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Pharmacology > Cardiotonics > Flashcards

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
Q

What does phenylephrine do?

A

Potent a1 stimulator, causes vasoconstriction; may cause reflex bradycardia. Also used in OTC cold medicine.

26
Q

What is dopamine used for in the ICU?

A

Vasopressor and inotrope (increases vasoconstriction and heart contractility)j

27
Q

What is dopamine used IV for?

A

Hypotension, cardiogenic or septic shock, any other situation resulting in poor cardiac output.

28
Q

What is dobutamine?

A

A synthetic catecholamine (trade name dobutrex)

29
Q

What receptor does dobutamine stimulate?

A

Inotropic effect on a1, b1, and b2 (increases contractility of heart).

30
Q

What is milrinone?

A

Phosphodiesterase inhibitor

31
Q

How do phosphodiesterase inhibitors work?

A

Phosphodiesterase removes P from cAMP to inactivate it. When we block its action it increases the contractility of the heart and improves CO.

32
Q

What effect does milrinone have?

A

Increases contractility and causes vasodilation (decreasing preload and afterload).

33
Q

What are some issues with milrinone?

A

It is controversial as a solo therapy drug, may decrease preload too much (dropping CO), and may cause arrhythmias.

34
Q

What is vasopressin?

A

Anti-diuretic hormone; a naturally occurring hormone released by the pituitary gland.

35
Q

When is ADH released?

A

When the body senses a decrease in the circulating volume.

36
Q

What does ADH do?

A

Increases reabsorption of water in the kidneys and causes peripheral vasoconstriction.

37
Q

What is ADH used for clinically?

A

Heart failure, septic shock, and diabetes insipidus.

38
Q

Where does Atropine work?

A

On the autonomic nervous system by blocking the cholinergic branch as a competitive antagonist.

39
Q

What does atropine do?

A

Blocks vagal stimulation to the SA and AV node to increase HR (positive chronotrope).

40
Q

When is atropine used?

A

Bradycardia, asytole, or PEA (resets heart). May also be used during intubation if vagal nerve stimulation is a concern.

41
Q

What are the two main ER/ICU drugs used to treat acute hypertension.

A

Nitro and Nipride

42
Q

What are the main effects of nitro?

A

Systemic vasodilation and coronary artery dilation.

43
Q

How does nitro work?

A

Converted to nitric oxide in vasculature which increases cGMP, decreasing intracellular calcium and reducing smooth muscle contraction.

44
Q

What is nitro used for?

A

acute hypertension, MI, ischemic heart failure, and angina. Increases blood flow to heart while decreasing resistance the heart has to push against.

45
Q

How is nitro delivered?

A

transdermally, sublingual, oral spray, extended release pills, and then IV for acute episodes in hospital.

46
Q

What does Sodium nitroprusside do?

A

Potent and profound vasodilator. Used for rapid reduction of acutely elevated BP.

47
Q

How does sodium nitroprusside work?

A

SNP binds to oxyhemoglobin and creates nitric oxide. Vasodilation occurs via same pathway as NO. Causes smooth muscle relaxation.

48
Q

What are the three ways we can treat chronic hypertension?

A

Lower circulating volume, lower force of cardiac contraction, and dilate vessels.

49
Q

Describe the renin-angiotensin pathway.

A

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
Q

What stimulates the release of aldosterone and what is the end result?

A

Angiotensin stimulates the release and aldosterone causes a reabsorption of fluid in the loop on Henle, decreasing urine output.

51
Q

How does the renin-angiotensin system increase blood pressure?

A

By increasing vasoconstriction and increasing intravascular volume.

52
Q

How do ACE inhibitors reduce blood pressure?

A

They interrupt the renin-angiotensin system to prevent vasoconstriction and fluid retention.

53
Q

What are ACE inhibitors usually combined with and why?

A

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
Q

What are the two ACE inhibitors we use?

A

Captopril and Ramipril

55
Q

What is a notable side effect of ACE inhibitors?

A

A persistent cough (ACE is active in the lungs)

Pharmacology (10 decks)

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