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Pharm II > Vasopressors/inotropes > Flashcards

Vasopressors/inotropes Flashcards

1
Q

CO=

A

HRxSV

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2
Q

Positive chronotropy

A

Increased heart rate

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3
Q

Negative chronotropy

A

Decreased heart rate

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4
Q

Dromotropy

A

Related to velocity of conduction (degree of delay in AV node)

Positive-increased speed of conduction
Negative-decreased speed of conduction

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5
Q

Inotropy

A

Strength of contraction

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6
Q

Preload

A

LV End diastolic volume just prior to contraction

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7
Q

Factors that impact preload

A

Changes in SVR
Intravascular volume
Sympathetic outflow
Skeletal muscle contraction- enhances venous return

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8
Q

Lusitropy

A

Rate of myocardial relaxation- impacts diastolic filling of LV

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9
Q

After load

A

Force opposing LV contraction

-tension or stress of LV wall during systole- not synonymous with SVR

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10
Q

Law of Laplace

A

-after load directly related to intraventricular pressure/size
-after load inversely related to wall thickness
-Thus, after load will vary continuously during systole

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11
Q

Variables impacting afterload

A

SVR

LV hypertrophy

LVEDP

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12
Q

Sympathomimetic

A

Drugs that mimic or modify actions of sympathetic nervous system via stimulation of alpha or beta adrenergic receptors.

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13
Q

Catecholamines

A

Subset of sympathomimetics with -OH substitutions on benzene ring

Epi
Norepi
Isoproterenol
Dopamine
Dobutamine

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14
Q

Sympathomimetics that are not catecholamines

A

Ephedrine and phenylephrine

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15
Q

Common action of increased inotropy

A

Enhancement of Ca interaction with actin and myosin in cardiac myocytes

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16
Q

Beta-1 agonist mechanism

A

Elevated cAMP followed by activation of protein kinase A

Opening of Ca channels

Ca influx and improved inotropy

Improved lusitropy due to PKA mediated activation of ATPase leading to increased calcium uptake in diastole

17
Q

Phosphodiesterase Type III inhibitor

A

Milrinone

Inhibition of PDE III causes intra-cytosol cAMP increase

18
Q

Levosimendan

A

Calcium sensitizer- does NOT increase cytosol Ca

Binds cardiac troponin C and stabilizes Ca bound form of the protein- prolonging contraction

19
Q

Factor influencing duration of action vasopressors/inotropes

A

elimination instead of redistribution!

20
Q

Catecholamine metabolism

A

MAO & COMT

Sequential metabolism to VMA- vanillylmandelic acid

21
Q

Phenylephrine metabolism

A

MAO

22
Q

Ephedrine and milrinone metabolism

A

Eliminated largely unchanged via kidneys

23
Q

Vasopressin elimination

A

2/3 unchanged

1/3 vasopressinases metabolize in liver and kidneys

24
Q

Levosimendan metabolism

A

Duration of action could be up to a week after a 24hr infusion

Metabolites form slowly

Actual drug levels fall rapidly after stopping the infusion

25
Q

Digoxin elimination

A

Unchanged via kidneys

Half-life is 32-40 hours

26
Q

Drug interactions!

A

MAO inhibitors

TCAs

27
Q

Unintended consequence of Epi induced B2 stimulation

A

Transient hyperkalemia
-potassium follows glucose out of hepatic cells, eventually leads to hypokalemia

28
Q

Why don’t we see an increase in heart rate with B1 activity in norepi?

A

Increase in SVR induces reflex vagal activity… baroreceptor?

29
Q

Consequences of low dose Vaso infusion and 1 adverse effect!

A

Potent vaso constrictor, however it selectively dilates renal afferent, pulmonary and cerebral arterioles

Increases blood pressure, urine output and creatinine clearance.

Gastrointestinal ischemia

30
Q

Why is ephedrine longer acting than epinephrine?

A

Lack of catechol structure- resistant to metabolism by MAO

31
Q

Why does ephedrine stop working?

A

Tachyphylaxis may develop with subsequent dosing because catecholamine stores become depleted

32
Q

Conducted responses (definition)

A

Vascular smooth muscle induced at one level of circulation can be electrically propagated to others via conducted responses-modulated by gap junctions

33
Q

Comparison of VSM to cardiac muscle

A

VSM is more dependent on extracellular Ca, contracts more slowly, develops greater force, and can function over a wider range of length

34
Q

Modulation of VSM tone

A

Influx of Ca
Release of Ca from SR
Ca-CaM activation of myosin light chain kinase
Phosphorylation causes linking of actin/myosin

35
Q

What is not required in the contraction of VSM?

A

Depolarization
-simply requires entry of Ca into the cytoplasm

36
Q

Mechanisms of Vasodilation

A

Decreased entry of Ca

Outward conductance of K

Decreased release of Ca from SR

Enhanced uptake of Ca into SR

Decreased myofilament sensitivity to Ca

Pharm II (8 decks)

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