Therapeutics - Shock 2

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  1. What is the goal Lactate when treating patient with shock?
    < 2.2 mMol/L
  2. When managing shock you should maintain urine output of what?
    > 0.5 ml/kg/hr
  3. 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
  4. 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
  5. 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
  6. What causes Hypovolemic shock?
    • Hemorrhage - Trauma
    • Dehydration
    • Vomiting
    • Diarrhea
    • Polyuria
    • Pancreatitis
    • Thermal injury
    • Trauma
  7. 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
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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
  13. 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
  14. ________________________should be corrected prior to vasopressor.
    Hypovolemia (give fluids)
  15. Dose of vasopressor is titrated to ____________ or _________________.
    • goal MAP
    • or
    • end organ perfusion
  16. Vasopressors are preferably administered via __________________________________.
    central venous catheter via infusion pump
  17. What are the Vasopressors?
    • Dopamine
    • Norepinephrine
    • Epinephrine
    • Phenylephrine
  18. What are the Inotropes?
    • Dobutamine
    • Phosphodiesterase inhibitors: Milrinone
  19. What physiological and Hemodynamic effects are produced through B2-agonism?
    • Physiologic Effects: Dilates arteries and veins
    • Hemodynamic Effects: Decreased SVR
  20. What physiological and Hemodynamic effects are produced through B1-agonism?
    • Physiologic Effects: Tachycardia, +inotropy
    • Hemodynamic Effects: Increased HR, CO, contractility
  21. What physiological and Hemodynamic effects are produced through a1-agonism?
    • Physiologic Effects: Constrict arteries and veins
    • Hemodynamic Effects: Increased SVR, MAP
  22. 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
  23. Moderate dose DA has what type of receptor effects?
    Beta effects
  24. High dose DA has what type of receptor effects?
    Alpha effects
  25. NE has what type of receptor effects?
    Mostly alpha effects
  26. EPI has what type of receptor effects?
    Non-selective Beta effects at low doses, primarily alpha effect at higher doses
  27. Phenylephrine has what type of receptor effects?
    Strictly alpha
  28. What receptors and physiologic effects does EPI have?
    • Receptors: B1 B2 and A1
    • Physiologic effects: increases CO, BP and HR
Card Set:
Therapeutics - Shock 2
2014-11-16 04:32:18
Therapeutics Shock
Therapeutics - Shock
Therapeutics - Shock
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