PAWP– Low Serum Osmolality – Hypertension– High Urine Osmolality – Concentrated And  UOP– Elevated Specific Gravity – Headache  Urine specific gravity > 1.030 – Altered LOC– Elevated Urine Osmolality – Seizures
    143. 143. SIADH CAUSES – Head Trauma – Medications – Oat Cell Carcinoma – Stress – Other Cancers – Mechanical Ventilation – Viral Pneumonia
    144. 144. SIADH 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
    145. 145. DI vs SIADH DI SIADH Too Little ADH  Too Much ADH Dehydration  Water Intoxication High Serum Sodium  Low Serum Sodium High Serum Osmolality  Low Serum Osmolality Low Urine Osmolality  High Urine Osmolality
    146. 146. DI vs SIADH Treatment DI SIADH Lots of Fluids  Fluid Restriction Hold Dilantin  May Give Dilantin Hold Lithium  May Give Lithium Give ADH  3% Saline
    147. 147. DIC What is DIC? – Disseminate Intravascular Coagulation – A clotting disorder that ultimately causes bleeding
    148. 148. DIC 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
    149. 149. Disseminated Intravascular Coagulation Systemic activation of coagulation Intravascular Depletion of platelets deposition of and coagulation fibrin factorsThrombosis of smalland midsize vessels BLEEDING with organ failure
    150. 150. DIC SIGNS & SYMPTOMS –Bleeding –Thrombosis –Organ Failure
    151. 151. DIC
    152. 152. DIC  CAUSES – Massive Tissue Injuries – Obstetric Emergencies – Septicemia – Cancers – Vascular Disorders – Systemic Disorders – Many More Causes
    153. 153. DIC Lab Results CLOTTING TESTS ELEVATED – PT ↑ – aPTT ↑ – Fibrin degradation products (D-dimer) ↑ CLOTTING FACTORS DEPLETED – Platelets ↓ – Fibrinogen ↓ – Protein C ↓ – Antithrombin ↓
    154. 154. DIC TREATMENT –Treat the Cause –Replace Clotting Factors –Anticoagulation Therapy (Heparin)
    155. 155. Shock DEFINITION –Inadequate perfusion to body tissues
    156. 156. Shock 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
    157. 157. Types of Shock 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
    158. 158. Hypovolemic Shock 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
    159. 159. Hypovolemic Shock TREATMENT –Volume (IVF, Blood)
    160. 160. Cardiogenic Shock 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
    161. 161. Cardiogenic Shock TREATMENT Bedrest O2 ↑ CO Positive Inotropes ↓ Preload & Afterload Diuretics ↓ Vasodilators Positioning ↓ Myocardial Demand IABP
    162. 162. Anaphylactic Shock 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
    163. 163. Anaphylactic Shock  TREATMENT – Epinephrine – IVF – Vasoconstrictors – Support/Maintain Airway
    164. 164. Septic Shock 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
    165. 165. Septic Shock TREATMENT – IVF (150cc/hr or wide open) – Treat Cause (Pan culture, antibiotics) – Vasoconstrictors in warm phase – Treat Temp as needed
    166. 166. Obstructive Shock CAUSES Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm TREATMENT Treat the Cause
    167. 167. Sepsis Syndrome SIRS Sepsis Severe Septic MODS DeathInfection Sepsis Shock
    168. 168. 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
    169. 169. Homeostasis Gets Lost
    170. 170. Treatment for Sepsis 1. Stabilize The Patient – Fluids (lots of fluids) – Vasoconstrictors 2. Treat The Cause – Seek primary site of infection – Direct therapy to primary cause 3. Improve Perfusion – Prevent organ dysfunction
    171. 171. PCCN REVIEW THE END PART 2
    172. 172. PCCN REVIEW THANK YOU!
    173. 173. PCCN REVIEW GOOD LUCK!
    174. 174. Resources American Stroke Association. (2007). Acute and Preventative Treatments. Retrieved March 4, 2007 from http://www.strokeassociation.org/presenter.jhtml?identifier =2532 Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):1–14, July 2001. 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. Impact of Stroke. (2007). American Stroke Association. Retrieved March 4, 2007 from http://www.strokeassociation.org/presenter.jhtml?identifier =1033
    175. 175. Resources Continued 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. Nettina, S. M. (2005). Diseases and Disorders in Lippincott Manual of Nursing Practice Handbook (3rd ed.), page 414. Rivers, E. P. (2006, February). Early goal-directed therapy in severe sepsis and septic shock: converting science to reality. Chest; 129(2):217-8. Rucker, D. (2006, June). Diabetic Ketoacidosis. Retrieved Feb 28, 2007 from http://www.emedicine.com/emerg/topic135.htm. Schmidt, T. (2000). “Assessing a Sodium and Fluid Imbalance”, Nursing 2000; (30) Number 1, p18. Sterns, R.H., Silver, S. M., Spital, A., Robertson, G. L., Seldin, D. W., Giebisch, G. (2000). The Kidney: Physiology & Pathophysiology. Philadelphia PA: Lippincott Williams & Wilkins, Inc; pgs. 1133–52 & 1217–38. Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188. Urden, L., Lough, M. E. & Stacy, K. L. (2005). Thelans Critical Care Nursing: Diagnosis and Management (5th ed). S