Shock Pharmacologics Flashcards

1
Q

Fluid Therapies

A
  • Crystalloids are initial fluid choice: 30 mL/kg until stable
  • Consider albumin if patients still requiring substantial amounts of crystalloids after initial resuscitation (otherwise, albumin doesn’t provide significant benefit and more costly)
  • CVP marker for fluid status (8-12, 12-15 if mechanically ventilated)
  • DONT USE HYDROXYETHYL STARCHES
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2
Q

Vasopressor Options/First Line

A
  • Goal: MAP >= 65
  • Arterial catheter should be placed ASAP
  • Norepi: first line - little change to HR/SV, may be more effective at reversing hypotension than dopamine
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3
Q

Vasopressor

A
  • Not recommended as single, initial vasopressor
  • Used in addition to NE to raise MAP
  • Increase BP in vasopressor refractory patients
  • Fewer kidney failure patient receive renal replacement compared to NE
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4
Q

Epi

A
  • Can be used in addition or as a substitute for NE

- Decreases renal/splanchnic blood flow

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5
Q

Phenylephrine

A
  • Not recommended unless NE causes serious arrhythmias
  • High CO and persistently low BP, salvage therapy
  • Least likely to produce tachycardia (only alpha) but can decrease SV
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6
Q

Dopamine

A
  • Alternative to NE when low risk of tachyarrhythmias and absolute/relative bradycardia
  • Don’t use low doses for renal perfusion
  • May be more arrhythmogenic than NE, but may be useful with compromised systolic fxn
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7
Q

Dobutamine

A
  • Inotropic Therapy
  • Can be initial or added to vasopressor therapy
  • May be useful for myocardial dysfxn (high pressures and low CO) and ongoing signs of hypoperfusion despite having good volume/MAP
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8
Q

Antimicrobial Therapy

A
  • Cultures (from two different sites) prior to antibiotic therapy if possible
  • IV antimicrobials should be given within the first hour with septic shock/severe sepsis patients (broad spectrum)
  • Each hour delayed, decrease in 7.6% survival
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9
Q

Corticosteroids

A
  • IV hydrocortisone is reserved for patients with hemodynamic instability despite fluid resuscitation and vasopressor therapy
  • Don’t administer in absence of shock
  • Taper steroids once vasopressors are no longer required
  • Combined with fludrocortisone may have better outcomes
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10
Q

Glucose Control

A
  • Initiate insulin when glucose > 180 (target =< 180)

- Blood glucose monitored every 1-2 hours until glucose/insulin infusion are stable, then every 4 hours thereafter

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11
Q

DVT Prophylaxis

A

Daily DVT prophylaxis with LMWH or UFH

  • Patients with CI to prophylaxis should receive intermittent compression devices
  • Use combination or intermittent pneumatic compression devices and pharm
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12
Q

Stress Ulcer Prophylaxis

A
  • H2 blocker or PPI with patients with bleeding risk factors
  • Bleeding risk factors: coagulopathy (INR > 1.5 or platelets <50,000), mechanical ventilation for > 48 hours and possibly hypotension
  • No risk factors shouldn’t get prophylaxis
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13
Q

Cardiac Term Definitions

A
  • Inotropy: altered contractility
  • Lusitropy: altered relaxation
  • Chronotropy: altered contraction rate (SA node conduction)
  • Dromotropy: altered AV node conduction
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14
Q

Alpha 1 Agonism

A
  • Agonist for alpha1 receptor GCPR that binds to PLC
  • Converts PIP2 to IP3 that opens calcium channel in SR
  • Increases calcium release within smooth muscles (contracts and increases BP)
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15
Q

Epi Sites/Uses

A
  • All alpha/beta receptors (NOT selective)
  • For anaphylactic shock and cardiac arrest/asystole
  • Improves breathing and clears airways as well
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16
Q

NE Sites/Uses

A
  • Alpha 1/2, Beta 1/3
  • Hypotensive shock (vasoconstricts through alpha1)
  • Cardiac arrest (increase HR/contractile strength)
17
Q

DA Sites/Uses

A
  • Alpha and beta 1
  • [High] bind to B1 - acute decompensated HR
  • [VERY high] binds to alpha1 - cardiogenic and septic shock
18
Q

Phenylephrine Sites/Uses

A
  • Alpha1 ONLY (semisynthetic)

- Septic shock, vasoconstriction, nasal decongestant, pupil dilation, hemorrhoids

19
Q

B-adrenergic System MoA

A
  • Agonist binds to B1 receptor GCPR which activated adenyl cyclase
  • Converts ATP into cAMP which activates PKA
  • Then phosphorylates LTCC and RyR which opens them more (more calcium)
  • Also phosphorylates PL which releases from SERCA and causes it to open more to allow more calcium to be available for successive contractions
20
Q

Dobutamine Sites/Uses

A
  • B1 ONLY
  • Cardiogenic shock and acute decompensated HF
  • Positive inotropy, little effect on chronotropy
  • Stereoisomeric specificity cancels out alpha activity
21
Q

Isoproterenol

A
  • Beta 1 and 2
  • Treats bradycardia, heart block, and cardiac arrest (positive inotropy and chronotropy)
  • Treats asthma (rarely used)
22
Q

Milrinone

A
  • Antagonist of PDE3
  • Similar end-result as dobutamine and EPI (positive inotropy)
  • Vasodilator effects
  • Potentiate the actions of catecholamines
23
Q

Vasopressin Receptors

A
  • V1R located on vascular smooth muscle cells, cardiomyocytes
  • Works same mechanism as alpha agonists via PLC
  • V2R: located in kidney, works via AC mechanisms and causes antidiuresis (volume retention)
  • Decreases in hemorrhagic and septic shock, increased sensitivity
24
Q

NO Vasodilators

A
  • Increases conversion of GTP to cGMP
  • Converts myosin and causes relaxation
  • Reduces preload and afterload by promoting vascular smooth muscle relaxation
  • Leads to decreased workload of the heart and increased CO
25
Q

Nesiritide

A
  • Recombinant BNP
  • B-type natriuretic peptides produced by heart due to excessive stretching of cardiomyocytes
  • Nesiritide binds to NPRs promotes vasodilation and diuresis by increase cGMP in smooth muscle and negatively regulating RAAS