CHAPTER 16- CRITICAL CARE.txt

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CHAPTER 16- CRITICAL CARE.txt
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  1. What is normal Cardiac output (CO) l/min:
    4-8
  2. What is normal cardiac index (L/min)?
    2.5-4
  3. What is normal systemic vascular resistance (SVR)?
    800-1400
  4. What is normal systemic vascular resistance index (SVRI)
    1500-2400
  5. What is normal pulmonary capillary wedge pressure (PCWP)?
    11+/- 4
  6. What is normal Central venous pressure?
    7+/- 2
  7. Pulmonary artery (PA)
    20-30/6-15
  8. Mixed venous oxygen saturation (SvO2)
    75 +/- 5
  9. Mean arterial pressure (formula):
    MAP = CO x SVR
  10. Cardiac index (formula):
    CO/BSA
  11. Systemic vascular resistance index (formula):
    SVRI= SVR x BSA
  12. What % of cardiac output goes to:
    -kidney
    -brain
    -heart
    • 1) kidney gets 25% of CO
    • 2) brain gets 15% of CO
    • 3) heart gets 5%
  13. Preload:
    • 1) end-diastolic length
    • 2) linearly related to end diastolic volume and filling pressure
  14. Afterload:
    1) resistance against the ventricle contracting (SVR)
  15. Stroke volume
    • 1) determined by:
    • 1- LVEDV
    • 2- contractility
    • 3- afterload

    2) stroke volume = LVEDV- LVESV
  16. Ejection fraction
    stroke volume/ EDV
  17. EDV (end-diastolic volume)
    determined by preload and distensibility of the ventricle
  18. ESV (end systolic volume)
    determined by contractility and afterload
  19. When does cardiac output increase in relation to heart rate and when does it go down?
    Cardiac output increases with HR up to 120-150 beats/min, then starts to go down because of decreased diastolic filling time
  20. Atrial kick
    accounts for 15-30% of LVEDV
  21. Anrep effect
    automatic increase in contractility secondary to increased afterload
  22. Bowditch effect
    automatic increase in contractility secondary to increased HR
  23. What is the relationship between aortic and radial pressures?
    • 1) Aortic mean and diastolic pressures are slightly greater than radial pressure.
    • 2) Radial systolic pressure are slightly higher than mean aortic pressure.
  24. O2 delivery formula:
    O2 delivery = CO x arterial O2 content (CaO2) = CO x (Hgb x 1.34 x O2 saturation + 1[Po2 x 0.003])
  25. O2 consumption (VO2) (formula):
    • O2 consumption = CO x (CaO2-CvO2).
    • CvO2= venous O2 content
  26. What is normal O2 delivery to consumptoin ratio?
    • 1) normal O2 delivery-to-consumption ratio is 5:1
    • 2) CO increases to keep this ratio constant
    • 3) O2 consumption is usually supply independent (consumption does not change until low levels of delivery are reached).
  27. Right shift on Oxygen-Hgb dissociation curve (O2 unloading)
    • 1- increased CO2
    • 2- increased temperature
    • 3- increased ATP production
    • 4- increased 2,3 DPG production
    • 5- decreased pH
  28. Normal p50:
    normal p50 (O2 at which 50% of O2 receptors are saturated) = 27mmHg
  29. When do you get increased SvO2?
    • 1) saturation of venous blood is normally 75%+/- 5%
    • 2) occurs with increased shunting of blood or decreased O2 extraction (sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation)
  30. When does decreased SvO2 occur?
    Decreased SvO2 occurs with increased O2 extraction or decreased O2 delivery (decreased O2 saturation, decreased CO)
  31. Wedge can be thrown off by:
    • 1- pulmonary hypertension
    • 2- aortic regurgitation
    • 3- mitral stenosis
    • 4- high PEEP
    • 5- poor LV compliance
  32. where should Swan-Ganz catheter be placed?
    should be placed in zone III (lower lung)
  33. What do you do if you have hemoptysis after flushing swan-ganz catheter
    • 1- increase PEEP (will tamponade the pulmonary artery bleed)
    • 2- mainstem intubate nonaffected side
    • 3- can try to place Fogarty baloon down the affected side
    • 4- may need thoracotomy and lobectomy
  34. Relative contraindications to swan ganz catheter-
    • 1) previous pneumonectomy
    • 2) left bundle branch block
  35. Approximate swan-ganz catheter distances to wedge
    • R SCV 45cm
    • R IJ 50cm
    • L SCV 55cm
    • LIJ 60cm
  36. What is the only way to measure pulmonary vascular resistance?
    pulmonary vascular resistance can be measured only by using a swan-ganz catheter
  37. What are the primary determinants of myocardial O2 consumption?
    • 1) increased ventricular wall tension
    • 2) increased HR

    are the primary determinants of myocardial O2 consumption--> can lead to myocardial ischemia
  38. Unsaturated bronchial blood
    empties into pulmonary veins; thus, LV blood is 5mmHg (PO2) lower than pulmonary capillaries
  39. Alveolar-arterial gradient
    1) 10-15mmHg normal in nonventilated patient
  40. What blood has the lowest venous saturation
    coronary venous blood (30%)
  41. Acute adrenal insufficiency
    • 1) cardiovascular collapse
    • 2) characteristically unresponsive to fluids and pressors
  42. Chronic adrenal insufficiency
    • 1) hyperpigmentation
    • 2) weakness
    • 3) weight loss
    • 4) GI symptoms
    • 5) increased K
    • 6) decreased Na
    • 7) fever
    • 8) hypotension
  43. Steroid potency:
    • 1x- cortisone, hydrocortisone
    • 5x- prednisone, prednisolone, methylprednisolone
    • 30x- dexamethasone
  44. Neurogenic shock
    • 1) loss of sympathetic tone
    • 2) Usually have decreased HR, decreased BP, warm skin
    • 3) Treatment:
    • 1- give volume 1st
    • 2- phenylephrine after resuscitation
    • 3- give steroids for blunt spinal trauma with deficit
  45. What is the initial alteration in hemorrhagic shock?
    increased diastolic pressure
  46. Cardiac tamponade
    • 1) causes decreased diastolic ventricular filling and hypotension
    • 2) Beck's triad:
    • 1- hypotension
    • 2- jugular venous distention
    • 3- muffled heart sounds
    • 3) Echocardiogram shows impaired diastolic filling of right atrium initially (1st sign of cardiac tamponade)
    • 4) pericardiocentesis blood does not form clot
    • 5) Treatment:
    • 1- fluid resuscitation initially
    • 2- need pericardial window or pericardiocentesis
  47. See types of shock chart pg 93
  48. Early sepsis triad:
    • 1) confusion
    • 2) hyperventilation
    • 3) respiratory alkalosis
  49. Early gram negative sepsis (what happens with insulin/glucose):
    • 1) decreased insulin
    • 2) increased glucose
    • (impaired utilization)
  50. Late gram negative sepsis (what happens with insulin/glucose)
    • 1) increased insulin
    • 2) increased glucose
    • (secondary to insulin resistance)
  51. What usually happens just before patient becomes clinically septic
    hyperglycemia
  52. Fat emboli
    • 1) Signs include:
    • 1- petechia
    • 2- hypoxia
    • 3- confusion
    • (can also be similar to pulmonary embolism)

    2) Sudan red stain may show fat in sputum and urine

    3) Most common with lower extremity (hip/femur) fractures/orthopaedic procedures
  53. Pulmonary thromboemboli
    • 1) echo will show RV strain
    • 2) suspect PE with:
    • 1- PA systolic pressures >40
    • 2- decreased PO2 and PCO2
    • 3- respiratory alkalosis
    • 4- chest pain
    • 5- cough
    • 6- dyspnea
    • 7- increased HR
  54. Air emboli
    1) place patient head down and roll to left (keeps air in RV and RA), then aspirate air would with central line or PA catheter to RA/RV
  55. Intra-aortic balloon pump (IABP)
    • 1) inflates on T-wave (diastole)
    • 2) deflates on P wave or start of Q wave (systole)
    • 3) aortic regurgitation is a contraindication
    • 4) place tip of the catheter just distal to left subclavian (1-2 cm below the top of the arch)
    • 5) used for cardiogenic shock (after CABG, MI) or in patient with refractory angina
    • 6) decreases afterload (deflation during ventricular systole)
    • 7) Improves SBP (inflation during ventricular diastole, which improves coronary perfusion
  56. Alpha-1 receptors
    • 1) vascular smooth muscle constriction
    • 2) gluconeogenesis
    • 3) glycogenolysis
  57. Alpha-2 receptor
    venous smooth muscle constriction
  58. Beta-1 receptors
    myocardial contraction and rate
  59. Beta-2 receptors
    • 1) relaxes bronchial smooth muscle
    • 2) relaxes vascular smooth muscle
    • 3) increases insulin, glucagon, rennin
  60. Dopamine receptors
    relax renal and splanchnic smooth muscle
  61. Dopamine
    • 1) (2-5ug/kg/min initially, 20-50 mg/kg/min for high dose)
    • 2) 0-5 ug/kg/min - dopamine receptors (renal)
    • 3) 6-10 ug/kg/min- beta-adrenergic (heart contractility)
    • 4) >10ug/kg/min- alpha-adrenergic (vasocontriction and increased BP)
  62. Dobutamine
    • 1) 3ug/kg/min initially
    • 2) 5-15ug/kg/min- beta-1 (increased contractility mostly)
    • 3) >15ug/kg/min- beta-2 (vasodilation and increased HR)
  63. Milrinone
    • 1) phosphodiesterase inhibitor (increased cAMP)
    • 2) results in increased calcium flux and increased myocardial contractility
    • 3) also causes vascular smooth muscle relaxation and vasodilation
  64. Phenylephrine
    1) alpha-1, vasocontriction
  65. Norepinephrine
    • 1) 4ug/min initially
    • 2)low dose- beta-1 (increased contractility)
    • 3) high dose- alpha-1 and alpha-2, potent splanchnic vasocontrictor
  66. Epinephrine
    • 1) 2ug/min initially
    • 2) Low dose- beta-1 and beta-2 (increased contractility and vasodilation)
    • 3) can decrease BP at low doses

    • 4) High Dose- alpha-1 and alpha-2 (vasocontriction)
    • - increased cardiac ectopic pacer activity and myocardial O2 demand
  67. Isoproterenol
    • 1) 1-2 ug/min initially
    • 2) beta-1 and beta-2, increases HR and contractility, vasodilates
    • 3) Side Effects:
    • 1- extremely arrhythmogenic
    • 2- increases heart metabolic demand (rarely used)
    • 3- may actually decrease BP
  68. Vasopressin
    • 1) V1 receptors- vasocontriction of vascular smooth muscle
    • 2) V2 receptors (intrarenal)- water reabsorption at collecting ducts
    • 3) V2 receptors (extrarenal)- mediate release of factor VIII and von willebrand factor
  69. Nipride
    arterial and venous dilator
  70. Cyanide toxicity
    • 1) at doses >3ug/kg/min for 72 hours
    • 2) can check thiocyanate levels and signs of metabolic acidosis
    • 3) treatment: amyl nitrite, then sodium nitrite
  71. Nitroglycerin
    • 1) predominantly venodilation
    • 2) modest effect on coronaries
    • 3) decreased myocardial wall tension by decreasing preload
  72. Hydralazine
    alpha blocker
  73. Pulmonary system:
    - compliance
    - aging
    - V/Q ratio
    • ´╗┐Compliance: (change in volume)/(change in pressure)
    • - high compliance means lungs are easy to ventilate
    • - Pulmonary compliance decreases in patients with:
    • 1) ARDS
    • 2) fibrotic lung diseases
    • 3) reperfusion injury
    • 4) pulmonary edema

    • Aging-
    • 1) decreases FEV1 and vital capacity
    • 2) increases functional residual capacity

    V/Q ratio- highest in upper lobes, lowest in lower lobes
  74. what happens when you increase PEEP?
    • 1) improve oxygenation (alveoli recruitment)
    • 2) improves FRC
  75. What happens when you increase rate or volume?
    decrease CO2
  76. Normal weaning parameters:
    • 1- negative inspiratory force (NIF) >20
    • 2- FiO2 <35%
    • 3- PEEP 5 (physiologic)
    • 4- pressure support 5
    • 5- RR <24/min
    • 6- HR <120 beats/min
    • 7- PO2 >60mmHg
    • 8- PCO2 <50mmHg
    • 9- pH 7.35-7.45
    • 10- saturations >93%
    • 11- off pressors
    • 12- follows comands and can protect airway
  77. What is pressure support?
    decreases the work of breathing (inspiratory pressure is held constant until minimum volume is achieved)
  78. FiO2 <60%
    prevents O2 radical toxicity
  79. Barotrauma
    high risk if plateaus >30 and peaks >50 --> consider prophylactic chest tube
  80. PEEP
    • 1) improves FRC and compliance by keeping alveoli open
    • 2) its the best way to improve oxygenation
  81. Excessive PEEP Complications:
    • 1) decreased RA filling
    • 2) decreased CO
    • 3) decreased renal blood flow
    • 4) decreased urine output
    • 5) increased pulmonary vascular resistance
  82. High-frequency ventilation
    used a lot in kids; tracheoesophageal fistula, bronchopleural fistula
  83. Inverse ratio ventilation
    helps reduce barotrauma (normal 1:2 I:E phase; go to 2:1)
  84. Total lung capacity (TLC):
    • 1) lung volume after maximal inspiration
    • 2) TLC= FVC +RV
  85. Forced vital capacity (FVC)
    1) maximal exhalation after maximal inhalation
  86. Residual volume (RV)
    lung volume after maximal expiration (20% TLC)
  87. Tidal volume
    1) volume of air with normal inspiration and expiration
  88. Functional residual capacity (FRC)
    • 1) lung volume after normal exhalation
    • 2) FRC= ERV + RV
  89. What things decrease FRC?
    • 1- surgery (atelectasis)
    • 2- sepsis (ARDS)
    • 3- trauma (contusion, atelectasis, ARDS)
  90. Expiratory reserve volume (ERV)
    volume of air that can be forcefully expired after normal expiration
  91. Inspiratory capacity
    maximum air breathed in from FRC
  92. FEV1
    forced expiratory volume in 1 second (after maximal inhalation)
  93. Minute ventilation
    Minute ventilation = TV x RR
  94. Restrictive lung disease
    • Decreased TLC
    • Decreased RV
    • Decreased FVC
    • FEV1 can be normal or increased
  95. Obstructive lung disease
    • Increased TLC
    • Increased RV
    • Decreased FEV1
    • FVC can be normal or decreased
  96. Dead space
    • 1) normally to the level of the bronchiole (150mL)
    • 2) increases with:
    • 1- drop in cardiac output
    • 2- PE
    • 3- pulmonary HTN
    • 4- ARDS
    • 5- excessive PEEP
    • 3) can lead to high CO2 buildup
    • 4) area of lung is ventilated but not perfused
  97. COPD
    • 1) increased work of breathing due to prolonged expiratory phase
    • 2) work of breathing normally 2% of total body VO2
  98. ARDS
    • 1) mediated by cellular inflammatory processes
    • 2) increased proteinaceous material
    • 3) increased gradient
    • 4) increased shunt
    • 5) most common cause is sepsis
  99. Diagnostic Criteria for Acute Lung Injury and Acute Respiratory Distress Syndrome
    • Acute Lung Injury
    • 1) Acute onset
    • 2) Bilateral pulmonary infiltrates
    • 3) PaO2/FiO2 <300
    • 4) PAOP <18 mmHg or no clinical evidence of LAH

    • Acute Respiratory Distress Syndrome
    • 1) all of the above criteria with PaO2/FiO2 <200
  100. SIRS--> Sepsis--> Severe Sepsis--> Septic Shock--> MOD
    1) Mediated by TNF-alpha and IL-1

    • Criteria for SIRS:
    • 1) Temperature >38C or <36C
    • 2) RR >20/min or PCO2 <32mmHg
    • 3) WBC >12 or <4
    • 4) HR >90

    • Sepsis
    • 1) SIRS with clinical evidence of infection
    • 2) Sepsis with organ dysfunction

    • Septic Shock
    • 1) sepsis and arterial hypotension despite adequate volume resuscitation

    • MOD
    • 1) progressive but reversible dysfunction of 2 or more organs arising from an acute disruption of normal homeostasis
  101. Diagnostic criteria for Significant Organ Dysfunction:
    Pulmonary: Need for mechanical ventilation; PaO2/FiO2 <300 for 24hrs

    Cardiovascular: Need for inotropic drugs to maintain adequate tissue perfusion or CI <2.5

    Kidney: Creatinine >2 times baseline on 2 consecutive days or need for renal replacement therapy

    Nutrition: 10% reduction in lean body mass; albumin <2g/dL or total lymphocyte count <1,000/uL

    CNS: glasgow coma scale <10 without sedation

    Coagulation- platelet count <50k/uL, fibrinogen <100mg/dL or need for factor replacement

    Host defenses: WBC <1,ooo/uL or invasive infection including bacteremia
  102. See page 98 for picture on multisystem organ dysfunctions
  103. Aspiration
    • 1) pH <2.5 and volume >0.4cc/kg associated with increased damage
    • 2) Mendelson's syndrome- chemical pneumonitis from aspiration of gastric secretions
    • 3) Most frequent site is the posterior portion of RUL and superior portion of RLL
  104. Atelectasis
    • 1) bronchial obstruction and respiratory failure are the main causes
    • 2) most common cause of fever in first 48 hrs after operation
    • 3) increased in patients with COPD, upper abdominal surgery, and obesity
    • 4) fever, tachycardia
    • 5) Treatment: incentive spirometer
  105. What things can throw off a pulse oximeter?
    • Lots of things can through off a pulse oximeter:
    • - nail polish
    • - dark skin
    • - low-flow states
    • - ambient light
    • -anemia
    • - vital dyes
  106. What things cause pulmonary vasodilation:
    • 1) bradykinin
    • 2) PGE1
    • 3) prostacyclin (PGI2)
    • 4) nitric oxide
  107. What things cause pulmonary vasoconstriction?
    • 1) histamine
    • 2) serotonin
    • 3) TXA2
    • 4) epinephrine + norepinephrine
    • 5) hypoxia
    • 6) acidosis
  108. Alkalosis
    pulmonary vasodilator
  109. Acidosis
    pulmonary vasocontrictor
  110. What causes pulmonary shunting?
    • 1) nitroprusside (nipride)
    • 2) nitroglycerin
    • 3) nifedipine
  111. What is the most common cause of postoperative renal failure?
    hypotension
  112. What percent of nephrons need to be damaged before renal dysfunction occurs?
    70%
  113. What is the best test for azotemia
    FeNa= (urine Na/Cr)/(plasma Na/Cr) --> best test for azotemia
  114. Prerenal cause of acute renal failure:
    • 1) FeNa <1%
    • 2) Urine Na <20
    • 3) BUN/Cr ratio >20
    • 4) urine osmolality >500mOsm
    • otherwise consider renal cause of azotemia
  115. Oliguria
    • 1st- make sure patient is volume loaded (CVP 11-15mmHg)
    • 2nd- try diuretic trial --> furosemide (lasix)/butanamide
    • 3rd- dialysis if needed
  116. Indications for dialysis:
    • 1) fluid overload
    • 2) high K
    • 3) metabolic acidosis
    • 4) uremic encephalopathy
    • 5) uremia coagulopathy
    • 6) poisoning
  117. hemodialysis
    • - rapid
    • - causes large volume shifts
  118. CVVH (continuous venovenous hemofiltration)
    • - slower
    • - good for ill patietns who cannot tolerate the volume shifts (septic shock, etc)
    • - Hct increases by 5-8 for each liter taken off
  119. Pg 100- chart on management of acute renal failure
  120. Advantages and Disadvantages of Intermittent Hemodialysis:
    • Advantages:
    • 1) lower risk of systemic bleeding
    • 2) facilitates transport for other interventions
    • 3) More suitable for severe hyperkalemia
    • 4) lower cost

    • Disadvantages
    • 1) availability of dialysis staff
    • 2) more difficult hemodynamic control
    • 3) inadequate dialysis dose (frequency)
    • 4) inadequate nutritional support
    • 5) not suitable for patients with intracranial hypertension
    • 6) no removal of cytokines (theoretical)
    • 7) potential complement activation by nonbiocompatible membranes
  121. Advantages and Disadvantages of Continuous renal replacement therapy:
    • Advantages:
    • 1) better hemodynamic stability
    • 2) fewer cardiac arrhythmias
    • 3) improved nutritional support
    • 4) better pulmonary gas exchange
    • 5) better fluid control

    • Disadvantages:
    • 1) greater vascular access problems
    • 2) higher risk of systemic bleeding
    • 3) long-term immobilization of patient
    • 4) more filter problems (rupture/clotting)
    • 5) greater cost
  122. Renin:
    • 1) released in response to decreased pressure sensed by the juxtaglomerular apparatus in kidney
    • 2) also released in response to increased Na concentrations sensed by the macula densa
    • 3) beta-adrenergic stimulation and hyperkalemia also cause release
    • 4) converts angiotensinogen (synthesized in liver) to angiotensin I
    • 5) angiotensin-converting enzyme (lung)- converts angiotensin I to angiotensin II
    • 6) adrenal cortex- releases aldosterone in response to angiotensin II
    • 7) Distal convoluted tubule- aldosterone acts here to reabsorb more water by increased Na/K ATPase on membrane (potassium secreted)
  123. Angiotensin II functions:
    • 1) vasoconstricts
    • 2) increases HR + contractility
    • 3) increases permeability
    • 4) glycogenolysis + gluconeogenesis
    • 5) inhibits renin release
  124. Atrial natriuretic peptide (or factor)
    • 1) released from atrial wall with atrial distention
    • 2) inhibits Na and water resorption in the collecting ducts
    • 3) also a vasodilator
  125. Which limb of the kidney controls GFR?
    efferent limb of kidney controls GFR
  126. Renal toxic drugs:
    • 1) NSAIDS- causes renal damage by inhibiting prostaglandin synthesis, resulting in renal arteriole vasocontriction
    • 2) Aminoglycosides- direct tubular injury and later renal vasoconstriction
    • 3) Myoglobin- direct tubular injury
    • Tx: alkalinize urine
    • 4) Contrast dyes- direct tubular injury
    • Tx: premedicate with N-acetylcysteine and volume
  127. What precludes the diagnosis of brain death:
    • Precludes Diagnosis:
    • 1) uremia
    • 2) temperature <30C
    • 3) BP <70/40mmHg
    • 4) desaturation with apnea test
    • 5) drugs (phenobarbital, pentobarbital)
    • 6) metabolic derangements
  128. Brain Death:
    • 1) must exist for 6-12 hours:
    • 1- unresponsive to pain
    • 2- absent caloric oculovestibular reflexes
    • 3- absent oculocephalic reflex
    • 4- positive apnea test
    • 5- no corneal reflex
    • 6- no gag reflex
    • 7- fixed and dilated pupils
  129. What will EEG and MRA show in a brain dead patient?
    EEG- electrical silence

    MRA- can be used--> will show no blood flow to brain
  130. Describe the apnea test:
    • 1) disconnect from ventilation
    • 2) CO2 >60mmHg or increase in CO2 by 20 is positive test for apnea
    • 3) if arterial pressure drops to <60 or patient desaturates, the test is terminated
  131. What can you still have with brain death?
    you can still have deep tendon reflexes with brain death
  132. Carbon monoxide:
    • 1) can falsely increase oxygen saturation reading on pulse oximeter
    • 2) binds hemoglobin directly (creates carboxyhemoglobin)
    • 3) can usually correct with 100% oxygen on ventilator (displaces carbon monoxide), may need hyperbaric O2 if really high
  133. Methemoglobinemia
    • 1) from nitrites such as Hurricain spray; nitrites bind Hgb
    • 2) O2 saturation reads 85%
    • 3) Tx: methylene blue
  134. Critical illness polyneuropathy:
    • 1) motor > sensory neuropathy
    • 2) occurs with sepsis; can lead to failure to wean from ventilation
  135. Xanthine oxidase:
    • 1) in endothelial cells, forms toxic oxygen radicals with reperfusion, involved in reperfusion injury
    • 2) also involved in the metabolism of purines and breakdown to uric acid
  136. symptoms and treatment of DKA:
    • 1) nausea + vomiting
    • 2) thirst
    • 3) polyuria
    • 4) abdominal pain
    • 5) increased glucose
    • 6) increased ketones
    • 7) increased K
    • 8) decreased Na

    • Treatment:
    • 1- insulin and eventually glucose, so patient does not bottom out
    • 2- isotonic solutions
    • 3- K+ (althuogh initial K wil be high, it will be driven back into cells by insulin)
    • 4- HCO3- for pH <7.25
  137. ETOH withdrawal
    • 1) HTN
    • 2) tachycardia
    • 3) delirium
    • 4) seizures after 48hrs

    • Treatment:
    • 1) Thiamine
    • 2) folate
    • 3) B12
    • 4) K
    • 5) Mg
    • 6) PRN lorazepam (ativan)
  138. ICU (or hospital psychosis):
    • 1) generally occurs after 3rd postoperative day and is frequently preceded by lucid interval
    • 2) need to rule out metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes

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