Hemodynamics/Sepsis: Pharmacotherapy Flashcards
Goals of therapy for shock management
Determine etiology: hypovolemia, cardiogenic, distributive, obstructive
Maintain adequate tissue perfusion:
Assess volume status: assess volume status (preload)
Restore MAP: goal MAP >65mmHg
Normalize lactate: Goal lactate <2mmol/L
Venous oxygen saturation (VBG): pulmonary artery catheter; assesses volume overload (MAP >65mmHg, goal lactate <2mmol.L)
Shock goals: hemodynamic optimization
MAP ≥65mmHg
HR <100bpm
CVP= 8-12 mmhg (12-15mmHg)
PCWP= 12-15 mmHg
Cardiac index >2.2L/min/m2
Shock goals: maintaining O2 delivery
Hgb 7-9gm/dl
Arterial saturation >88-92%
SVO2/SCVO2 >65%/70%
Shock goals: reversal of O2 dysfunction
lactate CL (<2 mmol/L) or normalization
Shock goals: urine output
> 0.5ml/kg/hr
Shock goals: reverse encephalopathy
improve cognition
Pharmacotherapy of shock
Initiation of vasoactive agents when MAP remains <65mmHg despite fluid administration
Shock pharmacotherapy: what do fluids do?
Increases SV, CO, DO2
Shock pharmacotherapy: fluids
Crystalloid fluid (LR, NS): 30ml/kg over 15-30 mins, then by 10ml/kg boluses
Cardiogenic shock: 100-200ml boluses
Shock pharmacotherapy: NE MoA
potent alpha-adrenergic agonist; increases MAP via peripheral vasoconstriction
NE dosing
0.01-3mcg/kg/min, or 5-65mcg/min
NE ADE
significant vasoconstriction
Shock pharmacotherapy: epinephrine MoA
potent alpha and beta-adrenergic agonist
Epinephrine dose-dependent activity
low-dose is predominantly beta-1 → increase HR and SV and beta-2 vasodilation, but higher doses produce increased alpha-1 stimulation
Epinephrine: dose
0.05-2mcg/kg/min
Epinephrine can increase aerobic lactate production by what?
Beta-2 skeletal muscle receptors
Epinephrine ADEs
tachycardia, arrhythmias, cardiac ischemia, peripheral vasoconstriction, reduced renal blood flow, hyperglycemia, hypokalemia
Epinephrine is good for what?
Anaphylaxis, cardiogenic shock
Dopamine MoA
Natural precursor of NE and epinephrine
Dopamine dosing
Dose-dependent pharmacology
Dopamine dosing: <5mcg/kg/min
Dopaminergic
Vasodilation of renal, mesenteric, and coronary
Increases renal blood flow, GFR, sodium excretion
Dopamine dosing: 5-10mcg/kg/min
Beta-1 adrenergic
Increases cardiac contractility, HR
Increases NE release from nerve terminals
Dopamine dosing: >10mcg/kg/min
alpha-1-adrenergic
Arterial vasoconstriction
Dopamine is effective in what patients
Hypotensive patients with depressed cardiac function/cardiac reserve
utilize when low risk for arrhythmia or with significant bradycardia
Dopamine ADEs
tachycardia, arrhythmogenesis, peripheral vasoconstriction at high doses
Phenylephrine MoA
selective alpha-1 adrenergic agonist, may stimulate beta receptors at high doses
Phenylephrine is NOT recommended in septic shock unless…
NE produces significant tachyarrhythmias
CO high, BP is persistently low
Salvage therapy when standard therapies are ineffective
Phenylephrine ADEs
ADEs: severe vasoconstriction, bradycardia, myocardial ischemia
Dobutamine MoA
inotrope (increases cardiac contractility), predominantly produces inotropic action via beta-1. Also produces vasodilation
When to give dobutamine
Added to treatment of shock when CO or SvO2/ScvO2 goals haven’t been achieved with vasopressor therapy
Often used for cardiogenic shock (pump failure)
Vasopressin MoA
released from the pituitary gland in response to decreased blood volume or increased plasma osmolarity
Vasopressin activity: V1
directly constricts smooth muscle and indirectly increases catecholamine release
Vasopressin activity: V2
ADH activity
Vasopressin activity: V3
increases ACTH release
Purpose of adding vasopressin
Decreasing doses of other pressors
Vasopressin ADEs
cardiac and mesenteric ischemia with higher doses
Angiotensin II MoA
Peptide hormone of the RAAS → produces vasoconstriction and aldosterone release to increase vascular tone
Angiotensin II benefit
reduce catecholamine response
Angiotensin caveat
Risk of thromboembolism, so all patients need to be on VTE prophy when getting this med (also mad expensive)
