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Anesthesia > Vasopressors > Flashcards

Vasopressors Flashcards

1
Q

Alpha 1 receptor mechanism and effects

A
  • G protein dependent increases in intracellular calcium (through phosphatidyl inositol)
  • densely found on smooth muscle
  • vasoconstriction, mydriasis, bronchoconstriction, sphincter contraction, uterine contraction
  • insulin and lipolysis is inhibited (anabolic effects inhibited)
  • mild positive inotropy (effects easily overshadowed by pronounced vasoconstriction, because receptors in myocardium much less densely populated)
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2
Q

Epinephrine vs norepinephrine

A
  • only epi has beta-2 receptor agonism
  • epi given for bronchospasm, not norepi
  • epi vasoconstricts (alpha-1) and vasodilates (beta-2) leading to more pronounced increases in SBP and minimal changes in DBP; whereas norepi has pronounced effect on both SBP and DBP (no beta-2 activity)
  • MAP more dependent on DBP (2/3 DBP + 1/3 SBP) so for an equal increase in MAP, epi causes a huge increase in SBP (and small increase in DBP) while norepi can produce the same MAP at a lower SBP
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3
Q

Norepinephrine and epinephrine effect on HR

A
  • norepinephrine- pronounced SVR and subsequent baroreceptor mediated bradycardia is offset by beta-1 chronotropic effects, leading to minimal changes in heart rate
  • epinephrine- pronounced effects on HR, and thus increase in CO
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4
Q

Best vasopressor to preserve renal function in sepsis

A

Norepinephrine- best evidence to maintain UOP and preserve kidney function

  • raises BP while preserving CO
  • in healthy patients, norepi decreases renal perfusion through vasoconstriction
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5
Q

Best vasopressor in patient with coexisting cardiogenic and septic shock

A

Norepinephrine + dobutamine

  • Septic shock- low SVR state, so increasing SVR and DBP (for pressure dependent perfusion) with norepi ideal
  • Cardiogenic shock- low contractility, so increasing CO with dobutamine is ideal
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6
Q

Surviving Sepsis vasopressor guidelines

A
  1. If hypotensive, use norepinephrine
    - Second line treatments for hypotension are epinephrine or vasopressin
  2. If cardiac performance compromised, add an inotrope (dobutamine)
  3. Consider dopamine under “special” circumstances only
    * never use dopamine for renal protection
  4. Phenylephrine reserved for refractory cases
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7
Q

Primary advantage of norepinephrine gtt compared to dopamine gtt

A

Norepi is associated with a lower rate of arrhythmias, especially high grade tachyarrhythmias (eg. a fib)

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8
Q

Catecholamine metabolism (hepatic v neural)

A
  • Liver: COMT then MAO (“Liver contains
  • Nerve endings: MAO then COMT
  • Final product in both: VMA
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9
Q

Dopamine doses and effects

A

2 mcg/kg/min: significant DA1 agonism (renal artery dilation) and relatively weak effects at other adrenergic receptors
-overall effect is minimal increase in HR and contractility and significant diuresis (increased UOP but no improvement in renal protection)

5 mcg/kg/min: beta > alpha effects (increased HR, contractility, vasodilation) leading to increased CO
-unfortunately, myocardial oxygen demand outpaces oxygen delivery (set up for non-STEMIs)

10 mcg/kg/min: alpha-1 effects predominate (increased SVR)
-renal blood flow decreases

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10
Q

Dopamine doses and effects

A

2 mcg/kg/min: significant DA1 agonism (renal artery dilation) and relatively weak effects at other adrenergic receptors
-overall effect is minimal increase in HR and contractility and significant diuresis (increased UOP but no improvement in renal protection)

5 mcg/kg/min: beta > alpha effects (increased HR, contractility, vasodilation) leading to increased CO
-unfortunately, myocardial oxygen demand outpaces oxygen delivery (set up for non-STEMIs)

10 mcg/kg/min: alpha-1 effects predominate (increased SVR)
-renal blood flow decreases

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11
Q

Mechanism and effects of dopexamine

A
  • B2»>B1 effects as well as potent DA agonism
  • think of as inverted dobutamine
  • used to increase CO in setting of CHF: strong beta 2 effects reduces afterload and weak beta 1 increases contractility and SV
  • however, since beta-2 (vasodilatory) effects are pronounced, BP will significantly decrease
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12
Q

Dobutamine MOA

A
  • racemic mixture: one enantiomer has beta 1»>beta 2, the other has alpha-1 agonism
  • overall effect is strong beta 1 effects and minimal reduction in SVR (nearly equal beta-2 and alpha-1)
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13
Q

Isoproterenol MOA

A

Beta-1 roughly equals beta-2

*“chemical pacemaker”

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14
Q

Dromotropy

A

Conduction speed of electrical impulses within the heart

  • primarily a result of AV node, as conduction through the his-purkinje system is far less variable
  • beta-1 agonism leads to increased dromotropy
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15
Q

Lusitropy

A

Definition: active process of myocardial relaxation in diastole

  • calcium increases isotropy (contractility) but decreases lusitropy
  • beta-1 agonism increases both isotropy (increasing calcium in myocyte during systole) and lusitropy (increasing rate of calcium uptake into SR during diastole)
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16
Q

SERCA

A

Sarco-endoplasmatic reticulum calcium ATPase

  • regulates uptake of calcium into the SR
  • impaired SERCA is a part of diastolic function (impaired lusitropy)
17
Q

Ephedrine MOA

A

Increased post-synaptic NE release and/or decreased NE reuptake

18
Q

Ephedrine MOA

A

Increased post-synaptic NE release and/or decreased NE reuptake

19
Q

Adrenergic receptor effect

A

Beta: G-protein (Gs) mediated stimulation of adenylate cyclase which converts ATP to cAMP, leading to increased intracellular calcium concentrations
Alpha-1: G-protein mediated stimulation of phospholipase C which splits phosphatidyl inositol into IP-3 and 1,2-DAG, leading to release of calcium from the SR

20
Q

Adrenergic receptor effect

A

Beta: G-protein (Gs) mediated stimulation of adenylate cyclase which converts ATP to cAMP, which activates PKA, which acts at the SR, leading to increased intracellular calcium concentrations
Alpha-1: G-protein mediated stimulation of phospholipase C which splits phosphatidyl inositol into IP-3 and 1,2-DAG, leading to release of calcium from the SR

21
Q

Calcium mediated contraction

A

Calcium released from SR binds to troponin, allowing actin/myosin mediated contraction

22
Q

Milrinone MOA and effects

A
  • Selective inhibition of PDE3, resulting in increased intracellular cAMP
  • increased isotropy (contractility), increased lusitropy (relaxation), increased chronotropy (HR), and significant arterial AND venous vasodilation (decreasing afterload AND preload)
23
Q

Fenoldopam MOA and effects

A
  • Pure DA1 agonist

- systemic vasodilation and increased renal blood flow

24
Q

Fenoldopam MOA and effects

A
  • Pure DA1 agonist

- systemic vasodilation and increased renal blood flow

25
Q

Nitric Oxide MOA, effects, metabolism, side effect

A
  • stimulates guanylate cyclase leading to increased cGMP levels, causing smooth muscle relaxation and vasodilation
  • broken down by PDE5 (inhibited by sildenafil)
  • inhaled NO: only active at vasculature near alveoli, increasing perfusion to well ventilated alveoli, decreasing V/Q mismatch
  • methhemoglobinemia (NO binds to heme moiety in hemoglobin)
26
Q

Nesiritde MOA, effects, indications

A
  • recombinant BNP- leads to stimulation of guanylate cyclase–>cGMP–>vasodilation
  • indicated as part of treatment in severe decompensated CHF for afterload reduction and improved forward flow
27
Q

SVR equation

A

SVR = (MAP-CVP)/CO *80

28
Q

PVR equation

A

PVR = (PAP-wedge)/CO *80

29
Q

Phentolamine MOA

A

Alpha blocker (both alpha-1 and alpha-2)

30
Q

Sodium nitroprusside MOA and two major side effects

A
  • nitrate that acts by a series of steps, first by entering RBCs, then accepting an electron from the 2+ ferrous oxy-Hb and oxidizes it to a +3 Met-Hb
  • heme in Hb has an iron atom which can have more electrons (Fe 2+) or less electrons (Fe 3+); oxygen only likes heme with more electrons, giving it a lower charge (+2) also known as ferrous state
  • when nitroprusside is exposed to ferrous (2+) hb, it takes an electron away, leaving iron in the ferric (3+) state, which is called met-Hb (ferr-IC state is ICky oxygen)
  • nitroprusside becomes unstable with the additional electron and breaks info five cyanide molecules (CN-) and nitric oxide
  • CN- binds one of three things: met-Hb (cyanmet-Hb), cytochrome oxidase (part of electron transport chain), or thiosulfate (thiocyanate- cleared by kidney)
31
Q

Sodium nitroprusside MOA and two major side effects

A
  • nitrate that acts by a series of steps, first by entering RBCs, then accepting an electron from the 2+ ferrous oxy-Hb and oxidizes it to a +3 Met-Hb
  • heme in Hb has an iron atom which can have more electrons (Fe 2+) or less electrons (Fe 3+); oxygen only likes heme with more electrons, giving it a lower charge (+2) also known as ferrous state
  • when nitroprusside is exposed to ferrous (2+) hb, it takes an electron away, leaving iron in the ferric (3+) state, which is called met-Hb (ferr-IC state is ICky oxygen)
  • nitroprusside becomes unstable with the additional electron and breaks info five cyanide molecules (CN-) and nitric oxide
  • CN- binds one of three things: met-Hb (cyanmet-Hb), cytochrome oxidase (part of electron transport chain), or thiosulfate (thiocyanate- cleared by kidney)
32
Q

Cyanide toxicity

  • cause and mechanism
  • treatment
A

Cause: nitroprusside

  • free CN- can bind to three things, with cytochrome oxidase being the most dangerous (ETC shuts down–>ATP not produced–>only anaerobic metabolism–>lactic acidosis)
  • inability of mitochondria to utilize oxygen resluts in decreased oxygen consumption and elevated mixed venous pO2

Treatment: increase other sinks of CN-

  • sodium nitrite- increases levels of methemoglobin (met-Hb) which acts as a sink for CN- by the production of cyan met-Hb
  • high levels of cyanmet-Hb leads to hypoxia, and is treated with methylene blue
  • sodium thiosulfate- binds with CN- to form thiocyanate (which is moderately toxic but slowly excreted by kidneys)
  • 100% and discontinuation of nitroprusside
33
Q

Nitroprusside effects on lungs and in ARDS

A

-vasodilates pulmonary vasculature and can counteract hypoxic pulmonary vasoconstriction (HPV), thereby increasing blood flow to poorly oxygenated alveoli (shunt)

34
Q

Cause of rebound HTN following sodium nitroprusside

A

Increased catecholamines

-during nipride treatment, there is increased catechol and renin-angiotensin release

35
Q

Nitroglycerin (NTG) MOA, function, and side effects

A
  • improves myocardial oxygen delivery to consumption ratio through multiple mechanisms
  • most important is through decreased preload (decreased LVEDP and wall tension)
  • in setting of ischemia, non-stenosed coronaries are maximally dilated, so NTG helps to redistribute blood flow to the subendocardium (where ischemia typically first presents during oxygen delivery/consumption mismatch)
36
Q

Venodilation versus arterial dilation with NTG, SNP and Nicardipine

A

NTG>SNP>nicardipine

  • NTG: primarily venodilator–>significant decreases in preload and small decreases in afterload
  • SNP: potently dilates both A and V–>significant reductions in afterload and preload (hypotension accounted for mostly by preload though)
  • Nicardipine: nearly exclusively dilates arterial bed (like hydralazine)
37
Q

Drug of choice in malignant hypertension and cerebral hemorrhage

A

Nicardipine- easily titrated, no metabolite concerns (like SNP), no tachyphylaxis (like SNP), and just as effective as SNP

Anesthesia (16 decks)

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