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Cardiotonics Flashcards

1
Q

What is the formula for cardiac output?

A

CO= HR x SV

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2
Q

Define inotrope

A

Drugs that improve contractility of the heart.

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3
Q

Define chronotrope.

A

Drugs that change the heart rate

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4
Q

Define Dromotrope.

A

Drugs that change the conduction velocity.

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5
Q

What is the difference between systole, diastole, and mean arterial pressure?

A

Systole is the peak pressure, diastole is the baseline pressure, and MAP is the average of the two.

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6
Q

What is afterload?

A

The force that the heart has to contract against.

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7
Q

What is preload?

A

The stretch of the cardiac muscle prior to contraction (main component of stroke volume).

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8
Q

What is the systemic vascular resistance and how does it affect CO?

A

It is a measure of the vascular tone (constriction of the vessels) and it tells us how much resistance the heart has to push against.

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9
Q

What are the coronary arteries fed by?

A

They exit from the base of the aorta.

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10
Q

What is the sympathetic control center?

A

The medulla oblongata

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11
Q

What does sympathetic innervation of the heart cause?

A

Vasoconstriction of the arterial system and increase of heart rate, contractility, and conduction velocity.

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12
Q

Where does parasympathetic innervation of the heart come from?

A

The vagus nerve

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13
Q

What does parasympathetic innervation of the heart do?

A

Causes a decrease in heart rate.

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14
Q

Where are the baroreceptors of the heart located?

A

Aortic arch and carotid sinus

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15
Q

What are the sympathetic receptors and what do they do?

A

a1: vasoconstriction
b1: increase HR and contractility
b2: bronchodilation but also minor vascular dilation

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16
Q

What is the first step in treating hypotension?

A

Giving fluid to increase the circulating volume.

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17
Q

What are the three endogenous catecholamines?

A

dopamine, norepinephrine (levophed), and epinephrine (adrenaline)

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18
Q

What does epinephrine stimulate?

A

a1: vasoconstriction and increase BP
b1: increases HR and myocardial contraction
b2: bronchodilation and vasodilation (but net vasoconstriction because of a1 effect)

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19
Q

_______ or leave em dead

A

Levophed (norepi)

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20
Q

What is norepi used for?

A

Hypotension, cardiogenic shock, and septic shock.

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21
Q

What happens in peripheries when norepi is given?

A

It is a profound vasoconstrictor, so extremities can lose perfusion, as well as kidneys and GI.

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22
Q

What does norepi do?

A

Increases BP by increasing preload and afterload, but at high levels the increase in afterload can cause decreased CO.

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23
Q

When should you not give norepi?

A

When pt is on MAO inhibitors

24
Q

What is the generic name for Neo-synephrine?

A

Phenylephrine

25
What does phenylephrine do?
Potent a1 stimulator, causes vasoconstriction; may cause reflex bradycardia. Also used in OTC cold medicine.
26
What is dopamine used for in the ICU?
Vasopressor and inotrope (increases vasoconstriction and heart contractility)j
27
What is dopamine used IV for?
Hypotension, cardiogenic or septic shock, any other situation resulting in poor cardiac output.
28
What is dobutamine?
A synthetic catecholamine (trade name dobutrex)
29
What receptor does dobutamine stimulate?
Inotropic effect on a1, b1, and b2 (increases contractility of heart).
30
What is milrinone?
Phosphodiesterase inhibitor
31
How do phosphodiesterase inhibitors work?
Phosphodiesterase removes P from cAMP to inactivate it. When we block its action it increases the contractility of the heart and improves CO.
32
What effect does milrinone have?
Increases contractility and causes vasodilation (decreasing preload and afterload).
33
What are some issues with milrinone?
It is controversial as a solo therapy drug, may decrease preload too much (dropping CO), and may cause arrhythmias.
34
What is vasopressin?
Anti-diuretic hormone; a naturally occurring hormone released by the pituitary gland.
35
When is ADH released?
When the body senses a decrease in the circulating volume.
36
What does ADH do?
Increases reabsorption of water in the kidneys and causes peripheral vasoconstriction.
37
What is ADH used for clinically?
Heart failure, septic shock, and diabetes insipidus.
38
Where does Atropine work?
On the autonomic nervous system by blocking the cholinergic branch as a competitive antagonist.
39
What does atropine do?
Blocks vagal stimulation to the SA and AV node to increase HR (positive chronotrope).
40
When is atropine used?
Bradycardia, asytole, or PEA (resets heart). May also be used during intubation if vagal nerve stimulation is a concern.
41
What are the two main ER/ICU drugs used to treat acute hypertension.
Nitro and Nipride
42
What are the main effects of nitro?
Systemic vasodilation and coronary artery dilation.
43
How does nitro work?
Converted to nitric oxide in vasculature which increases cGMP, decreasing intracellular calcium and reducing smooth muscle contraction.
44
What is nitro used for?
acute hypertension, MI, ischemic heart failure, and angina. Increases blood flow to heart while decreasing resistance the heart has to push against.
45
How is nitro delivered?
transdermally, sublingual, oral spray, extended release pills, and then IV for acute episodes in hospital.
46
What does Sodium nitroprusside do?
Potent and profound vasodilator. Used for rapid reduction of acutely elevated BP.
47
How does sodium nitroprusside work?
SNP binds to oxyhemoglobin and creates nitric oxide. Vasodilation occurs via same pathway as NO. Causes smooth muscle relaxation.
48
What are the three ways we can treat chronic hypertension?
Lower circulating volume, lower force of cardiac contraction, and dilate vessels.
49
Describe the renin-angiotensin pathway.
When bloodflow to the kidneys is decreased it releases renin into the bloodstream. Angiotensinogen is released by the liver and then converted to angiotensin I by renin. Angiotensin I is converted to angiotensin II by ACE. Angiotensin II binds to receptors in the vasculature and in the endocrine system. Overall causes vasoconstriction and decrease in urine production.
50
What stimulates the release of aldosterone and what is the end result?
Angiotensin stimulates the release and aldosterone causes a reabsorption of fluid in the loop on Henle, decreasing urine output.
51
How does the renin-angiotensin system increase blood pressure?
By increasing vasoconstriction and increasing intravascular volume.
52
How do ACE inhibitors reduce blood pressure?
They interrupt the renin-angiotensin system to prevent vasoconstriction and fluid retention.
53
What are ACE inhibitors usually combined with and why?
Neprilysin inhibitors because neprilysin is an enzyme that reverses some of our natural vasodilator and diuretic activity (the two inhibitors work together to lower BP)
54
What are the two ACE inhibitors we use?
Captopril and Ramipril
55
What is a notable side effect of ACE inhibitors?
A persistent cough (ACE is active in the lungs)

Pharmacology (10 decks)

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