CCP Fall 2013 - Week 3

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jmork
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242412
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CCP Fall 2013 - Week 3
Updated:
2013-11-09 16:07:20
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Critical Care Paramedic
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Endocrine & General Medical; Environmental Emergencies & Toxicology; Neurological Emergencies; Obstetrical/Gynecological Emergencies
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  1. Describe the dosing of insulin in DKA
    • 0.1 u/kg Bolus
    • Followed by drip at 0.1 u/kg/hr
  2. What is the max drop in BGL per hour in the treatment of DKA?
    100 mg/dl
  3. Once BGL = 300 what is added to the insulin drip?
    D5W
  4. What is the central health issue in HHNK?
    Too much sugar compared to their insulin production
  5. Describe the presentation of HHNK
    • SEVERE dehydration
    • Absence of ketosis – NO kussmaul breathing
    • Relative hypernatremia
    • Hyperglycemia [> 800 mg/dl common]Elevated BUN/Creatinine ratio
  6. Describe the treatment of HHNK
    AGGRESSIVE fluid rehydrationInsulinAnticipate severe hypokalemia
  7. What are the causes of Diabetes Insipidus (DI)?
    • Head Injury
    • Dilantin
  8. Describe the presentation of Diabetes Insipidus (DI)
    • Extreme urine output w/very low urine osmolarity/specific gravity
    • Hypernatremia
  9. Describe the treatment of Diabetes Insipidus
    • Aggressive fluid replacement
    • vasopressin (Pitressin©)dDAVP (DDAVP©, Stimate©, Minirin©)
  10. Describe the condition of Syndrome of Inappropriate ADH (SIADH)
    A syndrome of increased ADH activity despite reduced plasma osmolarity
  11. Describe the presentation of Syndrome of Inappropriate ADH
    • Dilutional hyponatremia
    • Cerebral edema
    • Seizures
    • Urine osmolarity/Specific gravity elevated
  12. Describe the treatment of Syndrom of Inappropriate ADH (SIADH)
    • Restrict fluids
    • Diuresis
    •     1° loop diuretics
    • Democlocycline (tetracycline family)
    •     ADH receptor antagonism
  13. Describe the treatment of GI hemorrhage
    • Essentially treat as a trauma pt
    • Also NGT/OGT & evacuate stomach
    • octreotide (Sandostatin) 25-50 mcg IVP followed by 25-50 mcg/hr IVgtt - Reduces hepatic portal pressures, allows relief of venous congestion
    • vasopressin (caution in CAD) - Decreases arterial pressure feeding to the hepatic portal system
  14. Describe the presentation of Graves Disease
    • Dramatic weight loss
    • CP, SOB & palpitations
    • Fever
    • Tremor, nervousness
    • Marked tachycardia (AF common)
    • ** Any new tach/AF in an otherwise healthy female **
  15. Describe the treatment of Graves Disease
    • Antithyroid meds needed
    • Antipyretics (Avoid ASA)
    • Fluids
    • Correct electrolytes: K+, Mg+
    • Supplement O2 delivery
    • Consider IV glucocorticoids, dexamethasone specifically inhibits hormone production & conversion from T4 to T3
    • Tachycardias not likely to respond to digitalis, will convert once antithyroid therapy initiated
  16. Describe the presentation of Myxedema Coma / Hypothyroidism
    • Primarily women
    • Almost exclusively > 60 YOA
    • > 90% of cases occur in winter
    • Fatigue & weight gain
    • Cold intolerance, deep voice, coarse hair
    • Officially “myxedema coma” upon any change in LOC
  17. Describe the treatment of Myxedema Coma / Hypothyroidism
    • Supportive during comatose states
    • IV levothyroxine (T4)
    • Watch for adrenal insufficiency (Etomidate issues)
  18. Describe the presentation of Addison's Disease / Adrenal Insufficiency
    • Inadequate aldosterone, cortisol & androgens
    • Fatigue, weakness, low BP 2°
    •     ↓ Na+/H2O retention
    •     Hypoglycemia
    •     Poor catecholamine production
    • Failure to respond to exogenous pressor agents 
  19. Describe the treatment of Addison's Disease / Adrenal Insufficiency
    • Avoid abrupt discontinuation of chronic glucocorticoid  use
    • May need to initiate steroids
    • Caution w/Etomidate (overstated)

  20. What are the causes of Cushing's disease?
    • Chronic glucocorticoid use w/abrupt cessation
    • Pituitary disorders (too much ACTH released
    • Oat Cell carcinoma (‘fake’ cortisol)
    • Adrenal carcinoma (too much cortisol produced/secreted)
  21. Describe the presentation of Cushing's disease
    • Upper body obesity w/thin arms & legs (muscle wasting)
    • Rounded face “buffalo hump”
    • Fatigue, HTN, hyperglycemia
    •     Incr. Norepinephrine/Epi
    •     Fatty & amino acids convert to glucose
    •       Type II DM (hyperglycemia wears out the pancreas)
  22. Describe the treatment for Cushing's disease
    • Initiation or reduction of glucocorticoids (Hydrocortisone)
    • Supportive
    • Need surgery
  23. What are the causes of pancreatitis?
    • EtOH abuse
    • Biliary stone disease
    • Steroids & antibiotics
    • Infections (viral/bacterial)
  24. Describe the presentation of pancreatitis
    • Low Ca+
    • Elevation of the left diaphragm w/left base atelectasis
    • Bilateral pleural effusions
    • Concomitant sepsis & ARDS
    • Renal failure
    • Cullen’s sign
  25. Describe the treatment of pancreatitis
    • Fluid resuscitation
    • NPO & place NGT/OGT
    • Meperidine vs. Morphine (Sphincter of Oddi spasticity)
    • Alternate use of atropine, β-blockers, Narcan® & tetrodotoxin
    • Anticipate progression
    •     Sepsis
    •     ARDS
    •     MODS
    •     DIC
    •     DEAD
    • Abx for sepsis (Rocephin, Ampicillin)
  26. What causes bowel obstructions?
    • Post operative adhesions
    • Malignancy
    • Crohn’s disease
    • Hernias
  27. Desccribe the presentation of bowel obstructions
    • Large vs. Small
    • Bowel ischemia results in sepsis
    • Pancreatitis is common
  28. Describe the treatment of bowel obstruction
    • NPO & place OGT/NGT
    • Aggressive fluid resuscitation
    • Aggressive pain control
    • Antiemetics
    • Antibiotics
    •     Ancef
  29. What are the primary issues with cirrhosis &/or hepatitis?
    • Ammonia toxicity
    •   By-product of protein metabolism
    •     TPN, blood, etc… Amine removal from amino acid
    •     NH3 converted to urea & glutamine for renal excretion
    •   Hypokalemia
    •     Diuretics
    •     Diarrhea
    •     Alkalotic states
  30. Describe the presentation of hepatic encephalopathy 2° to cirrhosis &/or hepatitis
    • ⇧ AST & ALT (SGOT/SPGT)
    • ⇧ BUN
    • Stuperous ⇨ obtunded ⇨ coma
    • “Coarse muscle flapping”
  31. Describe the treatment of hepatic encephalopathy 2° to cirrhosis &/or hepatitis
    • Stop GI bleeding & evacuate bowel of blood w/OGT/NGT
    • STOP protein intake (TPN, etc.)
    • Correct K+ levels
    •   Stop K+ retention
  32. What causes splenic rupture?
    Trauma - most commonly affected organ in blunt force trauma
  33. How does splenic rupture present?
    • Left shoulder pain (referred pain AKA Kehr’s sign)
    • Shock
  34. Describe the treatment of splenic rupture
    • Supportive
    • Aggressive fluid resuscitation & PRBCs
    • Get to surgeon
  35. Describe Brudzinski's sign & it's significance
    • Meningitis
    • Flex the neck & pt will bring up hamstring
  36. Describe Kernig's sign & it's significance
    • Meningitis
    • Bring up the pt's hamstring & the pt will flex their neck
  37. Describe Cullen's sign & it's significance
    • Pancreatitis
    • Periumbilical bruising
  38. Describe Grey-Turners sign & it's significance
    • Pancreatitis
    • Flank & groin bruising
  39. Describe Kehr's sign & it's significance
    • Splenic disease/rupture
    • Left shoulder referred pain
  40. Describe Murphy's sign & it's significance
    • Gallbladder
    • RUQ & push up, have pt take deep breath
    • + sign = pain & inability to take a full breath
  41. Describe Levine's sign & it's significance
    • Cardiac pain
    • Clenched fist over chest
  42. Describe the body's response to cold
    • Peripheral vasoconstriction
    • Skeletal muscle vasodilation
    • ⇧ Cardiac Output
    • Shivering
    •   Increases MRO2 by up to 600%
    •   Limited by available glycogen stores
    •   Loss of shivering @ 32°C (89.6° F)
  43. At what temperature does shivering stop?
    32° C (89.6° F)
  44. Describe the physiologic response to hypothermia
    • Initially metabolism⇧to produce heat
    • Metabolism ⇩ by ½ for every drop in core temp of 10° C
    • Pts BGL will ⇩ with mild chronic hypothermia
    • BGL is ⇧ w/severe hypothermia as insulin stops working
    • Respiratory minute volume (VE) ⇩ 
    • RR becomes inadequate to blow off CO2respiratory acidosis follows
    • ⇩ CO
    • ⇧ SVR
    •   Capillary leak decreases intravascular volume
    • Metabolic acidosis related to anaerobic metabolism
    • Enzyme function ⇩ dramatically
    •   Coagulation deficits
    •   Medication biometabolism deficits
  45. Describe mild hypothermia
    • >32-34°C
    • ⇧BMR, CO, HR begins to ⇩ @ 32° C
  46. Describe moderate hypothermia
    • 29 - < 32° C
    • Body stops attempting to conserve or produce heat @ 32° C, shivering stops, LOC & SVR fall, acidosis, hyperglycemia, CO falls
  47. Describe severe hypothermia
    • < - 28° C
    • Hypotension
    • ECG Δ: Prolonged QR, QRS, QT intervals, VF
    • risk highest @ 22° C. Osborn waves clear @ 25° C.
    • PT, PTT ⇧by 50%, Platelets ⇩ by 40%
  48. What is this? 
    Osborn wave
  49. Describe the treatment of hypothermia
    • Remove from cold & wet environment
    • Manage airway, consider ETI, Risk of VF
    • Handle gently
    • Only start CPR if monitor shows VF or asystole
    • Defer meds until core temp > 30° C
    • < 33° C we see enzymatic retardation
  50. How do you accomplish passive external re-warming?
    Pt allowed to re-warm self w/blankets & transport vehicle heater
  51. What comprises active external re-warming?
    • Heat placed on external body surfaces (neck, groin, axilla)
    • Watch for afterdrop
  52. What comprises active internal re-warming?
    • Heat directly to core
    • IVF, hemodialysis, gastric lavage, rectal lavage, ECMO
  53. Describe the neuro complications from hyperthermia
    Cerebral edema & seizure activity 2° to hyponatremia
  54. Describe the renal complications from hyperthermia
    Hypokalemia, ATN
  55. Describe the hepatic complications from hyperthermia
    Hypoglycemia & ⇧ clotting times
  56. Describe the muscular complications from hyperthermia
    Increased CK (CK-MM) & rhabdomyolosis
  57. Hyperthermia can also cause what conditions 2° lysosomal enzymes?
    • ARDS
    • DIC
  58. Where & under what conditions do heat cramps occur?
    • In heavily exercised muscles
    • High heat
  59. What causes heat cramps?
    • Hyponatremia
    • Associated w/only H2O replacement
  60. Describe the treatment of heat cramps
    • Cool
    • Rehydrate w/Salt containing solutions (0.9% saline)
  61. Define Heat Exhaustion
    Defined as an increase in core temp w/o neurologic impairment
  62. Describe Heat Exhaustion
    • Temperature is lower & symptoms less severe than heat STROKE
    • Pt retains ability to sweat
  63. Describe the treatment of Heat Exhaustion
    • Cooling
    • Fluid replacement
    • Electrolyte replacement
  64. What is Heatstroke?
    A life threatening emergency characterized by failure of the body to dissipate heat effectively
  65. Describe Heatstroke
    • LOC is altered
    • Core temp ⇧ 42° C
    • O2 demand exceeds supply
    • Respiratory alkalosis ⇨ Metabolic acidosis
    • High output cardiac failure (use caution w/over-aggressive cooling)
  66. Describe the treatment of heatstroke
    • Aggressive cooling
    •   Soak & air flow (Conduct/Convect)
    • Aggressive airway management
    •   Don’t under ventilate, use vent to reduce work load (use of AC mode ideal &/or pressure support)
    • Expose
    • IV fluids
    • Prevent shivering
    •   Phenothiazines & NMBAs
    •   MRO2 ⇧ x 600% w/shivering!
    • Place OGT/NGT & consider H2 blockers
    •   cimetidine (Tagamet®) * consider drug interactions
    • Foley & monitor
    •   Volume output
    •   Color/evidence of rhabdomyolosis
    • Monitor labs
    •   ABGs for acidosis
    •   Watch clotting factors for early onset DIC
    •   Monitor liver enzymes
    •   Watch Na+ for hyponatremia
  67. Describe the treatment of rhabdomylosis in heat related illness
    • ⇧ urine output to 2 mL/kg/hr
    • Alkalinize urine w/NaHCO3-
    • Assist diuresis w/Lasix &/or mannitol
  68. Describe the treatment of hyponatremia in heat related illness
    Replace by correcting Na+: 3.3% saline SLOWLY (central pontine myelinolysis)
  69. Describe the pathophysiology & presentation of TCA intoxication
    • Mimics Class I AAs (quinidine, lidocaine)
    •   Blocks Na+ Channels
    • Inhibits NE (norepinephrine) uptake [Like
    • cocaine]
    • Blocks PNS (Peripheral Nervous System) [Like jimson weed]
    •   Early tachycardia
    •   Widening of QRS
    •   Aberrant SVT
    •   Torsades de Pointes/VT/VF
  70. Describe the treatment of TCA intoxication
    • NaHCO3-
    • Norepinephrine: 1st choice pressor
    • Dialysis NOT helpful
  71. Identify the common cardioselective beta blockers
    • atenolol (Tenormin®),
    • metoprolol (Lopressor®),
    • esmolol (Brevibloc®),
    • betaxolol (Betoptic®)
  72. Identify the common non-cardioselective beta blockers
    • propanolol (Inderal®),
    • sotalol (Betapace®),
    • nadolol (Corgard®),
    • timolol (Timoptic®)
  73. Describe the presentation of a cardioselective β blocker OD
    • Bradycardias w/resultant hypotension
    • Look for escape rhythms
  74. Describe the potentials issues w/the use of Epi in the treatment of β-blocker OD
    • May result in an “Inverse Epinephrine Response”
    •   With β1 blocked, Epi can only stimulate β2 & α1
    •     β2 will vasodilate
    •       May attenuate α1 effect
    •       May override α1 completely ⇨ hypotension
    •       α1 will vasoconstrict ⇨ ⇧ BP ⇨ baroreceptors triggered ⇨ ⇩ HR = BAD
  75. Describe the presentation of a Non-cardioselective β blocker OD
    • Respiratory distress, exacerbation of RAD
    •   Beta2 blocked @ same time as Beta1
    •   Inhibits bronchodilation
  76. Describe the treatment of Beta-blocker OD
    • Atropine rule out / Parasympathetic tone/prasympathetic tone prophylaxis (will pay off post TCP capture)
    • TCP ASAP
    • Glucagon 2-5 mg IVP (incr. cAMP via glucagon receptor)
    • dopamine (Intropin) PRN for hypotension
  77. Describe the presentation of Cardiospecific Ca+ Channel Blocker OD
    • Severe bradycardias
    • AV Dissociation w/comcomitant hypotension
  78. Describe the presentation of Vasculomotor specific Ca+ Channel Blocker OD
    Severe hypotension
  79. Describe the treatment of Cardiospecific Ca+ Channel Blocker OD
    • CaCl/Ca+ Gluconate
    • TCP
    • Maintain Insulin Euglycemia
  80. Describe the treatment of Vasculomotor specific Ca+ Channel Blocker OD
    • CaCl/Ca+ Gluconate
    • TCP
    • Maintain Insulin Euglycemia
  81. Describe the presentation of Digitalis toxicity
    • Visual disturbances {Yellow/Green Halos}
    • Bradycardia, SVT, VT, AV Blocks
  82. Describe the treatment of Digitalis toxicity
    • Digoxin Immune Fab (Digibind)
    • Assure normal electroclytes
    •   K+ 1st, then Ca++ & Mg++
    • TCP
    • lidocaine (Xylocaine), MagSulfate & phenytoin (Dilantin) for tachyarrhythmias
    • Caution w/electricty
  83. Describe the presentation of hyperkalemia
    • Profound acidosis (DKA, vent mismanagement, etc)
    • K+ supplement OD
    • ECG: Flattening/slurring of P's w/peaked T's
  84. Describe the treatment of hyperkalemia
    • CaCl
    •   Raises the action potential threshold to compensate for hyperkalemic elevated resting potential
    •   CAUTION w/hyperkalemia secondary to malignant hyperthermia
    • NaHCO3- [Do not mix w/CaCl]
    • Insulin
    • D50
    • Beta2 agonists
    • sodium polystyrene sulfonate (Kayexalate)
    • furosemide (Lasix)
  85. Describe the presentation of hypokalemia (< 3.5)
    • Loop diuretic misuse/OD
    • Serum K+ important as well as pH
    • ECG: Peaked P's, flattened/slurred T's & apperance of U's
  86. Describe the treatment of hypokalemia
    • KCl, KPhos
    • Commonly 10-20 mEq/hr (10 mEq/hr peripheral, 20- central)
    •   Never more than 0.5-1.0 mEq/kg/hr
  87. Describe the presentation of mild ASA intoxication
    • Tinnitus
    • Headache
    • Vertigo
    • Mental confusion
    • Thirst
    • Sweating
    • N/V
    • Hyperventilation
  88. Describe the presentation of severe ASA intoxication
    • Agitation/restlessness
    • Coma
    • Seizures
    • Non-cardiac pulmonary edema
    • Electrolyte disturbances (TCO2, HCO3-)
  89. Describe the treatment of ASA poisoning
    • Gastric emptying
    • Charcoal
    • Alkaline diuresis using NaHCO3-
    •   Ion trapping mechanism
    • Hemodialysis
    • Management of Acid/Base & electrolyte disturbances
  90. Describe the presentation of acetaminophen (APAP) intoxication during Stage I
    • "Flu like symptoms"
    • Occurs w/in 30 min - 24 hrs
    • N/V/Anorexia
    • Malaise
    • Pallor
    • Diaphoresis
  91. Describe the presentation of acetaminophen (APAP) intoxication during Stage II
    • "Ow my liver!"
    • 24 - 48 hrs
    • RUQ pain/tenderness
    • Incr Liver enzymes
    • Incr serum bilirubin
    • Incr PT
    • Oliguria as a result of ATN
  92. Describe the presentation of acetaminophen (APAP) intoxication during Stage III
    • "Gonna die now"
    • 72-96 hrs
    • Peak for liver function abnormalities
    • Return of anorexia, N/V, Malaise
    • Jaundice becomes apparent
    • Hepatic encephalopathy
    • DIC
    • Death d/t fulminant hepatic necrosis
  93. Describe the presentation of acetaminophen (APAP) intoxication during Stage IV
    • "I'm not dead yet"
    • 4 days to 2 wks
    • Resolution period
    • Liver functions return to normal baseline values
    • Patients are asymptomatic
  94. What is a toxic level of acetaminophen poisoning?
    7.5 GM or 150 mg/kg
  95. How long post ingestion do you obtain serum levels in acetaminophen poisoning?
    4 hrs
  96. What is the treatment for acetaminophen poisoning?
    • n-acetylcysteine (Mucomyst)
    • Orally 140 mg/kg followed by 70 mg/kg Q 4 hrs for 17 dosings
  97. Describe the presentation of ethylene glycol / methanol poisoning
    • Profound anion gap
    • Osmolar gap
    • Nystagmus / blindness
    • Depressed DTRs
    • Stupor/Coma/Convulsions
    • Myoclonic jerks
    • Hypothermia/Low grade fever
    • Profound hypocalcemia
  98. Describe the treatment of ethylene glycol / methanol poisoning
    • IV ethanol drip
    • fomepizole (Antizol)
    • Thiamine
    • pyridoxine (Aminoxin)
  99. What are the treatment PEARLS for cocaine use?
    • Avoid beta-blockers
    • Utilize alpha-blockers for HTN
    • Use benzodiazipines for anxiety
  100. Identify a caution for treatment of the pt exposed to hallucinogens
    Beware of violent propensity
  101. What treatment may be required for alcohol intoxication?
    Dialysis
  102. What is the reversal agent & dosing schedcule for benzodiazepines?
    • 0.1 - 0.2 mg IVP, Max 3.0 - 5.0 mg
    • Caution w/Seizure or chronic use history
  103. What is the reversal agent and dosing schedule for opioids?
    • 0.4 - 2.0 mg IVP, Repeat PRN
    • Reverses all beneficial effects of opioids as well as problematic
    • Be alert for negative pressure induced pulmonary edema
  104. What is the treatment paradigm for Carbon Monoxide (CO) poisoning?
    • O2
    • Hyperbarics
  105. What is the treatment paradigm for Organophosphate (OGP)/Organocarbamate exposure?
    • atropine
    • 2-PAM
  106. What is the treatment paradigm for Methemoglobinemia?
    methylene blue
  107. Describe the presentation of anticholinergic crisis
    • Mad as a Hatter
    • Red as a Beet
    • Dry as a Bone
    • Blind as a Bat
  108. What is the treatment paradigm for anticholinergic crisis?
    physostigmine (Eserine)
  109. What is the mechanism of action for physostigmine in anticholinergic crisis?
    Inhibits acetylcholinesterase
  110. What is the treatment paradigm for coumadin poisoning?
    • Vitamin K (IV, IM)
    •   6 hr onset
    •   High rate of anaphylaxis when given IVP
    • FFP - for when 6 hrs is too long
  111. What is the treatment paradigm for heparin OD?
    • Protamine
    • Derived from whale sperm so watch for allergies to seafood & fish
    • Typical profile is to give a small test dose then give larger dose once risk of anaphylaxis is deemed low
  112. What is the treatment paradigm for Beta & Calcium channel blockers?
    • glucagon
    • CaCl/gluconate
  113. Where is CSF created?
    The Choroid Plexus
  114. Where is CSF reabsorbed?
    Arachnoid Villi
  115. What is the name of the thin cerebral cortex cover?
    Pia Mater
  116. What is the name of the tough outer covering?
    Dura Mater
  117. Where is CSF located?
    Subarachnoid space
  118. What is the significance of the finding on CT that a brain hemorrhage is lenticular in shape?
    Diagnostic for epidural bleed
  119. What is Cranial Nerve I?
    Olfactory
  120. What is Cranial Nerve II?
    Optic
  121. What is Cranial Nerve III?
    Oculomotor
  122. What is Cranial Nerve IV?
    Trochlear
  123. What is Cranial Nerve V?
    Trigeminal
  124. What is Cranial Nerve VI?
    Abducens
  125. What is Cranial Nerve VII?
    Facial
  126. What is Cranial Nerve VIII?
    Vestibulocochlear
  127. What is Cranial Nerve IX?
    Glossopharyngeal
  128. What is Cranial Nerve X?
    Vagus
  129. What is Cranial Nerve XI?
    Accessory
  130. What is Cranial Nerve XII?
    Hypoglossal
  131. What does the Olfactory Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Smell
    • Sensory
  132. What does the Optic Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Sight
    • Sensory
  133. What does the Oculomotor Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Eye movement [Adduction]
    • Motor
  134. What does the Trochlear Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Eye movement
    • Motor
  135. What does the Trigeminal Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Facial sensory, chewing
    • Both
  136. What does the Abducens Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Eye movement [Abduction]
    • Motor
  137. What does the Facial Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Facial muscles, taste
    • Both
  138. What does the Vestibulocochlear Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Balance / Position
    • Sensory
  139. What does the Glossopharyngeal Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Taste, baroreceptors
    • Both
  140. What does the Vagus Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Parasympathetic Nervous System (PNS), Motor of Larynx/Pharynx
    • Both
  141. What does the Accessory Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Shoulder / Head movement
    • Motor
  142. What does the Hypoglossal Cranial Nerve control?
    Also classify as Sensory, Motor or Both
    • Moves tongue
    • Motor
  143. What is the formula to calculate MAP?
    • or
  144. What is the normal range for ICP?
    0 - 10 mmHg
  145. What is the goal of CPP?
    > 60 mmHg
  146. What is the formula to calculate CPP?
  147. Describe the presentation of increased ICP
    • Change in LOC
    • Change in pupil size & reaction
    • Abnormal motor responses
    •   Decorticate
    •   Decerebrate
  148. Describe Decorticate posturing
    Adduction of upper extremities towards the "Core"
  149. What is the significance of decorticate posturing?
    Indicates damage above the cerebellum & brainstem (supra-tentorial)
  150. Describe decerebrate posturing
    Extension & hyperpronation of upper extremities
  151. What does decerebrate posturing indicate?
    Damage to brainstem or compression of the thalamus & brainstem
  152. Identify the 3 components of Cushing's Triad
    • HTN
    • Bradycardia
    • Respiratory changes
  153. Describe the treatment of the Increased ICP patient
    • Position patient
    •   Eyes forward
    •   15-30 degrees reverse trendelenburg
    • Limit noxious stimuli
    •   Suctioning/Invasive procedures
    •   Noise
    •   Atmospheric pressure changes
    • Maintain euvolemia, normothermia & normal electrolytes
    • Pharmacology:
    •   Sedation - benzos, propofol
    •   Analgesia - fentanyl
    •   NMBAs
    • Systematic Approach to Herniation
  154. Describe the Systematic Approach to Herniation
    • Paralyze, ETI & slightly hyperventilate to a PaCO2 of ~ 32-35 mmHg
    •   If using ETCO2 don’t forget gradient correction
    •   What happens w/hypoventilation?
    •     “Cerebral Steal or Luxury Perfusion”
    •   What happens w/hyperventilation?
    •     "Reverse Steal or Robin Hood Effect”
    • Assure adequate O2 delivery
    •   100% for duration of transport
    • Assure adequate fluid resuscitation 1st, then consider
    •   Mannitol
    •   Hypertonic saline
    • ⇩ O2 demand by induction of barbiturate coma
    •   thiopental (Pentothal®) TOO SHORT ACTING
    •   phenobarbital (Luminal®) DRUG OF CHOICE
  155. Describe subdural hematomas
    • Blood btn the Dura & Arachnoid membranes
    • Usually venous in nature
    • High morbidity/mortality
    • 3 types
    •   Acute: Symptomatic w/in 24°
    •   Subacute: Symptomatic w/in 2-10 days
    •   Chronic: Symptomatic after 2 weeks
  156. Describe subdural hematomas in the elderly
    Larger subdurals w/slowly developing symptoms d/t cerebral atrophy
  157. Describe subdural hematomas in younger pops
    • Rapid onset of symptoms w/marked ⇧ ICP
    •   Peds subdurals typically occur
    •     < 18 mos
    •     Look for bulging fontanelle & retinal hemorrhages
  158. Describe epidural hematomas
    • Bleeding btn the skull & the dura mater
    • Usually arterial but can be venous
    • Laceration of the middle meningeal artery in the temporal lobe area
  159. Describe the presentation of epidural hematomas
    • Classic symptomology – Transient loss of consciousness followed by a period of lucidity “Lucid Interval”
    • Epidural bleeds cause uncal herniation
    •   Will result in dilation of the ipsilateral pupil w/contralateral neuro deficits/posturing
  160. Describe subrachnoid hemorrhage
    • Bleeding btn the arachnoid membrane & the
    • pia mater
    • Trauma is the most common cause
    •   Berri aneurysm 2nd most common cause w/rupture 2° HTN
  161. Describe the presentation of subarachnoid hemorrhage
    • “Worst Headache of My Life”
    • N/V, stiff neck, visual disturbances, Δ LOC
    •   Confused w/meningitis
    •   No LP if Sub-A bleed possible
  162. Describe intracerebral hemorrhage
    • Hemorrhage in the brain parenchyma
    • Produced from shearing & tensile forces
    • Frequently occurs in the white matter of the frontal & temporal regions
    • May be single or multiple & is associated w/contusions, subdural hematoma & diffuse axonal injury (DAI)
    • Less common injury w/delayed onset of symptoms (24° or more after injury)
  163. Describe intraventricular hemorrhage
    • Bleeding into the ventricles as a result of severe brain trauma
    • Result of shearing forces
    • Greatly ⇧ mortality rate
    • Usually found in frontal or temporal lobes
  164. Describe mild concussion
    • Rotational Force
    • Reversible w/no persistent sequelae
    • Retrograde amnesia of short duration
  165. Describe Classic Concussion
    • Rotational or direct force
    • Reversible w/memory & info processing problems
    • Brief LOC, retrograde & post traumatic amnesia
  166. Describe Diffuse Axonal Injury [DAI]
    • Diffuse shearing injury – rotational acceleration
    • Irreversible w/profound neuro, psych & personality deficits
    • Usually coma
  167. Describe the 3 classifications of CVA
    • Embolic – Most common
    • Hemorrhagic – Bleeding into brain tissue
    • Thrombotic – Least common
  168. Describe the treatment of CVA
    • Prevent additional insult
    • Maximize Cerebral blood flow
    • Control ⇧ ICP
    • Manage associated conditions
    • Thrombolytic therapy w/i 3 hrs of neurologic deterioration onset
  169. Describe a linear skull fx
    A line that extends toward the base of the skull
  170. Describe a linear stellate skull fx
    Multiple Fx that radiate from the compressed area
  171. Describe a diastatic skull fx
    Involves a separation of the bones at a suture line or a marked separation of bone fragments
  172. Describe a depressed skull fx
    May be open or closed
  173. Describe a basilar skull fx
    Fx of the base of the skull
  174. Describe the signs of a basilar skull fx
    • Battle’s sign: Bruising behind the ear on the mastoid bone
    • Periorbital Ecchymosis (Raccoon Eyes): Ecchymosis around the eyes
    • Otorrhea: Bleeding from ear w/CSF leak 
    • Rhinorrhea: Bleeding from the nose w/a CSF leak
  175. What are the complications from skull fx?
    • Intracranial Infections
    • Hematomas
    • Meningeal & brain tissue damage
    • Pneumocephalus
    • Associated nerve damage & palsies
  176. Differentiate btn the LeFort Fx Classifications
    • LeFort I: Fx of the mandible
    • LeFort II: Nose & maxilla separate from skull
    • LeFort III: Through the zygomas; The face from the eyes down is free floating
  177. Define neurogenic shock
    • Areflexia w/flaccid paralysis immediately or shortly after injury
    • Parasympathetic dominance below the lesion
  178. Describe the classic presentation of neurogenic shock
    • Hypotension
    • Warm red skin below injury
    • Absence of tachycardia
  179. Management of CHI is typically referred to as Triple-H Therapy. This consists of:
    • HTN
    • Hypervolemia
    • Hemodilution
  180. Patients MOST likely to demonstrate an acute subdural include:
    Pediatric patients
  181. Describe maternal physiological Δs
    • HR ⇧ 15-20 bpm
    • BP ⇩ in 2nd Trimester 5-15 torr & ⇧ in 3rd trimester 10 torr
    • Cardiac Output ⇧ ~ 2 L/min
    • Plasma volume ⇧ 40% ⇨ ⇧ clotting factors
    • Placenta very high in tissue thromboplastin content
    • RBC’s ⇧ but not @ same rate as plasma ⇨ dilutional anemia
    • ⇧ volume ⇨ capillary engorgement ⇨ airway swelling
    •   Mallampati ⇧ 2-3 classes
    •   Failed airways 1:2230 vs 1:280 when Pg
    • Heart elevates anteriorly & ↺ to left
    • WBC ⇧ 
    • Progesterone relaxes everything (sphincters,
    • vasculature, etc)
    • ⇩ Functional Residual Capacity [FRC] by ~ 20%
  182. Define the obstetrical term 'Dilation'
    Refers to the extent of cervical dilation as judged by palpation
  183. Define the obstetrical term 'Effacement'
    Relates to the thickness of the cervix & is expressed as a %. The cervix is normally about 2 cm thick & thins during labor. When thinned to 1 cm would be said to be 50% effaced.
  184. Define the obstetrical term 'Lie'
    Refers to the longitudinal orientation of the fetus in relation to the longitudinal orientation of the mother
  185. Define the obstetrical term 'Station'
    Refers to the fetal head in relation to the mother’s pubic bone & is expressed as a + or a - number as measured in cm
  186. Define the obstetrical term 'Presentation'
    What is attempting to emerge 1st? Cephalic, breech or shoulder? (Cephalic – Vertex, brow or face)
  187. What are baseline FHTs?
    120-160/min
  188. Define the importance of 'variability' as it relates to FHTs
    The single most important predictor of fetal well-being
  189. What causes Poor variability in FHTs?
    • Fetal hypoxia
    • Meds given to mom
    • Smoking
    • Extreme prematurity
    • Fetal sleep
  190. What do accelerations indicate?
    • Usually GOOD
    • Usually associated w/fetal movement & CNS
    • response to stimuli
    • Hypoxic fetus w/metabolic acidosis cannot
    • accelerate the heart
  191. What causes Early Decelerations & of what diagnostic value are they?
    • OK sign
    • Typical vagal response to squeezing of head caused by contractions
  192. What are Late Decelerations & of what diagnostic value are they?
    • BAD
    • Indicate uteroplacental insufficiency causing the fetus to experience a hypoxic bradycardia
    • Commonly associated with:
    •   PIH
    •   DM
    •   Smoking
    •   Late Deliveries
  193. Describe Variable Decelerations in FHR monitoring
    • Not good but correctable
    • Common during contractions, typically V or W shaped
    • Caused by cord compression
    • Shouldering” is common
    • Look for ‘cord’ problems
    •   Prolapse
    •   Short
    •   Entanglement
    •   Nuchal
  194. What causes sinusoidal FHR patterns?
    • Typical of fetal hypovolemia OR anemia
    • Accidental tap of the umbilical cord during amniocentesis
    • Fetal maternal transfusion
    • Placental abruption
  195. Define fetal bradycardia
    FHR < 120 for 5-10 min
  196. Define fetal tachycardia
    FHR > 160 for 10 min
  197. Describe factors affecting fetal distress
    • Assure fetal oxygenation: Give mom High flow O2 by NRB
    • Maternal hypotension
    •   Initiate 250-500 cc IVF bolus
    •   Correct supine hypotension
    •   “Tank her up”
    • Hypertonic or tetanic contractions: D/C oxytocin infusion
    • R/O cord prolapse
    • Assess for placental abruption
    • Δ positions
  198. Describe S/S of Imminent Delivery
    • VB
    • Contractions more frequent than q 10 min
    • ⇧ intensity
    • Urge to push
    • Crowning
  199. What steps should you take when dealing w/Pre-Term labor?
    • ☑ 4 signs of Imminent Delivery
    • Obtain status of amniotic membranes
    • Determine cervical status
    • L Lateral Recumbent
    • Assess for infection
    •   Prophylactic Abx for Group B Strep
    • Tocolytics
    •   MgSO4-: Watch 4 toxicity
    •   Terbutaline
    • Monitor FHT, movement
  200. How do we monitor for mag toxicity?
    • DTRs
    • BP
    • LOC
    • Resps
  201. Describe the treatment of mag toxicity
    • CaCl 4 the acute OD
    • Push fluids w/diuresis [Renal excretion is very good]
  202. Drug Card: terbutaline
    • terbutaline
    • (Brethine®Breathaire®)
    • 0.25 mg sq q 15
    • Pre-Term Labor
  203. magnesium sulfate Drug Card
    • magnesium sulfate
    • (MgSO4-)
    • 4-6 gm bolus / 15-30 min, 2 gm/hr maint
    • Preeclampsia, Pre-Term Labor
  204. oxytocin Drug Card
    • oxytocin
    • (Pitocin®)
    • 20-40 units/1000 cc @ 125 cc/hr
    • Post-Partum hemorrhage
  205. hydralazine Drug Card
    • hydralazine
    • (Apresoline®)
    • 2 mg IVP q 5 min to DBP 90-100 mmHg OR 5-10 mg q 20 min
    • PIH, Preeclampsia
  206. What etiologies may account for PIH?
    • ⇧ Volume - Autoregulation Mismatch
    • Placental Toxins
  207. What does HELLP stand for?
    A syndrome where pts experience a myriad of symptoms including Hemolysis, Elevated Liver enzymes & a Low Platelet count
  208. Describe the presentation of PIH
    • HTN
    • Proteinuria
    • Edema
  209. What population most at risk for PIH?
    • African-American Females
    • Prima Gravida
    • Multi Gravida
    • Very young maternal
    • Advanced maternal age
  210. Describe guidelines for treatment of PIH, Preeclampsia & HELLP
    • Watch for late decels & ⇩ variability as well as fetal movement
    • MgSO4 4-6 G bolus followed by 1-2 G/hr
    • Steroids betamethasone (Celestone®) ASAP
    • Consider labetalol (Trandate®) 20 mg SIVP
    • Consider hydralazine (Apresoline®) 2 mg SIVP
    • Give diazepam (Valium®) PRN 4 seizure activity w/MgSO4 (MgSO4 inhibits cerebral vasospasm primarily)
  211. Describe the causes of AAA in pregnancy
    • Gravid uterus ⇧ clonic pressure on distal aorta & femoral arteries
    • ⇧ circulating volume
    • ⇧ aortic ejection pressures
  212. How may the parturient pt's AAA presentation be misleading?
    • CP similar to AMI
    •   May actually be complicated by an AMI
  213. How do you  maximize fetal viability in the pregnant trauma pt?
    Aggressively treat mom like you treat other trauma pts
  214. What are the risk factors for placenta previa?
    • Uterine scarring
    • Multiparity w/short intervals
    • Post D&C
  215. Describe the typical presentation of placenta previa
    Painless Bright red vaginal bleeding
  216. Describe the typical presentation of placental abruptio
    Ripping or tearing pain w/dark or no evident blood loss
  217. Describe the treats posed by placental abruptio
    • Exsanguination
    • Placental insufficiency
  218. What does bleeding in the uterus cause?
    Blood is irritating to the uterus ∴ it will initiate contractions
  219. Describe the management of the placental abruptio pt
    • High flow O2, VS, Fluids
    • Assess for contractions, fetal movement, FHTs, hemorrhage
    • Continually reassess fundal height
    • Consider tocolytics & blood products
    • Watch for signs of DIC
  220. What measurement is helpful in uterine rupture?
    Serial fundal height measurements
  221. How do FHTs respond to nuchal cord?
    Variable decelerations
  222. Describe management of nuchal cord
    • Gently loosen & draw down over head
    • Clamp & cut before shoulders deliver if it is too tight to remove
    • Focus is relieving cord tension before next contraction
  223. Describe treatment of umbilical cord prolapse
    • Elevate presenting part off the cord w/a hand in the vagina to prevent cord compression
    • Trendelenburg or knee-chest position
    • Tocolytics to reduce pressure on the cord during contractions
  224. Describe management of the breech presentation
    • Fetus should not be touched until cord has spontaneously delivered
    • Palpate the cord for FHR
    • After shoulders have delivered, rotate baby’s trunk so that the back is anterior & apply gentle downward traction
    • Apply suprapubic pressure to facilitate delivery of the head
    •   Mauriceau’s Maneuver
    • Do not attempt to deliver a footling breech
  225. Describe management of meconium delivery
    • Suction mouth, posterior pharynx & nose after delivery of head, but before delivery of
    • shoulders
    • If baby is vigorous continue w/supportive care
    • If baby is not vigorous suction mouth & trachea
  226. Define "vigorous" as it pertains to the newborn
    • Strong respiratory efforts
    • Good muscle tone
    • HR > 100 bpm
  227. Describe management of postpartum hemorrhage
    • Vigorous fundal massage
    • Rapid infusion of 20-40 units of oxytocin (Pitocin®)
    • methylergonovine (Methergine®) 0.2 mg IM
    • Assess blood loss
    • Replace fluids, blood
    • Bimanual uterine compression
  228. Describe the management of uterine inversion
    • Manual replacement if the uterus has not yet contracted down & cervix has not constricted
    • Tocolytics if the uterus has contracted to relax the uterus & allow replacement
    • DO NOT REMOVE THE PLACENTA
    • oxytocin use post replacement
  229. Describe management of Amniotic Fluid Embolism (AFE)
    • High flow O2, ETI PRN
    • PEEP may be required
    • Fluid resuscitation
    • Hemodynamic monitoring
    • Blood product replacement as needed
    •   FFP, Platelets, Cryo
    • Anticipate severe fetal distress if syndrome presents prepartum
    • Prepare for emergent post-mortum c-section
  230. Describe management of DIC
    • Airway management
    • Stop ongoing major hemorrhage
    • Volume replacement
    • Minimize needle sticks
    • Blood products (FFP, platelets)
  231. What airway issues are seen with DIC?
    • ⇧ sensitivity to aminosteroids (VEC & ROC)
    • Possible prolonged effects of SUX
    • Difficult airway/Failed airway more common

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