CV Drugs- ACE Inhibitors, Calcium Channel Blockers, Vasodilators Flashcards
(216 cards)
1
Q
concerns with antihypertensives and anesthesia- interference with the sympathetic nervous system’s activity resulting in
A
orthostatic hypotension related to hypovolemia, position change, or decreased venous return (PPV)
2
Q
concerns with antihypertensives and anesthesia- possible depletion of
A
norepinephrine stores- minimal response to indirect sympathomimetics
3
Q
concerns with antihypertensives and anesthesia- exaggerated response to
A
direct sympathomimetics- due to no counter- balancing beta 2 activity
4
Q
beta-blockers may improve
A
the outcome of patients with HTN
5
Q
other than __, HTN medication should be continued even on the morning of surgery- fewer alteration in BP and HR, fewer arrhythmias
A
diuretics
6
Q
antihypertensives drug classes
A
- beta-adrenergic blockers- negative chronotropic, inotropic
- combined alpha1 and beta-adrenergic blocker (labetolol)- negative inotropic, chronotropic, vasodilation; not as potent as beta-blockers or phentolamine
- alpha 1-adrenergic blocker (prazosin, phentolamine)- vasodilation
- centrally acting alpha 2-adrenergic agonist (clonidine, dex)- decrease sympathetic outflow
7
Q
ACEi MOA
A
- inhibit the ACE in both the plasma and in the vascular endothelium
- block the conversion of angiotensin I to angiotensin II
- prevent the vasoconstriction from angiotensin II and the stimulation of the SNS
- decrease aldosterone-decreased Na and water retention (however, increased K)
8
Q
ACEi advantage
A
minimal side effects compared to beta-blockers, diuretics
9
Q
ACEi indications
A
- HTN (in diabetes)
- CHF
- mitral regurgitation (F, F, V)
- development of CHF (regression of LVH)
10
Q
ACEi contraindications
A
patients with renal artery stenosis (their renal perfusion is highly dependent on angiotensin II)
11
Q
ACEi benefit
A
minimal side effects
12
Q
most common side effects
A
cough, upper respiratory congestion, rhinorrhea, allergic-like symptoms (potentiation of kinins and inhibition of breakdown of bradykinins)
13
Q
ACEi angioedema
A
potentially life-threatening (epi 0.30-0.5 ml of 1:1,000 dilution)
14
Q
ACEi hyperkalemia
A
due to decreased production of aldosterone (especially CHF with renal insufficiency)
15
Q
ACEi angioedema may occur
A
unexpectedly after prolonged drug use
16
Q
ACEi hereditary angioedema is due to
A
C1 esterase inhibitor deficiency
17
Q
ACEi induced angioedema is due to
A
increased availability of bradykinin because bradykinin catabolism is blocked
18
Q
how is angioedema treated?
A
- epi (catecholamines, antihistamines, and antifibrinolytics may be ineffective in acute episodes)
- tranexamic acid or aprotinin- inhibits plasmin activation
- Icatibant- a synthetic bradykinin receptor antagonist
- FFP- 2-4 units- to replace the deficient enzyme
19
Q
ACEi- captopril (Capoten)- causes
A
decreased SVR- especially in renal
20
Q
ACEi- captopril (Capoten)- __, __ not effected
A
CO, HR
21
Q
ACEi- captopril (Capoten)- __ reduced
A
baroreceptor sensitivity (HR does not increase with decreased BP)
22
Q
ACEi- captopril (Capoten)- may cause
A
hyperkalemia (related to blocking of aldosterone release)
23
Q
ACEi- captopril (Capoten)- onset
A
15 min
24
Q
ACEi- captopril (Capoten)- duration
A
6-10 hours
25
ACEi- enalapril (Vasotec)- dose PO
20 mg PO
26
ACEi- enalapril (Vasotec)- dose IV
0.625-1.25 mg
27
ACEi- enalapril (Vasotec)- onset
approx 1 hour
28
ACEi- enalapril (Vasotec)- duration
18-30 hours
29
ACEi- enalapril (Vasotec)- lacks
the rash and pruritus side effects of captopril; rarely angioedema of the face, lips, tongue, and glottis; watch for hypotension
30
losartan (Cozaar)- MOA
blocks the binding of angiotensin II to the receptors (type AT1- found in vascular smooth muscle) to prevent vasoconstriction and aldosterone release
31
losartan (Cozaar)- side effects
similar as ACEi
32
losartan (Cozaar)- risk of
stroke reduction 25% (compared to atenolol)
33
losartan (Cozaar)- dose
50mg
34
losartan (Cozaar)- may be combined with
thiazide diuretic or inhibitor of neprilysin (Entresto)
35
calcium channel blockers classifications
1. phenylalkylamines
2. 1,4-dihydropyridines
3. benzothiazepines
36
CCB- phenylalkylamines
occludes the channel (verapamil)
37
CCB- 1,4-dihydropryridines
arterial vascular smooth cells (nifedipine, nicardipine, nimodipine)
38
CCB- benzothiazepines
AV node, MOA? (diltiazem)
39
CCB MOA
1. bind to the alpha subunit of the slow L-type calcium ion channels
2. block calcium entering the cardiac and vascular smooth muscle cells (arterial specific)
3. reduction of calcium
40
CCB MOA of reduction of calcium
1. fails to activate myosin- which reduces contraction
2. slows depolarization of SA and AV nodal tissue
41
CCB effects- __ inotropic, chronotropic effects
negative
42
CCB effects- __ SA node activity
decreased
43
CCB effects- conduction slowed through the
AV node
44
CCB effects- vaso__, __ BP
dilation, decreased
45
CCB effects- relaxes
coronary artery spasm (complements nitrate- different MOA)
46
CCB uses
1. treatment of coronary artery spasm
2. unstable angina pectoris
3. chronic stable angina
4. essential hypertension
47
CCB increased risk with dihydrophyrimidine derivates (nifedipine)
1. CV complications (placebo)
2. perioperative bleeding, GI hemorrhage
3. development of cancer (beta-blockers, ACE inhibitors)
48
CCB- verapamil (Calan)- is a derivative of
papaverine
49
CCB- verapamil (Calan)- effects
1. decreases contractility
2. decreased HR
3. decreased conduction through AV node
4. relaxation of vascular smooth muscle, coronary arteries
50
CCB- verapamil (Calan)- uses
treatment of SVT (AV node), HTN
51
CCB- verapamil (Calan)- dose
75-150mcg/kg (2.5-5mg) IV slowly
52
CCB- verapamil (Calan)- onset
1-3 minutes
53
CCB- verapamil (Calan)- oral nearly complete __ metabolism
hepatic
54
CCB- verapamil (Calan)- IV metabolism
70% renal and 15% bile
55
CCB- verapamil (Calan)- elimination 1.2 life
6-12 hours
56
CCB- verapamil (Calan)- combination with volatile anesthesia
has additive myocardial depressant and vasodilation effects, even in normal LV function
57
CCB- nifedipine (Adalat, Procardia)-
dihydropyridine
58
CCB- nifedipine (Adalat, Procardia)- vasodilation of
coronary and peripheral arteries (>verapamil)
59
CCB- nifedipine (Adalat, Procardia)- __ BP
decreases
60
CCB- nifedipine (Adalat, Procardia)- ___HR
indirect baroreceptor-mediated increased
61
CCB- nifedipine (Adalat, Procardia)- __ contractility, __ chronotropic, and __ effects
directly decreased
decreased
dromotropic
62
CCB- nifedipine (Adalat, Procardia)- admin
PO, IV, SL
63
CCB- nifedipine (Adalat, Procardia)- uses
1. angina
2. especially coronary artery vasospasm
3. hypertension emergencies (CAUTION/STOP-cerebrovascular ischemia, MI, severe hypotension)
64
CCB- nifedipine (Adalat, Procardia)- dose
10-20 mg PO or SL
65
CCB- nifedipine (Adalat, Procardia)- onset
20 min
66
CCB- nifedipine (Adalat, Procardia)- metabolism
hepatic
67
CCB- nifedipine (Adalat, Procardia)- elimination 1/2 life
2-5 hours
68
CCB- nifedipine (Adalat, Procardia)- side effects
1. flushing
2. HA
3. vertigo
4. hypotension
5. may cause renal dysfunction
69
CCB- nifedipine (Adalat, Procardia)- abrupt stop has causes
coronary artery vasospasm
70
CCB- nicardipine (Cardene)- __ vasodilation
selective arterial (SVR)
71
CCB- nicardipine (Cardene)- __ vasodilation effects
greatest (especially coronary arteries)
72
CCB- nicardipine (Cardene)- does not effect
the SA node of AV node, minimal myocardial depressant effects
73
CCB- nicardipine (Cardene)- dose
25 mg in 240 ml (0.1mg/ml)
titrate- start at 5mg/hr (50ml/hr), increase by 2.5 mg/hr every 5-15 mins to a max of 15 mg/hr
74
CCB- nicardipine (Cardene)- not compatible with
LR
75
CCB- clevidipine (Cleviprex)-
3rd generation dihydropyridine
76
CCB- clevidipine (Cleviprex)- onset
rapid, titratable
77
CCB- clevidipine (Cleviprex)- __ emulsion
lipid (similar to propofol)
78
CCB- clevidipine (Cleviprex)- metabolism
plasma and tissue esterases (organ independent)
79
CCB- nimodipine (Nimotop)- highly
lipid soluble to cross BBB
80
CCB- nimodipine (Nimotop)- used to treat
vasospasm related to subarachnoid hemorrhage
81
CCB- nimodipine (Nimotop)- dose
0.7 mg/kg PO then 0.35 mg/kg q4 hours for 21 days
82
CCB- nimodipine (Nimotop)- if intracranial compliance is a concern,
an increase in ICP could occur
83
CCB- diltiazem (Cardizem, Dilacor, Tiazac)-
benzothiazepine
84
CCB- diltiazem (Cardizem, Dilacor, Tiazac)- blocks
channels in the AV node
85
CCB- diltiazem (Cardizem, Dilacor, Tiazac)- uses
treatment of SVT, angian pectoris
86
CCB- diltiazem (Cardizem, Dilacor, Tiazac)- dose
0.25 mg/kg IV over 2 minutes, may repeat in 15 min if needed
infusion 10mg/hr
87
CCB- diltiazem (Cardizem, Dilacor, Tiazac)- elimination
via bile (60%) and urine (35%)
88
CCB- diltiazem (Cardizem, Dilacor, Tiazac)- elimination 1.2 time
3-5 hours
89
CCB drug interactions- volatile anesthetics
additive myocardial depression and vasodilation, especially with preexisting LV dysfunction
90
CCB drug interactions- depolarizing and nondepolarizing NMB drugs like mucin antibiotics
potentiated (Ca ions are needed to release acetylcholine at the NM junction)
91
CCB drug interactions- LA
increased risk of toxicity (inhibition of Na ion movement via Na channels)
92
CCB drug interactions- K replacement
hyperkalemia due to inhibition of K moving into cell
93
CCB drug interactions- __ and __ cause hyperkalemia
verapamil and dantrolene
94
CCB drug interactions- digoxin
increase in digoxin plasma concentration- decreasing its clearance
95
vasodilators- indications
1. treat HTN
2. induce controlled hypotension
3. encourage LV SV
96
vasodilators- effects
1. decrease BP
2. decrease SVR (arterial)
3. decrease venous return and CO (ventilator)
97
nitric oxide- nitrovasodilators cause
both pulmonary and systemic vasodilation be producing NO
98
nitric oxide- increases
intracellular cGMP causing smooth muscle relaxation (results ultimately from decreased intracellular calcium similar to the effect of cAMP from beta 2 stimulation)
99
nitric oxide- can be
inhaled in the gaseous state to cause pulmonary vasodilation specifically
100
nitric oxide- endogenous- CV effects: release of NO from endothelial cells due to
shear stress and pulsatile arterial flow
101
nitric oxide- endogenous- CV effects: regulation
SVR and PVR- baseline
102
nitric oxide- endogenous- CV effects: impacts
distribution of cardiac output
103
nitric oxide- endogenous- CV effects: autoregulation
increased NO production with decreased oxygenation
104
nitric oxide- endogenous- CV effects: __ produce more NO than __
arteries
veins
(IMA remains patent longer than saphenous vein grafts)
105
nitric oxide- endogenous- pulmonary effects:
1. bronchodilation
2. selective dilation of vessels to ventilated alveoli
106
nitric oxide- endogenous- platelet effects:
inhibits plt activation, aggregation, and adhesion (antithrombotic)
107
nitric oxide- endogenous- nervous system effects: NT in
brain, spinal cord, and peripheral nervous system
108
nitric oxide- endogenous- nervous system effects: may be involved in
antinociception and anesthetic effects
109
nitric oxide- endogenous- nervous sytem effects: produce
relaxation of smooth muscle of the Gi tract
110
nitric oxide- endogenous- immune response: produced in response to
activation of macrophages
111
nitric oxide- endogenous- immune response: can damage
bacteria, fungi, and protozoa
112
pathophysiologic effects related to NO- essential hypertension
decreased NO release
113
pathophysiologic effects related to NO- sepsis shock
excessive NO release
114
pathophysiologic effects related to NO- atherosclerosis
decreased NO, plt aggregation, vasoconstriction
115
pathophysiologic effects related to NO- cirrhosis
excessive production of NO
116
anesthetic effects on NO- involved in the
excitatory neurotransmission
117
anesthetic effects on NO- anesthetics cause suppression of
formation of NO to decrease excitatory NT and enhance GABA inhibitory transmission
118
anesthetic effects on NO- administration of NO synthase inhibits have __ in MAC
dose dependent reduction in
119
uses of NO
1. inhaled form to treat PH (use in any other than neonates is "off label")
2. in neonates, its use has decreased the use of ECMO
120
sodium nitroprusside (SNP, nipride)- is a
direct-acting, arterial and venous vascular smooth muscle relaxant
121
sodium nitroprusside (SNP, nipride)- causes vasodilation of
arterial and venous
122
sodium nitroprusside (SNP, nipride)- onset
60-90 seconds
123
sodium nitroprusside (SNP, nipride)- duration
short requiring infusion, titration
124
sodium nitroprusside (SNP, nipride)- monitoring
careful, infusion device used
125
sodium nitroprusside (SNP, nipride)- dose
0.25-1 mcg/kg/min, up to 5 mcg/kg/min (body can handle only 2 mcg/kg/min continuous)
126
sodium nitroprusside (SNP, nipride)- MOA
reacts with hemoglobin to form methemoglobin and releases cyanide and NO; NO causes the vasodilation
127
sodium nitroprusside (SNP, nipride)- is __ cyanide and during metabolism __
44%
5 cyanide ions are release making cyanide toxicity possible0 causing tissue anoxia, anaerobic metabolism, and lactic acidosis
128
sodium nitroprusside (SNP, nipride)- susceptible to CN toxicity
1. receiving infusion of > 2 mcg/kg/min
2. children or young adults- baroreceptor reflexes cause stimulation of SNS, require larger dose
3. pregnancy- fetal cyanide toxicity
129
sodium nitroprusside (SNP, nipride)- signs and symptoms of CN toxicity
1. unresponsive to previously therapeutic doses of SNP
2. increased MvO2- inability of tissues to use oxygen
3. metabolic acidosis
4. CNS dysfunction, seizures
130
sodium nitroprusside (SNP, nipride)- treatment of CN toxicity
1. stop infusion
2. 100% O2
3. sodium bicarb to correct met acidosis
4. sodium thiosulfate to be a sulfur donor to convert cyanide to thiocyanate
131
sodium nitroprusside (SNP, nipride)- must be protected from
the light to prevent breakdown into cyanide; light-protected solution are safe for 24 hours
132
sodium nitroprusside (SNP, nipride)- CV effects:
direct partial and venous vasodilation
133
sodium nitroprusside (SNP, nipride)- CV effects: __ BP, SVR
decreased
134
sodium nitroprusside (SNP, nipride)- CV effects: __ HR and contractility
indirect increase in
135
sodium nitroprusside (SNP, nipride)- CV effects: __ CO
may have increased
136
sodium nitroprusside (SNP, nipride)- CV effects: ___ vasodilation which creates __
coronary artery
coronary steal from ischemic areas
137
sodium nitroprusside (SNP, nipride)- CV effects: __ diastolic pressure
decrease
138
sodium nitroprusside (SNP, nipride)- CNS effects: __ CBF
increased
139
sodium nitroprusside (SNP, nipride)- CNS effects: __ CBV
increased
140
sodium nitroprusside (SNP, nipride)- CNS effects: if pt has decreased intracranial compline,
ICP may become dangerously elevated
141
sodium nitroprusside (SNP, nipride)- CNS effects: ICP increases are maximal if
MAP decreases less than 30%; if >30% decrease in MAP, the ICP returns to normal
142
sodium nitroprusside (SNP, nipride)- CNS effects: to prevent the increase in ICP,
infuse SNP to slowly lower BP over 5 minutes along with hyperopia and hypocarbia
143
sodium nitroprusside (SNP, nipride)- CNS effects: once the dura is open, ICP
problems are not a problem
144
sodium nitroprusside (SNP, nipride)- CNS effects: contraindications
patients with increased ICP and inadequate CBF, and patents with carotid artery stenosis
145
sodium nitroprusside (SNP, nipride)- pulmonary effects:
decrease in the PaO2
146
sodium nitroprusside (SNP, nipride)- pulmonary effects: alteration of
HPV
147
sodium nitroprusside (SNP, nipride)- pulmonary effects: bigger problem in
healthy lungs
148
sodium nitroprusside (SNP, nipride)- pulmonary effects: COPD lungs develop
vascular changes that prevent the alteration of HPV
149
sodium nitroprusside (SNP, nipride)- pulmonary effects: treatment of alteration in HPV
add PEEP
150
sodium nitroprusside (SNP, nipride)- inhibits
platelet aggregation (>3 mcg/kg/min); not clinically significant- bleeding not increased
151
sodium nitroprusside (SNP, nipride)- clinical uses:
1. deliberate hypotension
2. hypertensive emergencies
3. cardiac disease
4. aortic surgery
5. cardiac surgery
152
sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- mostly likely to
maintain cerebral perfusion
153
sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- initial rate
0.3-0.5 mcg/kg/min
154
sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- should not exceed
2 mcg/kg/min
155
sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- combined with other agents to
minimize risk of CN toxicity
156
sodium nitroprusside (SNP, nipride)- clinical uses: HTN emergencies-
temporary initial treatment, effective no matter the cause, onset, tritration, quick offset
157
sodium nitroprusside (SNP, nipride)- clinical uses: cardiac disease-
decreased afterload (MR, AR, CHF, MI with LV failure but may also need inotrope)
158
sodium nitroprusside (SNP, nipride)- clinical uses: aortic surgery
treat HTN related to cross-clamp, spinal cord ischemia- distal hypotension
159
sodium nitroprusside (SNP, nipride)- clinical uses: cardiac surgery
1. rewarming period to cause vasodilation to distribute warmth to periphery
2. treat PH after valve replacement
160
nitroglycerin-
organic nitrate
161
nitroglycerin- dilates
venous side except, at elevated doses, it will relax arterial smooth muscle
162
nitroglycerin- MOA
produces NO which causes peripheral vasodilation
163
nitroglycerin- sublingual onset
4 minutes
164
nitroglycerin- transdermal
sustained protection from MI
165
nitroglycerin- infusion requires
special tubing and glass bottles to prevent absorption into the plastic
166
nitroglycerin- elimination 1/2 life
1.5 minutes; requires infusion
167
nitroglycerin- may cause
the production of methgb when the nitrite metabolite oxidizes the ferrous ion in hgb
168
nitroglycerin- methgb treatment
methylene blue 1-2 mg/kg IV over 5 minutes to convert back to hgb
169
nitroglycerin- CV effect: __ dilation
venous (up to 2mcg/kg/min)
170
nitroglycerin- CV effect: __ venous return, LVEDP, RVEDP
decreased
171
nitroglycerin- CV effect: CO __
decreased (in normal heart with no CHF; if patient in heart filature, the CO is improved, and pulmonary congestion is relieved)
172
nitroglycerin- CV effect: _ BP
decreased (related more to volume than SNP)
173
nitroglycerin- CV effect: __ DBP, coronary blood flow
decreased
174
nitroglycerin- CV effect: __ tachycardia, __ inotropic effect
baroreceptor-reflex
increased
(increased demand, decrease supply)
175
nitroglycerin- CV effect: dilates
larger conductance vessels of the coronary circulation- provides better blood flow to ischemic areas
176
nitroglycerin- CV effect: relaxes
pulmonary vessels
177
nitroglycerin- smooth muscle effect: relaxes
1. bronchial smooth muscle
2. biliary tract smooth muscle (sphincter of ddi)
3. esophageal muscles
4. uterine and ureteral smooth muscles
178
nitroglycerin- CNS effect:
1. cerebral vasodilation
2. inhibition of plt aggregation
179
nitroglycerin- clinical uses:
1. angina pectoris
2. cardiac failure
3. acute HTN
4. deliberate hypotension
180
nitroglycerin- clinical uses: angina pectoris
decrease myocardial oxygen demand and vasodilator coronaries to ischemic areas (decrease size of MI-not SNP)
181
nitroglycerin- clinical uses: cardiac failure
decrease preload and relieve pulmonary edema
182
nitroglycerin- clinical uses: acute HTN
maternal pt during C-section with no effects on fetus
183
nitroglycerin- clinical uses: deliberate hypotension
less potent than SNP; decrease in diastolic is less than SNP; intravascular volume has a bigger effect
184
isosorbide dinitrate-
oral nitrate- prophylaxis of angina pectoris
185
isosorbide dinitrate- prolonged __ effect, increased __
antianginal
exercise tolerance up to 6 hours
186
isosorbide dinitrate- vasodilation of
venous circulation and dilation of coronary arteries to redirect blood flow to ischemic areas
187
isosorbide dinitrate- given to
CABG patients preop
188
hydralazine (Apresoline)- direct dilation
arterial side, some venous
189
hydralazine (Apresoline)- vasodilates
coronary, cerebral, renal, and splanchnic, pulmonary vessels
190
hydralazine (Apresoline)- MOA
interferences with Ca ion transport
191
hydralazine (Apresoline)- decreases
diastolic more than systolic pressure
192
hydralazine (Apresoline)- increases
HR (baroreceptor and direct), SV, CO (can cause MI, prevented with beta-blocker)
193
hydralazine (Apresoline)- onset
10-20 minutes (prolonged)
194
hydralazine (Apresoline)- duration
2-4 hours (unpredictable)
195
hydralazine (Apresoline)- dose
10-20 mg
196
hydralazine (Apresoline)- metabolism
mostly hepatic
197
hydralazine (Apresoline)- side effects
1. lupus-like syndrome
2. peripheral neuropahties
3. vertigo
4. diaphoresis
5. nausea
6. tachycardia
uncommon in intermittent use
198
trimethaphan- is an
ganglionic blocker0 blocks autonomic nervous system reflexes
199
trimethaphan- vasodilation of
venous capacitance vessels
200
trimethaphan- __ CO, SVR
decreases
201
trimethaphan- blocks
receptors for ACh
202
trimethaphan- may have __ that offsets the benefit of __
tachycardia
decreased BP
203
trimethaphan- historical use
deliberate hypotension
204
adenosine- is an
endogenous nucleoside in all cells- maintain the balance of O2 supply and demand of the heart and other organs
205
adenosine- effects
dilation of coronary arteries (steal possible); negative chronotropic
206
adenosine- MOA
stimulation of K channels in supra ventricular cells to hyper polarize atrial cells and slowing of SA node (can also stimulate release of NO from endothelial cells)
207
adenosine- uses
1. SVT
2. deliberate hypotension
208
adenosine- uses: SVT for
paroxysmal SVT and narrow complex tachycardia (not atrial fib or v tach)
209
adenosine- for SVT dose
6 mg IV then 12 mg then 18 mg
210
adenosine- for SVT can repeat dose within
60 seconds
211
adenosine- for SVT elimination 1/2 life
0.6-1.5 seconds
212
adenosine- uses: deliberate hypotension because of
rapid responsiveness, onset and recovery
213
adenosine- for deliberate hypotension: __ SVR, __ HR, __ coronary flow, __ cardiac filling pressures
decreased
increased (reflex tachycardia)
increased
unchanged
214
adenosine- for deliberate hypotension: dose
220 mcg/kg/min- no tachyphylaxis
215
principle adenosine effects- adenosine 1 receptor effect
1. slowing of the rhythm neg inotropic effects
2. vasoconstriction
3. bronchoconstriction
4. sedation anticonvulsant effect; decrease of NT release
216
principle adenosine effects- adenosine 2 receptor effect
1. vasodilation
2. bronchodilation
3. complex stimulant effects
4. increase of NT release
5. plt aggregation inhibition
