Vasodilators, Negative Inotropes Flashcards
1
Q
What is the definition of idiopathic hypertension?
A
Related to overactivity of the ANS and an interaction with the RASS. Along with factors related to sodium homeostasis and intravascular volume.
2
Q
In the development of idiopathic hypertension, what occurs first? and it leads to what?
A
First, SVR is normal, but CO increases which increases BP.
SVR increases eventually increases to stop high BP from being transmitted to the capillary bed where it would affect cell homeostasis.
3
Q
What is the primary cause of perioperative hypertension?
A
Increased sympathetic discharge with systemic vasoconstriction
4
Q
What are the 4 types of vasodilators?
A
- Direct smooth muscle dilation
- Alpha-1 Antagonists
- Alpha-2 Agonists
- A.C.E. Inhibitors
5
Q
Afterload is improved by vasodilation of which vessels?
A
Arterial dilation
6
Q
Preload is improved by vasodilation of which vessels?
A
Venous dilation
7
Q
T/F: Pure venodilators are optimal in providing afterload reduction and pure arteriole dilators are not available?
A
False; Pure venodilators technically do not exist and arteriole dilation would cause reduction in afterload.
8
Q
What other hemodynamic effects might be seen with vasodilator administration?
A
- Reflex increase in HR to maintain CO.
2. Redistribution of coronary blood flow (some improve, some cause coronary steal).
9
Q
What percent of coronary artery perfusion occurs during systole?
A
10-20%. 70-90% occurs during diastole.
10
Q
T/F: In ischemic heart disease, the collateral arteries are maximally dilated and coronary perfusion pressure is largely pressure dependent?
A
True
11
Q
Describe coronary steal:
A
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.
12
Q
What are three examples of direct vasodilators?
A
- Hydralazine
- Nitroglycerine
- Sodium Nitroprusside
13
Q
What receptor does hydralazine stimulate?
A
Hydralazine Receptor
14
Q
Once the hydralazine Receptor is activated, what happens?
A
It is G protein coupled and has 2nd messenger pathways which amplify the signal. GC (Guanilate Cyclase) changes GTP to cGMP.
15
Q
What action does cGMP perform?
A
It blocks calcium absorption and slows down the influx of calcium which promotes relaxation.
16
Q
What CV effects will be seen with hydralazine administration?
A
- Reflex increase in HR
- Renin activity- fluid retention
- Can even see peripheral edema
- Decreased BP and SVR
17
Q
Will diastolic or systolic pressure be decreased more with hydralazine administration?
A
Diastolic>Systolic
18
Q
Hydralazine may also cause hyperpolarization of smooth muscle cells by influx of what electrolyte?
A
Potassium.
19
Q
Does hydralazine increase or decrease myocardial oxygen demand and why?
A
It increases and leads to ischemia d/t an increase in HR.
20
Q
Which patients should hydralazine be avoided in?
A
CAD, increased ICP, Lupus
21
Q
Side effects of hydralazine to be concerned with?
A
Anemia, agranulocytosis, nasal congestion, muscle cramps, edema, Hydralazine-Induced Lupus
22
Q
What is the dose, onset, and duration of hydralazine?
A
10-20mg IV
Onset 30min
Duration 4-6hrs
23
Q
Advantages of hydralazine?
A
- Maintains/increases cerebral blood flow
2. Increased CO and SV
24
Q
Disadvantages of hydralazine?
A
- Reflex tachycardia
- Sodium/water retention
- Long duration of action
- Tachyphylaxis with monotherapy.
25
What is Sodium Nitroprusside broken down into?
1 Nitrous Oxide and 5 Cyanide molecules.
26
Ultimately, what are the effects of Nitroglycerine and Sodium Nitroprusside on smooth muscle?
Relaxation. This is achieved via Nitric Oxide promoting GC (guanilate cyclase) which converts GTP to cGMP
27
What effect dose nitroglycerine have on smooth muscle?
Causes release of Nitric Oxide which dilates primarily veins, but has some arterial dilation.
28
What CV effects can be seen with nitroglycerine administration?
1. Decreased peripheral vascular resistance
2. Decreases Venous return
3. Decreased Myocardial oxygen consumption
(Overall, reduces workload of the heart).
29
What effect does NTG have on coronary vessels?
Relaxation of coronary vessels and relieves spasm (Pritzmetal angina).
30
What are the non-cardiac effects of NTG?
1. Dilates minigeal vessesl (caution with inc ICP).
2. Decreased RBF with dec BP
3. Dilates pulmonary vessels.
31
What is dose, onset, and duration of NTG?
0.5mcg/kg/min, onset 1 min, duration 3-5
32
How is NTG metabolized?
By Glutathione Nitrate Reductase in the liver.
33
Nitrite Ion oxidizes Hgb into what?
Methemoglobin.
34
T/F: Tolerance in venous vessels occurs with chronic administration, but not in arterial vessels?
False; venous vessels do not, arterial vessel become tolerant.
35
5 contraindications for Nitroglycerine?
1. PDE5 inhibitors
2. Narrow angle glaucoma
3. Head trauma, cerebral hemorrhage
4. Severe anemia
5. Hypotension.
36
What is the issue co-administration of NTG and PDE5 Inhibitors?
Severe hypotension (even death).
37
Advantages of NTG?
1. Rapid onset and short duration
2. Coronary dilation
3. Dec. myocardial O2 consumption
4. No major toxicities
5. No coronary steal
6. Reduced PVR
38
Disadvantages of NTG?
1. Dec diastolic BP
2. Reflex tachycardia
3. Possibly HoTN
4. Variable efficacy
5. Tachyphylaxis
6. Methemoglobinemia
7. Intrapulmonary shunting
8. Prolonged bleeding time
39
What vessels does Sodium Nitroprusside dilate?
Both arteries and veins
40
What can be seen with abrupt discontinuation of Sodium Nitroprusside?
Reflex tachycardia and hypertension
41
Is there an increase or decrease in myocardial O2 demand with SNP?
Overall reduction
42
What is the dose, onset, and duration of SNP?
Dose 0.5-10mcg/kg/min
Onset <1min
Duration 5-10min
43
Side effects of SNP?
Cyanide toxicity, increased serum creatinine
44
Contraindications of SNP?
1. Congenital optic atrophy
2. Hypovolemia
3. Compensatory HTN (AV shunting, aortic coarctation)
4. Inc ICP
5. Severe renal/hepatic impairment
45
How does cyanide toxicity present? (7)
1. Hypotension
2. Blurred vision
3. Fatigue
4. Metabolic acidosis
5. Pink skin
6. Absence of reflexes
7. Faint heart sounds
(breathe smells like almonds)
46
Do smokers have a higher or lower tolerance for cyanide levels?
```
Higher tolerance (<0.4mcg/ml)
Non-smokers <0.2mcg/ml
```
47
What are two risk factors for cyanide toxicity with SNP administration?
1. Doses over 4mcg/kg/min
| 2. >2 days of therapy
48
What is treatment of cyanide toxicity from SNP?
1. Stop infusion
2. Admin 100% oxygen
3. Correct metabolic acidosis
4. Admin 3% Sodium Nitrite IV
5. Admin Sodium Thiosulfate
6. Consider Vit B12 administration
49
Which two methods of administration are available for Sodium Thiosulfate?
Prophylaxis or treatment
50
SNP advantages:
1. Immediate onset
2. Short duration
3. Reduced myocardial O2 demand
51
SNP disadvantages:
```
Reflex tachycardia.
Cyanide toxicity.
Intrapulmonary shunting.
Precipitous drop in BP
Methemoglobinemia
Coronary steal.
Cerebral vasodilator
```
52
MOA of Alpha Antagonists?
Blocks alpha-1 receptor from converting Inositol triphosphate into a contraction
53
Which alpha antagonist irreversibly binds to the receptor?
Phenoxybenzamine (dibenzyline)
54
In what situations is phenoxylbenzamine used?
Long term preoperative control of pheochromocytoma (chemical sympathectomy).
and in BPH to improve flow
55
Since phenoxybenzamine is a non-selective alpha antagonist, what are signs/symptoms you will see with administration?
1. Reduced SVR
2. Reduced BP
3. Secondary increase in NE due to alpha 2 blockade can increase HR and CO
56
What are uses for phentolamine?
1. HTN secondary to pheochromocytoma
2. Clonidine withdrawal HTN
3. Erectile dysfunction
4. Extravasation of catacholamines
57
Which medications may not have the same level of effect when a patient is on an Alpha 1 antagonist?
Alpha 1 Agonists like phenylephrine or norephinephrine
58
What medication can be administered to potentially see a reduction in post-op delirium?
Precedex
59
Cochrane Review on Alpha 2 Agonists concluded that...?
Overall mortality, cardiac mortality, and MI are all reduced with clonidine use peri-operatively.
60
What is clonidine's affinity for Alpha 2 vs Alpha 1 receptors?
Alpha-2 220:1
61
What two main results are seen from clonidine adminsitration?
1. Decrease release of sympathetic neurotrasmitters
| 2. Inhibits renin release
62
T/F: Clonidine cessation must be done abruptly as to not produce down-regulation of receptors?
False; Abrupt cessation of clonidine may lead to rebound HTN. This withdrawal is very common and is significant
63
Why/how does clonidine withdrawal occur?
Up-regulation occurs because Alpha 2 agonism means less NE "floating around". Body begins to produce more Alpha 1 Receptors in response.
64
How many days of therapy are required before abrupt cessation of clonidine leads to withdrawal?
Usually 6 or more.
65
How quickly does peak effect of PO clonidine take?
60-90 mins
66
Which patients should clonidine be avoided?
Severe coronary insufficiency.
Conduction disturbances.
Recent MI, CVA.
CKD
67
During withdrawal from clonidine, which medication can be given to correct HTN/tachycardia?
Coreg or labetolol
68
What effects on anesthesia administration does clonidine have?
1. Reduces propofol/thiopental requirements
2. Alternative to N2O for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia
3. Supplement of regional blocks
69
What is Precedex's affinity for a given Alpha receptor?
Alpha 2>Alpha 1 1620:1
70
Which patients can clinically significant bradycardia and sinus arrest be seen in with precedex use?
Young, healthy patients with high vagal tone
71
Will you more likely see HTN or HoTN with bolus of precedex?
| With infusion?
Bolus=HTN
| Infusion=Hypotension
72
MOA of methyldopa?
Acts as a "false" neurotransmitter and is apart of a negative feedback loop. Falsely makes the body think it is breaking down into NE, but it isnt.
Further, it is broken down from Alpha-methyl-NE to Alpha-methyl-epinephrine which acts at alpha 2 receptors to decrease sympathetic outflow
73
What are uses for methyldopa?
treatment of HTN during pregnancy
74
What are side effects of methyldopa?
1. Sedation, H/A, dizzy
2. Fluid retention
3. Orthostasis/bradycardia
75
MOA of ACE Inhibitors
By inhibiting Angiotensin converting enzyme which ultimately stops angiotensin I from converting to angiotensin II
76
Ultimately, how do ACE inhibitors decrease BP?
Predominantly arterial vasodilation because angiotensin II is not binding to arterial receptors
77
Uses of ACE Inhibitors?
1. Treat CHF and MR by afterload reduction
| 2. Increase CO without excessive decrease in preload
78
If a patient is Normotensive and an ACE inhibitor is administered, what is the effect on renal function?
Renal function may deteriorate because compensatory efferent arteriolar constriction mediated by angiotensin II is blocked and decreased GFR may result in acute hyperkalemia
79
Which two patients is an ACE inhibitor the anti-HTN drug of choice?
1. DMII
| 2. Renal failure
80
What are the side effects of ACE Inhibitors?
1. Respiratory (cough, congestion, rhinorrhea)
| 2. Angioedema
81
T/F: ACE Inhibitors and methyldopa are the only two anti-HTN medications safe to use in pregnancy?
False; ACE Inhibitors are CONTRAINDICATED in pregnancy
82
Two major outcomes of Hollman et al 2018?
1. Overall 30% increase in risk of HoTN associated with continued ACEI preoperatively
2. Patients that withheld 24hrs prior had lower incidence of all-cause death, stroke, MI
83
Which medications when given with ACE inhibitors decrease the anti-HTN effects of the ACEI?
NSAIDs and ASA because they effect the way the afferent arteriole constricts and dilates
84
What class of drug is Cozaar (losartan)?
Angiotensin II Receptor Antagonist (ARB).
85
What other medication class are ARBs most alike in SE profile and use?
A.C.E. Inhibitors
86
What three major locations do Calcium Channel Blocks typically work?
Peripheral smooth muscle, Cardiac Smooth muscle, and SA/AV nodes
87
What electrolyte is the driving force for action potentials in the pacemaker cells?
Calcium
88
What are the 3 primary actions of Calcium Channel Blockers?
1. Negative Inotropic effect
2. Negative dromotropic effect (AV conduction mostly)
3. Vasodilation of systemic, splanchnic, coronary, and pulmonary beds
89
What are the two classes of Calcium Channel Blockers?
1. Dihydropyridines
| 2. Non-Dihydropyridines (Phenylalkylamines and Benzothiazines)
90
What are 3 examples of Dihydropyridine Calcium Channel Blockers?
1. Nifedipine
2. Nicardipine
3. Amlodipine
91
How do dihydropyridine Calcium channel blockers lower BP?
Pure arterial vasodilators, but with minimal reflex tachycardia
Also have minimal negative inotropic and dromotropic effects
92
Do Dihydropyridines have any effect on Ca+ channels in the heart?
No, hence why there is no change in HR
93
Nicardipine is a ___ specific vasodilator
arteriole
94
What is a unique feature of nicardipine?
There is no coronary steal syndrome, so it has favorable myocardial O2 supply/demand
95
What is the onset of nicardipine?
Less than minute
96
What is the DOA of nicardipine?
15-20 mins
97
What is the dose of nicardipine to attenuate the hypertensive response to intubation?
0.5mg to 1mg boluses
Give 1mg/min to achieve a systolic arterial pressure decrease of up to 30mmHg or until 5mg has been administered
98
How does nicardipine compare to nitro and SNP?
- longer DOA compared to nitro
| - slower onset and offset than SNP
99
Why is nicardipine useful for IV control of HTN in the PACU and ICU?
- Easier to use with less swings in BP bc of longer half life
- No rebound hypertension with withdrawal (actually with any CCB)
- Reflex tachycardia <10 bpm
- Prolonged duration of action may be a benefit postop
100
Advantages of nicardipine
- Dose dependent arterial vasodilation
- no aterial cath,
- no coronary steal
- cerebral and coronary vasodilation
- minimal effects on contractility/ conduction
- mild natriuretic effect
101
Disadvantages of nicardpine
- May accumulate (this can actually be a good thing per Emily)
- Variable DOA
- Hypotension
- Venous irritation
- May cause tachycardia
102
Clevdipine is a _____
Dihydropyridine
103
MOA of Clevidine
Vasodilation reduces PVR (arteriole specific)
104
Is Clevidine is long acting or short actin?
Ultra-short acting
105
Onset, peak, DOA of Clevipine
Onset < 5 min
Peak 10 min
Duration 10-20 min
Quickly cleared after administration due to half life of 1 min
106
The dose of Clevidipine can be double every ___
90 seconds
107
Once a vial of Clevidipine is open, use within ____
12 hours ( due to being in a lipid emulsion like propofol
108
What has a faster onset, Clevidipine or Nicardipine?
Nicardipine
109
Advantages of Clevidine
- Reduced need for other antihypertensives
- Reliable control
- No dose adjustments for renal/hepatic disease
- Ready to use vial
- No sig myocardial depression
- No effect on preload
- Low potential for drug interactions
110
Disadvantages of Clevidpine
- Lipid emulsion (no more that 1 L or 21 mg/h recommended)
- Continuous monitoring required,
- Contraindicated with egg and soy bean allergy, pancreatitis, and HLD
111
Verapamil is ____ CCB
phenylalkylamine
112
Verapamil is a potent _____
negative inotrope, dromotrope, and vasodilator
113
What are 3 uses of Verapamil?
- Aortic Stenosis and IHSS
- Conversion of atrial re-entry tachyarrhythmias
- Coronary artery vasospasm (Prinzmetal angina)
114
What 2 big side effects of Verapamil?
- Lower extremity edema
| - Constipation
115
Diltiazem is a ____ CCB
Benzothiazine
116
In regards to action, where does Diltiazem fit with phenylakylamine and dihydropyrdinces?
Right in b/w them
117
What is Diltiazem used for?
- Rate control of fib and atrial tachycardia vs a conversion agent such as verapamil
118
Describe the dosing of IV Diltiazem
- Dose 20mg IV bolus over 2 min
- If no response, in 15 min give 25mg IV over 2 min
- Infusion 10-20mg/hr.
119
Verapamil vs Diltiazem vs Dihydropyridnes
VERAPAMIL:
- Potent negative inotrope and negative dromotrope
- Mild vasodilator
- Useful in the treatment of vasospastic angina and essential hypertension.
DILTIAZEM(Cardizem®):
- Fits between verapamil (phenylakylamine) and dihydropyridines in action
- Less negative inotropic and dromotropic effects than verapamil but more than dihydropyridines.
- Mild vasodilator like verapamil
DIHYDROPYRIDNES:
- Virtually pure arterial vasodilator
- Lack clinically significant negative inotropic and dromotropic effects.
120
Which CCB's have the the most potent vasodilation effect?
NIcarpdine and Nifedipine
121
Do Nicardipine and Nifedipine have any effect on negative inotropy and AV block?
No
122
Which CCB has the most potent negative isotropy and AV block effects?
Verapamil
Diltiazem is 2nd
123
Do Diltiazem and Verapamil have any effect any vasodilation?
Yes, but mild
124
Is constipation more common with dihydropyramines (DHP) or non-dihydropyramines (NDHP)?
NDHP
125
Adverse CNS effects of CCB's
- Dizziness,
- HA
- Fatigue
- Insomnia
- Nervousness
126
Adverse CV effects of CCB's
- Flushing,
- Edema,
- Palpitations (DHP)
- Bradycardia (NDHP)
127
Adverse Respiratory effects of CCB's
- Nasal congestion
- Dyspnea
- Cough (nifedipine mostly)
128
Adverse GI effects of CCB's
N/V/D
129
Other adverse effects of CCB's
- Arthralgias/joint stiffness,
| - Itching
130
When would give a NDHP vs a DHP CCB?
NDHP is given when you want the HR to come down, not given just for BP control. If that’s the case, just give DHP
131
How do Verapamil and Diltiazem enhance myocardial O2 balance?
- Decreasing myocardial oxygen consumption by afterload reduction and/or negative inotropic effect.
- Increasing O2 delivery through coronary vasodilation.
132
How do DHP CCB's effect myocardial O2 balance?
Dihydropyridine vasodilators may worsen MvO2 by causing diastolic hypotension and reflex tachycardia (except nicardipine).
133
T/F
| CCB decrease reperfusion injury after ischemia
True
134
Are there any significant benefits of CCB's on the kidneys
No, they are not nephroprotective
135
What are the effects of CCB's on renal function?
Increase RBF and GFR and induce a naturesis
Benefits can be reversed if they cause hypotension, reflex catecholamine release and angiotensin activation leading to decreases in RBF and GFR
136
What are the recommendations of CCB and surgery
Continue up to the time of surgery without risk of significant drug interactions
137
CCB's ___ the effects of neuromuscular blocking agents
Potentiate
138
What are some anesthetic considerations with CCB's?
- May enhance hypotensive, CV depressant, and vasodilating effects of anesthetics and analgesics
- Use adequate hydration to avoid hypotension due to inc fluid requirements
- Clevidipine reduces gastric emptying
- Diltiazem inc sedative effects of midazolam
139
How does Diltiazem increase the sedative effect of Midazolam?
Diltaizem is a CYP3A4 inhibitor and Midazolam is a CYP3A4 substrate, so may see prolonged DOA of versed and also propofol
140
T/F
Beta blockers cause vasodilation
False
141
2 actions of beta blockers
- Decrease C.O. (HR and contractility)
| - Decrease renin release
142
What are the advantages of beta blockers over vasodilators?
- No reflex tachycardia or widening of pulse pressure
- Improved MvO2 (decrease HR and decrease contractility)
- Intrinsic antiarrhythmic activity
143
3 classifications of beta blockers
- Beta-1 selectives (Metoprolol, Atenolol, Acebutolol, Bisoprolol, Esmolol)
- Non-selective (Propranolol, Nadolol, Timolol, Pindolol, Carteolol)
- Combined Alpha-1 and non-selective beta(Carvedilol and Labetalol)
144
MOA of beta-1 selective BB's
Decrease velocity of A-V conduction, HR, contractility, renin release and lipolysis
145
MOA of non-selective BB's
Block Beta-1 receptors
Also act at Beta-2 receptor to cause bronchoconstriction, peripheral vasoconstriction and decrease glycogenolysis.
146
Which class of BB's is useful for cocaine overdose?
Combined alpha-1 and non-selective beta
147
What class of BB's cannot be used in asthmatics?
Non-selectives
b/c they cause bronchoconstriction
148
T/F
Propanolol can be used to treat tremors and portal HTN
True
149
How do beta blockers work at the cellular level?
Block beta receptors, which block adenyl cyclase (AC) which block the conversion of ATP to cAMP
150
How are long-acting BB's metabolized?
Glucuronide hepatic biotransformation
Ex. Atenolol and metoprolol XL
151
How are intermediate-acting BB's metabolized?
Rapidly hydroxylated by the liver, 1st pass effect
152
How are short-acting BB's metabolized?
By red cell esterase. These attack esmolol immediately
153
What are the routes of elimination of long-acting, intermediate-acting, and short-acting BB's?
Long-acting: Kidney
Intermediate-acting: Liver
Short-acting: Red cell esterase
154
Why is lipophilicity important for classifying BB's?
BB's can cause CNS depression
155
What are examples of low lipophilicity BB's?
```
Acebutolol
Atenolol
Bisoprolol
Carteolol,
Nadolol
```
156
What are examples of moderate lipophilicity BB's?
Metoprolol
Pindolol
Coreg
Labetalol
157
What are examples of high lipophilicity BB's?
Propanolol
| Penbutolol
158
What happens when you begin to increase the dose of beta blockers?
The selecetivity goes away, can cause beta-2 effects
Ex. Loppressor 100mg q8 PO
159
Which BB class has more adverse effects?
Non-selective
160
What are the adverse effects of BB's
Non-selective blockade of Beta-2 receptors:
- Vasoconstriction and worsening PVD
- Bronchospasm
Myocardial depression:
- Decreased contractility could precipitate CHF
Life-threatening bradycardia or asystole
Hyperkalemia in renal failure
161
What is the treatment for BB overdose?
- Treat with atropine
- May need Isoproterenol, dobutamine and/or glucagon infusion
- Could ultimately need pacing
162
Glucagon ____ cAMP
Increases
163
What can occur when combining Verapamil and BB's?
Decrease HR and contractility
164
What can occur when combining Digoxin and BB's?
Decrease HR and conduction
165
Which beta blocker is effective in limiting HTN during induction and emergence?
Esmolol
166
what are 4 perioperatve indications for BB's?
- 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, AS or IHSS
- Peripheral manifestations of hyperthyroidism – propranolol given most often for this
167
What are BB contraindications?
- Severe bradycardia
- > 1st degree heart block
- Cardiogenic shock
- Raynaud’s disease
168
What types of patients should BB be used with caution?
- Asthma/COPD
- DM
- CHF
169
What was the prototype non-selective BB?s
Propranolol
170
Can propranolol cross the BBB?
yes, b/c its lipid soluble
this is why it's a good drug for people with public speaking anxiety/fear
171
What % of propranolol undergoes metabolism in the liver?
70% (undergoes 1st pass effect)
172
What class of BB is esmolol?
Beta-1 selective
173
What are 3 intraoperative uses of esmolol?
- Blunt the CV response to intubation
- Control of SVT and A. Fib.
- Intraop and postop HTN and tachycardia
174
T/F
Esmolol is more likely than Verapamil to convert fib to SR
True
175
Is Esmolol's onset/offest rapid or slow?
Rapid, b/c its metabolized by red cell esterases
176
Which BB is approved for the the treatment of angina, acute MI, and HTN?
Metoprolol
177
What class of BB is metoprolol?
Beta-1 selective
178
What can occur when BB's and general anesthetics interact?
Negative inotropic effects and conduction delays are potentiated by many general anesthetics
179
What can happen if BB's are stopped abruptly?
Rebound HTN and tachycardia
180
What 2 problems can BB's mask?
- Hypoglycemia
| - Hyperthyroidism
181
When a patient is on BB's, what is the best way to prevent orthostasis?
Adequate IVF
182
T/F
If a patient is on BB's, anticholinesteras may increase bradycardia
True
183
If a patient develops HTN intraoperatively, what steps should be taken?
1. Check depth of anesthesia
2. Administer sufficient analgesia
3. R/O hypercarbia, distended bladder, hyperthermia, hypoxia, thyroid storm, malignant hyperthermia
4. When vasodilators are used, watch for reflex tachycardia as BP decreases
184
What is the drug of choice for HTN during pregnancy?
Alpha-methyldopa
185
Can labetalol be used during pregnancy ?
Yes, in 2nd and 3rd trimesters only
Beta blockers are associated with growth retardation in the 1st trimester
186
Can ACEI's be used for HTN during pregnancy?
No
ACEI have demonstrated fetal morbidity and mortality in all 3 trimesters.
187
Can hydralaizne be used during pregnancy?
Yes, during delivery
188
What can nifedipine be administered during pregnancy?
PO only (not SL)
189
T/F
SNP is regular used to treat HTN during pregnancy
False
It is rarely used
190
What is considered a HTN emergency?
Acute elevation of SBP > 180 or DBP > 120 with target organ damage
191
What can occur if excessive correction happens for a HTN emergency?
Renal, cerebral, and coronary ischemia
192
What is the definition of HTN urgencies?
Accelerated, malignant, or perioperative inc in BP without target organ damage
193
T/F
For HTN urgencies, PO therapy is preferred and immediate BP lowering is not required
True
194
What drug should NOT be used to treat HTN urgencies?
IR nifedipine
195
What are 7 examples of target organ damage related to HTN?
1. Encephalopathy
2. ICH
3. Unstable angina
4. Acute MI
5. Acute LV failure with pulmonary edema
6. Dissecting aortic aneurysm
7. Eclampsia
196
T/F
Labetolol does not increase ICP
True
This is why its a good choice for ICH patients
197
What is the ratio of beta/alpha blockade with labetalol
7:1 (Beta:alpha)
198
What happens if you give labetalol for vasoconstrictor HTN?
vasodilation without reflex tachycardia
199
What happens if you give labetalol for hyper dynamic HTN?
Beta blocker without reflex vasoconstriction
200
What can occur with giving SNP with labetalol?
tachyphylaxis with SNP
201
How should labetalol be administered?
- “Test dose” of “baby dose” 2.5-5mg IV to make sure there isn’t CV collapse.
- If no change in HR in 5-10 min, progressively double the dose every 5-10 min. to a max. dose of 100mg
- Dose can be repeated every 2-4 hours.
202
What can occur with labetalol in large doses?
1. Bronchoconstriction
| 2. Acute hyperkalemia in renal failure
