Surgical Critical Care Flashcards
Know the receptors relevant to pressor management and their effect on cardiovascular physiology (5)
- α1 - peripheral vasc; stim - vasoconstriction
- β1 - cardiac muscle, JG cells of the kidney; stim - inotropy (contractility), chronotropy (rate), conduction, release of renin
- β2 - heart, peripheral vasc, and bronchial SM; stim - diastolic relaxation, vasodilation, bronchodilation
- D - renal, mesenteric/splanchnic, coronary vascular beds; stim - vasodilation
- V1 - mesenteric/splanchnic vascular beds; stim - vasoconstriction
Understand common risks and complications of vasopressor and inotrope usage.
- All vasopressors/inotropes have arrhythmogenic potential; DA notably high
- Inc cardiac O2 consumption via inotropy/chronotropy - worse MI
- HR increases myocardial O2 use > contractility alone
- In shock, worsens splanchnic vasoconsx - mesenteric/renal ischemia
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Cutaneous extravasation of vasopressors, and norepinephrine in particular, carry risk of local tissue necrosis and compartment syndrome.
- Treat NE extrav w/ local inj of 5-10 mg in 10 mL phentolamine (α-antag).
Describe the mechanism of action, indications, and dosages for common vasopressors (epinephrine).
Epinephrine has both α and β1/2 effects. At lower doses β1 effect predominates, resulting in increased heart rate and contractility, with some degree of β2 effect causing peripheral vasodilation. At higher rates, α effect predominates with increased peripheral vascular resistance and blood pressure. Epinephrine is indicated for anaphylactic shock, and as a second line agent for septic shock unresponsive to norepinephrine or dopamine. Typical dosage is 1-200 µg/min.
Describe the mechanism of action, indications, and dosages for common vasopressors (norepinephrine).
Norepinephrine has both α and β1 effects (less β2 effect than epinephrine). β1 effect is more prominent at lower dosages resulting in increased cardiac contractility and heart rate. At higher dosages, α effects dominate with increasing peripheral vascular resistance and blood pressure. Norepinephrine exhibits preferential splanchnic vasoconstriction and is a first line agent for septic shock. Typical dosage is 0.5-80 µg/min.
Describe the mechanism of action, indications, and dosages for common vasopressors (dopamine).
Dopamine has α, β, and D receptor effects. Low doses (1-3 µg/kg/min) stimulate D receptors which may increase renal blood flow. Moderate doses (5-10 µ/kg/min) stimulate β1/2 receptors with increasing contractility and cardiac output, but have little effect on heart rate or blood pressure. High doses (10-30 µg/kg/min) stimulate α receptors increasing peripheral vasoconstriction with increased blood pressure. Dopamine is indicated for septic shock, although norepinephrine has a more reliable dosage profile.
Describe the mechanism of action, indications, and dosages for common vasopressors (phenylephrine).
Phenylephrine has predominantly α effect that results in peripheral vasoconstriction, and may cause a degree of reflex bradycardia. It is useful in hypotension in the setting of decreased peripheral vascular resistance (hyperdynamic septic shock, neurogenic shock, post-anesthesia), but rarely used as a first line medication. Typical dosage is 20-200 µg/min.
Describe the mechanism of action, indications, and dosages of common inotropes (dobutamine).
Dobutamine has predominantly β1/2 effect with minimal α effect. It produces increased contractility with reduced peripheral vascular resistance (afterload) and may lower blood pressure. It is a good agent for patients in cardiogenic shock when the primary goal is to improve cardiac output. Dobutamine does not dramatically increase myocardial oxygen consumption. Typical dose is 2-30 µg/kg/min.
Describe the mechanism of action, indications, and dosages of common inotropes (milrinone).
Milrinone is a synthetic phosphodiesterase III inhibitor and does not act along the typical α/β mechanism. Reduced activity of phosphodiesterase III increases cAMP concentration, which increases cardiac contractility and reduces peripheral vascular resistance. The net effect is to increase cardiac output and reduce afterload. Milrinone is indicated for cardiogenic shock. Typical dose is 50 µg/kg load over 10 mins, then 0.375-0.75 µg/kg/min.
Be able to select the appropriate vasopressor and inotrope medications depending on the clinical situation (spetic shock).
Septic shock - norepinephrine should be provided as the first line vasoprossor with non-titrated vasopressin as an adjunct. In hyperdynamic septic shock, phenylephrine can be consider as the second line agent; otherwise, epinephrine should be provided as the second line agent.
Describe the mechanism of action, indications, and dosage of vasopressin.
Vasopressin acts on V1 receptors to contract splanchnic and peripheral vascular beds. Research suggests vasopressin secretion may be impaired in patients in shock and catecholamine-resistant septic shock in particular. It is indicated as an adjunct to reduce norepinephrine dosages in septic shock. Typical dose is 0.04 U/min (not titrated).
Be able to select the appropriate vasopressor and inotrope medications depending on the clinical situation (anaphylaxis).
Anaphylactic shock - epinephrine should be provided as the first line vasopressor.
Be able to select the appropriate vasopressor and inotrope medications depending on the clinical situation (cardiogenic).
Cardiogenic shock - dobutamine or milrinone should be provided as the first line inotrope.
Be able to select the appropriate vasopressor and inotrope medications depending on the clinical situation (neurogenic).
Neurogenic shock - norepinephrine or dopamine should be provided as the first line vasopressor. Phenylephrine can be considered if bradycardia is not an issue.
Be aware of inappropriate uses of vasopressors and inotropes.
Prelim steps? Renal protection? Definitive therapy?
- Always provide adequate volume resuscitation before pressors.
- Low dose dopamine is NOT appropriate for “renal protection.”
- Pressors are bridging measures used while underlying pathophysiology is diagnosed/corrected. They are not a definitive therapy.
Septic shock is defined as
sepsis-induced hypotension that persists despite adequate fluid resuscitation and requires vasopressor therapy to maintain MAP >65, AND lactate >2
hospital mortality >40%