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
*how empty the heart gets after systole (how strongly the heart can contract & how difficult it is to eject the blood from the LV)
*the appropriate heart rate
*the degree of resistance to blood flow as it travels through the systemic vasculature
*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 increase LVESV AFTERLOAD (increase afterload, with the ultimate goal of increasing blood pressure)
VASODILATORS/AFTERLOAD REDUCERS:
*ACE inhibitors, nitroprusside
*phosphodiesterase (PDE) inhibitors
