Antihypertensives Flashcards
(173 cards)
1
Q
Main concern of antihypertensives + anesthesia is due to interference with which system?
A
Interference with SNS activity
Resulting in orthostatic hypotension, or exaggerated hypotension
2
Q
What are reasons for hypotension during anesthesia that may be exaggerated when patient has taken an antihypertensive
A
- Hypovolemia
- Position change
- Decreased venous return related to positive pressure ventilation
3
Q
Which catecholamine may be depleted when a surgical patient is on antihypertensives?
A
Norepinephrine
4
Q
How might a patient taking antihypertensives respond to indirect sympathomimetics like ephedrine?
A
Minimal response due to depletion of norepinephrine
5
Q
Which drugs may a surgical patient on antihypertensives have an exaggerated response to? Why?
A
Direct sympathomimetics, due to no counter balancing of beta2
6
Q
Why were antihypertensives always withheld before surgery before the mid 1970’s
A
Due to their myocardial depressant nature
The drugs then caused severe perioperative lability
7
Q
What do we know now about patients with HTN taking beta-blockers prior to surgery?
A
May improve outcomes of patients with hypertension
8
Q
Antihypertensives should be taken the morning of surgery except for what drugs?
A
Diuretics
9
Q
Benefits of taking most antihypertensives the morning of surgery?
A
Fewer alterations in BP and HR
Fewer arrhythmias
10
Q
Beta-blockers effect on HR and contractility
A
Negative chronotropic and inotropic effect
11
Q
What receptors does Labetalol work on?
A
Combined alpha1 and beta adrenergic blcoker
12
Q
Effect of Labetalol on HR, contractility, and vessel tone
A
Negative inotropic and chronotropic
Vasodilation
13
Q
Which is more potent?
Labetalol vs beta-blockers or phentolamine
A
Beta-blockers or phentolamine
14
Q
Two Alpha1 adrenergic blocking drugs
How do they reduce blood pressure?
A
Prazosin and phentolamine
Vasodilation
15
Q
Two centrally acting alpha2 adrenergic agonists
How do they decrease blood pressure?
A
Clonidine and dexmedetomidine
Decrease sympathetic outflow
16
Q
Neurogenic control of vasomotor tone through SNS
A
Cortex–> hypothalamus –> vasomotor center –> sympathetic ganglia –> adrenergic nerves –> adrenergic receptors (alpha1 and beta 2) –> calcium channels
17
Q
Neurogenic control of vasomotor tone through PNS
A
Cortex –> hypothalamus –> PNS ganglia –> cholinergic receptors –> endothelium –> EDRF (NO)
18
Q
Where do diuretics work in the body?
A
Kidney tubules and vascular smooth muscle
19
Q
Where do ACE-inhibitors work in the body?
A
Kidney tubules, angiotensin receptors on vessels, and adrenal medulla
20
Q
Where do beta-blockers work in the body?
A
B-adrenoreceptors on heart and juxtaglomerular cells that release renin
21
Q
How do ACE inhibitors work?
A
Inhibit ACE in plasma and vascular endothelium to block conversion of angiotensin I to angiotensin II
Prevents vasoconstriction effect of angiotensin II and stimulation of SNS
Also causes decreased aldosterone
22
Q
What effect do ACE inhibitors have on aldosterone?
What are the effects?
A
- Decreased aldosterone
- Causes decreased Na and water retention
- Increased potassium retention
23
Q
Advantage of ACE inhibitors vs beta blockers and diuretics
A
minimal side effects
24
Q
Indications of ACE inhibitors
A
- Hypertension in diabetes
- CHF
- Mitral regurg (F, F, V)
- Development of CHF (regression of LVH)
25
In which patients are ACE-inhibitors contraindicated?
* Renal artery stenosis
* their renal perfusion is highly dependent on angiotensin II
26
Where is angiotensin I converted to angiotensin II?
Lungs
27
There is great controversy on whether to continue your ACE inhibitor the morning of surgery. If you patient does, what should you absolutely be prepared for during their surgery?
They will become hypotensive
28
Most common side effects of ACE-inhibitors
What causes these?
* Cough, upper respiratory congestion, rhinorrhea allergic symptoms
* Potentiation of kinins and inhibition of breakdown of bradykinins
29
Two potentially life-threatening side effects of ACE-inhibitors
Angioedema and hyperkalemia
30
How to treat angioedema with ACE-inhibitors
* Epinephrine 0.3-0.5 ml of 1:1,000 dilution (assuming this is IM?)
* FFP: 2-4 units to replace deficient enzyme
31
What causes hyperkalemia with ACE inhibitors?
Who is it more common in?
Decreased production of aldosterone
More common in CHF with Renal insufficiency
32
2 ACE-inhibitors
Which is available IV route?
- Captopril (Capoten)
- Enalapril (Vasotec) - IV option
33
Which ACE-inhibitor is available IV?
IV dose?
Enalapril (Vasotec)
0.625- 1.25 mg
34
Angiotensin receptor blocking drug
What drugs are these simlar to?
Losartan (Cozaar)
Similar to ACE-inhibitors
35
Compare onset and duration of Captopril (capoten) and enalapril (vasotec)
Captopril has faster onset and shorter duration than enalapril
Captopril: Onset 15 mins and duration 6-10 hours
Enalapril: Onset 1 hour and duration 18-30 hours
36
Between the two ACE-inhibitors discussed, which one does not cause rash and pruritis side effect and rarely causes angioedema?
Enalapril
37
Effects of captopril on CO, SVR, HR, and electrolytes
* Decreased SVR (especially in renal)
* CO and HR not effected
* Baroreceptor sensitivity is reduced so you do not see increased HR with decreased BP
* May cause hyperkalemia due to blocking of aldosterone release
38
MOA of losartan (cozaar)
Blocks binding of angiotensin II to receptors
Type AT1- found in vascular smooth muscle to prevent vasoconstriction and aldosterone release
39
What drug showed 25% in stroke risk reduction when compared with atenolol
Losartan (Cozaar)
40
Entresto is a combination of what two drug classes
ARB + neprilysin inhibitor
\*also can combine losartan (cozaar) with a thiazide diuretic
41
3 classifications of calcium channel blockers
1. phenylalkylamines
2. 1,4 dihydropyridines
3. benzothiazepines
42
MOA of phenylalkylamines
Name the drug in this class
MOA: occludes the calcium channel
Verapamil
43
MOA of dihydropyridines
Name the 3 drugs in this class
Act on arterial vascular smooth muscle cells to cause vasodilation
Nifedipine, nicardipine, nimodipine
44
MOA of benzothiazepines
Drug in this class
Blocks calcium channels in AV node
Diltiazem (cardizem)
45
General MOA of Calcium channel blockers
Bind to alpha1 subunit of slow L-type calcium ion channels to block Calcium from entering cardiac and vascular smooth muscle cells (particularly in arteries
46
Two main effects of reduction of calcium in heart and nodal tissue
1. Fails to activate myosin which reduces contraction
2. Slows depolarization of SA and AV nodal tissue
47
Effects of ca++ channel blockers on HR, contractility, nodal tissue, vessels
Negative inotropic and chronotropic
Decreased SA node activity and slowed conduction through AV node
Vasodilation and deceased BP
Relaxes coronary artery vasospasm (in complement to nitrates)
48
4 main uses of calcium channel blockers
1. Coronary artery vasospasm
2. Unstable angina pectoris
3. Chronic stable angina
4. Essential hypertension
49
Which class of calcium channel blcoker carries increased risk?
"Almost too potent" as TC says
What are the increased risks?
Dihydropyrimidine derivatives (nifidepine)
Increased risks:
- CV complications (hypotension, strokes, MI)
- Perioperative bleeding, GI hemorrhage
- Development of cancer (compared to beta-blockers, ACE-Is)
Anyone know if this just applies to nifedipine or all 3 of them?
50
Verapamil is a deriverate of \_\_\_\_\_\_\_\_
Papaverine
51
How does verapamil affect contractility, HR, conduction, and vasculature?
* Decreased contractility
* Decreased HR
* Decreased conduction through AV node
* Relaxation of vascular smooth muscle, coronary arteries
52
Uses of Verapamil
Treatment of SVT and HTN
53
metabolism of Verapamil for IV and PO forms
Elimination 1/2 life
IV: 70% renal, 15% bile
Oral: nearly complete hepatic
6-10 hours
54
Effect of combining verapamil and volatiles
Additive myocardial depressant and vasodilation effects, even in normal LV function
55
which drug vasodilates coronary and peripheral arteries even better than verapamil?
Nifedipine
56
Effects of nifedepine on vessels, BP, contractility
Vasodilation of coronary and peripheral arteries
Decreased BP
Directly decreased contractility, chronotropic, and dromotropic effects
57
Explain effects of nifedipine on HR
Directly decreases chronotopic (HR)
However, indirectly may cause baroreceptor mediated increase in HR that may outweigh direct decrease
58
Metabolism of nifedipine
Elimination half life
Hepatic
2-5 hours
59
Uses of nifedipine
* Angina
* Especially coronary artery vasospasm
* Hypertension emergencies
60
Contraindications/caution/reasons to stop nifedepine
- Severe hypotension (duh?)
- MI
- Cerebrovascular ischemia
61
Side effects of nifedipine
* Flushing
* Headache
* Vertigo
* Hypotension
* may cause renal dysfunction
62
What can occur from abrupt discontinuation of nifedipine
Soooo should you take it the day of surgery?
Coronary artery vasospasm
TC says take it the morning of surgery because that would be bad during surgery
63
Which Calcium channel blocker has the greatest vasodilating effects, especially on coronary arteries?
Does this drug affect conduction?
Nicardipine (Cardene)- selective arterial vasodilator
Does not effect SA or AV node and has minimal myocardial depressant effects
64
Which Calcium channel blocker is incompatible with LR?
Cardene
65
Concentration and dose of cardene
25 mg in 240 ml solution (0.1 mg/ml)
Start at 5 mg/hr (50 ml/hr) and titrate by 2.5 mg/hr every 5-15 mins to a max of 15 mg/hr
66
3rd generation dihydropyride
Fast or slow onset?
Bolus or titratable?
Clevidipine (cleviprex)
Rapid onset
Titrable
67
Which calcium channel blocker is a lipid emulsion?
What is the max dose and why is it important to know?
Clevidipine (cleviprex)
Max dose is 32 mg/hr because of risk of increased triglycerides
68
Which calcium channel blocker would be useful in patient with severe organ dysfunction? Why?
Clevedipine
Because it is metabolized by plasma and tissue esterases independent of organs
69
Calcium channel blocker used to treat vasospasms related to subarachnoid hemorrhage
What unique property allows this
Nimodipine (Nimotop)
Highly lipid soluble allows it to cross BBB
70
Potential adverse effect of Nimodipine if intracranial compliance is a concern
Increase in ICP can occur due to vasodilation
71
Is nimodipine short term or long term use?
Dosage forms available
Short term use (~21 days)
PO form only makes it a realy pain in the butt apparently
72
Which calcium channel blocker is given more for conduction issues?
how does it work?
Diltiazem
Blocks calcium channels in the AV node
73
Uses of diltiazem
SVT, angina pectoris
74
Dose of diltiazem
Elimination of diltiazem
Dose 0.25 mg/kg IV over 2 mins
May repeat in 15 mins if needed
Elimination: 60% in bile and 35% in urine
75
Which calcium channel blocker may be used to decrease HR significantly for off-pump CABG?
Diltiazem
76
Name some drugs that may interact with calcium channel blockers
* Volatiles
* NMB
* Local anesthetics
* Potassium replacement
* dantrolene (with verapamil)
* Digoxin
77
Reaction between Calcium channel blockers and volatiles
Additive myocardial depression, especially with pre-existing LV dysfunction
78
Calcium channel blockers effect on NMB
Why?
What drug is this similar to?
Potentiates/ prolongs both depolarizing and non-depolarizine NMB
Calcium ions are needed to release acetylcholine at the NMJ
similar to mycin antibiotics
79
Why do calcium channel blockers increase risk of LAST?
Inhibition of NA ion movement via Na channels
80
How do Ca channel blockers increase risk of hyperkalemia with K replacement?
Inhibition of K moving into cell
81
Potential adverse effect of combining verapamil + dantrolene
hyperkalemia
82
Effect of calcium channel blockers on digoxin
Increased digoxin plasma concentration
Decreases its clearance
83
Uses for vasodilators
- hypertension
- induce controlled hypotension
- encourage LV stroke volume
84
effects of vasodilators
- decreased BP
- decrease SVR
- decrease VR and CO
85
How do nitrovasodilators work?
Cause both pulmonary and systemic vasodilation by producing nitric oxide
More specifically, nitric oxide increases intracellular cGMP causing smooth muscle relaxation resulting in decreased intracellular calcium
Similar to effect of cAMP from beta2 stimulation
86
How can nitric cause pulmonary vasoconstriction specifically
can be inhaled in the gaseous state
87
Effect of essential hypertention on endogenous nitric oxide
Decreased NO release
88
Effect of septic shock on endogenous NO
Excessive NO release
89
Effect of atherosclerosis on endogenous NO
Decreased NO causing platelet aggregation and vasoconstriction
90
Effect of cirrhosis on endogenous NO
Excessive production of NO
Responsible for hyperdynamic state (decreased SVR, increased CO)
91
CV effects of NO
* Release from NO from endothelial cells due to shear stress and pulsatile arterial flow
* Regulates baseline SVR and PVR
* Impacts distribution of CO
* Autoregulation- increased NO production with decreased oxygenation
92
Which produces more NO, arteries or veins?
Impact?
Arteries
This is why the IMA remains patent longer than saphenous vein grafts
93
Pulmonary effects of NO
Bronchodilation
Selective dilation of vessels to ventilated alveoli
94
Platelet effects of NO
inhibits platelet activation, aggregation, and adhesion (antithrombotic)
95
Nervous systom effects of NO
Neurotransmitter in the brain, spinal cord, and peripheral nervous system
- may be involved in antinociception and anesthetic effects
96
GI effects of NO
Produces relaxation of smooth muscle in the GI tract
97
Immune response of NO
Produced in response to activation of macrophages
- Can damage bacteria, fungi, and protozoa
98
Anesthetic effects of NO
* NO involved in excitatory neurotransmission
* Anesthetics suppress formation of NO to decrease excitatory neurotransmission and enhance GABA inhibitor effects
* NO synthase inhibitors have dose-dependent reduction in MAC
99
What populations is NO approved for use?
Neonates- has decreased use of ECMO
Use in adults is off label
100
Nipride is a direct acting vasodilator
Does it dilate arterial, venous or both?
Both
101
Onset and duration of nitroprusside
Considerations?
Rapid onset (60-90 seconds)
Short duration
Requires infusion and titration
Needs to be on pump (not roller clamp) and patient needs art line
102
Dose of Nitroprusside
Max dose
0.25-1 mcg/kg/min up to 5 mcg/kg/min
BUT Max infusion dose is 2 mcg/kg/min to prevent cyanide toxicity??
103
MOA of nitroprusside
Reacts with hemoglobin to form methemoglobin and release cyanide and NO which causes vasodilation
104
Why can nitroprusside cause cyanide toxicity?
Nipride is 44% cyanide
During metabolism five cyanide ions are released
105
Who is more susceptible to cyanide toxicity
* Infusion dose \>2 mcg/kg/min
* Children or young adults due to baroreceptor reflexes causing SNS stimulation requiring larger dose
* In pregnancy, fetus is more at risk
* If the drug is not protected from light, it can breakdown into cyanide
106
How long is nitroprusside safe for when protected from light?
24 hours
107
S/S of cyanide toxicity
* Tissue anoxia
* Anaerobic metabolism
* Lactic acidosis
* Unresponsive to previously therapeutic doses
* Increased MvO2 due to inability of tissues to use O2
* CNS dysfunction, seizures
108
Treatment for cyanide toxicity
* Stop infusion
* 100% O2
* May need to use a different anti-hypertensive
* Sodium bicarb to correct acidosis
* Sodium thiosulfate to be a sulfur donor to convert cyanide to thiocyanate
109
Nipride is a coronary artery vasodilator
In a good or bad way?
BAD- Can cause coronary steal
Potential for preferential blood flow to bigger vessels
110
CV effects of nitroprusside
* Direct arterial and venous dilation
* Decreased BP, SVR
* Indirect increase in HR and contractility (reflex)
* May have increased CO due to heart pumping agianst lower afterload
* Coronary artery vasodilation (steal)
* Decrease in diastolic blood pressure
111
CNS effects of nitroprusside
- Increased CBF and CBV
- If decreased compliance can dangerously increase ICP
112
With nitroprusside, when are ICP increases maximal
When are they maintained normal
Maximal ICP increase if MAP decreases \<30%
Maintained if MAP decreases \>30%
113
How to prevent increase in ICP with nipride/SNP
Influse slowly to lower BP over 5 minutes
Along with hyperoxia and hypocarbia
Also could just wait until dura is open
114
Contraindications to nitroprusside
Increased ICP and inadequate CBF
Patients with carotid artery stenosis
115
Pulmonary effects of nitroprusside
How to treat
- Decrease in PaO2
- Alteration of hypoxic pulmonary vasoconstriction
- More of an issue in healthy lungs than COPD patients (develop vascular changes to prevent)
Treatment: add PEEP
116
What dose of nipride can inhibit platelet aggregation?
Is it clinically significant?
Dose \>3 mcg/kg/min
Not clinically significant
117
Which drug used for deliberate hypotension is most likely to maintain cerebral perfusion?
(not 100% sure this is what this means but we will go with it)
Nitroprusside
118
Why is nitroprusside good for hypertensive emergencies?
- effective no matter the cause so good for inital temporary treatment until you can figure something else out
- Onset, titration, and offset are all quick
119
Use of nitroprusside in cardiac diseases
* MR
* AR
* CHF
* MI with LV failure (but may combine with inotrope)
120
use of nitroprusside in aortic surgery
- to treat HTN related to cross-clamping
SOS idk what this means but- may cause spinal cord ischemia related to distal hypotenion and something about the artery of adamkiewicz
121
Use of nitroprusside at the end of cardiac surgery
- Used in the rewarming period to caue vasodilation to distribute warmth to periphery
- To treat pulmonary HTN after valve replacement
122
Nitroglycerine vasodilates
Arteries, veins, both?
Venous \> arterial
- only vasodilates arterial at elevated doses
123
MOA of nitroglycerine
- Produces NO which causes peripheral vasodilation
124
Routes of nitroglycerine
IV, sublingual, transdermal
Sublingual- onset 4 minutes
Transdermal - sustained protection from MI
125
Special considerations with nitroglycerine infusion
Requires special tubing and glass bottles to prevent absorption into plastic
126
Elimination 1/2 life of nitroglycerine
1.5 minutes
So requires infusion
127
AE of nitroglycerine
May cause production of methemoglobin when the nitrite metabolite oxidizes the ferrous ion in hemoglobin
128
Treatment of methemoglobinemia with nitroglycerine
- Methylene blue 1-2 mg/kg IV over 5 minutes to convert back to hemoglobin
129
At what dose of nitroglycerine can arterial vasodilation occur
\>2 mcg/kg/min
130
Which is more potent, nipride or nitroglycerine?
Nipride
131
Effects of nitroglycerin on vessels
* Venous dilation (and arterial \>2 mcg/kg/min)
* Decreased venous return, LVEDP, RVEDP
* Dilates larger conductance vessels of coronary circulaiton
* Relaxes pulmonary vessels
132
Does nitroglycerine cause coronary steal?
No
Provides better flow to ischemic areas
133
Smooth muscle effects of nitroglycerine
* Relaxes bronchial smooth muscle
* Relaxes biliary tract smooth muscles (sphincter of Oddi)
* Relaxes esophageal muscles
* Relaxes uterine and ureteral smooth muscle
134
Which is more likely to cause increased ICP, nitroglycerine or nipride?
More likely with nipride but both can cause
135
Effect of nitroglycerine on platelet
inhibits aggregation
136
Clinical uses of nitroglycerine
- Angina pectoris
- Cardiac failure
- Acute hypertension
- Deliberate hypotension
137
Effect of nitroglycerine on angina
- Decrease CMRO2 and vasodilates coronary arteries to ischemic areas
Decreases size of MI
138
Effect of nitroglycerine on cardiac failure
- Decrease preload and relieve pulmonary edema
139
Consideration with use of nitroglycerine for acute hypertension in pregnant mom
Better for maternal patient during C-section with no effects on fetus
140
Use of nitroglycerine for deliberate hypotension compared to SNP
Less potent than SNP
Less decrease in DBP than SNP
Decrease is more related to intravascular volume
141
Uses of isosorbide dinitrate
- Prophylaxis of angina pectoris (chronic)
- Prolonged antianginal effect
- Increases exercise tolerance up to 6 hours
142
Vasodilation with isosorbide dinitrate
arteries, veins, or both?
Venous \> arterial
143
Does isosorbide dinitrate cause steal?
No, redirects blood flow to ischemic areas
144
Isosorbide is given to what patients preop
CABG
TC says maybe to vasodilate their saphenous but she doesnt really know ?
145
Vasodilation with hydralazine
Arterial, venous, or both?
Arterial \> venous
Dilates coronary, cerebral, renal, splanchnic, and pulmonary vessels
146
MOA of hydralazine
Interference with calcium ion transport
147
Hydralazine effect on BP, HR, SV, and CO
Possible adverse effect
Decreases diastolic more than systolic (so not good for coronary perfusion)
Increases HR both directly and baroreceptor mediated
Increases SV and CO
Can cause MI, prevent with Beta-blocker
148
Onset and duration of hydralazine
- 10 -20 minutes (TC says be patient)
- Duration 2-4 hours but very unpredictable
149
Hydralazine metabolism
Mostly hepatic
150
Side effects of hydralazine
| (more with chronic use)
* Lupus like autoimmune syndrome
* Peripheral neuropathies
* Vertigo
* Diaphoresis
* Nausea
* Tachycardia - uncommon
151
What may offset benefit of decreased BP with trimethorphan
Increased HR
152
Effects of trimethorphan
- Ganglion blocker- blocks ANS reflexes
- Vasodilation of venous capacitance vessels
- Decreases CO, SVR
- Blocks receptors for acetylcholine
153
What is adenosine and what is its role?
An endogenous nucleotide in all cells
Maintains balance of oxygen supply and demand of heart and all other organs
154
Effects of adenosine
- Dilation of coronary arteries
- Negative chronotropic
155
MOA of adenosine
Stimulation of K channels in supraventricular cells to hyperpolarize atrial cells and slow SA node
Can also stimulate release of NO from endothelial cells
156
Uses of adenosine
- SVT and narrow complex tachycardia (not a fib or v tac)
- Deliberate hypotension
157
Dose and elimination 1/2 life of adenosine
6 mg IV, 12 mg, then 18 (some say repeat 12 mg dose)
Can repeat within 60 seconds
1/2 life 0.6-1.5 seconds
158
Adenosine for deliberate hypotension
Why is it good?
General effects
Rapid responsiveness, onset and recovery (must be used as infusion)
Decreases SVR, increases HR, coronary flowincreased, cardiac filling pressures unchanged
220 mcg/kg/min
159
Does adenosine cause coronary steal?
Yes
160
Dose of adenosine for deliberate hypotension
Tachyphylaxis?
220 mcg/kg/min
No tachypylaxis
161
Effects of adenosine 1 receptor activation
* Slowing of rhythm
* Negative inotropic
* Vasoconstriction
* Bronchoconstriction
* Sedation
* Anticonvulsant
* Decreased neurotransmitter release
162
Effect of Adenosine 2 receptor activation
- vasodilation
- Bronchodilation
- Complex stimulant effects
- Increased neurotransmitter release
- Platelet aggregation inhibition
163
Effect of nitroglycerine on CO
* CO decreased in normal heart with no CHF
* CO improved if patient in HF, and pulmonary congestion is relieved
164
Effect of nitroglycerine on BP
* Decreased BP (related more to volume than SNP)
* Decreased DBP, decreased coronary blood flow
165
Effect of nitroglycerine on HR and contractility
* Baroreceptor reflex tachycardia
* Increased ionotropic
166
anesthesia challenges for pts with untreated HTN
likely to be vasoconstricted, volume depleted, autoregulation shifted higher
167
AEs of Nipride
| (table 9-1)
* hypotension
* N/V
* apprehension
* increased cyanide tox with sucky kidneys
168
AEs of labetolol
| (table 9-1)
* hypotension
* heart block
* heart failure
* bronchospasm
* N/V
* scalp tingling
* paradoxical pressor response
169
AEs of nitroglycerin
| (table 9-1)
* headache
* N/V
* beta tolerance with prolonged use (?)
170
AEs of phentolamine
| (table 9-1)
* hypotension
* tachycardia
* headache
* angina
* paradoxical pressor response
171
AEs of hydralazine for treatment of eclampsia
(table 9-1)
* hypotension
* fetal distress
* tachycardia
* headache
* N/V
* local thrombophlebitis
172
AEs of nicardipine
| (table 9-1)
* hypotension
* headache
* N/V
173
to summarize table 9-1:
all the anti hypertensives can cause hypotension (shocker), N/V, and headache
:)
