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What is the goal Lactate when treating patient with shock?
< 2.2 mMol/L
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When managing shock you should maintain urine output of what?
> 0.5 ml/kg/hr
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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
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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
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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
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What causes Hypovolemic shock?
- Hemorrhage - Trauma
- Dehydration
- Vomiting
- Diarrhea
- Polyuria
- Pancreatitis
- Thermal injury
- Trauma
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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
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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
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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
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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
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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
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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
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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
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________________________should be corrected prior to vasopressor.
Hypovolemia (give fluids)
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Dose of vasopressor is titrated to ____________ or _________________.
- goal MAP
- or
- end organ perfusion
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Vasopressors are preferably administered via __________________________________.
central venous catheter via infusion pump
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What are the Vasopressors?
- Dopamine
- Norepinephrine
- Epinephrine
- Phenylephrine
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What are the Inotropes?
- Dobutamine
- Phosphodiesterase inhibitors: Milrinone
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What physiological and Hemodynamic effects are produced through B2-agonism?
- Physiologic Effects: Dilates arteries and veins
- Hemodynamic Effects: Decreased SVR
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What physiological and Hemodynamic effects are produced through B1-agonism?
- Physiologic Effects: Tachycardia, +inotropy
- Hemodynamic Effects: Increased HR, CO, contractility
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What physiological and Hemodynamic effects are produced through a1-agonism?
- Physiologic Effects: Constrict arteries and veins
- Hemodynamic Effects: Increased SVR, MAP
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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
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Moderate dose DA has what type of receptor effects?
Beta effects
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High dose DA has what type of receptor effects?
Alpha effects
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NE has what type of receptor effects?
Mostly alpha effects
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EPI has what type of receptor effects?
Non-selective Beta effects at low doses, primarily alpha effect at higher doses
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Phenylephrine has what type of receptor effects?
Strictly alpha
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What receptors and physiologic effects does EPI have?
- Receptors: B1 B2 and A1
- Physiologic effects: increases CO, BP and HR
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