Inotropes & Vasopressors Flashcards
Ohm’s Law
V = I x R
*the voltage drop across an electrical circuit equals the current flowing through the circuit multiplied by the resistance to that circuit
Ohm’s Law in Hydraulics/Hemodynamics
ΔP = Q x R
*instead of a voltage drop with electrical circuits, there is a PRESSURE DROP across a FLUID-FILLED circuit
*the pressure drop equals the flow through the circuit (Q) multiplied by the resistance to that flow
Ohm’s Law applied to Systemic Circulation
BP = CO x SVR
*consider the circuit as the left ventricle to the tissues
*the pressure change is simply our blood pressure (BP)
*flow through our circulation is the cardiac output (CO)
*resistance to blood flow through the systemic circulation is systemic vascular resistance (SVR)
Ohm’s Law applied to Systemic Circulation - expanded
BP = CO x SVR → BP = [LVEDV - LVESV] x HR x SVR
*CO = stroke volume x heart rate
*stroke volume = left ventricular end-diastolic volume - left ventricular end-systolic volume = LVEDV - LVESV
based on Ohm’s Law as applied to systemic circulation, a patient’s blood pressure depends on…
*how full the heart gets at the end of diastole (EDV)
*how empty the heart gets after systole (how strongly the heart can contract & how difficult it is to eject the blood from the LV) (ESV)
*the appropriate heart rate
*the degree of resistance to blood flow as it travels through the systemic vasculature (SVR)
*CHANGING EACH OF THESE VARIABLES IS HOW WE INCREASE BP WHEN NEEDED
recall: BP = [LVEDV - LVESV] x HR x SVR
alpha1 receptors
*found in peripheral & splanchnic vasculature, and also on “capacitance vessels” (can regulate blood volume)
*stimulation → smooth muscle CONTRACTION
*stimulation in blood vessels → VASCULAR CONSTRICTION (Pressor effect), and may increase blood volume
alpha2 receptors
*found in peripheral & splanchnic vasculature
*stimulation → smooth muscle contraction & vascular constriction (Pressor effect)
*found in the pre-synaptic receptors, so stimulation → NEGATIVE FEEDBACK
*CNS: role in pain and sedation
beta1 receptors
*found in cardiac tissue & peripheral vasculature
*stimulation of beta1 receptors in cardiac tissue:
→ inotropic effect (increased contractility; cAMP modulated)
→ chronotropic effect (increased HR)
→ lusitropic effect (relaxation)
*stimulation of beta1 receptors in peripheral vasculature → VASODILATION (smooth muscle relaxation) [cGMP modulated]
*pre-synaptic receptors provide positive feedback
beta2 receptors
*found in cardiac tissue & peripheral vasculature
*same effects as beta1 receptors (increased contractility, increased HR, vasodilation of vasculature)
*many more beta1 receptors than beta2 in normal hearts, but in advanced CHF, the ratio decreases
*stimulation of beta2 receptors in bronchial smooth muscle → BRONCHODILATION
dopamine receptors
*found in:
-cardiac tissue (inotropic & CHRONOTROPIC [increased HR])
-peripheral vasculature
-splanchnic vasculature (vasodilation)
-renal (multiple effects, including diuretic & natriuretic)
*CNS
vasopressin receptors
*stimulation → marked VASOCONSTRICTION, esp in peripheral & splanchnic vasculature
*renal effects (V2): Na+ reabsorption & ADH
*CNS (V3): corticotropin release
angiotensin receptors
*stimulation → marked VASOCONSTRICTION in peripheral vasculature
*adrenal effects: increased aldosterone release → Na+ and H2O retention
Rx to increase LVEDV (increase preload, with the ultimate goal of increasing blood pressure)
*fluids
*alpha-agonists (at low doses)
Rx to increase LVESV CONTRACILITY (increase contractility, with the ultimate goal of increasing blood pressure)
INOTROPES:
*beta-adrenergic agonists
*phosphodiesterase (PDE) inhibitors
Rx to decrease AFTERLOAD
VASODILATORS/AFTERLOAD REDUCERS:
*ACE inhibitors, nitroprusside
*phosphodiesterase (PDE) inhibitors
Rx to increase HEART RATE (increase HR, with the ultimate goal of increasing blood pressure)
CHRONOTROPES:
*beta-adrenergic agents
*atropine, aminophylline, others
*pacemakers
Rx to increase systemic vascular resistance (increase SVR, with the ultimate goal of increasing blood pressure)
VASOCONSTRICTORS (pressors):
*alpha-adrenergic agonists
*vasopressin
*angiotensin
Ohm’s Law & treatment to increase blood pressure - summary
*increase LVEDV: fluids, low dose alpha agonists
*increase LVESV:
-afterload reduction: ACE inhibitors, PDE inhibitors, vasodilators
-contractility: beta agonists, PDE inhibitors
*increase HR: beta agonists, atropine, pacemaker
*increase SVR: alpha agonists, vasopressin, angiotensin
epinephrine - overview
*“God’s inotrope” - from adrenal glands
*beta-effects predominate at low doses (non-selective beta1 and beta2)
*alpha-effects occur at high doses
*INOTROPIC (increased contractility) & CHRONOTROPIC (increased HR)
*used for cardiogenic shock, post-CABG, sepsis
note - do NOT use in an acute MI
dobutamine - overview
*beta agonist (mostly beta1)
*inotrope with some vasodilatory effects
*INCREASES CONTRACTILITY & HR
*vasodilates & reduces afterload
*INOTROPIC & CHRONOTROPIC
*uses: acute MI, mild cardiogenic shock
isoproterenol - overview
*beta agonist
*inotrope with vasodilatory effects
*INCREASES CONTRACTILITY & HR
*vasodilates & reduces afterload, esp in pulmonary circulation (may improve pulmonary blood flow)
*INOTROPIC & CHRONOTROPIC
*uses: congenital heart repairs, pulmonary HTN
norepinephrine - overview
*“God’s pressor”
*alpha-effects predominate at low doses (vasoconstriction)
*beta effects are present at higher doses
*VASOCONSTRICTION & INCREASED SVR
*uses: SEPSIS, distributive shock (sepsis) with good CO
phenylephrine - overview
*pure alpha agonist
*vasoconstriction & increased SVR
*not as potent/effective as norepi
*uses: mild sepsis, hypotension with good CO
dopamine - overview
*dose-dependent pharmacology
*stimulates dopamine receptors at low doses, beta receptors at medium doses, alpha receptors at high doses
*not used with much frequency due to side effects (tachycardia)
vasopressin - overview
*intense vasoconstriction through V-receptors
*no alpha or beta stimulation (non-adrenergic vasoconstriction, no direct cardiac effects)
*may have predilection for splanchnic vessels (beware of gut ischemia)
*uses: ACLS, severe shock, CABG (on ACEi), with norepi in sepsis
angiotensin II - overview
*intense vasoconstriction through AT-receptors
*no alpha or beta stimulation (non-adrenergic vasoconstrictor, no direct cardiac effects)
*may stimulate aldosterone production (retention of Na+ and H2O)
*uses: severe shock, CABG, combinations
phosphodiesterase inhibitors (PDEi) - overview
*examples: milrinone, amrinone
*VASODILATORS & INOTROPES
*augments beta-adrenergic stimulation (prevents breakdown of cAMP)
*smooth muscle relaxation
*uses: CABG, vasoconstricted with low CO
treatment strategy for: hypotension with high CO
*phenylephrine for more SVR
*norepinephrine might be necessary
treatment strategy for: hypotension with low CO with low LVEDV
*crystalloid volume (GIVE FLUIDS)
treatment strategy for: low CO with adequate LVEDV
*dobutamine for inotropy
*milrinone if high SVR by exam
treatment strategy for: decompensated septic shock with vasodilation from mediators
*need exogenous vasoconstriction (alpha, V, AT):
-phenylephrine, NOREPINEPHRINE, AT-2, epi
-vasopressin or angiotensin II
treatment strategy for: decompensated septic shock with depressed myocardial contractility
*need inotropic support (beta):
-dobutamine
-EPINEPHRINE
-norepinephrine
treatment strategy for: decompensated septic shock with third space fluid losses
*need FLUIDS
