CCRN Review part 2

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The CCRN Review prepares critical care nurses for the CCRN and PCCN certification exams and is an excellent review for other nurses and other health care professionals.

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  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Network of Tubes Each kidney has approximately 1 million nephrons Most parts of the Nephron are in the renal cortex
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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) Proximal convoluted tubule reabsorbs 75 % of the filterate 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 Countercurrent Multiplier System The countercurrent flow within the descending and ascending limb increases (multiplies) the osmotic gradient between tubular fluid and interstitial space
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Nitrogenous Wastes = Ammonia (NH 3 ) = Urea ( CH 4 N 2 O) = Uric Acid ( C 5 H 4 N 4 O 3 )
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Glomerular Filtration Rate Normal = 90 - 120 mL/min/1.73 m 2 GFR decreases with age Levels below 60 mL/min/1.73 m 2 for 3 or more months are a sign of chronic kidney disease A GFR result below 15 mL/min/1.73 m 2 is a sign of kidney failure and requires immediate medical attention GFR Normal: 100-140 ml/min, Mild Kidney Failure < 90 ml/min, Moderate Kidney Failure < 60ml/min, Severe Kidney Failure < 30 ml/min, and End-stage Kidney Failure < 15ml/min, which is incompatible with life, without dialysis or transplantation
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 24hr urine creatine most definitive test for kidney function
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 MAP < 60 X > 40 min = ARF
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 BUN / Cr ratio normally 12:1-20:1 Lab Test Prerenal Value Intrarenal Value Urine Specific Gravity Greater than 1.020 1.010 to 1.020
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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 Renal Failure Diet Low Protein Low Phosphorus Low Potassium Low Sodium
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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 Renal Failure Diet Low Protein Low Phosphorus Low Potassium Low Sodium
  • Chronic renal failure is associated with insulin resistance. COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Neurological signs due to sympathetic nervous system stimulation
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Carpopedal spasm  = spasm of the hand or foot May see Chvostek & Trousseau signs in hypomagnesemia, hypocalcemia, hypo and hyperkalemia and alkalosis
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Need Vitamin D to absorb calcium
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Need Vitamin D to absorb calcium
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Inversely related to calcium (Hypophosphatemia = Hypercalcemia, Hypocalcemia – hyperphosphatemia) Need Vitamin D to absorb calcium
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Inversely related to calcium (Hypophosphatemia = Hypercalcemia, Hypocalcemia – hyperphosphatemia)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Inversely related to calcium (Hypophosphatemia = Hypercalcemia, Hypocalcemia – hyperphosphatemia)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Increase osmolality with Hyperglycemia Glucose is a large molecule Increased osmolality in hyperglycemia pulls water into vascular space and ultimately increases UOP
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • 5% Albumin = Isotonic 25% Albumin = Hypertonic COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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).
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • Lactate is metabolized into bicarbonate by the liver, which can lead to metabolic alkalosis. COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Increased ICP: Cushing’s Triad: 1. A change in respirations, often irregular and deep, such as cheyne stokes 2. A widening pulse pressure (the difference between the Systolic and the Diastolic BP) 3. Bradycardia
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • The Spinothalamic tract crosses over in the spinal cord before traveling up the spine. The Corticospinal Tract crosses in the medulla before traveling down the spine. COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • Brown-Séquard syndrome results from incomplete lateral injury (hemisection) of the spinal cord. COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • Central Cord Compression COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Ho monymous hemianopia is the loss of half of the visual field on the same side in both eyes. Brain injury is on the opposite side of the visual deficit in homonymous hemianopia.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Pheochromocytoma Cocaine
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Pheochromocytoma Cocaine
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 20% have ECG evidence of myocardial ischemia • ST segment elevation, T wave changes ( Due to high levels of circulating catecholamines)
  • Papaverine Infusion (antispasmodic) COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Papaverine is an opium alkaloid with vasodilatory action.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 High BP : weakens and damages blood vessels High cholesterol : increase risks of arthrosclerosis and plaque buildup in arteries.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Metabolizes fats for energy resulting in buildup of fatty acids. Kussmaul = Rapid and deep respirations Polyuria Unconsciousness
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Similar Symptoms include: Hypotension, LOC Changes, N/V, Polyuria, Thirst, Dry Mouth, Dry Skin, Weakness,
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 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
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Decreased ADH Causes Inability To Concentrate Urine, Thereby Losing Water (Polyuria) Severe Hypovolemia
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Watch for chest pain or abdominal cramps. Watch for for ST depressions.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Seizures due to cerebral edema
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Holding onto water Water Intoxication
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Activation of intrinsic or extrinsic pathways
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Fibrin deposition in organs, leading to organ failure
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Replacement Therapy FFP Platelets Cryoprecipitate Packed Red Blood Cells Anticoagulation Therapy Heparin Antithrombin III Recombinant tissue plasminogen activator Activated Protein C
  • CCRN Review part 2

    1. 1. ““Education is a progressiveEducation is a progressivediscovery of our own ignorance”discovery of our own ignorance”-- Will Durant -Will Durant -CCRN REVIEW PART 2CCRN REVIEW PART 2Sherry L. Knowles, RN, CCRN, CRNISherry L. Knowles, RN, CCRN, CRNI
    2. 2. TOPICSTOPICSRenal AlterationsRenal Alterations– Acute Renal FailureAcute Renal Failure– ElectrolytesElectrolytes– IV Fluid TherapyIV Fluid TherapyNeurological AlterationsNeurological Alterations– AVM’s & CerebralAVM’s & CerebralAneurysmsAneurysms– Intracranial HemorrhageIntracranial Hemorrhage– StrokeStrokeCCRN REVIEW PART 2CCRN REVIEW PART 2Metabolic AlterationsMetabolic Alterations– DKA & HNNKDKA & HNNK– DI & SIADHDI & SIADH– DICDIC– Shock StatesShock States– SepsisSepsis
    3. 3. OBJECTIVESOBJECTIVES1.1. List the main functions of the kidney.List the main functions of the kidney.2.2. List the common diagnostic tests associated with renal function.List the common diagnostic tests associated with renal function.3.3. List the complications associated with acute renal failure.List the complications associated with acute renal failure.4.4. Describe the common treatments of acute renal failure.Describe the common treatments of acute renal failure.5.5. List the major signs & symptoms associated with electrolyte disturbances ofList the major signs & symptoms associated with electrolyte disturbances ofsodium, potassium magnesium and calcium and phosphorus.sodium, potassium magnesium and calcium and phosphorus.6.6. Define serum osmolality.Define serum osmolality.7.7. List the intracellular & extracellular fluid compartments of the body.List the intracellular & extracellular fluid compartments of the body.8.8. Describe the effects of hypotonic, isotonic and hypertonic IV fluids.Describe the effects of hypotonic, isotonic and hypertonic IV fluids.9.9. Describe the different treatments for intravascular depletion verses cellularDescribe the different treatments for intravascular depletion verses cellulardehydration.dehydration.10.10. Identify the risk factors and signs & symptoms of brain aneurysms andIdentify the risk factors and signs & symptoms of brain aneurysms andAVM’s.AVM’s.11.11. Explain the current treatments available for brain aneurysms and AVM’s.Explain the current treatments available for brain aneurysms and AVM’s.12.12. Describe the different types of intracranial hemorrhage and their associatedDescribe the different types of intracranial hemorrhage and their associatedsigns & symptoms.signs & symptoms.CCRN REVIEW PART 2CCRN REVIEW PART 2
    4. 4. OBJECTIVESOBJECTIVES13.13. List the potential complications of associated with intracranial hemorrhages,List the potential complications of associated with intracranial hemorrhages,brain aneurysms and AVM repairs.brain aneurysms and AVM repairs.14.14. List the types of CVA’s, their risk factors and related pathophysiology.List the types of CVA’s, their risk factors and related pathophysiology.15.15. Identify the recommended treatments for CVA’s.Identify the recommended treatments for CVA’s.16.16. Differentiate between the signs and symptoms of DKA and HHNK.Differentiate between the signs and symptoms of DKA and HHNK.17.17. Describe the treatment of DKA and HHNK.Describe the treatment of DKA and HHNK.18.18. Differentiate between the signs and symptoms of DI and SIADH.Differentiate between the signs and symptoms of DI and SIADH.19.19. Describe the treatment of DI and SIADH.Describe the treatment of DI and SIADH.20.20. List the signs & symptoms of Disseminated Intravascular Coagulation.List the signs & symptoms of Disseminated Intravascular Coagulation.21.21. Explain the treatments for disseminated intravascular coagulation.Explain the treatments for disseminated intravascular coagulation.22.22. Understand the different stages of shock.Understand the different stages of shock.23.23. Differentiate between different types of shock.Differentiate between different types of shock.24.24. Identify the different treatments used for the different types of shock.Identify the different treatments used for the different types of shock.25.25. Describe the stages of the sepsis syndrome.Describe the stages of the sepsis syndrome.26.26. Explain the treatment of septic shock.Explain the treatment of septic shock.CCRN REVIEW PART 2CCRN REVIEW PART 2
    5. 5. Acute Renal FailureAcute Renal FailureElectrolytesElectrolytesIV Fluid TherapyIV Fluid TherapyRenalRenal AlterationsAlterations
    6. 6. AcuteAcute RenalRenal FailureFailureWHAT DO THE KIDNEYS DO?WHAT DO THE KIDNEYS DO?– Filter bloodFilter bloodRegulates electrolytesRegulates electrolytes– Regulate blood pressureRegulate blood pressureRenin-angiotensin system (RAS)Renin-angiotensin system (RAS)– Maintain acid/base balanceMaintain acid/base balanceRemoves wastes, detoxifies bloodRemoves wastes, detoxifies blood
    7. 7. AcuteAcute RenalRenal FailureFailureWHAT ELSE DO THE KIDNEYS DO?WHAT ELSE DO THE KIDNEYS DO?– Stimulate RBC productionStimulate RBC productionMake erythopoietinMake erythopoietin– Make corticosteroidsMake corticosteroidsRegulate kidney functionRegulate kidney function– Increase calcium absorptionIncrease calcium absorptionConvert Vitamin D to its active formConvert Vitamin D to its active form CalcitriolCalcitriol
    8. 8. TheThe KidneyKidney
    9. 9. TheThe NephronNephron
    10. 10. GlomerulusGlomerulus– Network of capillariesNetwork of capillariesBowman’sBowman’s capsulecapsule– Membrane that surroundsMembrane that surroundsthe glomerulusthe glomerulusRenal TubulesRenal Tubules– Travel from cortex toTravel from cortex tomedulla and back to cortexmedulla and back to cortexCollecting ductCollecting duct– Within the medullaWithin the medullaTheThe NephronNephron
    11. 11. TheThe KidneyKidneyThe Renal Cortex ContainsThe Renal Cortex Contains– Bowmans CapsulesBowmans Capsules– GlomerulusGlomerulus– Proximal TubulesProximal Tubules– Distal Convoluted TubulesDistal Convoluted TubulesThe Renal Medulla ContainsThe Renal Medulla Contains– The PyramidsThe PyramidsLoop of HenleLoop of HenleCollecting DuctCollecting DuctBlood VesselsBlood Vessels
    12. 12. Lies within CortexLies within CortexControls the activity ofControls the activity ofthe nephronthe nephronPlays major role in thePlays major role in therenin-angiontension-renin-angiontension-aldosterone systemaldosterone systemThe Juxtaglomerular ApparatusThe Juxtaglomerular Apparatus
    13. 13. UrineUrine FormationFormation
    14. 14. AcuteAcute RenalRenal FailureFailureDEFINITIONSDEFINITIONS– Sudden interruption of kidney function resultingSudden interruption of kidney function resultingfrom obstruction, reduced circulation, or disease offrom obstruction, reduced circulation, or disease ofthe renal tissuethe renal tissue– Rapid deterioration of renal functionRapid deterioration of renal functionincrease of creatinine of >0.5 mg/dl in <72hrsincrease of creatinine of >0.5 mg/dl in <72hrs““azotemia” (accumulation of nitrogenous wastes)azotemia” (accumulation of nitrogenous wastes)elevated BUN and Creatinine levelselevated BUN and Creatinine levelsdecreased urine output (usually but not always)decreased urine output (usually but not always)
    15. 15. AcuteAcute RenalRenal FailureFailureTERMINOLOGYTERMINOLOGY– Anuria:Anuria: No UOP (or <100mL/24hrs)No UOP (or <100mL/24hrs)– OliguriaOliguria:: UOP<400-500 mL/24hrsUOP<400-500 mL/24hrs– AzotemiaAzotemia:: (Increased BUN, Cr, Urea)(Increased BUN, Cr, Urea)May be prerenal, renal, postrenalMay be prerenal, renal, postrenalDoes not require any clinical findingsDoes not require any clinical findings– Chronic Renal InsufficiencyChronic Renal InsufficiencyDeterioration over months-yearsDeterioration over months-yearsGFR 10-20 mL/min, or 20-50% of normalGFR 10-20 mL/min, or 20-50% of normal– ESRD:ESRD: GFR <5% of mL/minGFR <5% of mL/min
    16. 16. AcuteAcute RenalRenal FailureFailurePERSONS AT RISKPERSONS AT RISK– Major surgeryMajor surgery– Major traumaMajor trauma– Receiving nephrotoxic medicationsReceiving nephrotoxic medications– Hypovolemia > 40 minutesHypovolemia > 40 minutes– ElderlyElderly
    17. 17. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– AzotemiaAzotemia– HyperkalemiaHyperkalemia– Electrolyte DisturbancesElectrolyte Disturbances⇑⇑ K+K+ ⇑⇑ phosphatephosphate⇓⇓ Na+Na+ ⇓⇓ calciumcalcium⇑⇑ CrCr ⇑⇑ BUNBUN– Metabolic acidosisMetabolic acidosis– Nausea/VomitingNausea/Vomiting– Oliguria - anuriaOliguria - anuria– HTNHTN– HypovolemiaHypovolemia– Pulmonary edemaPulmonary edema– AscitesAscites– Metabolic acidosisMetabolic acidosis– AsterixisAsterixis– EncephalopathyEncephalopathyAcuteAcute RenalRenal FailureFailure
    18. 18. AcuteAcute RenalRenal FailureFailureCOMPLICATIONSCOMPLICATIONS– Results in retention of toxins, fluids, and endResults in retention of toxins, fluids, and endproducts of metabolismproducts of metabolism– May be reversible with medical treatmentMay be reversible with medical treatment
    19. 19. DIAGNOSTIC TESTSDIAGNOSTIC TESTS– H&PH&P– BUN, creatinine, sodium, potassium, pH,BUN, creatinine, sodium, potassium, pH,bicarb, Hgb and Hctbicarb, Hgb and Hct– Urine studiesUrine studies– US of kidneysUS of kidneys– 24 hour urine for protein and creatinine24 hour urine for protein and creatinine– Urine eosinophilsUrine eosinophilsAcuteAcute RenalRenal FailureFailure
    20. 20. OTHER DIAGNOSTIC TESTSOTHER DIAGNOSTIC TESTS– Albumin, glucose, prealbuminAlbumin, glucose, prealbumin– KUBKUB– Abd and Renal CT/MRIAbd and Renal CT/MRI– Retrograde pyloegramRetrograde pyloegram– Renal biopsyRenal biopsy– Post-void residual or catheterizationPost-void residual or catheterizationAcuteAcute RenalRenal FailureFailure
    21. 21. AcuteAcute RenalRenal FailureFailurePHASESPHASES– OnsetOnset1-3 days with1-3 days with ⇑⇑ BUN andBUN and ⇑⇑ creatinine andcreatinine andpossible decreased UOPpossible decreased UOP– OliguricOliguricUOP < 400/day,UOP < 400/day, ⇑⇑ BUN,BUN, ⇑⇑ Cr,Cr, ⇑⇑ P04,P04, ⇑⇑ K, mayK, maylast up to 14 dayslast up to 14 days– DiureticDiureticUOPUOP ⇑⇑ to as much as 4000 mL/day but withoutto as much as 4000 mL/day but withoutwaste products, may begin to see improvement atwaste products, may begin to see improvement atend of this stageend of this stage– RecoveryRecoveryThings go back to normal or may remainThings go back to normal or may remaininsufficient and become chronicinsufficient and become chronic
    22. 22. AcuteAcute RenalRenal FailureFailureCAUSESCAUSES– Pre-renalPre-renal (hypoperfusion)(hypoperfusion)– RenalRenal (intrinsic)(intrinsic)– Post-renalPost-renal (obstructive)(obstructive)
    23. 23. AcuteAcute RenalRenal FailureFailureSPECIFIC CAUSESSPECIFIC CAUSES– PrerenalPrerenalHypovolemia, shock, blood loss, embolism,Hypovolemia, shock, blood loss, embolism,pooling of fluid due to ascites or burns,pooling of fluid due to ascites or burns,cardiovascular disorders, sepsiscardiovascular disorders, sepsis– IntrarenalIntrarenalATN, nephrotoxic agents, infections, ischemiaATN, nephrotoxic agents, infections, ischemiaacute tubular necrosis, acute nephritis, polycysticacute tubular necrosis, acute nephritis, polycystickidney diseasekidney disease– PostrenalPostrenalStones, blood clots, BPH, urethral edema fromStones, blood clots, BPH, urethral edema frominvasive procedures, renal calculiinvasive procedures, renal calculi
    24. 24. Pre-Renal or Intra-Renal?Pre-Renal or Intra-Renal?Pre-renal Intra-renalBUN/Cr > 20 < 20Urine Na(mEq/L)< 20 > 40UrineSpecific GravityHigh LowBUN/CR Ratio > 20:1 < 10-15:1
    25. 25. TREATMENTTREATMENT– Make/consider the diagnosisMake/consider the diagnosis– Treat life threatening conditionsTreat life threatening conditions– Identify the cause if possibleIdentify the cause if possibleHypovolemiaHypovolemiaToxic agents (drugs, myoglobin)Toxic agents (drugs, myoglobin)ObstructionObstruction– Treat reversible elementsTreat reversible elementsHydrateHydrateRemove drugRemove drugRelieve obstructionRelieve obstructionAcuteAcute RenalRenal FailureFailure
    26. 26. NURSING CARENURSING CARE– Fluid and dietary restrictionsFluid and dietary restrictionsProtein, potassium & phosphate restrictionProtein, potassium & phosphate restriction– Maintain electrolytesMaintain electrolytes– D/C or reduce causative agentD/C or reduce causative agent– Adjust medication dosesAdjust medication doses– May need dialysis to jump start renal functionMay need dialysis to jump start renal function– May need to stimulate production of urine withMay need to stimulate production of urine withIV fluids, Dopamine, diuretics, etc.IV fluids, Dopamine, diuretics, etc.AcuteAcute RenalRenal FailureFailure
    27. 27. DIALYSISDIALYSIS– HemodialysisHemodialysis– Peritoneal DialysisPeritoneal Dialysis– Continuous Renal Replacement Therapy (CRRT)Continuous Renal Replacement Therapy (CRRT)AcuteAcute RenalRenal FailureFailure
    28. 28. TREATMENTTREATMENT– Strict I&OStrict I&O– Daily weightsDaily weights– Watch for heart failureWatch for heart failure– Monitor lab resultsMonitor lab results– Watch for hyperkalemiaWatch for hyperkalemia– Watch forWatch forhyper/hypoglycemiahyper/hypoglycemia– Maintain nutritionMaintain nutrition– Mouth careMouth care– Monitor skinMonitor skin– S & S of Hyperkalemia: Malaise, anorexia,S & S of Hyperkalemia: Malaise, anorexia,parenthesia, muscle weakness, EKG changesparenthesia, muscle weakness, EKG changesChronic RenalChronic Renal FailureFailureS & S
    29. 29. BREAKBREAKCCRN REVIEW PART 2CCRN REVIEW PART 2
    30. 30. ElectrolyteElectrolyteDisturbancesDisturbancesNa+Ca++Cl-Mg+K+PO4NH3CuHCO3-NaCl
    31. 31. Dominant intracellular electrolyteDominant intracellular electrolytePrimary buffer in the cellPrimary buffer in the cellK+K+Potassium (KPotassium (K++))Normal serum K+ level: 3.5-5.5 mEq/LNormal serum K+ level: 3.5-5.5 mEq/L
    32. 32. INVOLVED ININVOLVED IN– Muscle contractionMuscle contraction– Nerve impulsesNerve impulses– Cell membrane functionCell membrane function– Attracting water into the ICFAttracting water into the ICF– Imbalances interfere with neuromuscular functionImbalances interfere with neuromuscular functionand may cause cardiac rhythm disturbancesand may cause cardiac rhythm disturbancesPotassium (KPotassium (K++))
    33. 33. HyperkalemiaHyperkalemiaSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Weakness, malaise, lethargyWeakness, malaise, lethargy– AnorexiaAnorexia– Muscle crampsMuscle cramps– ParesthesiasParesthesias– DysrhythmiasDysrhythmias
    34. 34. K > 5.5 -6K > 5.5 -6Tall, peaked T’sTall, peaked T’sWide QRSWide QRSProlong PRProlong PRDiminished PDiminished PProlonged QTProlonged QTQRS-T waveQRS-T wavemerge = “sine wave”merge = “sine wave”HyperkalemiaHyperkalemia
    35. 35. Sine (Off) WaveSine (Off) Wave
    36. 36. HyperkalemiaHyperkalemiaCAUSESCAUSES– Chronic or acute renal failureChronic or acute renal failure– BurnsBurns– Crush injuriesCrush injuries– Excessive use of Potassium saltsExcessive use of Potassium salts
    37. 37. TREATMENTTREATMENT– Calcium Gluconate (carbonate)Calcium Gluconate (carbonate)– Calcium ChlorideCalcium Chloride– Sodium BicarbonateSodium Bicarbonate– Insulin/glucoseInsulin/glucose– KayexalateKayexalate– LasixLasix– AlbuterolAlbuterol– HemodialysisHemodialysisHyperkalemiaHyperkalemia
    38. 38. SIGNS & SYMPTOMSSIGNS & SYMPTOMS–MalaiseMalaise–Skeletal muscle weaknessSkeletal muscle weakness–Decreased reflexesDecreased reflexes–HypotensionHypotension–VomitingVomiting–Excessive thirstExcessive thirst–Cardiac arrhythmias and cardiac arrestCardiac arrhythmias and cardiac arrest–Flattened T waveFlattened T wave–U waveU waveHypokalemiaHypokalemia
    39. 39. HypokalemiaHypokalemiaCAUSESCAUSES– Reduced dietary intakeReduced dietary intake– Poor absorption by the bodyPoor absorption by the body– Vomiting and/or diarrheaVomiting and/or diarrhea– Renal diseaseRenal disease– Medications (typically diuretics)Medications (typically diuretics)
    40. 40. Hypo Verses Hyper PotassiumHypo Verses Hyper Potassium
    41. 41.  SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Cold, clammy, pale skinCold, clammy, pale skin– NervousnessNervousness– Shakiness, lack of coordination, staggering gaitShakiness, lack of coordination, staggering gait– Irritability, hostility, and strange behaviorIrritability, hostility, and strange behavior– Difficulty concentratingDifficulty concentrating– FatigueFatigue– Excessive hungerExcessive hunger– HeadacheHeadache– Blurred vision and dizzinessBlurred vision and dizziness– Abdominal pain or nauseaAbdominal pain or nausea– Fainting and unconsciousnessFainting and unconsciousnessHypoglycemiaHypoglycemia
    42. 42. SIGNS & SYMPTOMSSIGNS & SYMPTOMSCardiovascular SignsCardiovascular SignsPalpitationsPalpitationsTachycardiaTachycardiaAnxietyAnxietyIrritabilityIrritabilityDiaphoresisDiaphoresisPale, cool skinPale, cool skinTachypneaTachypneaNeurological SignsNeurological SignsAgitationAgitationConfusionConfusionSlurred SpeechSlurred SpeechStaggering GaitStaggering GaitParaplegiaParaplegiaSeizuresSeizuresComaComaAcute HypoglycemiaAcute Hypoglycemia
    43. 43. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– ThirstThirst– PolyuriaPolyuria– DehydrationDehydration– Nausea, vomitingNausea, vomiting– DKADKA– HNNKHNNKHyperglycemiaHyperglycemiaNormal serum Glu level:Normal serum Glu level: 70 - 110 mg/dL70 - 110 mg/dL
    44. 44. Dominant extracellur electrolyteDominant extracellur electrolyteChief determinant of osmolalityChief determinant of osmolalityNaClNaClSodium (NaSodium (Na++))Normal serum Na+ level: 135-145 mEq/LNormal serum Na+ level: 135-145 mEq/L
    45. 45. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Deficiency of sodium in the bloodDeficiency of sodium in the blood– HypotensionHypotension– TachycardiaTachycardia– Muscle weaknessMuscle weakness– Mental ConfusionMental ConfusionHyponatremiaHyponatremia
    46. 46. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Excess sodium in the bloodExcess sodium in the blood– HypertensionHypertension– Muscle twitchingMuscle twitching– Mental confusionMental confusion– ComaComaHypernatremiaHypernatremia
    47. 47. Activates many enzymesActivates many enzymes50% is insoluble in bone50% is insoluble in bone45% is intracellular45% is intracellular5% is extracellular5% is extracellularMg+Mg+Magnesium (MgMagnesium (Mg++))Normal serum Mg+ level: 1.5 - 2.5 mg/dLNormal serum Mg+ level: 1.5 - 2.5 mg/dL
    48. 48. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– TremorsTremors– Positive Chvostek & TrousseauPositive Chvostek & Trousseau– NystagmusNystagmus– Confusion/HallucinationsConfusion/Hallucinations– DiarrheaDiarrhea– Hyperactive deep reflexesHyperactive deep reflexes– SeizuresSeizuresHypomagnesemiaHypomagnesemia– DysrhythmiasDysrhythmias– ECG ChangesECG ChangesFlat T waveFlat T waveST interval depressionST interval depressionProlonged QT intervalProlonged QT interval– May lead toMay lead toTorsade deTorsade dePointesPointes
    49. 49. CAUSESCAUSES–AlcoholismAlcoholism–MalabsorptionMalabsorption–StarvationStarvation–DiarrheaDiarrhea–DiuresisDiuresisHypomagnesemiaHypomagnesemia
    50. 50. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Peaked T wavePeaked T wave– BradycardiaBradycardia– CNS DepressionCNS Depression– AreflexiaAreflexia– SedationSedation– Respiratory paralysisRespiratory paralysisHypermagnesemiaHypermagnesemia
    51. 51. CAUSESCAUSES– Not commonNot common– Occurs with chronic renal insufficiencyOccurs with chronic renal insufficiency– Treatment is hemodialysisTreatment is hemodialysisHypermagnesemiaHypermagnesemia
    52. 52. – ESSENTIAL FORESSENTIAL FOR– Neuromuscular transmissionNeuromuscular transmission– Growth and ossification of bonesGrowth and ossification of bones– Muscle contractionMuscle contractionCa++Ca++Calcium (CaCalcium (Ca++++))Normal serum Ca++ level: 8 - 11 mg/dLNormal serum Ca++ level: 8 - 11 mg/dL
    53. 53. – INVOLVED ININVOLVED IN– Blood clottingBlood clotting– Nerve impulseNerve impulse– Muscle contractionMuscle contractionCa++Ca++Calcium (CaCalcium (Ca++++))Excreted through urine, feces, and perspirationExcreted through urine, feces, and perspiration
    54. 54. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– TetanyTetany (cramps/convulsions in wrists and ankles)(cramps/convulsions in wrists and ankles)– Weak heart muscleWeak heart muscle– Increased clotting timeIncreased clotting time– Prolonged QT intervalProlonged QT intervalMay lead to Torsade de PointesMay lead to Torsade de Pointes– Abnormal behaviorAbnormal behavior– Chvosteks sign (facial twitching)Chvosteks sign (facial twitching)– Trousseau”s Sign (carpopedal spasm)Trousseau”s Sign (carpopedal spasm)– ParesthesiaParesthesiaHypocalcemiaHypocalcemia
    55. 55. CAUSESCAUSES– Renal insufficiencyRenal insufficiency– Decreased intake or malabsorption of CalciumDecreased intake or malabsorption of Calcium– Deficiency in or inability to activate Vitamin DDeficiency in or inability to activate Vitamin DHypocalcemiaHypocalcemia
    56. 56. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Kidney stonesKidney stones– Bone painBone pain– Hypotonicity of musclesHypotonicity of muscles (decreased tone)(decreased tone)– Altered mental statusAltered mental status– Cardiac arrhythmiasCardiac arrhythmias– Shortened QT intervalShortened QT intervalHypercalcemiaHypercalcemia
    57. 57. CAUSESCAUSES– Neoplasms (tumors)Neoplasms (tumors)– Excessive administration of Vitamin DExcessive administration of Vitamin DHypercalcemiaHypercalcemiaTREATMENTTREATMENT– Usually aimed at underlying disease andUsually aimed at underlying disease andhydrationhydration– Severe hypercalcemia may be treated withSevere hypercalcemia may be treated withforced diuresisforced diuresis
    58. 58. INVOLVED ININVOLVED IN–Energy metabolismEnergy metabolism–Genetic codingGenetic coding–Cell functionCell function–Bone formationBone formationPOPO44Phosphorus (P, POPhosphorus (P, PO44))Normal serum PO4 level: 2.5-4.5 mg/dLNormal serum PO4 level: 2.5-4.5 mg/dL
    59. 59. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Respiratory difficultyRespiratory difficulty– ConfusionConfusion– IrritabilityIrritability– ComaComaHypophosphatemiaHypophosphatemia
    60. 60. CAUSESCAUSES– Severe infectionsSevere infections– Kidney failureKidney failure– Thyroid failureThyroid failure– Parathyroid FailureParathyroid Failure– Often associated with hypercalcemia orOften associated with hypercalcemia orhypomagnesemia or too much Vitamin Dhypomagnesemia or too much Vitamin D– Cell destruction - from chemotherapy, when theCell destruction - from chemotherapy, when thetumor cells die at a fast ratetumor cells die at a fast rateCan cause tumor lysis syndromeCan cause tumor lysis syndromeHypophosphatemiaHypophosphatemia
    61. 61. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Elevated blood phosphate levelElevated blood phosphate level– There are no symptoms of hyperphosphatemiaThere are no symptoms of hyperphosphatemiaHyperphosphatemiaHyperphosphatemia
    62. 62. TREATMENTTREATMENT– Calcium Carbonate tabletsCalcium Carbonate tablets– Aluminum hydroxideAluminum hydroxideCan cause aluminum toxicityCan cause aluminum toxicityHyperphosphatemiaHyperphosphatemia
    63. 63. IV Fluid TherapyIV Fluid TherapyOSMOLALITYOSMOLALITY– Concentration of a solutionConcentration of a solution– Concentration of solutes per kilogramConcentration of solutes per kilogram– The higher the osmolality the greaterThe higher the osmolality the greaterits pulling power for waterits pulling power for waterNormal serum osmolality isNormal serum osmolality is 275 to 295275 to 295 mOsm/LmOsm/L
    64. 64. Serum OsmolalitySerum OsmolalitySodium = major solute in plasmaSodium = major solute in plasma– Estimated serum osmolality = 2 X serum NaEstimated serum osmolality = 2 X serum NaUrea (BUN) and Glucose are large moleculesUrea (BUN) and Glucose are large moleculesthatthat ↑↑ serum osmolalityserum osmolality– When either or both are elevated, the serum osmolalityWhen either or both are elevated, the serum osmolalitywill be higher than 2 times the sodium level, so thewill be higher than 2 times the sodium level, so thefollowing formula is more accurate:following formula is more accurate:Serum osmolality = 2 X serum Na +Serum osmolality = 2 X serum Na + BUNBUN ++ glucoseglucose3 183 18
    65. 65. Major Mediators ofMajor Mediators ofSodium and Water BalanceSodium and Water BalanceAngiotensin IIAngiotensin IIAldosteroneAldosteroneAntidiuretic hormone (ADH)Antidiuretic hormone (ADH)
    66. 66. Renin-Angiotensin-AldosteroneRenin-Angiotensin-AldosteroneAngiotensin IIAngiotensin II  1. Stimulates production of aldosterone1. Stimulates production of aldosterone2. Acts directly on arterioles to cause vasoconstriction2. Acts directly on arterioles to cause vasoconstriction3. Stimulates Na3. Stimulates Na++/H/H++exchange in the proximal tubuleexchange in the proximal tubuleAldosteroneAldosterone  1. Stimulates reabsorption of Na1. Stimulates reabsorption of Na++and excretion of Kand excretion of K++ininthe late distal tubulethe late distal tubule2. Stimulates activity of H2. Stimulates activity of H++ATPase pumps in the lateATPase pumps in the latedistal tubuledistal tubule
    67. 67. Antidiuretic Hormone (ADH)Antidiuretic Hormone (ADH)Synthesized in the hypothalamus and stored in theSynthesized in the hypothalamus and stored in theposterior pituitaryposterior pituitaryReleased in response to plasma hyperosmolalityReleased in response to plasma hyperosmolalityand decreased circulating volumeand decreased circulating volumeActions of ADHActions of ADH– Increases the water permeability of the collecting tubuleIncreases the water permeability of the collecting tubule(makes kidneys reabsorb more water)(makes kidneys reabsorb more water)– Mildly increases vascular resistanceMildly increases vascular resistance
    68. 68. IsotonicIsotonic – same osmolality as serum– same osmolality as serumHypotonicHypotonic – lower osmolality than serum– lower osmolality than serumHypertonicHypertonic – higher osmolality than serum– higher osmolality than serumIV Fluid TherapyIV Fluid Therapy
    69. 69. Effect on CellsEffect on Cells
    70. 70. IV SolutionsIV SolutionsD5WD5W Hypotonic in the bodyHypotonic in the bodyHypotonicHypotonicSolutionsSolutionsUsed for cellular dehydrationUsed for cellular dehydrationNot used with head injuriesNot used with head injuriesIsotonicIsotonicSolutionsSolutionsHydrates extracellular compartmentHydrates extracellular compartmentHypertonicHypertonicSolutionsSolutionsPulls fluid into vascular spacePulls fluid into vascular space
    71. 71. IV SolutionsIV SolutionsD5WD5WD10WD10WD50WD50W½ NS½ NSNSNSD51/2 NSD51/2 NSD5NSD5NSD5WD5W Hypotonic in the bodyHypotonic in the bodyIsotonicIsotonicHypertonicHypertonicHypertonicHypertonicHypotonicHypotonicIsotonicIsotonicHypertonicHypertonicHypertonicHypertonicHypertonicHypertonicIsotonicIsotonicHypertonicHypertonicHypertonicHypertonicHypertonicHypertonicHypertonicHypertonicHypertonicHypertonic3% NaCl3% NaClLRLRD5LRD5LRAlbuminAlbuminDextranDextranHetastarchHetastarchPRBC’sPRBC’s
    72. 72. Daily Fluid BalanceDaily Fluid BalanceIntake:Intake:1-1.5 L1-1.5 LInsensible LossInsensible Loss- Lungs 0.3 L- Lungs 0.3 L- Sweat 0.1 L- Sweat 0.1 LUrine: 1.0 to 1.5 LUrine: 1.0 to 1.5 L
    73. 73. IntracellularIntracellular(2/3)(2/3)ExtracellularExtracellular(1/3)(1/3)Solids 40% of WtSolids 40% of WtHH22OO HH22OONaNa
    74. 74. Intra-Intra-vascularvascular((1/4)1/4)E.CE.C..FF.. COMPARTMENTSCOMPARTMENTSInterstitial (3/4)Interstitial (3/4)HH22OO HH22OONaNaNaNaColloidsColloids& RBC’s& RBC’s
    75. 75. ““Third Space”Third Space”Third space refers to collection of fluids (usuallyThird space refers to collection of fluids (usuallyisotonic) that is sequestered in potential spaces.isotonic) that is sequestered in potential spaces.This situation is not normal and the fluid is derivedThis situation is not normal and the fluid is derivedfrom extracellular fluid.from extracellular fluid.
    76. 76. Principles of TreatmentPrinciples of TreatmentHow much volume?How much volume?– Need to estimate fluid deficitNeed to estimate fluid deficitWhich fluid?Which fluid?– Which fluid compartment is predominantly affected?Which fluid compartment is predominantly affected?– Must evaluate other acid/base, electrolyte &Must evaluate other acid/base, electrolyte &nutrition needsnutrition needs
    77. 77. Fluid Replacement ProductsFluid Replacement ProductsCrystalloidsCrystalloids –– able to pass through semi permeable membranesable to pass through semi permeable membranes–Isotonic solutionsIsotonic solutions–Hypotonic solutionsHypotonic solutions–Hypertonic solutionsHypertonic solutionsColloidsColloids – do not cross the semi permeable membrane and remain– do not cross the semi permeable membrane and remainin the intravascular space for several days (pulling fluidin the intravascular space for several days (pulling fluidout of the intracellular and interstitial space)out of the intracellular and interstitial space)–AlbuminAlbumin–DextranDextran–HetastarchHetastarch
    78. 78. 1 liter 5% Albumin1 liter 5% AlbuminIntravascularIntravascular=1 liter=1 literTotal body waterTotal body waterECFECFICFICF
    79. 79. Total body waterTotal body waterECF=1 literECF=1 liter ICF=0ICF=0IntravascularIntravascular=1/4 ECF=250 ml=1/4 ECF=250 ml1 Liter 0.9% saline1 Liter 0.9% salineInterstitial=3/4Interstitial=3/4of ECF=750mlof ECF=750ml
    80. 80. 1 liter 5% Dextrose1 liter 5% DextroseTotal body waterTotal body waterECF=1/3 = 300mlECF=1/3 = 300ml ICF=2/3 = 700mlICF=2/3 = 700mlIntravascularIntravascular=1/4 of ECF~75ml=1/4 of ECF~75ml
    81. 81. Ringers LactateRingers LactateInfusion of Ringer Lactate solution may lead to metabolicInfusion of Ringer Lactate solution may lead to metabolicalkalosis because of the presence of lactate ionsalkalosis because of the presence of lactate ionsLactated Ringer’s should be used with great care withLactated Ringer’s should be used with great care withpatients with hyperkalemia, severe renal failure, andpatients with hyperkalemia, severe renal failure, andhepatic insufficiencyhepatic insufficiencySolutions containing lactate are not for use in theSolutions containing lactate are not for use in thetreatment of lactic acidosistreatment of lactic acidosis
    82. 82. BREAKBREAKCCRN REVIEW PART 2CCRN REVIEW PART 2
    83. 83. NeurologicalNeurological AlterationsAlterationsBrain Aneurysms & AVM’sBrain Aneurysms & AVM’sIntracranial HemorrhageIntracranial HemorrhageStrokeStroke
    84. 84. TheThe HumanHuman BrainBrain
    85. 85. CerebralCerebral SpinalSpinal FluidFluidThe serum-like fluid that circulates through the ventricles of theThe serum-like fluid that circulates through the ventricles of thebrain, the cavity of the spinal cord, and the subarachnoid spacebrain, the cavity of the spinal cord, and the subarachnoid space
    86. 86. Spinal Cord Nerve TractsSpinal Cord Nerve TractsAscendingSensoryTractDescendingMotor Tract(Corticospinal Tract)(Spinothalmic Tract)
    87. 87. Brown-Séquard syndromeBrown-Séquard syndromeIncompleteSpinal CordInjury(Hemi-section)
    88. 88. Central Cord SyndromeCentral Cord SyndromeWalkingQuads
    89. 89. Homonymous HemianopiaHomonymous Hemianopia
    90. 90.  Brain AneurysmBrain Aneurysm– An intracranial aneurysm is a weak or thin spot on a bloodAn intracranial aneurysm is a weak or thin spot on a bloodvessel in the brain that balloons out and fills with bloodvessel in the brain that balloons out and fills with blood AV Malformation (AVM)AV Malformation (AVM)– Arteriovenous malformation (AVM)Arteriovenous malformation (AVM) of the brain is a "shortof the brain is a "shortcircuit“circuit“ between the arteries and veinsbetween the arteries and veinsBrain Aneurysms & AVM’sBrain Aneurysms & AVM’s
    91. 91. Intracranial AneurysmsIntracranial AneurysmsUsually occur at bifurcations and branches of theUsually occur at bifurcations and branches of thelarge arterieslarge arteries located in the Circle of Willislocated in the Circle of WillisThe most common sites include the:The most common sites include the:– Anterior Communicating artery (30 - 35%)Anterior Communicating artery (30 - 35%)– Bifurcation of the Internal Carotid and PosteriorBifurcation of the Internal Carotid and PosteriorCommunicating artery (30 - 35%)Communicating artery (30 - 35%)– Bifurcation of Middle cerebral (20%)Bifurcation of Middle cerebral (20%)– Basilar artery bifurcation (5%)Basilar artery bifurcation (5%)– Remaining posterior circulation arteries (5%)Remaining posterior circulation arteries (5%)
    92. 92. Types of AneurysmsTypes of Aneurysms Saccular aneurysmSaccular aneurysm– Occurs at bifurcationsOccurs at bifurcations Fusiform aneurysmFusiform aneurysm– Often in basilar arteryOften in basilar artery Dissecting aneurysmDissecting aneurysm Ruptured aneurysmRuptured aneurysm
    93. 93. Brain CirculationBrain Circulation
    94. 94. Arterial Circulation in the BrainArterial Circulation in the Brain
    95. 95. RISK FACTORSRISK FACTORS– SmokingSmoking– HypertensionHypertension– Coarctation of the aortaCoarctation of the aorta– Dissections/traumaDissections/trauma– Intracranial neoplasmIntracranial neoplasm– Polycystic kidney diseasePolycystic kidney disease– Abnormal vessels or High-flow states (eg, vascularAbnormal vessels or High-flow states (eg, vascularmalformations, fistulae)malformations, fistulae)– HypercholesterolemiaHypercholesterolemia– Connective tissue disorders (eg, Marfan, Ehlers-Danlos)Connective tissue disorders (eg, Marfan, Ehlers-Danlos)Intracranial AneurysmsIntracranial Aneurysms
    96. 96. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Usually asymptomatic until ruptureUsually asymptomatic until ruptureCranial Nerve PalsyCranial Nerve PalsyDilated PupilsDilated PupilsDouble VisionDouble VisionPain Above and Behind EyePain Above and Behind EyeLocalized HeadacheLocalized Headache– Warning signs prior ruptureWarning signs prior ruptureLocalized HeadacheLocalized HeadacheNausea & VomitingNausea & VomitingStiff NeckStiff NeckBlurred or Double VisionBlurred or Double VisionSensitivity to Light (photophobia)Sensitivity to Light (photophobia)Loss of SensationLoss of SensationIntracranial AneurysmsIntracranial Aneurysms
    97. 97. Treatment of Brain AneurysmsTreatment of Brain AneurysmsSurgerySurgery–– Craniotomy and clippingCraniotomy and clippingEndovascular coilingEndovascular coiling
    98. 98. Aneurysm Post-Op RisksAneurysm Post-Op RisksRebleedingRebleeding– Most frequently within the first 24 hoursMost frequently within the first 24 hours– Up to 20% of patients rebleed within 14 daysUp to 20% of patients rebleed within 14 days– Main preventative measure is control of blood pressureMain preventative measure is control of blood pressure(preferably beta blockers)(preferably beta blockers)VasospasmVasospasm– Usually occurs before 3 days or after 10 days (post bleed)Usually occurs before 3 days or after 10 days (post bleed)– May require hypervolemic therapyMay require hypervolemic therapyHydrocephalusHydrocephalusHyponatremiaHyponatremiaFluids / ElectrolytesFluids / Electrolytes
    99. 99. Arterio-Venous MalformationArterio-Venous Malformation
    100. 100.  The arteries and veins have a direct connection,The arteries and veins have a direct connection,bypassing the capillary networkbypassing the capillary network Presents with ongoing headaches, seizures,Presents with ongoing headaches, seizures,hemorrhage, or progressive neurologicalhemorrhage, or progressive neurologicaldysfunctiondysfunctionArterio-Venous MalformationArterio-Venous Malformation
    101. 101. Arterio-Venous MalformationArterio-Venous MalformationSIGNS & SYMPTOMSSIGNS & SYMPTOMS– SeizuresSeizures– HeadachesHeadaches– ““Whooshing" Sound (Bruit)Whooshing" Sound (Bruit)– Other SignsOther SignsSubtle behavioral changesSubtle behavioral changesCommunication or thinking disturbancesCommunication or thinking disturbancesLoss of coordination and balanceLoss of coordination and balanceParalysis or weakness in one part of the bodyParalysis or weakness in one part of the bodyVisual disturbancesVisual disturbancesAbnormal sensationsAbnormal sensations
    102. 102. Arterio-Venous MalformationArterio-Venous MalformationCOMPLICATIONSCOMPLICATIONS– HemorrhageHemorrhage (into surrounding tissue)(into surrounding tissue)– IschemiaIschemia– SeizuresSeizures– Brain Cell DeathBrain Cell Death
    103. 103. Arterio-Venous MalformationArterio-Venous MalformationDIAGNOSISDIAGNOSIS– MRIMRI (including MR Angiography) as well as(including MR Angiography) as well as CTCTAngiography help identify AVM’sAngiography help identify AVM’s– Cerebral AngiographyCerebral Angiography is a prerequisite tois a prerequisite totreatmenttreatmentTo identify the precise anatomy and configurationTo identify the precise anatomy and configurationof both the lesion and the feeding and drainingof both the lesion and the feeding and drainingvesselsvessels
    104. 104. Arterio-Venous MalformationArterio-Venous MalformationTREATMENTTREATMENT– SurgerySurgeryUsually delayedUsually delayedOpen ligation and/or resection of the AVMOpen ligation and/or resection of the AVM– RadiosurgeryRadiosurgery– EmbolizationEmbolizationUsually as adjunct to surgeryUsually as adjunct to surgery– ObservationObservation
    105. 105. Arterio-Venous MalformationArterio-Venous MalformationRADIOSURGERYRADIOSURGERY– Believed to "work" by initiating an "inflammatory"Believed to "work" by initiating an "inflammatory"response in the pathological blood vesselsresponse in the pathological blood vesselsultimately resulting in their progressive narrowingultimately resulting in their progressive narrowingand ultimate closureand ultimate closure– The risk for hemorrhage is not reduced during thisThe risk for hemorrhage is not reduced during thislag timelag time– There is the added risk of radiation necrosis ofThere is the added risk of radiation necrosis ofadjacent healthy brain tissue or brain cyst formationadjacent healthy brain tissue or brain cyst formation
    106. 106. Brain RadiosurgeryBrain RadiosurgeryADVANTAGESADVANTAGES– NoninvasiveNoninvasive– Can access all anatomic locations of the brainCan access all anatomic locations of the brainDISADVANTAGESDISADVANTAGES– Can only treat smaller lesionsCan only treat smaller lesions(<3 cm in diameter)(<3 cm in diameter)– Requires 2 or more years to completeRequires 2 or more years to complete
    107. 107. AVM Post-Op RisksAVM Post-Op RisksPerfusion-breakthrough bleedingPerfusion-breakthrough bleedingEndovascular occlusionEndovascular occlusion
    108. 108. Sudden onset of “the worst headache of my life”Sudden onset of “the worst headache of my life”IntracranialIntracranial HemorrhageHemorrhage
    109. 109. IntracranialIntracranial HemorrhageHemorrhageEpiduralEpiduralSubduralSubduralSubarachnoidSubarachnoidIntraparencymalIntraparencymalIntraventricularIntraventricularCerebellarCerebellar
    110. 110. ICH is a dynamic, not a static processICH is a dynamic, not a static processHemorrhage volume can increase over timeHemorrhage volume can increase over timeCT scan is the most important diagnostic toolCT scan is the most important diagnostic toolManaging blood pressure is extremely importantManaging blood pressure is extremely importantMust aggressively manage fever and seizuresMust aggressively manage fever and seizuresConsider hyperventilation and paralytics in settingConsider hyperventilation and paralytics in settingof increased ICP and deteriorationof increased ICP and deteriorationIntracranialIntracranial HemorrhageHemorrhage
    111. 111. Treatment of ICHTreatment of ICHKEY CONCEPTSKEY CONCEPTS1)1) Intracranial PressureIntracranial Pressure– Elevated when ICP >20 mm HgElevated when ICP >20 mm Hg2)2) Cerebral Perfusion PressureCerebral Perfusion Pressure– CPP = MAP - ICPCPP = MAP - ICP– Must maintain CPP > 70 mm HgMust maintain CPP > 70 mm Hg– Example: MAP = 100, ICP = 20Example: MAP = 100, ICP = 20CPP = 80 mmHgCPP = 80 mmHg
    112. 112. Subarachnoid Hemorrhage (SAH)Subarachnoid Hemorrhage (SAH)DEFINITIONDEFINITION–When a blood vessel just outside the brain ruptures, theWhen a blood vessel just outside the brain ruptures, thearea of the skull surrounding the brain (the subarachnoidarea of the skull surrounding the brain (the subarachnoidspace) rapidly fills with bloodspace) rapidly fills with blood
    113. 113. Subarachnoid Hemorrhage (SAH)Subarachnoid Hemorrhage (SAH)SIGNS & SYMPTOMSSIGNS & SYMPTOMS–Sudden, intense headacheSudden, intense headache–Neck painNeck pain–Nausea or vomitingNausea or vomiting–Neck stiffnessNeck stiffness–PhotophobiaPhotophobiaSudden onset of “the worst headache of my life”Sudden onset of “the worst headache of my life”
    114. 114. Subarachnoid Hemorrhage (SAH)Subarachnoid Hemorrhage (SAH)SAH may be spontaneous or traumaticSAH may be spontaneous or traumaticSpontaneous SAH causesSpontaneous SAH causes–Cerebral aneurysmsCerebral aneurysms–AV malformationsAV malformations–TraumaTraumaUncommon causesUncommon causes–Neoplasms, venous angiomas, infectionsNeoplasms, venous angiomas, infections
    115. 115. Warning bleeds” are relatively commonWarning bleeds” are relatively commonSentinel headache 30-50%Sentinel headache 30-50%Early diagnosis prior to rupture will improve outcomesEarly diagnosis prior to rupture will improve outcomes50% of patients die within 48 hours irrespective of50% of patients die within 48 hours irrespective oftherapytherapySubarachnoid HemorrhageSubarachnoid Hemorrhage
    116. 116. Often accompanied by a period of unconsciousnessOften accompanied by a period of unconsciousness(50% never wake up)(50% never wake up)Common signs include neck stiffness, photophobia,Common signs include neck stiffness, photophobia,headacheheadache20% have ECG evidence of myocardial ischemia20% have ECG evidence of myocardial ischemiaSubarachnoid HemorrhageSubarachnoid Hemorrhage
    117. 117. Complications of SAHComplications of SAHHydrocephalusHydrocephalus may develop within the first 24may develop within the first 24hours because of obstruction of CSF outflow in thehours because of obstruction of CSF outflow in theventricular system by clotted bloodventricular system by clotted bloodRebleedingRebleeding of SAH occurs in 20% of patients in theof SAH occurs in 20% of patients in thefirst 2 weeks. Peak incidence of rebleeding occurs the dayfirst 2 weeks. Peak incidence of rebleeding occurs the dayafter SAH and may be from lysis of the aneurysmal clotafter SAH and may be from lysis of the aneurysmal clotVasospasmVasospasm from arterial smooth muscle contractionfrom arterial smooth muscle contraction(symptomatic in 36% of patients)(symptomatic in 36% of patients)
    118. 118. Re-bleeding After SAHRe-bleeding After SAHRe-bleeding occurs most frequently within the first 24 hrsRe-bleeding occurs most frequently within the first 24 hrsUp to 20% of patients rebleed within 14 daysUp to 20% of patients rebleed within 14 daysThe main preventative measure is to control the bloodThe main preventative measure is to control the bloodpressure – preferably beta blockerspressure – preferably beta blockersEarly clipping of the aneurysm allows hypertensive andEarly clipping of the aneurysm allows hypertensive andhypervolemic therapy to prevent vasospasmhypervolemic therapy to prevent vasospasm
    119. 119. Vasospasm After SAHVasospasm After SAHWorst time is day 7 to day 10 (most frequent time forWorst time is day 7 to day 10 (most frequent time forvasospasms)vasospasms)Diagnosed by neurologic exam, transcranial doppler andDiagnosed by neurologic exam, transcranial doppler andangiographyangiographyMay use calcium channel blockersMay use calcium channel blockers– Reduces vasospasm, neurological deficit, cerebral infarctionReduces vasospasm, neurological deficit, cerebral infarctionand mortalityand mortalityMay use some antispasmodicsMay use some antispasmodics
    120. 120. Vasospasm & HHH TherapyVasospasm & HHH TherapyHemodilutionHemodilution–Hct 30-35%Hct 30-35%HypertensionHypertension–Phenylephrine / NorepinephrinePhenylephrine / Norepinephrine–BP titration to CPP/examBP titration to CPP/examHypervolemiaHypervolemia–Colloids/crystalloidsColloids/crystalloids
    121. 121. Other Vasospasm TherapyOther Vasospasm TherapyAngioplastyAngioplasty–BP management during procedureBP management during procedure–Reperfusion issuesReperfusion issues–TimingTimingPapaverine InfusionPapaverine Infusion–Side effectsSide effects–Repeated tripsRepeated trips
    122. 122. Neurologic deficitsNeurologic deficits from cerebral ischemia, peaks at days 4-12from cerebral ischemia, peaks at days 4-12Hypothalamic dysfunctionHypothalamic dysfunction causes excessive sympatheticcauses excessive sympatheticstimulation, which may lead to myocardial ischemia or labile BPstimulation, which may lead to myocardial ischemia or labile BPHyponatremiaHyponatremia may result from cerebral salt wasting / SIADHmay result from cerebral salt wasting / SIADHNosocomial pneumoniaNosocomial pneumonia and other such complicationsand other such complicationsPulmonary edemaPulmonary edema neurogenic & non-neurogenicneurogenic & non-neurogenicOther Complications of SAHOther Complications of SAH
    123. 123. 1)1) Identify and treat the causative lesionIdentify and treat the causative lesion– Thus preventing re-bleedingThus preventing re-bleeding1)1) Treat hydrocephalusTreat hydrocephalus2)2) Treating and prevent vasospasmTreating and prevent vasospasmTreatment of SAHTreatment of SAH
    124. 124. Maintain systolic BP >130mmHgMaintain systolic BP >130mmHg– Use vasopressors if necessary to maintain CPPUse vasopressors if necessary to maintain CPPand reduce ischemic complications from vasospasmand reduce ischemic complications from vasospasm– Generally avoid vasodilators (except calciumGenerally avoid vasodilators (except calciumchannel blockers)channel blockers)Treatment of SAHTreatment of SAH
    125. 125. BREAKBREAKCCRN REVIEW PART 2CCRN REVIEW PART 2
    126. 126. StrokeStroke
    127. 127. StrokeStroke
    128. 128.  RISK FACTORSRISK FACTORS TIATIA CADCAD High Blood PressureHigh Blood Pressure High CholesterolHigh Cholesterol SmokingSmoking Heart DiseaseHeart Disease DiabetesDiabetes Excessive alcoholExcessive alcohol Family HistoryFamily History AgeAge SexSex RaceRace ObesityObesityAnnual risk of stroke: Increases with ageAnnual risk of stroke: Increases with ageStrokeStroke
    129. 129. Computed Tomography (CT)Computed Tomography (CT)Magnetic Resonance Imaging (MRI)Magnetic Resonance Imaging (MRI)Cerebral Angiography: identify responsible vesselCerebral Angiography: identify responsible vesselCarotid Ultrasound: carotid artery stenosisCarotid Ultrasound: carotid artery stenosisEchocardiogram: identify blood clot from heartEchocardiogram: identify blood clot from heartElectrocardiogram (ECG): underlying heart conditionsElectrocardiogram (ECG): underlying heart conditionsHeart monitors, blood work and more tests!!Heart monitors, blood work and more tests!!Stroke TestsStroke Tests
    130. 130. CT MRICT MRIpp::////wwwwww..ssttrrookkeecceenntteerr..oorrgg//eedduuccaattiioonn//aaiiss__cctt__ttooooll//cctt0044//cctt0044--ffrraammeess..hhttmmhttp://www.strokecenter.org/education/ais_ct_tool/index.htmhttp://www.strokecenter.org/education/ais_ct_tool/index.htm
    131. 131. Tissue plasminogen activator (tPA) can be givenTissue plasminogen activator (tPA) can be givenwithin three hours from the onset of symptomswithin three hours from the onset of symptomsHeparinHeparinIntra-arterial thrombolysisIntra-arterial thrombolysisHemicraniectomyHemicraniectomyIn addition to being used to treat strokes, theIn addition to being used to treat strokes, thefollowing can also be used as preventativefollowing can also be used as preventativemeasuresmeasures–Anticoagulants/AntiplateletsAnticoagulants/Antiplatelets–Carotid EndarterectomyCarotid Endarterectomy–Angioplasty/StentsAngioplasty/StentsTreatment of Ischemic CVATreatment of Ischemic CVA
    132. 132. Surgery is often required to remove pooled bloodSurgery is often required to remove pooled bloodfrom the brain and to repair damaged blood vesselsfrom the brain and to repair damaged blood vesselsPrevention:Prevention:– An obstruction is introduced to prevent rupture andAn obstruction is introduced to prevent rupture andbleeding of aneurysms and AVM’sbleeding of aneurysms and AVM’s– Surgical InterventionSurgical Intervention– Endovascular ProceduresEndovascular ProceduresTreatment of Hemorrhagic CVATreatment of Hemorrhagic CVA
    133. 133. Control high Blood PressureControl high Blood PressureLower cholesterolLower cholesterolQuit smokingQuit smokingControl diabetesControl diabetesMaintain healthy weightMaintain healthy weightExerciseExerciseManage stressManage stressEat a healthy dietEat a healthy dietPrevention of CVAPrevention of CVA
    134. 134. BREAKBREAKCCRN REVIEW PART 2CCRN REVIEW PART 2
    135. 135. DKA & HHNKDKA & HHNKDI & SIADHDI & SIADHDICDICShock StatesShock StatesSepsisSepsisMetabolicMetabolic AlterationsAlterations
    136. 136. Diabetic KetoacidosisDiabetic KetoacidosisWhat is DKA?What is DKA?– Diabetic KetoacidosisDiabetic Ketoacidosis– A life-threatening complication seen withA life-threatening complication seen withDiabetes Mellitus Type 1Diabetes Mellitus Type 1
    137. 137. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Serum Glucose 300-800Serum Glucose 300-800– Ketoacidosis PresentKetoacidosis Present– Large Serum And Urine KetonesLarge Serum And Urine Ketones– Fruity BreathFruity Breath– Kussmaul RespirationsKussmaul Respirations– Serum pH < 7.3Serum pH < 7.3– DehydrationDehydrationDiabetic KetoacidosisDiabetic Ketoacidosis
    138. 138. HHNKHHNKWhat is HHNK?What is HHNK?– Hyperglycemic Hyperosmolar Nonketonic ComaHyperglycemic Hyperosmolar Nonketonic Coma– A life threatening complication seen withA life threatening complication seen withDiabetes Mellitus Type 2Diabetes Mellitus Type 2
    139. 139. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Serum Glucose 600-2000Serum Glucose 600-2000– Ketoacidosis Not PresentKetoacidosis Not Present– Absent Or Slight Serum And Urine KetonesAbsent Or Slight Serum And Urine Ketones– Normal BreathNormal Breath– Shallow RespirationsShallow Respirations– Serum pH NormalSerum pH Normal– Severe DehydrationSevere DehydrationHHNKHHNK
    140. 140. DKA vs HHNKDKA vs HHNKDKADKA Faster OnsetFaster Onset Glucose 300-800Glucose 300-800 AcidosisAcidosis Fruity BreathFruity Breath Kussmaul RespirationsKussmaul RespirationsHHNKHHNK Slower OnsetSlower Onset Glucose 600-2000Glucose 600-2000 No AcidosisNo Acidosis Normal BreathNormal Breath Shallow RespirationsShallow Respirations
    141. 141. Treatment of DKA & HHNKTreatment of DKA & HHNKReverse DehydrationReverse DehydrationNS, then ½ NSNS, then ½ NSRestore Glucose LevelsRestore Glucose LevelsDD55 ½ NS When Glu 250½ NS When Glu 250Restore ElectrolytesRestore Electrolytes
    142. 142. Diabetes InsipitusDiabetes InsipitusWhat is Diabetes Insipitus?What is Diabetes Insipitus?– A Condition resulting from too little ADHA Condition resulting from too little ADHWhy is it called Diabetes Insipitus?Why is it called Diabetes Insipitus?– The term Diabetes refers to polyuriaThe term Diabetes refers to polyuria
    143. 143. Diabetes InsipitusDiabetes InsipitusSIGNS & SYMPTOMSSIGNS & SYMPTOMS– PolyuriaPolyuria– Severe HypovolemiaSevere Hypovolemia– Severe DehydrationSevere Dehydration– Elevated Serum OsmolalityElevated Serum Osmolality– Elevated Serum SodiumElevated Serum Sodium– ShockShock
    144. 144. Diabetes InsipitusDiabetes InsipitusCAUSESCAUSES– Decreased ADHDecreased ADH– Neurological SurgeryNeurological Surgery– Head TraumaHead Trauma– Dilantin or LithiumDilantin or Lithium
    145. 145. Diabetes InsipitusDiabetes InsipitusTREATMENTTREATMENT– Fluid ResuscitationFluid Resuscitation– ADH ReplacementADH ReplacementVasopressin, Pitressin, DDAVPVasopressin, Pitressin, DDAVP– Treat The CauseTreat The Cause
    146. 146. SIADHSIADHWhat is SIADH?What is SIADH?– Syndrome of Inappropriate ADHSyndrome of Inappropriate ADH– Too much ADHToo much ADH
    147. 147. SIADHSIADH SIGNS & SYMPTOMSSIGNS & SYMPTOMS–HyponatremiaHyponatremia–Low Serum SodiumLow Serum Sodium Serum NA < 135Serum NA < 135– Low Serum OsmolalityLow Serum Osmolality– High Urine OsmolalityHigh Urine Osmolality– Elevated Specific GravityElevated Specific Gravity Urine specific gravityUrine specific gravity> 1.030> 1.030– Elevated Urine OsmolalityElevated Urine Osmolality– Elevated ADH LevelElevated ADH Level– Weight Gain Without EdemaWeight Gain Without Edema– Elevated CVP, PAP, PAWPElevated CVP, PAP, PAWP– HypertensionHypertension– Concentrated AndConcentrated And  UOPUOP– HeadacheHeadache– Altered LOCAltered LOC– SeizuresSeizures
    148. 148. CAUSESCAUSES– Head TraumaHead Trauma– Oat Cell CarcinomaOat Cell Carcinoma– Other CancersOther Cancers– Viral PneumoniaViral PneumoniaSIADHSIADH– MedicationsMedications– StressStress– Mechanical VentilationMechanical Ventilation
    149. 149. TREATMENTTREATMENT– Monitor Fluid Balance, Monitor I & OMonitor Fluid Balance, Monitor I & O– Restrict FluidsRestrict Fluids– Replace Na+ loss when necessaryReplace Na+ loss when necessary– May Give 3% (Hypertonic) SalineMay Give 3% (Hypertonic) Saline– May Give Dilantin or LithiumMay Give Dilantin or Lithium– May require PA Catheter For MonitoringMay require PA Catheter For Monitoring– May Give DiureticsMay Give DiureticsSIADHSIADH
    150. 150. DI vs SIADHDI vs SIADHDIDIToo Little ADHToo Little ADHDehydrationDehydrationHigh Serum SodiumHigh Serum SodiumHigh Serum OsmolalityHigh Serum OsmolalityLow Urine OsmolalityLow Urine OsmolalitySIADHSIADHToo Much ADHToo Much ADHWater IntoxicationWater IntoxicationLow Serum SodiumLow Serum SodiumLow Serum OsmolalityLow Serum OsmolalityHigh Urine OsmolalityHigh Urine Osmolality
    151. 151. DI vs SIADH TreatmentDI vs SIADH TreatmentDIDILots of FluidsLots of FluidsHold DilantinHold DilantinHold LithiumHold LithiumGive ADHGive ADHSIADHSIADHFluid RestrictionFluid RestrictionMay Give DilantinMay Give DilantinMay Give LithiumMay Give Lithium3% Saline3% Saline
    152. 152. DICDICWhat is DIC?What is DIC?– Disseminate Intravascular CoagulationDisseminate Intravascular Coagulation– A clotting disorder that ultimately causesA clotting disorder that ultimately causesbleedingbleeding
    153. 153. Caused by over-activation of the clotting pathwaysCaused by over-activation of the clotting pathwaysCauses widespread fibrin depositsCauses widespread fibrin depositsBleeding and renal failure are most common manifestationsBleeding and renal failure are most common manifestationsTreating the underlying disease is the most important stepTreating the underlying disease is the most important stepDICDIC
    154. 154. Disseminated IntravascularDisseminated IntravascularCoagulationCoagulationSystemic activationSystemic activationof coagulationof coagulationIntravascularIntravasculardeposition ofdeposition offibrinfibrinDepletionDepletion of plateletsof plateletsand coagulationand coagulationfactorsfactorsBLEEDINGBLEEDINGThrombosis of smallThrombosis of smalland midsize vesselsand midsize vesselswith organ failurewith organ failure
    155. 155. SIGNS & SYMPTOMSSIGNS & SYMPTOMS–BleedingBleeding–ThrombosisThrombosis–Organ FailureOrgan FailureDICDIC
    156. 156. DICDIC
    157. 157. CAUSESCAUSES– Massive Tissue InjuriesMassive Tissue Injuries– Obstetric EmergenciesObstetric Emergencies– SepticemiaSepticemia– CancersCancers– Vascular DisordersVascular Disorders– Systemic DisordersSystemic Disorders– Many More CausesMany More CausesDICDIC
    158. 158. CLOTTING FACTORS DEPLETEDCLOTTING FACTORS DEPLETED– PlateletsPlatelets ↓↓– FibrinogenFibrinogen ↓↓– Protein Activated CProtein Activated C ↓↓– AntithrombinAntithrombin ↓↓DIC Lab ResultsDIC Lab ResultsCLOTTING TESTS ELEVATEDCLOTTING TESTS ELEVATED– PTPT ↑↑– aPTTaPTT ↑↑– Fibrin degradation products (D-dimer)Fibrin degradation products (D-dimer) ↑↑
    159. 159. TREATMENTTREATMENT–Treat the CauseTreat the Cause–Replace Clotting FactorsReplace Clotting Factors–Anticoagulation Therapy (Heparin)Anticoagulation Therapy (Heparin)DICDIC
    160. 160. THE ENDTHE ENDPART 2PART 2CCRN REVIEWCCRN REVIEW
    161. 161. THANK YOU!THANK YOU!CCRN REVIEW PART 2CCRN REVIEW PART 2
    162. 162. GOOD LUCK!GOOD LUCK!CCRNCCRN REVIEWREVIEW
    163. 163. ReferencesReferences American Stroke Association. (2007). Acute and PreventativeTreatments. Retrieved March 4, 2007 fromhttp://www.strokeassociation.org/presenter.jhtml?identifier=2532. Block, C., and Manning, H. (2002). Prevention of acute renal failure inthe critically ill. American Journal of Respiratory and Critical CareMedicine; (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. AACNClinical Issues; (16)515-525. Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranialaneurysms? Lancet; (366)783-785. Campbell, D. (2003). How acute renal failure puts the breaks on kidneyfunction. Nursing 2003; (33)59-63.
    164. 164. References ContinuedReferences Continued Campbell, D. (2003). How acute renal failure puts the breaks on kidneyfunction. Nursing 2003; (33)59-63. Carlson, K. (2009) Advanced Critical Care Nursing. Philadelphia, Pa:Saunders/Elsevier. Guyton, A. C., and Hall, J. E. (2000). Unit V: The kidneys and body fluids. InA. 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. Lynn-Mchale Wiegand, D. J. (ed.). (2011). AACN Procedure Manual forCritical Care. 6th ed. St. Louis, MO: Saunders. Pagana, K. D. & Pagana, T. J. (2008). Mosby’s Diagnostic and LaboratoryTest Reference. 9th ed. St. Louis, MO: Mosby/Elsevier. Stillwell, S. (2006). Mosby’s Critical Care Nursing Reference. 4th ed. St.Louis, MO: Mosby/Elsevier.: Diagnosis and Management (5th ed).

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