Hemodynamics/Sepsis: Pharmacotherapy

Question 1

Goals of therapy for shock management

Answer 1

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)

Question 2

Shock goals: hemodynamic optimization

Answer 2

MAP ≥65mmHg
HR <100bpm
CVP= 8-12 mmhg (12-15mmHg)
PCWP= 12-15 mmHg
Cardiac index >2.2L/min/m2

Question 3

Shock goals: maintaining O2 delivery

Answer 3

Hgb 7-9gm/dl
Arterial saturation >88-92%
SVO2/SCVO2 >65%/70%

Question 4

Shock goals: reversal of O2 dysfunction

Answer 4

lactate CL (<2 mmol/L) or normalization

Question 5

Shock goals: urine output

Answer 5

> 0.5ml/kg/hr

Question 6

Shock goals: reverse encephalopathy

Answer 6

improve cognition

Question 7

Pharmacotherapy of shock

Answer 7

Initiation of vasoactive agents when MAP remains <65mmHg despite fluid administration

Question 8

Shock pharmacotherapy: what do fluids do?

Answer 8

Increases SV, CO, DO2

Question 9

Shock pharmacotherapy: fluids

Answer 9

Crystalloid fluid (LR, NS): 30ml/kg over 15-30 mins, then by 10ml/kg boluses
Cardiogenic shock: 100-200ml boluses

Question 10

Shock pharmacotherapy: NE MoA

Answer 10

potent alpha-adrenergic agonist; increases MAP via peripheral vasoconstriction

Question 11

NE dosing

Answer 11

0.01-3mcg/kg/min, or 5-65mcg/min

Question 12

NE ADE

Answer 12

significant vasoconstriction

Question 13

Shock pharmacotherapy: epinephrine MoA

Answer 13

potent alpha and beta-adrenergic agonist

Question 14

Epinephrine dose-dependent activity

Answer 14

low-dose is predominantly beta-1 → increase HR and SV and beta-2 vasodilation, but higher doses produce increased alpha-1 stimulation

Question 15

Epinephrine: dose

Answer 15

0.05-2mcg/kg/min

Question 16

Epinephrine can increase aerobic lactate production by what?

Answer 16

Beta-2 skeletal muscle receptors

Question 17

Epinephrine ADEs

Answer 17

tachycardia, arrhythmias, cardiac ischemia, peripheral vasoconstriction, reduced renal blood flow, hyperglycemia, hypokalemia

Question 18

Epinephrine is good for what?

Answer 18

Anaphylaxis, cardiogenic shock

Question 19

Dopamine MoA

Answer 19

Natural precursor of NE and epinephrine

Question 20

Dopamine dosing

Answer 20

Dose-dependent pharmacology

Question 21

Dopamine dosing: <5mcg/kg/min

Answer 21

Dopaminergic
Vasodilation of renal, mesenteric, and coronary
Increases renal blood flow, GFR, sodium excretion

Question 22

Dopamine dosing: 5-10mcg/kg/min

Answer 22

Beta-1 adrenergic
Increases cardiac contractility, HR
Increases NE release from nerve terminals

Question 23

Dopamine dosing: >10mcg/kg/min

Answer 23

alpha-1-adrenergic
Arterial vasoconstriction

Question 24

Dopamine is effective in what patients

Answer 24

Hypotensive patients with depressed cardiac function/cardiac reserve

utilize when low risk for arrhythmia or with significant bradycardia

Question 25

Dopamine ADEs

Answer 25

tachycardia, arrhythmogenesis, peripheral vasoconstriction at high doses

Question 26

Phenylephrine MoA

Answer 26

selective alpha-1 adrenergic agonist, may stimulate beta receptors at high doses

Question 27

Phenylephrine is NOT recommended in septic shock unless…

Answer 27

NE produces significant tachyarrhythmias
CO high, BP is persistently low
Salvage therapy when standard therapies are ineffective

Question 28

Phenylephrine ADEs

Answer 28

ADEs: severe vasoconstriction, bradycardia, myocardial ischemia

Question 29

Dobutamine MoA

Answer 29

inotrope (increases cardiac contractility), predominantly produces inotropic action via beta-1. Also produces vasodilation

Question 30

When to give dobutamine

Answer 30

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)

Question 31

Vasopressin MoA

Answer 31

released from the pituitary gland in response to decreased blood volume or increased plasma osmolarity

Question 32

Vasopressin activity: V1

Answer 32

directly constricts smooth muscle and indirectly increases catecholamine release

Question 33

Vasopressin activity: V2

Answer 33

ADH activity

Question 34

Vasopressin activity: V3

Answer 34

increases ACTH release

Question 35

Purpose of adding vasopressin

Answer 35

Decreasing doses of other pressors

Question 36

Vasopressin ADEs

Answer 36

cardiac and mesenteric ischemia with higher doses

Question 37

Angiotensin II MoA

Answer 37

Peptide hormone of the RAAS → produces vasoconstriction and aldosterone release to increase vascular tone

Question 38

Angiotensin II benefit

Answer 38

reduce catecholamine response

Question 39

Angiotensin caveat

Answer 39

Risk of thromboembolism, so all patients need to be on VTE prophy when getting this med (also mad expensive)