Cardiovascular drug tracings

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jknell
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209655
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Cardiovascular drug tracings
Updated:
2013-03-26 23:22:54
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Cardio Drug tracings
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  1. Drug tracings
    • Pulse
    • Blood pressure
    • Peripheral resistance
  2. Systematic approach:
    • 1. Look at the diastolic blood pressure
    • -what does the drug due to total peripheral vascular resistance (i.e. SVR)

    • 2. Pulse pressure:
    • -Stroke volume (preload, afterload, contractility, heart rate)
    • -Inotropic state

    • 3. Heart rate tracing: increased, decreased, stays the same
    • -direct: effect on SA node (automaticity, threshold potential, APD, maximal diastolic potential)
    • -Indirect: baroreceptor reflex

    • X - Y - X format
    • -X is usually an agonist
    • -Y is usally an antagonist
  3. General principles for antagonists
    1. Antagonists occupy the receptor, but have no efficacy. Can cause physiological response by blocking normal tone

    2. Antagonists typically cause effects that are longer lasting than the effects of the agonists
  4. General principle
    Baroreceptor reflex
    Don't forget baroreceptor reflex!!

    • Baroreceptors:
    • -carotid sinus (afferents on: CN IX)
    • -aortic arch (afferants on: CN X)

    →NTS (control center)

    • Efferents:
    • - (-/+) Sympathetic outflow: to heart and blood vessels
    • - (+/-) Parasympathetic outflow: to heart
    • Norepinephrine
    • α, β1
    • direct and indirect effects on heart rate
    • Baroreceptor effects override direct affects
    • Epinephrine
    • α, β1, β2
    • Moderate pressor
    • Physiologic/Low dose: ↓ diastolic BP: β2 vasodilation > α vasoconstriction
    • High dose: ↑ diastolic BP: α vasoconstriction > β2 vasodilation
    • Isoproterenol
    • β1, β2
  5. Baseline tone
    • Heart rate: parasympathetic tone (70bpm) > sympathetic tone (110bpm); intrinsic: 100bpm
    • Blood vessels: sympathetic tone (vasoconstriction)
    • Airway: parasympathetic tone (bronchoconstrictor) > sympathetic tone (bronchodilator)
    • Sweat glands: sympathetic cholinergic tone (stimulate sweating)
    • Pupillary diameter: parasympathetic tone (constriction) sympathetic tone (dilation)
  6. Agonists
    • NE: α, β1
    • EPI: α, β1, β2
    • Isoproterenol: β1, β2
    • ACh: NN, NM and M1, M2, M3
    •      -Low dose: (↓BP; ↑ HR)
    •      -High dose: (???)
    • Carotid occlusion: ↓ nerve traffic to nucleus of solitary tract → NTS "thinks" BP has fallen → ↑ sympathetic tone to CV system, ↓ parasympathetic tone to heart
  7. Antagonists
    • Atropine: mAChR antagonist (BP unchanged; ↑ HR)
    • Trimethaphan: NN antagonist (ganglionic blocking agent) (↓ BP; ↑ HR)
    • Phentolamine: α antagonist (↓ BP; ↑ HR)
    • Vagotomy: (↑ BP; ↑ HR)
    •      - loss of afferent info from Aortic Arch baroreceptor to NTS
    •     - loss of parasympathetic efferent to heart
    • X = NE: α, β1
    • Y = Atropine: mAChR antagonist

    • NE
    • -α vasoconstriction → ↑ diastolic blood pressure 
    • 1 ↑ Inotropic state → ↑ pulse pressure
    • 1 ↑ HR, but baroreceptor reflex overrides: ↓ HR

    • Atropine: blocks parasympathetic (vagus) tone on heart (Min SA node)
    • - no effect on BP
    • - ↑ HR

    • NE:
    • -same effect on diastolic BP and pulse pressure
    • 1 ↑ HR; BRR blocked by atropine!
    • X = NE:  α, β1
    • Y = Trimethaphan: NN antagonist - anglionic blocking agent

    • NE: as before
    • -α vasoconstriction → ↑ diastolic blood pressure 
    • -β1 ↑ Inotropic state → ↑ pulse pressure
    • -β1 ↑ HR, but baroreceptor reflex overrides: ↓ HR

    • Trimethaphan: (blocks NN in glanglia)
    • -blocks baseline sympathetic tone (vasoconstrictor tone) → ↓ SVR
    • -blocks baseline parasympathetic tone to heart → ↑ HR

    • NE:
    • -same effect on diastolic BP and pulse pressure
    • -β1 ↑ HR; BRR blocked by trimethaphan!
    • X = EPI: α, β1, β2
    • Y = Phentolamine: α antagonist
    • "EPI reversal" (pressor → depressor)

    • EPI:
    • - ↓ diastolic BP: β2 vasodilation > α vasoconstriction
    • - ↑ pulse pressure: β1 ↑ inotropic state
    •      →Mild pressor; not enough to cause BRR to ↓ HR
    • -↑ HR: β1

    • Phentolamine:
    • -↓ Diastolic BP: block α vasoconstriction
    • - BRR → ↑ HR

    • NE:
    • -↓↓ diastolic BP: β2 vasodilation; α vasoconstriction is blocked by phentolamine
    • - ↑ pulse pressure: β1 ↑ inotropic state
    •      → Depressor
    • -↑ HR: β1
    • * β1 β2 effects only: EPI looks like Isoproterenol!
    • X = Low Dose ACh: M1, M2, M3
    • Y = Atropine: mAChR antagonist

    • ACh:
    • - ↓ diastolic BP: non-innervated M3 receptors on endothelial cells (indirect, via NO)
    • - BRR → ↑ HR (β1; overrides M2 ↓ HR)

    • Atropine: mAChR antagonist
    • -Diastolic BP unchanged; normal vascular tone unaffected
    • -Pulse pressure unchanged; inotropic state not affected
    • -↑ HR: block normal parasympathetic (M2) tone on heart

    • ACh:
    • -low dose cannot overcome mAChR blockade
    • Carotid occlusion:
    • -↑ BP: ↑ sympathetic to blood vessels (α)
    • -↑ HR: ↑ sympathetic to heart (β1); ↓ parasympathetic to heart (M2)

    • Atropine: mAChR antagonist
    • -BP unchanged; normal vascular tone unaffected
    • - ↑ HR: parasympathetic to heart blocked (M2)

    • Carotid occlusion:
    • -As before; M2 blocked on heart from atropine

    • Vagotomy:
    • -NTS losses afferent from Aortic arch baroreceptors
    • -NTS only has afferent from Carotid sinus
    •      → ↑ sympathetic/↓ parasympathetic output from NTS (due to lack of signal from AoA receptors)
    • - ↑ BP
    • - ↑ HR

    • Carotid occlusion:
    • - ↑ BP; ↑ HR more than before vagotomy (no balance of input to NTS from the Aortic Arch baroreceptor
  8. What would happen (in the last tracing) if we gave trimethaphan?
    (NN antagonist)
    • ↓ BP: blocks basal sympathetic tone to blood vessels
    • ↓ HR: blocks sympathetic tone to heart (β1); parasympathetic tone already blocked (atropine)
  9. What would be the affect of carotid occlusion after this?
    • Nothing...
    • parasympathetic input to heart is out (vagotomy; atropine)
    • sympathetic output (to blood vessels and heart) are out (trimethaphan)

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