Pharmacology: Vasoactive Agents Flashcards

1
Q

How do inotropes, vasopressors and chronotropes affect cardiac aspects

A

contractility: inotropes

SVR: vasopressors

HR: chronotropes

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2
Q

2 aspects of the PNS

A

somatic and autonomic (broken down to parasympathetic and sympathetic)

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3
Q

end organ receptor of the parasympathetic NS (Autonomic)

A

muscarinic (ACh)

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4
Q

end organ receptor of thesympathetic NS (Autonomic)

end organ receptor for the parasympathetic NS

A

end organ receptor is the adrenergic alpha and beta receptors.

end organ receptor for the parasympathetic NS is muscarinic (Ach)

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5
Q

Alpha 1 receptors:

__- synaptic

affects ___ muscle.

activation leads to:

A

post-synaptic.

  • affects VASCULAR SMOOTH MUSCLE HEART.
  • Activation Leads to:
  • contraction vascular smooth muscle
  • increased cardiac contractility
  • increased heart rate.
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6
Q

Beta 1 receptors are ___ synaptic and can be found in the ___. activation leads to:

A

beta 1 receptors are POST SYNPATIC and found in the HEART .

-activation leads to increased contractility and increased heart rate

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7
Q

beta 2 receptors are ___ synaptic and affects ___ muscle. They are located in the muscle of the ___ and ___. activation leads to:

A

beta 2 receptors are PRE AND EXTRA SYNAPTIC

  • affects smooth muscle of vessels and bronchi
  • activation leads to:

- vasodilation and bronchial dilation

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8
Q

fill table out

A
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9
Q

match the action to the receptor that is involved

  1. vasoconstriction
  2. increased contractility
  3. bronchodiltation
  4. decrease SVR
A
  1. vasocontriction = alpha 1
  2. increased contractility = beta. 1
  3. bronchodilation = beta 2
  4. beta 2
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10
Q

which receptors does epinpehrine affect? Where it is released from?

A

affects A1, B1, B2

  • inotropy
  • dilation skeletal muscle in small doses
  • vasocontsrictin in large doses
  • bronchodilation
  • released from adrenal medulla
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11
Q

typical uses of epinephrine

A
  • anaphylaxis, cardiac arrest
  • severe shock
  • status asthmaticus
  • local anesthetics
  • upper airway edema (croup)
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12
Q

• 68 yo woman • No previous CAD • Onset of CP 60 minutes ago

  • wheres the problem in the vasculature
A

looks like a heart block.

  • ventricel could be overly constricted/ contractility or thickened causing a poor conduction
  • afterload is increased because of poorly contracting ventricle.
  • rate and rhythm is thus affected.
  • wanna increase the contractility of the ventricle to help with the afterload. therefore we want a beta 1 stimulator: DOPAMINE
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13
Q

DA is a precursor to ___. Effects are dose related. It a Beta 1, beta 2 and.a alpha 1 agonist.

A

precursor to norepinephrine. efects are dose related-

  • increased renal blood flow
  • increases heart rate
  • increases contractility
  • increases vasconstriction.
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14
Q

explain how a 0.5 – 2 μg/kg/min dose of dopamine causes systemic effects different than 2 – 10 μg/kg/min vs 10 – 20 μg/kg/min:

A

• 0.5 – 2 μg/kg/min
– Dopamine receptor activity
Vasodilation renal, mesenteric, coronary and intracerebral vessels

• 2 – 10 μg/kg/min:
– β-1 activity
– Increased heart rate and contractility

• 10 – 20 μg/kg/min:
– α-1 activity
– Increased vasoconstriction

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15
Q

Dopamine Dosages:

• 0.5 – 2 μg/kg/min
– ___ receptor activity
– ___ renal, mesenteric, coronary and intracerebral vessels

• 2 – 10 μg/kg/min:
– ___ recepor activity
– Increased heart rate and ___

• 10 – 20 μg/kg/min:
– ___ receptoractivity
– Increased __

A

• 0.5 – 2 μg/kg/min
Dopamine receptor activity
– Vasodilation renal, mesenteric, coronary and intracerebral vessels

• 2 – 10 μg/kg/min:
– β-1 activity
– Increased heart rate and contractility

• 10 – 20 μg/kg/min:
– α-1 activity
– Increased vasoconstriction

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16
Q

T/F you can give inotropes alone

A

false. inotropes are only a bridge to definitive therapy. inotropes stimulate contractility which helps short term but you’ll burn the heart out.— gotta figure out what’s wrong with them overall that’s causing high afterload or cardiac weakness.

17
Q
A
18
Q
  • POD #1 – AAA Repair
  • Unconscious
  • Faint Carotid Pulse

Where is the problem? What is the approach/treatment to this?

A

ECG looks normal BUT she is brady-cardic.

  • might be due to an overactive parasympathetic nervous system inducing a reduction in heart rate. Blocking the PNS shoud increase the heartrate. recall that the post synaptic junction is a muscarininc (Ach) receptor.
  • we need to block this receptor.

ATROPINE. inhibitor of the muscarinic Ach receptor. blocks vagus nerve action on heart leading to icnrease in heart rate.

19
Q

atropine is a ___ ____ of muscarinic receptors

A

competitive inhibitors

20
Q
  • 66 yo woman
  • Pneumonia

• Overwhealming Sepsis pneumonosepsis

• 4 L of fluid, still 80/30

  • where is the problem? what should be done to help the issue?
A

pneumonia causes a lot of edema/obstruction in the lungs. the afterload is decreased because of the leaky lungs. need to increase SVR.

Afterload can be helped by norepinephrine.????

21
Q

dobutamine is a ___ receptor agonist. It is weak with B2 and A activity. it ___ contractility, and thus ___ CO.

A

β-1 receptor agonist, weak β-2 and minimal α activity.
• Increased contractility = CO ↑

Vasodilation: – β-2 activation – Reflex vasodilation due to increased CO

22
Q

typical uses of dobutamine

A
  • cardiogenic shock
  • decompensated distributive shock
23
Q
A
24
Q

outline the dosages of epinephrine during acrdiac arrset, anaphylaxis, or status asthmaticus.

A

watch the dosages in terms of concentration!!!

25
Q
A
26
Q

where is the problem and what si going on? what should we do?

A

he has decompensated heart dailure. ventrile is crappy because of the chronic hypertorophy. it was working hard to compensate, but now the ventricel is crapping out and probalby cant contract well anymore.

  • afterload– high.
  • contractility is too high,

A1 stimulation would not help. would increase SVR. would increase after load

Beta 1- would help. increase the contractility.

Beta 2= decrease SVR

Would help with DOBUTAMINE INJECTION