Lecture 2-Antihypertensives, Negative Inotropes, Negative Chronotropes Flashcards
1
Q
This type of hypertension is related to overactivity of the ANS and an interaction with the renin-angiotensin system, along with factors related to sodium homeostasis and intravascular volume
A
Idiopathic hypertension
2
Q
Primary cause of perioperative hypertension is increased ___ (sympathetic/parasympathetic) discharge with systemic vaso___
A
Increased sympathetic discharge with systemic vasoconstriction
3
Q
Potential complications related to perioperative hypertension include CVA, MI, ischemia, LV dysfunction, arrhythmias, increased suture tension, hemorrhage, pulmonary edema, cognitive dysfunction—T/F?
A
True
4
Q
Vasodilators are classified according to their predominate effect on the circulation—arterial dilators reduce ___
A
Afterload
Most vasodilators are arterial vasodilators
5
Q
Vasodilators are classified according to their predominate effect on the circulation—venodilators reduce ___
A
Preload
6
Q
Vasodilators act primarily to cause systemic vasodilation—T/F?
A
True
7
Q
Pure arteriole dilators cause minimal effect on preload—T/F?
A
True—arteriole dilators affect afterload
8
Q
“Pure” venodilators are not available—T/F?
A
True—NTG acts primarily on the venous circulation but also affects arterioles
9
Q
Balanced vasodilators (i.e.: SNP) decrease afterload and preload—T/F?
A
True
10
Q
Hemodynamic effects of vasodilators—reflex increase in ___
A
Heart rate—baroreceptors pick up on vasodilation in the periphery, resulting in a reflex tachycardia
11
Q
Hemodynamic effects of vasodilators—redistribution of ___ blood flow; NTG may improve ___ circulation; other vasodilators may cause coronary ___
A
Coronary blood flow; NTG may improve collateral circulation; other vasodilators may cause coronary steal
12
Q
What is coronary steal?
A
Stealing blood flow away from ischemic areas, making coronary artery disease/ischemia even worse. Can occur with use of vasodilators
13
Q
70-90% of coronary artery perfusion to the LV occurs during ___ (systole/diastole)
A
Diastole
14
Q
Aortic ___ (systolic/diastolic) pressure governs perfusion
A
Aortic diastolic pressure
15
Q
In the presence of ischemic heart disease, collateral arteries are maximally dilated and coronary perfusion is largely pressure dependent—T/F?
A
True
16
Q
Beta blockers/calcium channel blockers reduce myocardial oxygen demand and improve myocardial oxygen use—T/F?
A
True
17
Q
What is this phenomenon?—narrowed coronary arteries are always maximally dilated to compensate for the decreased blood supply; dilating the other arterioles causes blood to be shunted away from the coronary vessels
A
Coronary steal
18
Q
Vasodilators and coronary perfusion pressure—in the myocardium, ___ (what vasodilator?) dilates both epicardial conductance and intramyocardial resistance vessels; in the presence of CAD, this vasodilator shunts blood away from ischemic zones
A
SNP—sodium nitroprusside
This increases coronary steal and makes ischemia even worse
19
Q
Vasodilators and coronary perfusion pressure—___ (what vasodilator?) preferentially dilates conductance vessels and directs more blood toward ischemic zones
A
NTG
20
Q
(3) vasodilator medications that we use:
A
- Hydralazine
- Nitroglycerine (NTG)
- Sodium nitroprusside (SNP)
21
Q
Hydralazine is a direct acting ___ (arterial/venous) vasodilator; it alters ___ metabolism and movement
A
Arterial vasodilator; it alters calcium metabolism and movement
22
Q
Hydralazine ___ (increases/decreases) HR, contractility, renin activity, fluid retention, CO, and SV
A
Increases
Reflex tachycardia results from drops in BP
Stimulates the RAAS system as pressures begin to drop, leading to increased renin activity/fluid retention
23
Q
Hydralazine ___ (increases/decreases) BP—it decreases ___ BP more than ___ BP; ___ (increases/decreases) SVR
A
Decreases BP—it decreases diastolic BP more than systolic BP; decreases SVR
24
Q
Hydralazine acts on a specific receptor—T/F?
A
False—does not act on a specific receptor
Hydralazine acts through a second messenger pathway with cyclic GMP as the second messenger protein; results in an increase in cyclic GMP which reduces afterload (arterial vasodilator)
25
Hydralazine ___ (increases/decreases) myocardial oxygen demand, leading to ischemia
Increases myocardial oxygen demand
26
Hydralazine should be avoided in patients with ___, increased ___, and ___...why?
CAD, increased ICP, and lupus
Avoid in CAD because Hydralazine can cause reflex tachycardia, resulting in ischemia
Avoid with increased ICP d/t fluid shifts (stimulates RAAS system, leading to increased renin/fluid retention)
Avoid in lupus—interesting side effect with lupus—will see positive ANA [antinuclear antibody] titers in 5-10% of patients treated with Hydralazine; patients won’t get butterfly rash or organ damage but will get arthralgias and painful components of lupus from hydralazine
27
Hydralazine CNS side effects—___ache, ___ness, ___ from increased ICP
Headache, dizziness, tremor from increased ICP
28
Hydralazine CV side effects—___tations, ___ina, ___cardia, ___ from vasodilation
Palpitations, angina, tachycardia, flushing from vasodilation
29
Hydralazine GI side effects—___xia, ___/___, ___ pain, paralytic ___
Anorexia, nausea/vomiting, abdominal pain, paralytic ileus
30
Hydralazine other side effects—___ia, ___osis, ___ congestion, muscle ___, ___ from activation of RAAS system
Anemia, agranulocytosis, nasal congestion, muscle cramps, edema from activation of RAAS system
31
Hydralazine pharmacokinetics—onset ___ mins (IV and PO); peak ___-___ mins (IV and PO); duration ___-___ hours (PO), ___-___ hours (IV); half life ___-___ hours (IV and PO); metabolized in ___, excreted by ___; highly ___ bound
Onset 30-60 mins (IV and PO); peak 30-60 mins (IV and PO); duration 4-6 hours (PO), 2-6 hours (IV); half life 3-7 hours (IV and PO); metabolized in liver, excreted by kidney; highly protein bound
32
Hydralazine is good for acute BP management—T/F?
False—not good for acute BP management because it takes ~30 mins to kick in, peak effect in 60 mins
Pros = lasts longer
Cons = tachycardia and fluid shifts
33
Nitroglycerine causes a release of ___ for ___ (specific/non-specific) relaxation of vascular smooth muscle
Causes a release of nitric oxide for non-specific relaxation of vascular smooth muscle
34
Nitroglycerine dilates ___ > ___
Veins > arteries
35
Nitroglycerine ___ (increases/decreases) PVR, venous return, and myocardial oxygen consumption
Decreases
Venous dilation = decreased venous return, reducing preload
Decreased venous return = pooling of blood/edema in lower extremities
36
Nitroglycerine relaxes ___ vessels and relieves ___ spasms
Relaxes coronary vessels and relieves coronary spasms
37
What is an advantage of using nitroglycerine?
It preferentially shifts blood flow to areas that need it—don’t have coronary steal like you do with SNP
38
NTG non-cardiac effects—dilates ___ vessels (caution in patients with increased ___); decreased ___ blood flow with decreased BP; dilates ___ vessels and reduces ___ vascular resistance
Dilates meningeal vessels (caution in patients with increased ICP); decreased renal blood flow with decreased BP; dilates pulmonary vessels and reduces pulmonary vascular resistance
39
Pharmacokinetics of NTG—onset ___ min; duration ___-___ min; half life ___-___ min
Onset 1 min; duration 3-5 min; half life 1-4 min
Much faster onset than hydralazine, much shorter duration
40
Nitroglycerine/SNP are good for acute BP management, unlike hydralazine—T/F?
True
41
Metabolism of NTG—metabolized by ___ in the ___
Glutathione nitrate reductase in the liver
42
Metabolism of NTG—nitrite ion oxidizes ___ to ___
Hemoglobin to methemoglobin
43
What is a risk of using nitroglycerin in patients at risk for developing anemia? (i.e.: patients with CKD or CLD)
If you have a patient at risk for developing anemia (i.e.: patients with CKD or CLD), the more the methemoglobin builds up from NTG metabolism into nitrite ions, the less O2 delivery and higher risk for ischemia
44
Tolerance with NTG—tolerance in ___ (arterial/venous) vessels can occur with chronic NTG administration
Tolerance in arterial vessels can occur with chronic NTG administration, but not in the venous vessels
45
Tachyphylaxis can occur with NTG over time—T/F?
True—can start to lose effect in arterial vessels
46
NTG CNS side effects—___ache, appre___, ___ vision, ___go, ___ness, ___ness
Headache, apprehension, blurred vision, vertigo, dizziness, faintness
47
NTG CV side effects—___ hypotension d/t vaso___ and ___ of blood in the periphery, ___tations, ___ (increased/decreased) heart rate, ___cope
Postural hypotension d/t vasodilation and pooling of blood in the periphery, palpitations, increased heart rate, syncope
48
NTG GI side effects—___/___, ___ pain, ___ mouth
Nausea/vomiting, abdominal pain, dry mouth
49
NTG other side effects—___hemoglobinemia, ___ from vasodilation, ___, ana___, ___ and ___ edema (potentially d/t fluid shifts)
Methemoglobinemia, flushing from vasodilation, rash, anaphylaxis, oral and conjunctival edema (potentially d/t fluid shifts)
50
Warnings/contraindications with NTG—___ inhibitors; ___ glaucoma; ___ trauma, cerebral ___; severe ___; ___tension
PDE5 inhibitors (used to treat erectile dysfunction/pulmonary HTN); narrow angle glaucoma; head trauma, cerebral hemorrhage; severe anemia; hypotension
51
If you give NTG with PDE5 inhibitors, it can lead to fatal ___
Fatal hypotension
52
Advantages of NTG—___ (rapid/slow) onset; ___ (short/long) duration; coronary vaso___; ___ (increased/decreased) myocardial O2 consumption; no major ___; no coronary ___; reduced ___ vascular resistance
Rapid onset; short duration; coronary vasodilation; decreased myocardial O2 consumption; no major toxicities; no coronary steal; reduced pulmonary vascular resistance
53
Disadvantages of NTG—decreased ___ (systolic/diastolic) BP; reflex ___cardia; possible ___tension; variable efficacy; ___phylaxis
Decreased diastolic BP; reflex tachycardia; possible hypotension; variable efficacy; tachyphylaxis
54
Within 3-5 days of NTG use—___hemoglobinemia; intrapulmonary ___; prolonged ___ time
Methemoglobinemia; intrapulmonary shunting; prolonged bleeding time
55
NTG is best used to treat ___
Emergent HTN—fast onset, short duration, and easy to titrate
56
SNP directly vasodilates ___ and ___
Arteries and veins
57
SNP ___ (increases/decreases) BP with slight ___ (increase/decrease) in HR; ___ (increases/decreases) cerebral blood flow and ICP; ___ (increases/decreases/maintains) renal blood flow; ___ (increases/decreases) myocardial O2 demand
SNP decreases BP with slight increase in HR; increases cerebral blood flow and ICP; maintains renal blood flow, slight reduction; decreases myocardial O2 demand
58
What occurs with abrupt discontinuation of SNP?—___cardia and ___tension
Reflex tachycardia and hypertension
59
SNP pharmacokinetics—onset less than ___; peak ___-___ min; duration ___-___ min; half life ___ to ___ days
Onset less than 1 min; peak 2-3 min; duration 5-10 min; half life 2.7 to 7 days
60
Even though SNP has a much longer half life than NTG, the risk of toxicity is low because it doesn’t actually exert its effects for a full 7 days—T/F?
True
Half life of NTG = 1-4 min
Half life of SNP = 2.7 to 7 days
61
SNP CNS side effects—___lessness, appre___, muscle ___, ___ache, ___ness
Restlessness, apprehension, muscle twitching, headache, dizziness
62
SNP CV side effects—profound ___tension, ___tations, fluctuations in ___, ___ discomfort
Profound hypotension, palpitations, fluctuations in heart rate, retrosternal discomfort
63
SNP GI side effects—___/___, ___ pain
Nausea/vomiting, abdominal pain
64
SNP other side effects—nasal ___; ___ (increased/decreased) serum creatinine with ___/___ doses; ___/___ toxicity that can lead to ___ via ___
Nasal stuffiness, increased serum creatinine with higher/longer doses; thiocyanate/cyanide toxicity that can lead to end organ damage via hypoxia
65
SNP warnings/contraindications—congenital optic ___; ___volemia; compensatory ___tension (i.e.: AV shunting, aortic coarctation); ___ (increased/decreased) ICP; severe ___/___ impairment
Congenital optic atrophy; hypovolemia; compensatory hypertension (i.e.: AV shunting, aortic coarctation); increased ICP; severe renal/hepatic impairment
66
Why should SNP be avoided in severe renal/hepatic impairment?
Because you need the liver to breakdown cyanide (byproduct of SNP)
Thiocyanate is a byproduct of cyanide metabolism and is broken down by the kidneys
67
Thiocyanate/cyanide toxicity presentation—___tension; ___ vision; ___gue; metabolic ___osis; ___ skin; absence of ___; ___ heart sounds
Hypotension; blurred vision; fatigue; metabolic acidosis; pink skin; absence of reflexes; faint heart sounds
68
Risk of thiocyanate/cyanide toxicity increases with doses over ___mcg/kg/min, > ___ days of therapy
Doses over 4 mcg/kg/min, > 2 days of therapy
69
Thiocyanate levels—therapeutic = ___-___ mcg/ml; toxic = ___-___ mcg/ml; fatal > ___ mcg/ml
Therapeutic = 6-29 mcg/ml
Toxic = 35-100 mcg/ml
Fatal > 200 mcg/ml
70
Cyanide levels—normal is < ___ mcg/ml, < ___ mcg/ml for smokers; toxic > ___ mcg/ml; fatal > ___ mcg/ml
Normal is < 0.2 mcg/ml, < 0.4 mcg/ml for smokers
Toxic > 2 mcg/ml
Fatal > 3 mcg/ml
71
Thiocyanate/cyanide toxicity—what happens? ___ binds to hemoglobin very quickly; iron in hemoglobin cannot bind to ___ when cyanide is bound; patients can die of ___ dysfunction because they are ___ and no ___ exchange is occurring
Cyanide binds to hemoglobin very quickly; iron in hemoglobin cannot bind to oxygen when cyanide is bound; patients can die of multiorgan dysfunction because they are hypoxic and no oxygen exchange is occurring
72
What is one distinct feature in patients with thiocyanate/cyanide toxicity?
Can smell almonds on patient’s breath
73
SNP—treatment of cyanide toxicity—___ infusion; administer ___; correct ___
Stop SNP infusion; administer 100% oxygen; correct metabolic acidosis
74
SNP—treatment of cyanide toxicity—sodium thiosulfate donates a ___ group to remove ___/___ molecules from hemoglobin so that hemoglobin can bind to ___
Sodium thiosulfate donates a sulfate group to remove thiocyanate/cyanide molecules from hemoglobin (they will bind to the sulfate instead) so that hemoglobin can bind to oxygen
75
SNP—treatment of cyanide toxicity—hydroxocobalamin is a precursor to vitamin ___; binds ___ molecules
Precursor to vitamin B12; binds cyanide molecules
Can consider Vitamin B12 for treatment of cyanide toxicity as well
76
SNP—treatment of cyanide toxicity—3% sodium nitrite has become a medication of last resort because it causes ___ and can worsen ___
Has become a medication of last resort because it causes anemia and can worsen ischemia
77
SNP advantages—___ onset, ___ (short/long) duration, ___ (increased/decreased) myocardial O2 demand
Immediate onset, short duration, decreased myocardial O2 demand
78
SNP disadvantages—reflex ___cardia; ___ toxicity; intrapulmonary ___; precipitous drop in ___ is possible; ___degradation; ___hemoglobinemia; coronary ___; enhanced ___; cerebral vaso___
Reflex tachycardia; cyanide toxicity; intrapulmonary shunting; precipitous drop in BP is possible; photodegradation; methemoglobinemia; coronary steal; enhanced bleeding; cerebral vasodilator
79
Always use ___ for CAD patients, not ___
NTG for CAD patients, not SNP
Because NTG does not cause coronary steal and SNP does, which further worsens ischemia
80
Alpha 1 receptor activation—increases intracellular ___; smooth muscle ___ (contraction/relaxation); peripheral vaso___; broncho___; ___ (inhibits/stimulates) insulin secretion; ___ (inhibits/stimulates) glycogenolysis and gluconeogenesis; ___ (mydriasis/miosis); GI ___ (contraction/relaxation)
Increases intracellular calcium; smooth muscle contraction; peripheral vasoconstriction; bronchoconstriction; inhibits insulin secretion; stimulates glycogenolysis and gluconeogenesis; mydriasis; GI relaxation
81
Alpha 2 receptor activation ___ (stimulates/inhibits) neuronal firing in the CNS and peripheral NS; results in ___tension, ___cardia, ___ation, ___gesia
Inhibits neuronal firing in the CNS and peripheral NS; results in hypotension, bradycardia, sedation, analgesia
82
Alpha 2 receptor activation—effects on other organs—___ (increased/decreased) salivation and secretions; ___ (increased/decreased) GI motility; ___ (stimulates/inhibits) renin release; ___ (increases/decreases) GFR; ___ (increases/decreases) sodium and water secretion; ___ (increased/decreased) insulin release
Decreased salivation and secretions; decreased GI motility; inhibits renin release; increases GFR; increases sodium and water secretion; decreased insulin release
83
Phenoxybenzamine (Dibenzyline) is a ___
Nonselective alpha antagonist—it irreversibly binds to alpha 1 and alpha 2 receptors
84
Main use of phenoxybenzamine (dibenzyline)—long-term preoperative treatment to control the effects of ___
Pheochromocytoma
“Chemical sympathectomy”
85
Other uses of phenoxybenzamine (dibenzyline)—relieve ischemia in ___; ___ to improve flow
Relieve ischemia in PVD; BPH to improve flow (was used before flomax, rapaflo, and hytrin came around)
86
Effects of phenoxybenzamine (dibenzyline)—reduced ___ to reduced ___; secondary increases in ___ due to ___ blockade can increase ___ and ___
Reduced peripheral vascular resistance (PVR) to reduced BP; secondary increases in NE due to alpha 2 blockade can increase HR and CO (beta 1 effects)
87
Phenoxybenzamine (dibenzyline) does not cross the BBB—T/F?
False—crosses the BBB
88
Phenoxybenzamine (dibenzyline) CNS side effects—___ation, ___ssion, ___ness, ___gy, ___ache
Sedation, depression, tiredness, lethargy, headache
89
Phenoxybenzamine (dibenzyline) GI side effects—___/___
Nausea/vomiting
90
Phenoxybenzamine (dibenzyline) CV side effects—___tension, ___cardia, ___mias
Postural hypotension, tachycardia, arrhythmias
91
Phenoxybenzamine (dibenzyline) pharmacokinetics—half life ___ hours; duration of action ___ days; route of administration ___
Half life 24 hours; duration of action 4 days; route of administration PO
92
May see up regulation of alpha receptors with phenoxybenzamine (dibenzyline)—T/F?
True—because it is a nonselective alpha antagonist—blocks alpha 1 and alpha 2 receptors
93
Phentolamine is a ___
Nonselective alpha antagonist—blocks alpha 1 and alpha 2 receptors just like phenoxybenzamine
94
Phentolamine uses—hypertension secondary to ___; ___ withdrawal hypertension; ___ dysfunction; ___ of catecholamines
Hypertension secondary to pheochromocytoma; clonidine withdrawal hypertension; erectile dysfunction; extravasation of catecholamines
95
Phentolamine pharmacokinetics—half life ___ minutes; onset ___-___ minutes IM, ___ IV
Half life 19 minutes; onset 15-20 minutes IM, immediate IV
96
Oral alpha 1 antagonists are ___ (selective/non-selective)
Selective
97
Alpha 1 antagonists end in -___
-zosin or -osin
Examples = prazosin (minipres); terazosin (hytrin); doxazosin (cardura); tamsulosin (flomax); silodosin (rapaflo); afluzosin (uroxatral)
98
What did Cochrane review demonstrate about the use of Alpha 2 agonists and risk of cardiac complications after surgery?
Alpha 2 agonists had no effect on reducing cardiac complications after surgery—specifically, they had no effect on overall mortality, cardiac mortality, and prevention of MI
99
Alpha 2 agonists and cardiac complications—monitor patients for excessive ___ and ___
Excessive hypotension and bradycardia
100
Clonidine is a ___ (central/peripheral) acting alpha-___ ___ that leads to inhibition of ___ (sympathetic/parasympathetic) outflow
Clonidine is a central acting alpha-2 agonist that leads to inhibition of sympathetic outflow
101
Clonidine affinity for alpha 2 over alpha 1 receptors is ___:___
220:1
102
Clonidine ___ (increases/decreases) the release of sympathetic neurotransmitters, ___ (stimulates/inhibits) renin release
Decreases the release of sympathetic neurotransmitters, inhibits renin release
103
Clonidine can be administered orally and by patch, as well as by IV, intrathecal, and epidural—T/F?
True
104
Clonidine actions/effects—___ (increases/decreases) HR, BP, CO, and SVR
Decreases
105
Baroreceptor reflexes are preserved in patients on clonidine—T/F?
True
106
Abrupt cessation of clonidine may lead to rebound ___
Rebound hypertension
Clonidine blocks NE from binding to alpha 2 receptors, so there is an upregulation of alpha receptors; with abrupt discontinuation, there is a risk for accelerated HTN, because all of the NE that was blocked now binds to the upregulated receptors—can push systolic pressures into the 200s
107
If patient has been on clonidine for 6 days or more, abrupt discontinuation will cause accelerated HTN—T/F?
True
108
Clonidine withdrawal occurs with ___ discontinuation; due to ___; manifestations include excessive ___tension, ___cardia, ___lessness, ___mnia, ___ache, ___ea
Abrupt discontinuation; due to NE; manifestations include excessive hypertension, tachycardia, restlessness, insomnia, headache, nausea
109
Patients are at risk for clonidine withdrawal if they have taken clonidine for at least 6 days—T/F?
True
110
Clonidine pharmacokinetics—rapidly and completely absorbed from PO dosing with peak in ___-___ minutes; patch takes about ___ days to reach full potential; half life ___-___ hours
Peak in 60-90 minutes; patch takes about 2 days to reach full potential; half life 9-12 hours
111
Clonidine side effects—___siness, ___ness, ___ mouth, ___stasis
Drowsiness, dizziness, dry mouth, orthostasis
112
Caution using clonidine in patients with severe ___ insufficiency, ___ disturbances, recent ___/___, ___
Severe coronary insufficiency, conduction disturbances, recent MI/CVA, CKD
Because clonidine decreases HR, BP, CO, and SVR
113
It is recommended to give clonidine via epidural route for the perioperative period—T/F?
False—not recommended
114
Clonidine effects on anesthesia—___ (increases/decreases) propofol and thiopental requirements; can be used as an alternative to ___ for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia; supplement to ___
Decreases propofol and thiopental requirements; can be used as an alternative to nitrous for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia; supplement to regional blocks
115
Dexmedetomidine (precedex) is a relatively ___ (selective/non-selective) alpha-___ ___ used for continuous IV ___ in the ICU
Relatively selective alpha-2 agonist used for continuous IV sedation in the ICU (package insert says it should be used as a continuous infusion for < 24 hours)
116
Precedex affinity for alpha 2 over alpha 1 receptors = ___:___
1620:1
117
Precedex maintains ___ stability in intubated or extubated patients; patients are ___ and ___ when stimulated; sedation resembles natural ___
Precedex maintains respiratory stability in intubated or extubated patients; patients are arousable and alert when stimulated; sedation resembles natural sleep
118
Precedex may be useful for ___ sedation, i.e.: sedation for awake ___ intubation, during ___ anesthesia or other procedures
Procedural sedation, i.e.: sedation for awake fiberoptic intubation, during regional anesthesia or other procedures
119
Precedex allows patients to maintain ___ respirations; sedation is more like natural ___; has some ___ effects, no ___ effects
Maintain spontaneous respirations; sedation is more like natural sleep; has some analgesic effects, no amnesic effects
120
Precedex is safe for use by nonanesthesia providers—T/F?
True
121
There are no studies regarding the safety of precedex use in children—T/F?
True
122
Precedex may reduce post-op opiate use by as much as ___ and can be used to reduce post-op ___
By as much as half and can be used to reduce post-op shivering
123
Precedex adverse effects—___/___, ___, ___ia
Nausea/vomiting, fever, hypoxia
124
Precedex BOLUS adverse effects—___tension, ___cardia
Hypertension, bradycardia
125
Clinically significant bradycardia and sinus arrest has been seen in young, healthy volunteers with high vagal tone when bolused with precedex—T/F?
True
126
Precedex INFUSION adverse effects—___tension
Hypotension
127
Safety precautions for precedex—exercise caution in patients with advanced heart ___ or severe ___ dysfunction; significant ___cardia and sinus ___ are possible, especially with high vagal tone or rapid bolus
Exercise caution in patients with advanced heart block or severe ventricular dysfunction; significant bradycardia and sinus arrest are possible, especially with high vagal tone or rapid bolus
128
Less than 1% of patients have respiratory adverse events with continuous precedex infusion—T/F?
True
129
As per the package insert, do not give precedex > 24 hours continuous infusion—T/F?
True
130
Methyldopa (aldomet) is initially thought to act as a false transmitter in the periphery (alpha-methyl-NE)—T/F?
True
131
Alpha-methyl-NE (methyldopa/aldomet) is almost as potent as NE—T/F?
True
132
In the CNS, methyldopa (aldomet) is further metabolized to alpha-methyl___
Alpha-methylepinephrine
133
Alpha-methylepinephrine (metabolite of methyldopa) acts at alpha-___ receptors to decrease ___ outflow
Acts at alpha-2 receptors to decrease sympathetic outflow
134
Methyldopa is used to treat ___
Hypertension during pregnancy, usually third trimester
135
RAAS review
- Renin is released by the kidneys in response to low BP/decreased renal perfusion
- Angiotensinogen released by the liver converts renin into angiotensin I
- ACE (angiotensin converting enzyme) released by the lungs converts angiotensin I to angiotensin II
- Angiotensin II is a potent vasoconstrictor—increases BP
- Angiotensin II stimulates the adrenal cortex to release aldosterone, which results in sodium/water retention, H+/K+ excretion
- Angiotensin II stimulates the pituitary gland to release ADH—increases water reabsorption
136
Angiotensin II participates in cardiac remodeling; it slows down cardiomegaly/ischemia that occurs from longstanding CV disease—T/F?
True
137
ACE inhibitors are predominantly ___ (arterial/venous) vasodilators
Arterial vasodilators
138
ACE inhibitors treat CHF and MR by ___ (preload/afterload) reduction; are used post-___; have improved outcomes in ___
Treat CHF and MR by afterload reduction; are used post-MI; have improved outcomes in DM
139
ACE inhibitors are the antihypertensive of choice for patients with ___
Chronic illnesses
140
ACE inhibitors effect on renal function—biphasic effect depending on baseline BP—if patient is baseline ___tensive, decreased renal vascular resistance improves RBF and GFR
If patient is baseline hypertensive, decreased renal vascular resistance improves RBF and GFR
141
ACE inhibitors effect on renal function—biphasic effect depending on baseline BP—if patient is baseline ___tensive, if BP is decreased, renal function may deteriorate because compensatory efferent arteriolar constriction mediated by angiotensin II is blocked and decreased glomerular filtration pressure and GFR may result in acute hyperkalemia
If patient is baseline hypotensive...
142
ACE inhibitors should be avoided in patients with significant ___ dysfunction or renal artery ___
Should be avoided in patients with significant renal dysfunction or renal artery stenosis
143
Constriction of the efferent arteriole is mediated by ___; with ACE inhibitors, the kidney can’t regulate its own blood flow via constriction of the ___ arteriole; this leads to further vaso___/___perfusion of the kidney and massive reduction in ___
Angiotensin II; with ACE inhibitors, the kidney can’t regulate its own blood flow via constriction of the efferent arteriole; this leads to further vasodilation/hypoperfusion of the kidney and massive reduction in GFR
144
ACE inhibitors end in -___
-pril
145
ACE inhibitors—enalaprilat (vasotec) IV—defer or avoid if there is ___ or ___ postoperatively
Hemodynamic instability or renal insufficiency postoperatively
146
Respiratory side effects of ACE inhibitors—___, ___, and ___ are most common side effects; ___ is a serious side effect; ___kalemia, ___mias
Cough, congestion, and rhinorrhea are most common side effects; angioedema is a serious side effect; hyperkalemia, arrhythmias
147
It is not safe to d/c ACE inhibitors without tapering—T/F?
False—it is safe to d/c without taper
CHF, bronchospasm, hypokalemia, hyponatremia, and rebound hypertension NOT seen with abrupt withdrawal
148
Angioedema from ACE inhibitors can lead to ___ compromise
Airway compromise
149
Caution using ACE inhibitors in ___ failure and ___kalemia; these effects are reversible with withdrawal of the drug
Acute renal failure and hyperkalemia
150
ACEI ___ (have/have not) demonstrated fetal morbidity and mortality
Have
151
It is safe to use ACEIs during pregnancy—T/F?
False—do NOT use at all during pregnancy
152
ACE inhibitors and perioperative issues—prolonged ___tension can occur in patients being treated with ACE inhibitors and undergoing general anesthesia
Prolonged hypotension
153
Risk of ___ in the intra- and postoperative periods in patients on ACEIs or ARBs; ___tension and ___volemia seem to contribute to this risk
Risk of acute renal failure in the intra- and postoperative periods in patients on ACEIs or ARBs; hypotension and hypovolemia seem to contribute to this risk
154
What should patients on ACEIs or ARBs do the day of surgery?
Hold medication on the day of surgery
155
Preop ACEIs in CABG patients may contribute to significant reduction in glomerular perfusion pressure and postop acute renal failure; the risk is especially high if large blood or fluid shifts occur—T/F?
True
156
There is loss of the compensatory mechanism of constriction of the efferent arteriole in people taking ACE inhibitors; acute renal failure can occur with hypotension because they don’t have this compensatory mechanism available—T/F?
True
157
Toronto 2011 study on ACE inhibitors
Found no difference between taking ACEI vs. holding it before surgery; patients on ACEI had lower 30 day mortality post procedure
158
Roshanov et al Anesthesiology 2017 study on ACE inhibitors
Holding ACEIs/ARBs the morning of surgery reduced death/stroke/myocardial injury by 18% and hypotension by 20%
159
Hollmann et al Anesth Analg. 2018 study on ACE inhibitors
No difference if withheld the day of surgery; higher rates of hypotension in those who continued the medication, but no significant increase in mortality found
160
ACC and AHA recommend ___ (continuing/not continuing) for major non-cardiovascular surgery; ___ (continue/do not continue) for cardiovascular surgery
Recommend continuing ACEIs for major non-cardiovascular surgery; do not continue for cardiovascular surgery
161
ACEIs have increased hypotensive effects with ___, ___, and ___
Diuretics, vasodilators, and anesthetics
162
ACEIs + NSAIDs/ASA interaction—reduce anti___ effect, increased risk of ___kalemia and ___ failure
Reduce antihypertensive effect, increased risk of hyperkalemia and acute renal failure
163
For patients on ACEIs, check fluids for ___ (what electrolyte?)
Potassium
164
Angiotensin II receptor antagonists end in -___
-sartan
I.e.: losartan (cozaar), irbesartan (avapro)
165
Angiotensin II receptor antagonists have the same hemodynamic effects and uses as ___
ACEIs
166
Angiotensin II receptor antagonists have ___ (more/less) cough/angioedema than ACEIs
Less
167
Angiotensin II receptor antagonists are available ___
PO, no IV available yet
168
Angiotensin II receptor antagonists have a similar side effect profile and considerations with anesthesia as ACEIs—T/F?
True
169
Other RAS medications—aliskiren (tekturna) is a ___
Direct renin inhibitor
170
Other RAS medications—sacubitril/valsartan (entresto); combination medication—sacubitril is a ___ inhibitor that reduces ___ peptide degradation; valsartan is an ___
Sacubitril is a neprilysin inhibitor that reduces natriuretic peptide degradation; valsartan is an angiotensin II receptor blocker (ARB)
171
How do calcium channel blockers work?—they block ___ channels that move ___ into the cell; need this for ___/___; by blocking, less ___ = more ___
They block calcium channels that move calcium into the cell; need this for contraction/constriction; by blocking, less calcium = more relaxation
172
Functions of calcium—signal transduction in the ___, ___; muscle contraction—___ muscle, ___ muscle, ___ walls; ___ health; ___ cascade
Signal transduction in the CNS, heart; muscle contraction—smooth muscle, cardiac muscle, vessel walls; bone health; clotting cascade
173
Calcium channel blockers primary actions—negative ___ effect; negative ___ effect; vasodilation of ___, ___, ___, and ___ beds
Negative inotropic (force of contraction) effect
Negative dromotropic (speed of conduction in the AV node) effect (AV conduction block)
Vasodilation of systemic, splanchnic, coronary, and pulmonary beds
174
Calcium channel blockers—dihydropyridines end in -___
- dipine
| i. e.: nifedipine (adalat/procardia); nicardipine (cardene); amlodipine (norvasc)
175
Dihydropyridine CCBs are pure ___ (arterial/venous) vasodilators, but with minimal ___; they have minimal negative ___/___ effects
Pure arterial vasodilators, but with minimal reflex tachycardia (usually < 10 bpm); they have minimal negative inotropic/dromotropic effects
176
Nicardipine is a potent vasodilator of ___, ___, and ___ circulations without important negative ___ or ___ effects
Potent vasodilator of systemic, coronary, and cerebral circulations without important negative inotropic or dromotropic effects
177
Nicardipine is a/an ___ (arteriole/venous) specific vasodilator
Arteriole
178
Nicardipine has no ___, which allows for favorable myocardial oxygen supply/demand
No coronary steal syndrome
179
Nicardipine is useful for IV control of ___tension in the PACU or ICU
Hypertension
180
Nicardipine has ___ (slower/faster) onset and offset than SNP; has ___ (more/less) swings in BP; no rebound ___ with withdrawal; reflex tachycardia is usually < ___ bpm; ___ (short/long) duration of action may be a benefit postop
Nicardipine has a slower onset and offset than SNP; has less swings in BP; no rebound hypertension with withdrawal; reflex tachycardia is usually < 10 bpm; long duration of action may be a benefit postop
181
Advantages of nicardipine—dose dependent ___ (arterial/venous) vasodilation; ___ (does/does not) cause coronary steal; cerebral and coronary vaso___; minimal effects on ___/___; mild ___ effect
Dose dependent arterial vasodilation; does not cause coronary steal; cerebral and coronary vasodilation; minimal effects on contractility/conduction; mild natriuretic effect
182
Disadvantages of nicardipine—may ___; ___ (predictable/variable) duration of action; ___tension; ___ irritation; may cause ___cardia
May accumulate; variable duration of action; hypotension; venous irritation; may cause tachycardia
183
Clevidipine is an IV ___; ___pyridine; vasodilation reduces ___ vascular resistance; ___ (arteriole/venous) specific
IV calcium channel blocker; dihydropyridine; vasodilation reduces peripheral vascular resistance; arteriole specific
184
Clevidipine is cleared much ___ (slower/faster) than nicardipine
Much faster than nicardipine—half life of 1 min
185
Disadvantages of clevidipine—___ emulsion; contraindicated with ___ and ___ allergy, ___titis, and hyper___
Lipid emulsion; contraindicated with egg and soy bean allergy, pancreatitis, and hyperlipidemia
186
Verapamil is part of the ___ class
Phenylalkylamine class
187
Verapamil is a potent negative ___trope, ___trope, and vaso___
Potent negative inotrope, dromotrope, and vasodilator
188
Verapamil is used for aortic ___; conversion of atrial re-entry ___arrhythmias; coronary artery ___
Verapamil is used for aortic stenosis; conversion of atrial re-entry tachyarrhythmias; coronary artery vasospasm (Prinzmetal angina)
189
70% of verapamil is excreted via ___; 20-30% of verapamil is excreted via ___/___
70% of verapamil is excreted via urine; 20-30% of verapamil is excreted via bile/feces
190
Diltiazem (cardizem) is part of the ___ class
Benzothiazine class
191
Diltiazem (cardizem) is used as a ___ agent in a-fib/atrial tachycardia versus a ___ agent like verapamil
Diltiazem (cardizem) is used as a rate-control agent in a-fib/atrial tachycardia versus a conversion agent like verapamil
192
Diltiazem drug interactions—CYP ___ (inhibitor/inducer)
Inhibitor
193
Review of CCBs—which CCB is this describing?—potent negative inotrope and negative dromotrope; mild vasodilator; useful in the treatment of vasospastic angina and essential hypertension
Verapamil
194
Review of CCBs—which CCB is this describing?—fits between verapamil (phenylakylamine) and dihydropyridines in action; less negative inotropic/dromotropic effects than verapamil but more than dihydropyridines; mild vasodilator like verapamil
Diltiazem
195
Review of CCBs—which CCB is this describing?—virtually pure arterial vasodilator; lack clinically significant negative inotropic and dromotropic effects
Dihydropyridines—nifedipine, nicardipine, amlodipine
196
CCBs—dihydropyridines may cause ___ from a reflex ___cardia d/t ___ (arterial/venous) vasodilation
May cause palpitations from a reflex tachycardia d/t arterial vasodilation
197
CCBs—non-dihydropyridines may cause ___cardia
Bradycardia
198
Which CCB mostly causes cough?
Nifedipine
199
Verapamil and diltiazem ___ (enhance/worsen) myocardial oxygen balance by ___ reduction and/or negative ___tropic effect; they increase O2 delivery through coronary vaso___
Enhance myocardial oxygen balance by afterload reduction and/or negative inotropic effect; they increase O2 delivery through coronary vasodilation
200
Dihydropyridine vasodilators may ___ (enhance/worsen) MvO2 (myocardial oxygen consumption) by causing diastolic ___tension and reflex ___cardia
Worsen MvO2 by causing diastolic hypotension and reflex tachycardia
201
Which dihydropyridine does not cause reflex tachycardia to a great extent and thus does not worsen MvO2 as much as other dihydropyridine vasodilators?
Nicardipine
202
CCBs ___ (increase/decrease) reperfusion injury after ischemia
Decrease
203
CCBs effect on renal function—___ (increase/decrease) renal blood flow and GFR; induce a ___
Increase renal blood flow and GFR; induce a naturesis
204
CCB benefits on renal function can be reversed if they cause hypotension because reflex catecholamine release and angiotensin activation lead to decreases in RBF and GFR—T/F?
True
205
Overall, CCB effects on renal function are not significantly beneficial or detrimental—T/F?
True
206
CCBs should be continued up to the time of surgery without risk of significant drug interactions—T/F?
True
207
CCBs may potentiate the effects of ___ agents
Neuromuscular blocking agents
208
CCBs block ___-type calcium channels in the CV system; by blocking this type of calcium channel, more NDNMB may bind to ___-type channels that affect ACh calcium mediated release (and thus prolonging the block)
L-type calcium channels in the CV system; by blocking this type of calcium channel, more NDNMB may bind to P-type channels that affect ACh calcium mediated release (and thus prolonging the block)
209
CCBs—anesthetic considerations—they may enhance ___tensive, CV ___, vaso___ effects of anesthetics and analgesics
They may enhance hypotensive, CV depressant, vasodilating effects of anesthetics and analgesics
210
Clevidipine reduces ___; what post-op issues can this cause?
Reduces gastric emptying—post-op can cause nausea/vomiting, aspiration
211
Diltiazem can increase sedative effects of ___
Midazolam
212
Beta receptor activation—beta-1 ___ (increases/decreases) HR, conduction velocity, myocardial contractility
Increases HR, conduction velocity, myocardial contractility
213
Beta receptor activation—beta-2–stimulation leads to smooth muscle ___; peripheral vaso___; ___ (increases/decreases) BP; broncho___; ___ (increases/decreases) insulin secretion; ___ (increases/decreases) glycogenolysis, gluconeogenesis; ___ (increases/decreases) GI mobility
Smooth muscle relaxation; peripheral vasodilation; decreases BP; bronchodilation; increases insulin secretion; increases glycogenolysis, gluconeogenesis; decreases GI mobility
214
Beta blockers ___ (increase/decrease) cardiac output; ___ (increase/decrease) renin release; ___ (do/do not) vasodilate
Decrease cardiac output (HR and contractility); decrease renin release; do NOT vasodilate
215
Advantages of beta blockers over vasodilators—no reflex ___cardia or ___ of pulse pressure; improved ___ through decreased HR and contractility; intrinsic anti___ activity
No reflex tachycardia or widening of pulse pressure; improved MvO2 through decreased HR and contractility; intrinsic antiarrhythmic activity
216
Pure beta blockers vasodilate—T/F?
False—pure beta blockers do NOT vasodilate
217
Labetalol and carvedilol do not vasodilate—T/F?
False—they are alpha/beta blockers, so they do vasodilate
Pure beta blockers do NOT vasodilate
218
Classifications of beta blockers—beta selectivity—beta-1 selective beta blockers (metoprolol, atenolol, acebutolol, bisoprolol, esmolol) ___ (increase/decrease) velocity of AV conduction, HR, contractility, renin release, and lipolysis
Decrease
219
Classifications of beta blockers—beta selectivity—non-selective beta blockers (propranolol, nadolol, timolol, pindolol, carteolol) block both ___ and ___ receptors; action at beta-2 receptor causes broncho___, peripheral vaso___, and ___ (increased/decreased) glycogenolysis
Block both beta 1 and beta 2 receptors; action at beta-2 receptor causes bronchoconstriction, peripheral vasoconstriction, and decreased glycogenolysis
220
What two beta blockers have combined alpha 1 and non selective beta effects?
Labetalol and carvedilol
221
What two beta blockers are the top choices to treat cocaine OD or Clonidine withdrawal?
Labetalol and carvedilol because they provide both alpha and beta blockade
222
Nadolol is a ___ (short/long)-acting; ___ (selective/nonselective); and is eliminated via the ___
Long-acting; nonselective; and is eliminated via the kidney
223
Atenolol is a ___ (short/long)-acting; ___ (selective/nonselective); and is eliminated via the ___
Long-acting; selective; and is eliminated via the kidney
224
Propranolol is a ___ (short/long/intermediate)-acting; ___ (selective/nonselective); and is eliminated via the ___
Is an intermediate-acting; nonselective; and is eliminated via the liver
225
Metoprolol is a ___ (short/long/intermediate)-acting; ___ (selective/nonselective); and is eliminated via the ___
Intermediate acting; selective; and is eliminated via the liver
226
Esmolol is an ___ (ultra short/long)-acting; ___ (selective/nonselective); and is eliminated via ___
Ultra short-acting; selective; and is eliminated via red cell esterases
227
Atenolol and nadolol have a ___ (low/moderate/high) lipophilicity
Low lipophilicity
228
Metoprolol, Coreg, and labetalol have a ___ (low/moderate/high) lipophilicity
Moderate lipophilicity
229
Propranolol has a ___ (low/moderate/high) lipophilicity
High lipophilicity
230
Adverse effects of beta blockers—non-selective beta blockers (i.e.: propranolol) can cause vaso___ and worsen ___; can also cause broncho___; caution using non-selective beta blockers in patients with ___
Can cause vasoconstriction and worsen PVD; can also cause bronchospasm; caution using non-selective beta blockers in patients with asthma
231
Adverse effects of beta blockers—myocardial ___; decreased contractility could precipitate ___
Myocardial depression; decreased contractility could precipitate CHF
232
Adverse effects of beta blockers—life-threatening ___cardia or ___
Bradycardia or asystole
233
Adverse effects of beta blockers—___kalemia in patients with ___
Hyperkalemia in patients with renal failure
234
Caution using beta blockers with ___ (decreased HR and contractility) and ___ (decreased HR and conduction)
Verapamil and digoxin
235
Beta blocker overdose—treat with ___; may need ___, ___, and/or ___ infusion; patient may ultimately need ___
Treat with atropine; may need isoproterenol, dobutamine, and/or glucagon infusion; patient may ultimately need pacing
236
Perioperative indications for beta blocker—control intra- and postoperative ___tension and ___cardia; ___ control and/or conversion of SVT, a-fib, and a-flutter; myocardial protection in ___ heart disease; peripheral manifestations of ___thyroidism
Control intra- and postoperative hypertension and tachycardia; rate control and/or conversion of SVT, a-fib, and a-flutter; myocardial protection in ischemic heart disease; peripheral manifestations of hyperthyroidism
237
Which beta blocker is effective in limiting hypertension during induction and emergence?
Esmolol
238
Contraindications to beta blockers—severe ___cardia; > ___ degree heart block; ___ shock; ___ disease
Severe bradycardia; > 1st degree heart block; cardiogenic shock; Raynaud’s disease
239
Caution using nonselective beta blockers in patients with ___/___ because they increase the risk of broncho___
Asthma/COPD because they increase the risk of bronchospasm
240
Caution using beta blockers in patients with ___ because they can mask symptoms of ___glycemia
In patients with diabetes because they can mask symptoms of hypoglycemia
241
Caution using beta blockers in patients with ___ failure because they can make symptoms even worse
Heart failure
242
Propranolol is a ___ (selective/non-selective) beta blocker; it is ___ soluble and can penetrate the ___; it is metabolized in the ___
Non-selective beta blocker; it is lipid soluble and can penetrate the CNS; it is metabolized in the liver
243
Esmolol is a beta ___ selective agent; it can blunt the CV response to ___; can control ___ and ___; it is more likely than ___ to convert a-fib to sinus rhythm; can be used to treat intraop/postop ___tension and ___cardia
Esmolol is a beta 1 selective agent; it can blunt the CV response to intubation; can control SVT and a-fib; it is more likely than verapamil to convert a-fib to sinus rhythm; can be used to treat intraop/postop hypertension and tachycardia
244
Esmolol has a ___ (slow/rapid) onset and offset; it is metabolized by ___
Rapid onset and offset; it is metabolized by red cell esterases
245
Metoprolol is a beta ___ selective agent; approved for the treatment of ___ and acute ___
Beta 1 selective agent; approved for the treatment of angina and acute MI
246
Labetalol combines weak alpha blockade with weak non-selective beta blockade—T/F?
True
247
Labetalol beta:alpha ratio = ___:___
Beta:alpha ratio = 7:1 (5-10:1)
248
Labetalol is a negative ___trope and ___trope with vaso___; it provides effective anti___tensive action
Negative inotrope and chronotrope with vasodilation; it provides effective antihypertensive action
249
Labetalol indications—hyperdynamic ___tension—blunts CV response to ___; treatment of aortic ___; tachyphylaxis with ___; intracranial ___tension—does not increase ___
Hyperdynamic hypertension—blunts CV response to tracheal intubation; treatment of aortic dissection; tachyphylaxis with SNP; intracranial hypertension—does not increase ICP
250
Beta blockers—negative inotropic effects and conduction delays are potentiated by many general anesthetics—T/F?
True
251
Beta blockers should be continued preoperatively—T/F?
True
252
Do not stop beta blockers abruptly d/t rebound ___tension and ___cardia
Rebound hypertension and tachycardia
253
Beta blockers may mask ___glycemia and ___thyroidism
Hypoglycemia and hyperthyroidism
254
Beta blocker overdose—give ___; ___; beta 1 ___; high dose euglycemic ___ therapy; intravenous ___ emulsion
Glucagon; atropine; beta 1 agonists; high dose euglycemic insulin therapy; intravenous lipid emulsion
255
There is no data to support use of calcium and sodium bicarb for treatment of beta blocker overdose—T/F?
True
256
What antihypertensive medication is favored to use in pregnant patients?
Alpha-methyldopa (aldimet)
257
What beta blocker can be used in the 2nd and 3rd trimesters?
Labetalol
258
Beta blockers are associated with growth retardation if given during the first trimester of pregnancy—T/F?
True
259
What medication class has demonstrated fetal morbidity and mortality in all 3 trimesters?
ACE inhibitors
260
Hydralazine may be used during delivery—T/F?
True
261
Nifedipine can be used PO but not sublingual in pregnant patients—T/F?
True
262
SNP is often used to treat hypertension in pregnancy—T/F?
False—rarely used in pregnancy
