The use of Vasspressor Therapy in the ICU

Keith Habeeb MS4

Shock
Shock is hypotension with associated hypoperfusion abnormalities or impaired cell oxygen utilization. In adults, a systolic blood pressure (BP) <90 mm Hg, a mean arterial pressure <60 mm Hg, or a decrease in systolic BP of >40 mm Hg from the patients baseline pressure constitutes significant hypotension. Evidence of hypoperfusion includes mental status changes, oliguria, or lactic acidosis. However, hypoperfusion may be present in the absence of significant hypotension.

Types of Shock
Cardiogenic Shock: Inadequate blood flow due to primary
defect in cardiac pumping function.

Distributive Shock: Loss of peripheral vascular tone with the

effect of hypovolemia (Septic, anapylaxis, acute adrenal insuff, neurogenic and liver failure).

Obstructive Shock: The impedance of adequate cardiac

filling (Tamponade, PE, Tension pneumothorax).

Hypovolemic Shock: Depletion of intravascular volume

(Hemorrhage, vomiting, severe diarrhea, dehydration)

Hemodynamic profile of shock

Types of Shock
Cardiogenic

PCWP

CO

SVR

Distributive
Obstructive Hypovolemic

/
Tamponade: PE: or

Sympathetic Receptor
a1: Vascular smooth muscle contraction. B1: Contractility and chronicity of the Heart B2: Vasodilation. D1 and D2: renal and splanchic vasculature resulting in dilation.

Dopamine
MOA + EFFECT + Dosing
-Low Dose (3mcg/kg/min): Affects DA receptors in the renal and splanchnic circulation = Blood flow to these regions and natriuresis in the kidneys. -Intermediate dose (3-10mcg/kg/min): Affects the B1 and B2 receptors = CO ( HR+ Intropy+Vasodilation). -High dose (>10mcg/kg/min): Above + a1 receptors = Vasoconstriction + Negates the Intermediate dose effect on CO + PWCP (constriction of pulmonary vein). renders the use of PCWP as a measurement of LV fill pressure unreliable. -Where both cardiac stimulation + pressor effect is desired (Cardiogenic shock w/ or N BP). -2nd line treatment for septic shock. -Renoprotective theory has not been proven beneficial. -DA as an endogonous agent has the potential for prolactin release, and lymphocyte apoptosis. Leading to immunosuppressio -Tachycardia arrhythmias, and ischemic limb necrosis. Extravasation into the perivascular tissue. Use a large central line to infuse.

Use

Issues
SE

Dobutamine
MOA
-Potent B1 agonist/weak B2 agonist = Produces both positive inotropic and chronotropic effect along with peripheral vasodilation Preload.

Effect - CO with variable effect on BP (//) Use

-Decompensate HF w/ systolic dysfxn and a N/Low BP. -R sided HF. -First line intropic agent for a small subset of pt with septic shock and CO w/ adequate filling pressures.

- HR leads to O2 demand which can exacerbate cardiac Issues ischemia in cardiogenic shock.

Dose

3-15 mg/kg/min (Max 200mg/kg/min) Titrate dose for maximal effect while min toxicity. -Tachycardia, Ventricular ectopic beats

SE

Norepinephrine
MOA -Primarily an a1 agonist with a small effect on B1 receptors. -Potent vasopressor + decreases organ blood flow particularly in the kidneys. Except in septic shock -Pressor of choice in septic shock. -Last measure of choice in HoTN refractory to volume infusion and other drug. -andomized data comparing norepinephrine with other catecholamines have previously been limited to one small trial in which norepinephrine was compared with dopamine in 32 volume-resuscitated septic patients, and proved better at achieving and maintaining normal hemodynamic and oxygen transport parameters (36) therapies (Dopamine/Dobutamine). -0.5mcg/kg/min and titrate to effect. -Tachycardia, local tissue necrosis, and organ ischemia.

Effect

Use

Dose SE

Epinephrine
-Affects both the a1 receptors and the B1>B2 adrenergic MOA receptors.
- both Cardiac index and vascular tone. O2 Effect consumption

Use

-Cardiogenic shock/ Vasodilatory shock. -Cardiac Arrest/ Bradycardia unresponsive to pacing / atropine

-Not a first line agent for other types of shock due to Issues regional ischemia and lactic acid build up.

SE

-Tachycardia, arrhythmias.

Vasopressin
MOA
Effect
- Directly affecs the V1 receptors and may inhibit endogenous NO production.
-Causes direct vasoconstriction of the vascular smooth muscle and the response to catacholamines.

Use

- Cardiac arrest - May be used in low doses to the requirement of pressor therapy in shock (Septic, cardiogenic, hypovolemic and distributive). - Meta analysis of 6 trials show no decrease in mortality when used in septic shock as compared to placebo but pts who receive vasopressin did require less norepi.
Coronary/mesenteric ischemia, hyponatremia, pulmonary vasoconstriction, and skin necrosis from peripheral infusion.

Issues

SE

Pressing a Failing Heart

L-Sided Systolic Failure HIGH BP
(PWCP/ CO)

First line Treatment

-Vasodilator Therapy (NITRO)
-Dobutamine/ milrinone or Vasodilator Therapy (NITRO). -Dopamine w/ Dobutamine.

Second Line Treatment

-PCWP > 20 then diuretic therapy with IV furosimide. -PCWP > 20 then diuretic therapy with IV furosimide.

Note

-Promotes vasodilation= Afterload+CO+BP -Vasodilation is preferred due to the the in O2 consumption caused by dobutamine may cause ischemia. -Dopamine vasoconstriction + mild Intropy -Add dobutamine to enhance the effect of DA negative effect on CO.

N BP
(PWCP/ CO)

LOW BP
(PWCP/ CO)

-Mechanical support devices if postbypass or when bypass is planned.

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