Shock Drugs (Inotropes and Vasopressors)

What does blood pressure depend on (components of equation)

BP= (LVEDV-LVESV) x HR x SVR: depends on CO(SVxHR) and SVR, so drugs target LVEDV (preload), LVESV (contractility/afterload), HR (chronotropy), or SVR (vasoconstriction) to correct hypotension.

Which hemodynamic variable does epinephrine primarily modify, and how does this help differentiate shock types?

Epinephrine increases CO (β1/β2) and SVR (α1 at higher doses), improving hypotension in distributive(low SVR) or cardiogenic shock depending on the dominant deficit.

How does norepinephrine’s receptor profile help identify distributive shock physiology?

Norepinephrine’s strong α1 vasoconstriction corrects low SVR, the hallmark of distributive shock (e.g., sepsis), while modest β1 support maintains CO.

Why is phenylephrine inappropriate for cardiogenic shock when analyzing pump function?

Phenylephrine is a pure α1 vasoconstrictor that increases SVR/afterload without improving contractility, worsening CO in cardiogenic shock.

How does dobutamine’s effect on LVESV help differentiate cardiogenic shock from hypovolemic shock?

Dobutamine(b1 agonist) reduces LVESV by increasing contractility (β1) and decreasing afterload (β2), improving CO in cardiogenic shock but ineffective if preload is low (hypovolemia).

How does isoproterenol’s physiology help identify obstructive vs cardiogenic shock?

Isoproterenol increases HR/contractility (beta agonist) and causes pulmonary vasodilation, improving RV output—useful in pulmonary hypertension or RV failure but not in tamponade or PE obstruction.

How does angiotensin II help differentiate shock states with preserved CO but severe vasoplegia?

AT1 vasoconstriction rapidly increases SVR and BP, identifying distributive shock with intact cardiac function.

How do PDE inhibitors (milrinone) help evaluate afterload vs contractility problems?

Milrinone increases contractility and decreases SVR

Why does norepinephrine improve MAP more predictably than epinephrine in septic shock?

Norepinephrine’s dominant α1 vasoconstriction increases SVR without β2 vasodilation, producing a more stable MAP rise in vasoplegic states.

Why is dopamine avoided in modern shock algorithms?

Tachyarrhythmias from β1 stimulation worsen CO and oxygen demand, complicating diagnosis and increasing mortality in septic shock.

How does vasopressin’s splanchnic vasoconstriction help critique its risks?

V1 constriction may cause gut ischemia, limiting use in patients with mesenteric hypoperfusion.

How does angiotensin II’s aldosterone stimulation affect fluid resuscitation strategy?

AT2 increases Na/H2O retention, supporting intravascular volume but risking fluid overload in cardiogenic shock.

How does analysis of LVEDV guide the choice between fluids vs pressors?

Low LVEDV → fluids first

What is isoproterenol useful in?

Pulmonary hypertension or congenital heart repairs bc it vasodilates(especially pulmonary circulation)

How does myocardial oxygen demand critique epinephrine use?

Epinephrine increases HR/contractility → ↑O2 demand → risk of ischemia in cardiogenic shock(pulls O2 away from other areas)

How does obstructive shock physiology limit drug effectiveness?

Tamponade/PE prevent LV filling regardless of drugs

Alpha 1 agonists do

vasoconstrict peripheral arteries

Alpha 2 agonists do

mainly inihibit presynaptic receptors and act as negative feedback for sympathetic NS, vasoconstrict

B1 agonists do

Inc HR(chronotropic) and contractility(inotropic); vasodilate in peripheral vasculature

B2 agonists do

Inc HR(chronotrope) and contractility(Inotrope), vasodilate in periphery, bronchodilate!; **In advanced CHF»they are better target than B1

Dopamine agonist do

Increase HR, vasodilation in splanchnic and peripheral, diuretic

Vasopressin agonist do

Vasoconstriction, inc water reabsorption

Angiotensin agonist do

Inc vasoconstriction, inc aldosterone release (inc water and Na retention)

Drugs to increase LVEDV

Fluids, low dose a agonists

Drugs to dec LVESV

Afterload reduction: ACEi, PDEi, vasodilators

Contractility: B agonists, PDEi

Drugs to inc HR

B agonists, atropine, pacemaker

Drugs to inc SVR

Alpha agonists, vasopressin, angiotensin