Therapeutics - Shock Combined

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kyleannkelsey
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289593
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Therapeutics - Shock Combined
Updated:
2014-11-18 23:38:40
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Therapeutics Shock
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Therapeutics - Shock
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Therapeutics - Shock
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  1. What receptors and physiologic effects does NE have?
    • Receptors: B1 B2 and A1
    • Physiologic effects: increases CO and BP
  2. What receptors and physiologic effects does DA have?
    • Receptors: B1 DA and A1
    • Physiologic effects: increases CO, BP and HR and RBF
  3. What receptors and physiologic effects does Phhenylephrine have?
    • Receptors: A1
    • Physiologic effects: increases BP, decrease HR and +/- CO
  4. EPI (adrenalin) is used for what?
    Uses: anaphylaxis, anaphylactoid reactions or cardiac arrest (pulseless VT or VF, asystole, PEA), refractory shock (EPI infusion), especiallu w/ norepinephrine failure
  5. What drug can increase BP in patients unresponsive to other agents?
    EPI (adrenalin)
  6. EPI is considered a second or first line agent?
    2nd
  7. What is a normal dose of EPI?
    • Infusion at 1-10 mcg/min (max 30 mcg/min)
    • or 0.01 to 0.1 mcg/kg/min
  8. What are the precautions for EPI (adrenalin) use?
    • Raising blood pressure may cause myocardial ischemia
    • Higher doses may be required to treat poison/drug induced shock
    • Incompatible with alkaline solutions (NaHCO3)
    • Side effects: tachyarrhythmias, ischemia, hyperglycemia, lactic acidosis, extravasation
  9. Norepinephrine (Levophed) is primarily an ____ agonist
    Alpha
  10. What is the MOA of Norepinephrine (Levophed)?
    Increases MAP by vasoconstriction
  11. What drug is considered FIRST-LINE THERAPY for maintenance of blood pressure and tissue perfusion in septic shock?
    Norepinephrine (Levophed)
  12. What is the dose for Norepinephrine (Levophed)?
    0.1 to 2.0 mcg/kg/min (2-30 mcg/min)
  13. What are the Side effects of Norepinephrine (Levophed)?
    Increased myocardial oxygen demand, ischemia/dysrrhythmias (alpha effects), peripheral hypoperfusion (potent vasoconstriction), tissue necrosis
  14. What are the Drug interactions of Norepinephrine (Levophed)?
    TCAs, leads to prolonged hypotension
  15. Morality is lower when what drug is used for cardiogenic shock?
    NE
  16. What drug is a pure alpha agonist?
    Phenylephrine (Neo-Synephrine)
  17. What is Phenylephrine (Neo-Synephrine)useful for treating?
    • Shock due to peripheral vasodilation
    • Effective in patients with hypotension and tachydysrhythmias where avoidance of myocardial stimulation is desirable
  18. Is Phenylephrine (Neo-Synephrine) a first or second line agent?
    Regarded as a second line agent
  19. What is the dose of Phenylephrine (Neo-Synephrine)?
    0.5-10 mcg/kg/min (30-300 mcg/min)
  20. What are the Side effects of Phenylephrine (Neo-Synephrine)?
    Reflex bradycardia, hypertension, headache, dysrhythmia, mesenteric ischemia (potent alpha effects)
  21. Dopamine (Intropin) is an Immediate precursor of both _________________ and ___________________.
    Norepinephrine and epinephrine
  22. What drug has variable effects depending upon dose administered?
    Dopamine (Intropin)
  23. What is Dopamine (Intropin) used for?
    Used for hypotension due to sepsis or cardiac failure
  24. When should Dopamine (Intropin) not be used?
    Should not be used for renal protection
  25. How does Dopamine (Intropin) improve splanchnic/mesenteric flow?
    Mainly by increasing cardiac output
  26. What is the dose of Dopamine (Intropin)?
    Start at 2.5-5 mcg/kg/min in cardiogenic shock (range 2.5-20 mcg/kg/min)
  27. What are the Side effects of Dopamine (Intropin)?
    Tachycardia, tachydysrhythmias, extravasation, contains sulfites
  28. What are the drug-drug interactions of Dopamine (Intropin)?
    MAOIs, α and ß-blockers, phenytoin
  29. What actions does low dose dopamine have?
    • Worsens splanchnic oxygenation via redistribution
    • Impair GI function
    • Impair endocrine and immune systems
    • Blunt hypoxemic respiratory drive
  30. Vasopressin is AKA:
    Antidiuretic hormone or ADH
  31. What endogenous molecule is at inappropriately low levels in patients with shock?
    Vasopressin
  32. What effect does Vasopressin have?
    • Exogenous administration can restore vascular tone
    • Acts on V1 and V2 receptors
    • V1”vasopressin” receptors: Direct vasoconstriction of systemic vasculature
    • V2 “ADH” receptors: Osmoregulation and maintenance of normovolemia
    • Vasopressin enhances the sensitivity of the vascular system to other pressor agents
  33. What is the Second line agent for refractory vasodilatory shock?
    Vasopressin
  34. What is the dose of Vasopressin?
    • 0.01-0.04 U/min added to catecholamines (like NE) can raise blood pressure in patients with pressor-refractory septic shock
    • Not titrated like traditional vasopressors
    • Prone to dosing errors – Units/minute
    • Dose is 40 U for cardiac arrest
  35. What are the Side effects of Vasopressin?
    Arrhythmias, myocardial/gut/digit/skin ischemia, increased bilirubin
  36. Dobutamine (Dobutrex) has what MOA?
    • Positive inotropic, chronotropic, lusitropic effects
    • Improves oxygen delivery, may improve mesenteric flow
  37. What is the agent of choice for low-output states with elevated cardiac filling pressures (ADHF, cardiogenic shock)?
    Dobutamine (Dobutrex)
  38. What is the dose for Dobutamine (Dobutrex)?
    Begin at 2.5-5 mcg/kg/min, titrate to 20 mcg/kg/min
  39. When does Dobutamine (Dobutrex) its peak effect?
    Peak effect within 10 minutes
  40. What are the Side effects of Dobutamine (Dobutrex)?
    Ventricular arrhythmias, tachycardia, hypokalemia, myocardial ischemia, tachyphylaxis
  41. What are the Drug interactions of Dobutamine (Dobutrex)?
    ß-blocking agents, incompatible with alkaline solutions
  42. What are the classical findings of Shock?
    • “Low” BP
    • Tachycardia
    • Cool, clammy skin (not in distributive/septic shock)
    • Warm, flushed skin (distributive shock)
    • Altered mental status
    • Oliguria
    • Metabolic Acidosis
  43. What constitutes shock?
    • MAP < 60 mm Hg or
    • SBP < 90 mm Hg
    • (Relative for patient)
  44. In the presence of Low BP and the HR is too fast/slow, what is the likely eitiology?
    Pump/heart problem
  45. In the presence of Low BP and the Stroke Volume (SV) is low, what is the likely eitiology?
    • Fluid problem = not enough fluid
    • Could also be a pump/heart problem
  46. In the presence of Low BP and the SVR is low, what is the likely eitiology?
    Container/systemic problem
  47. What should you monitor for (labs) if a person has shock?
    Hemoglobin, WBC, platelets, PT/PTT/INR, electrolytes, ABG, Ca, Mg, BUN, Cr, LFTS, bilirubin, lactate, toxicology screen, cardiac enzymes
  48. What is the basic framework to the clinical approach for Shock treatment?
    • Monitor hemodynamics and enhance perfusion:
    • -Stop any adverse medications
    • -Control heart rhythm
    • -IV fluid
    • -Vasopressors and/or inotropes
    • Ensure O2 delivery:
    • -Protect airway
    • - Minimize consumption
    • Pain control, sedation, paralytic:
    • - Support with mechanical ventilation if needed
    • Identify (and treat) the source
    • Monitor for developing organ failures
  49. What is a normal Systolic blood pressure (SBP)?
    108-140 mm Hg
  50. What is a normal Mean arterial pressure (MAP)?
    80-100 mm Hg
  51. What is a normal Heart rate (HR)?
    60-100 beats/min
  52. What is a normal Cardiac output (CO)?
    4-7 L/min
  53. What is a normal Cardiac index (CI)?
    2.8-3.6 L/min/m2
  54. What is a normal Ejection fraction (EF)?
    50-70%
  55. What is a normal Diastolic blood pressure (DBP)?
    70-90 mm Hg
  56. When performing hemodynamic monitoring of a shock patient are BP, HR, oxygen saturation sufficient in sepsis?
    • No, need MAP
    • Need to monitor S/S of hypoperfusion
  57. What type of line, used to measure MAP, can also be used to deliver medications?
    Pulmonary aterial catheter and Central venous catheter
  58. What type of line, used to measure MAP, cannot also be used to deliver medications?
    Arterial line
  59. What can an arterial line be used to assess?
    • Continuous blood pressure monitoring (MAP)
    • Line used for blood draws, ABGs, not to administer meds
  60. What can a Central venous catheter be used to monitor?
    • Marker of volume status and systolic return to heart
    • Validity in sepsis questioned
    • Can administer fluids and vasoactive agents
    • Assess changes in fluid status
  61. What is a Quinton catheter?
    Non-tunneled central venous catheter
  62. What is a Hickman or Groshong catheter?
    Tunneled central venous catheter
  63. Which type of line can be used to assess the type of shock?
    Pulmonary Artery Catheter
  64. What does CV measure and what is a normal value?
    • Right heart preload
    • 2-6 mm Hg
  65. What does the Pulmonary capillary wedge pressure (PCWP) measure?
    • Left heart preload
    • 8-12 mm Hg
  66. What does Pulmonary vascular resistance (PVR) measure?
    • Right heart afterload
    • 80-120 dynes/s/cm-5
  67. What does Systemic vascular resistance (SVR) and what is a normal value?
    • Left heart afterload
    • 800-1200 dynes/s/cm-5
  68. What hemodynamic effects does Hypovolemic shock present with?
    • Decreased: Preload/PCWP, CO/Pump function, Mixed venous O2 saturation/tissue perfusion
    • Increased: SVR
  69. What cardiogenic effects does Hypovolemic shock present with?
    • Decreased: CO/Pump function, Mixed venous O2 saturation/tissue perfusion
    • Increased: Preload/PCWP and SVR
  70. What cardiogenic effects does Hypovolemic shock present with?
    • Decreased: Preload/PCWP and SVR
    • Increased: CO/Pump function, Mixed venous O2 saturation/tissue perfusion
  71. Why do the peripheries feel warmer in Distributve shock?
    Increased CO and decreased SVR (dilation) leads to well perfused peripheries
  72. What is the goal MAP when treating patient with shock?
    > 60 mm Hg
  73. What is the goal PCWP when treating patient with shock?
    15 - 18 mm Hg
  74. What is the goal Cardiac Index (CI) when treating patient with shock?
    • > 2.1 (cardiogenic/obstructive shock)
    • > 4.0 - 4.5 (septic/hemorrahgic shock)
  75. What is the goal Hemoglobin when treating patient with shock?
    > 10 g/dL
  76. What is the goal SaO2 when treating patient with shock?
    > 92%
  77. What is the goal SvO2 when treating patient with shock?
    > 60%
  78. What is the goal PaO2 when treating patient with shock?
    > 60 mm Hg
  79. What is the goal Lactate when treating patient with shock?
    < 2.2 mMol/L
  80. When managing shock you should maintain urine output of what?
    > 0.5 ml/kg/hr
  81. Why is the blood pressure low in Cardiogenic shock?
    • Low CO (Low HR and SV, which when multiplied = CO)
    • Caused by: direct myocardial damage, arrhythmia, or a mechanical abnormality of the heart
  82. How do you treat Cardiogenic Shock?
    • Rate and rhythm control
    • Ventricular assist device
    • Emergent coronary revascularization
    • Surgical repair of valvular abnormalities or septal defects
    • Venoarterial extracorporeal membrane oxygenation (ECMO)
    • IABC (intraaortic balloon counterpulsation) – balloon pump
    • Vasopressors and inotropes
    • Goal MAP > 60 mm Hg and CI > 2.2 L/min/m2
  83. What causes Hypovolemic shock?
    • Result of blood or fluid loss (internal or external)
    • Leads to decreased circulating blood volume and reduced diastolic filling pressures and volume
    • Low CI, low PCWP, high SVR
    • Decreased CO due to decreased SV
  84. What causes Hypovolemic shock?
    • Hemorrhage - Trauma
    • Dehydration
    • Vomiting
    • Diarrhea
    • Polyuria
    • Pancreatitis
    • Thermal injury
    • Trauma
  85. How is Hypovolemic shock treated?
    • Hemorrhagic Shock: Transfusion of PRBC and aggressive evaluation of source of bleeding
    • Crystalloids: Normal Saline or Lactated Ringers
    • Colloids not commonly used
  86. What causes Extracardiac Obstructive Shock?
    • Obstruction to flow in the cardiovascular circuit
    • Leads to inadequate diastolic filling or decreased systolic function due to increased afterload
    • Low CO due to low SV
  87. What are the treatments for Obstructive shock?
    • Tension pneumothorax: Needle thoracostomy
    • Cardiac tamponade: Fluids and vasopressors, Pericardiocentesis or pericardotomy (remove fluid around myocardium)
    • Massive pulmonary embolism: Thrombolytic therapy, Embolectomy
  88. What characterizes Distributive shock?
    • Peripheral vasodilation
    • High CI, low PCWP, low SVR
    • Low BP because of low SVR
    • Increased venous capacitance
    • Decreased effective blood volume
    • Decreased MAP
  89. What are the etiologies of Distributive shock?
    • Sepsis – MAJOR CAUSE
    • Toxic shock syndrome
    • Drugs or toxins
    • Anaphylaxis
    • Neurogenic or “spinal shock”
    • Adrenal crisis
    • Myxedema coma – in patients that stop taking Thyroid meds
  90. What is the treatment of distributive shock?
    • Stop offending drug (anti-hypertensive, opioid analgesic, etc.)
    • Anaphylaxis:
    • Epinephrine 0.1mg (1 cc of 1:10,000) IVP
    • Epinephrine 0.3mg (3 cc of 1:1,000) SQ (epipen)
    • Adrenal Insufficiency:
    • Stress dose hydrocortisone – very high doses
    • Culture all sites of infection, remove any origin of infection (drainage) and start antibiotics – right away
    • Fluid, fluid, and more fluid
    • Appropriately monitor hemodynamics and restore blood pressure (vasopressors)
    • Ventilator support
    • Monitor and correct metabolic derangements
  91. What action do Vasopressors have?
    • Produce vasoconstriction and elevate MAP
    • Used for drop in systolic blood pressure (>30 mmHg) or MAP (<60 mmHg) when associated with end-organ dysfunction due to hypoperfusion
  92. ________________________should be corrected prior to vasopressor.
    Hypovolemia (give fluids)
  93. Dose of vasopressor is titrated to ____________ or _________________.
    • goal MAP
    • or
    • end organ perfusion
  94. Vasopressors are preferably administered via __________________________________.
    central venous catheter via infusion pump
  95. What are the Vasopressors?
    • Dopamine
    • Norepinephrine
    • Epinephrine
    • Phenylephrine
  96. What are the Inotropes?
    • Dobutamine
    • Phosphodiesterase inhibitors: Milrinone
  97. What physiological and Hemodynamic effects are produced through B2-agonism?
    • Physiologic Effects: Dilates arteries and veins
    • Hemodynamic Effects: Decreased SVR
  98. What physiological and Hemodynamic effects are produced through B1-agonism?
    • Physiologic Effects: Tachycardia, +inotropy
    • Hemodynamic Effects: Increased HR, CO, contractility
  99. What physiological and Hemodynamic effects are produced through a1-agonism?
    • Physiologic Effects: Constrict arteries and veins
    • Hemodynamic Effects: Increased SVR, MAP
  100. What physiological and Hemodynamic effects are produced through DA-agonism?
    • Physiologic Effects: Vaosdilate and increase blood flow GI, kidney, brain
    • Hemodynamic Effects: Increased urine output
  101. Moderate dose DA has what type of receptor effects?
    Beta effects
  102. High dose DA has what type of receptor effects?
    Alpha effects
  103. NE has what type of receptor effects?
    Mostly alpha effects
  104. EPI has what type of receptor effects?
    Non-selective Beta effects at low doses, primarily alpha effect at higher doses
  105. Phenylephrine has what type of receptor effects?
    Strictly alpha
  106. What receptors and physiologic effects does EPI have?
    • Receptors: B1 B2 and A1
    • Physiologic effects: increases CO, BP and HR

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