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N929 - Anesthesia Pharmacology > CV Drugs III > Flashcards

CV Drugs III Flashcards

(94 cards)

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1
Q

Nitric oxide

A
  • endogenous gas messenger

- lipophilic, highly reactive, labile free radical

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2
Q

NO formation

A

from L-arginine with NOS (nitric oxide synthase enzyme)

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3
Q

NO elimination

A

oxidation to form either nitrate or nitrite; nitrosylation of hemoglobin

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4
Q

NO half-life

A

a few seconds

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5
Q

NO Protective biological roles

A
  • NT
  • immune cytotoxicity
  • inhibit platelet aggregation
  • cyto-protection
  • vasodilator, smooth muscle relaxation
  • decreased cell adhesion, proliferation
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6
Q

NO pathogenic biological roles

A
  • neuronal injury (NMDA)
  • cell proliferation
  • shock, hypotension,
  • inflammation, tissue injury
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7
Q

NO Donor Drugs

A
  • Organic Nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
  • sodium nitroprusside
  • amyl nitrite
  • nitric oxide gas
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8
Q

Sodium nitroprusside structure

A

complex of 1 iron, 5 cyanide, and 1 NO group

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9
Q

sodium nitroprusside MOA

A
  • spontaneous breakdown to NO and cyanide
  • NO release resulting in activation of guanylyl cyclase in vascular smooth muscle, formation of cGMP, VSMC relaxation and vasodilation
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10
Q

sodium nitroprusside PK/PD

A
  • metabolism – cyanide combines with sulfur groups  thiocyanate
  • renal excretion; but some exhaled in air or excreted in feces
  • onset < 2 min
  • DOA 1-10 min
  • half-life ~2 min
  • half-life thiocyanate 2-7 days (increased with impaired renal fxn)
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11
Q

sodium nitroprusside administration parameters

A
  • IV infusion via pump
  • dilute in 5% dextrose
  • shortest infusion possible to avoid toxicity, if reduction in BP not obtained within 10 min, d/c
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12
Q

sodium nitroprusside clinical uses

A
  • HTN crisis – BP reduction to prevent/limit target organ damage
  • controlled hypotension during surgery – to reduce bleeding when indicated
  • CHF (acute, decompensated)
  • acute MI – improve CO; limited use due to coronary steal effect
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13
Q

sodium nitroprusside effects

A

CV:
-decreased arterial/venous pressure
-decreased PVR
-decreased afterload (in HF or acute MI – CO may increase due to decreased afterload)
-slight increased HR
Renal – vasodilation without significant change in GFR
CNS – increase CBF and ICP
Blood – inhibits plt aggregation
-Stability – unstable, light and temp sensitive; protect from light and store at 20-25 C; deterioration = blue color

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14
Q

sodium nitroprusside adverse effects

A
  • profound hypotension (potential for impaired organ perfusion)
  • cyanide toxicity
  • methemoglobinemia
  • thiocyanate accumulation
  • renal – transient increased serum Cr
  • others – increased ICP, nausea, HA, restlessness, flushing, dizziness, palpitation
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15
Q

Cyanide toxicity

A

often dose/duration dependent, but may occur at recommended dose; tissue anoxia; venous hyperoxemia (tissues can’t extract oxygen); lactic acidosis; confusion; death

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16
Q

methemoglobinemia

A

iron becomes ferric (3+) and has reduced O2 affinity; decreased O2 to tissues; symptomatic metHb>10%; reversal = methylene blue

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17
Q

Thiocyanate accumulation

A

increased with prolonged infusion and renal impairment; neurotoxicity (tinnitus, miosis, hyperreflexia); hypothyroid d/t impaired iodine uptake

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18
Q

Sodium Nitroprusside drug interactions

A
  • hypotensive drugs (negative inotropes, general anesthetics, circulatory depressants)
  • PDE 5 inhibitors
  • soluble guanylate cyclase stimulators
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19
Q

organic nitrates

A
  • nitroglycerin
  • isosorbide dinitrate
  • isosorbide mononitrate
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20
Q

nitroglycerin MOA

A
  • NO release through cellular metabolism – glutathione dependent pathway
  • requires thiols
  • NO release resulting in activation of guanylyl cyclase in vascular smooth muscle, formation of cGMP, VSMC relaxation and vasodilation
  • PRIMARY ACTION – at venous capacitance vessels; venodilation –> decreased VR –> decreased RVEDP and LVEDP –> decreased MVO2
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21
Q

nitroglycerin PK/PD

A
  • large first pass (90%) after oral admin
  • metabolized in liver –> denitrated by glutathione-organic nitrate reductase to glyceryl dinitrate and then mononitrate
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22
Q

nitroglycerin administration notes

A

Route – IV, SL, translingual spray, transdermal ointment

-tolerance after 8-10 hours; diminishing effectiveness –> have to have an off period

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23
Q

nitroglycerin clinical uses

A
  • angina – acute (sublingual) and prevention (longer acting oral, transdermal, or ointment)
  • HTN – peri or postop; HTN emergencies
  • controlled hypotension
  • NSTEMI ACS
  • acute MI (limits damage)
  • HF, low output syndromes –> decreases preload and relieves pulmonary edema
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24
Q

nitroglycerin effects

A

CV:
-venous capacitance vessels – decreased preload and MVO2
-arteriolar resistance (mild) – modest decreased afterload and MVO2
-myocardial arteries – increased O2 supply
-no change in SVR
-decrease VR, and LVEDP/RVEDP
-decrease CO
-increase corrP to ischemic areas
Pulm – bronchial dilation; inhibit HPV
Other – smooth muscle relaxation in bronchi, GI tract; inhibit plt aggregation

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25
nitroglycerin adverse effects
CNS: -throbbing HA -increased ICP CV: -orthostatic hypotension, dizziness, syncope -reflex tachycardia (arterial barorecptors) -flushing -vasodilation, venous pooling, decreased CO Heme – methemoglobinemia (rare) Tolerance – limitation of use of nitrates
26
nitroglycerin cautions
volume depletion, hypotension, brady- or tachycardia, constrictive pericarditis, AS, MS, inferior wall MI, RV involvement
27
nitroglycerin drug interactions
- antihypertensive drugs - selective PDE-5 inhibitor drugs - guanylate cyclase stimulating drugs
28
nitroglycerin and PDE-5 inhibitors
- absolute contraindication - will get profound potentiation - possible life-threatening hypotension and/or hemodynamic compromise - accumulation of cGMP by inhibiting its breakdown
29
isosorbide mononitrate or dinitrate PK/PD
- well absorbed orally from GI tract - DOA 6 hrs - dinitrate – metabolized to mononitrate (active) - mononitrate – metabolized to isosorbide to sorbitol (inactive)
30
isosorbide mononitrate or dinitrate administration
- regular and extended release forms | - need nitrate-free period to prevent tolerance
31
isosorbide mononitrate or dinitrate clinical uses
- prophylaxis of angina | - HF in Black patients combined with hydralazine
32
isosorbide mononitrate or dinitrate considerations
-avoid concomitant use with PDE5 inhibitor drugs
33
Phosphodiesterase enzymes
- family of enzymes that breakdown cyclic nucleotides - regulate intracellular levels of 2nd messengers (cAMP and cGMP) - 11 subfamilies - inhibitors - boost levels of cyclic nucleotides by preventing their breakdown
34
older non-selective drugs that inhibit PDE
caffeine | theophylline
35
PDE3
- broad distribution that includes heart and VSMC - substrates include cAMP, cGMP - function has to do with cardiac contractility and platelet aggregation
36
PDE 3 inhibitor drugs
amirone, milrinone, cilastazol
37
PDE 3 inhibitor clinical use #1
- positive inotrope (increase force of contraction) - peripheral vasodilator - limited for acute HF - milrinone, amirone
38
PDE 3 inhibitor clinical use #2
- intermittent claudication | - cilastazol
39
PDE4
- broad distribution including CV, neural, and immune/inflammatory - substrate includes cAMP - immune, inflammatory function
40
PDE4 inhibitor clinical use/drugs
- COPD - decrease inflammation, decrease remodeling | - roflumilast
41
PDE5
- broad distribution in VSMC especially erectile tissue, retina, lungs - substrate is cGMP - causes vascular smooth muscle relaxation, especially erectile tissue and lung
42
PDE5 inhibitor clinical uses
- erectile dysfunction | - pulmonary hypertension
43
PDE5 inhibitor drugs
- sildenafil - tadalafil - vardenafil
44
milrinone class
PDE 3 inihibitor
45
milrinone MOA
inhibit breakdown of cAMP
46
milrinone PK/PD
- onset (IV) 5-15 min - half-life ~3-6 hrs - majority not metabolized - renally excreted >80% unchanged
47
milrinone clinical uses
- acute HF or severe chronic HF - cardiogenic shock - heart transplant bridge or post-op
48
milrinone effects
- inotropic, increase cardiac contractility - vasodilation - little chronotropic activity
49
milrinone adverse effects
- arrhythmias | - hypotension
50
Key components of RAAS
- renin - angiotensin I - ACE (kinase II) - angiotensin II - aldosterone
51
Goal of RAAS
maintain tissue perfusion through increase in extracellular fluid volume
52
renin
- formed/secreted from JG cells - release stimulated by decreased BP or Na+ load, beta 1 receptor activation - protease - cleaves angiotensinogen to form ANGI
53
angiotensin I
inert, inactive form of ANGII
54
ACE (Kinase II)
- broad protease action --> forms ANGII from ANGI - metabolism of bradykinin to inactive form - located in membrane of EC cells
55
angiotensin II
- vasoconstriction (AT1 receptor) - aldosterone secretion (AT1 receptor) - other - increase ADH, increase proximal tubule Na reabsorption
56
aldosterone
- steroid formed in adrenal cortex - regulates gene expression, increases Na+ reabsorption - H2O retained - K+ excreted
57
angiotensin II receptors
- GPCR - subtypes are AT1R and AT2R - current antagonist drugs block AT1R
58
normal functions of AT1 Receptor
- regulate BP - regulate body fluid balance - vasoconstriction - inflammation - platelet aggregation/adhesion - reactive oxygen species - proliferative - hypertrophy - fibrosis
59
ACE inhibitor drugs
-Captopril -Enalapril -Lisinopril (ends in pril)
60
ACE inhibitor MOA
- decreases ANGII by preventing conversion of ANGI to ANGII - prevent vasoconstriction - prevent aldosterone secretion, decreasing sodium and water retention - increases bradykinin by inhibiting the breakdown
61
ACE inhibitor PK/PD
- many are prodrugs | - usually renal metabolism and elimination
62
ACE inhibitor clinical uses
- HTN - CHF - mitral regurgitation - post MI - more effective in DM for diabetic nephropathy - delay progression of renal disease
63
ACE inhibitor clinical effects
- decreased ANGII --> vasodilation, decreased remodeling, decreased aldosterone, (less Na/H2O retention, increased K+), decreased SNS output, increased natriuresis - increased BKN --> vasodilation, cough, angioedema - decreased BP, PVR - decreased preload, afterload - decreased cardiac workload - no reflex tachycardia - improve/prevent LV hypertrophy and remodeling - improved morbidity/mortality in HF - delays progression of diabetic nephropathy (improves renal hemodynamics)
64
ACE inhibitor adverse effects
- CV – hypotensive symptoms, syncope; 1st dose effect - electrolyte – hyperkalemia; caution with K+ sparing diuretics or supplements - renal – decreased GFR, increased BUN/Cr; renal dysfunction; contraindicated in bilateral renal artery stenosis - inflammatory – dry cough (r/t BKN, reversible), angioedema (r/t BKN) - fetal development – teratogenic; contraindicated in pregnancy bc can cause fetal anuria, RF, skull hypoplasia, death
65
ACE inhibitor surgical considerations
potential for prolonged hypotension, hold DOS
66
Captopril duration of BP lowering effects
~6 hours
67
Enalapril duration of BP lowering effects
12-24 hours
68
Lisinopril duration of BP lowering effects
24 hours
69
Angiotensin Receptor Blocker (ARB) Drugs
Losartan | ends in sartan
70
Angiotensin Receptor Blocker (ARB) MOA
- competitive antagonist at AT1 receptor - blocks effects of ANGII mediated by AT1 receptor - does not block breakdown of BKN, so no accumulation of BKN
71
Angiotensin Receptor Blocker (ARB) PK/PD
- varies | - metabolized in liver by CYP450
72
Angiotensin Receptor Blocker (ARB) clinical uses
uses similar to ACEi
73
Angiotensin Receptor Blocker (ARB) effects/considerations
- adverse effects similar to ACEi - less incidence of cough/angioedema because no buildup of BKN - contraindication --> renal artery stenosis, pregnancy - more tolerable than ACEi
74
Differences between ACEi and ARB?
- efficacy in HTN - ARBs slightly more tolerable, less likely to be d/c (main reason for d/c would be dry cough) - ACEi - higher quality of data; ARBs don't have a comparison vs placebo
75
Aldosterone Antagonist Drugs
Spironolactone | Eplerenone
76
Aldosterone Antagonist MOA
- competitive antagonist at mineralocorticoid receptor (kidney, heart, blood vessels, brain) - prevent nuclear translocation of receptor - block transcription of genes coding for Na+ Ch
77
Aldosterone Antagonist PK/PD
- Spironolactone = hepatic metabolism; active metabolites; P-gp inhibitor - eplerenone = CYP3A4
78
Aldosterone Antagonist clinical uses
- HTN, HF - K+ sparing diuresis - primary hyperaldosteronism - off label --> acne, hirsutism, PCOS
79
Aldosterone Antagonist effects
increased Na+/H2O excretion (mild diuresis); increased K+ reabsorption
80
Aldosterone Antagonist adverse effects
hyperkalemia; spironolactone has broad effects
81
Aldosterone Antagonist drug interactions
- other K+ sparing - K+ supplements - NSAIDs (increased renal risks) - eplerenone - CYP3A4 inhibitors
82
Direct Arterial Vasodilators
- hydralazine | - minoxidil
83
hydralazine MOA
- release of NO from endothelial cells | - potential inhibition of calcium release from SR
84
hydralazine PK/PD
- extensive first pass - bioavail ~25% - half-life 1.5-3 hrs
85
hydralazine clinical uses
- HTN (in combo with beta blocker and diuretic to limit SNS effects) - HF (reduced EF)
86
hydralazine effects
vasodilates arterioles, minimal venous effect, decreased SVR, DBP reduced > SBP, increased HR/SV/CO
87
hydralazine adverse effects
HA, nausea, palpitations, sweating, flushing, reflex tachy, tolerance/tachyphylaxis, Na/H2O retention, angina with EKG changes, lupus (reversible)
88
hydralazine contraindications
CAD, mitral valve RH disease
89
minoxidil MOA
- direct relaxation of arteriolar smooth muscle, little effect on venous capacitance - increases efflux of K+ form VSMC resulting in hyperpolarization and vasodilation
90
minoxidil PK/PD
- 90% oral dose absorbed from GI tract - peak 2-3 hrs - half-life ~ 4 hrs - 10% drug recovered unchanged in urine
91
minoxidil clinical uses
HTN (limited to later line)
92
minoxidil effects
vasodilation of arterioles, not veins
93
minoxidil adverse effects
tachycardia, increased MVO2, palpitations, angina, sodium/fluid retention, edema, weight gain, hypertrichosis
94
minoxidil warnings
fluid retention, pericardial effusion or tamponade, sinus tahcy, rapid BP response, elderly

N929 - Anesthesia Pharmacology (12 decks)

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