Vasodilators Flashcards
1
Q
SV is determined by?
A
- Preload
- Afterload
- Contractility
2
Q
What effect will an increase of B1 receptors do?
Where is it located?
A
B1 receptors are located on the heart
and activation of this receptor results in INCREASED CO
3
Q
What does the activation of ALPHA 1 receptors do? where is it located?
A
Activation of alpha 1 receptors on the peripheral vasculature results in an increase in SVR
4
Q
Causes of systemic hypertension
A
- renal artery stenosis
- Pheochromocytoma
- withdrawal from alcohol
- sympathomimetics
- rebound
5
Q
How do you manage hypertension?
A
- Inhibit RAAS
- direct peripheral vasodilation
- effects of autonomic receptor
6
Q
The patient population that should be started on B BLOCKERS as long as there is not overt HF
A
Acute Coronary Syndrome
–> as long as there is no exacerbation of HF or BB could cause worsening hypotension
7
Q
When do you use B blockers as first-line agents for the management of hypertension
A
ACS [w/o HF]
Cardiac Dysrhythmias
8
Q
Receptos sites where B- blockers may act upon (competitive inhibition)
B1 sites and effects
A
B1 - CARDIAC
- Decrease heart rate (negative chronotropic effects)
- Decrease cardiac output (negative inotropic effects)
- Inhibit the release of renin from the kidneys
9
Q
Where can we find B2 receptors?
A
B2 found in the vascular and bronchial smooth muscle, metabolic
- B2 agonist –> albuterol will cause bronchial relaxation
10
Q
Where can we find Alpha 1 receptors?
what do we get when we block alpha 1 receptors?
A
Alpha 1 is found in the vasculature
– decrease in peripheral resistance when blocked
11
Q
Which ones are beta selective among the beta-blockers
A
MEAN
Metoprolol
Esmolol
Atenolol
Nebivolol
12
Q
beta-blockers consideration / special population
A
beta 1 selectivity is overcome with large doses
–> if we give massive doses of metoprolol sometime we will hit the beta 2 receptors ;
- COPD patients on high dose beta-blockers may end up with blocked beta 2 receptors and this may cause vasoconstriction
13
Q
What is the ratio of beta:alpha blockade on IV Labetalol
how about oral?
A
Beta:alpha (IV) = 7:1
Oral: 3:1
14
Q
ratio of Metoprolol oral:iv
A
2.5 mg oral: 1 mg IV
15
Q
When do you use Beta-blockers that are cardioselective??
A
- May be more preferable in patients with
- asthma/COPD,
- peripheral vascular disease, vulnerable to hypoglycemia
- Tachyarrhythmias
- Decrease risk of postoperative myocardial ischemia in patients at high risk for cardiovascular disease with perioperative administration
-
Prophylaxis against tachycardia/hypertension around procedures (e.g., laryngoscopy, tracheal intubation)
- Esmolol
16
Q
Common adverse effects of Beta-blockers
A
- Hypotension
- Bronchospasm
- Bradycardia/heart block
- Possible worsening CHF
- masking of hypoglycemia (tremors and tachycardia)
- Angina and MI –> HIGHER RISK PATIENTS upon abrupt discontinuation
17
Q
How can poorly controlled diabetes management be affected by B- blockers?
A
- May block the release of insulin from pancreatic β cells –> hyperglycemia
- Initial signs of hypoglycemia (tremors, tachycardia) can be masked
18
Q
If a patient has known CAD and at risk for MI what should you do with the beta-blocker?
A
Perioperative management of β-blockers
-
Continue in patients at risk for myocardial infarction (e.g., known CAD, perioperative stress tests, diabetes treated with insulin, LV hypertrophy) during high-risk surgery (e.g., vascular, thoracic, intraperitoneal surgery, large blood loss)
- Pre- and post- non-cardiac surgery shown to decrease mortality, CV complications, myocardial ischemia
- Consider baseline blood pressure, possible intraoperative complications and start low dose postoperatively
19
Q
What are the common selective alpha 1 blockers?
A
“zosin”
- Prazosin
- Terazosin
- Doxazosin
- Tamsulosin
20
Q
what is the MOA of selective alpha 1 blockers
what is the downside?
A
Mechanism of action
- Post-synaptic α1 blockade: vasodilation of arterial and venous vessels
- downside: Usually long/longer half-lives
- common uses: hypertension, benign prostatic hyperplasia
- prazosin, terazosin, doxazosin, tamsulosin
21
Q
MOA of non-selective alpha-blockers
when is it commonly used?
A
- Phenoxybenzamine, phentolamine
Mechanism of action
- Post-synaptic α1 blockade: vasodilation of arterial and venous vessels
- Pre-synaptic synaptic competitive α2 blockade–> release of presynaptic norepinephrine
Common uses: *pheochromocytoma management*
22
Q
Adverse effects of alpha receptors blockers
A
- orthostatic hypotension
- Hypotension
- exaggeration of hypotension during epidural anesthesia –> alpha 1 receptor blockers tend to have a longer half-life [mind prolong hypotension even more] but can really happen to any antihypertensive
23
Q
How do you overcome the effects of alpha-receptor blockers in the OR?
A
use vasoactive agents with alpha1 agonist activity
—> PHENYLEPHRINE [POTENT], NOREPINEPHRINE
Other atypical agents could include (not recommended as first line): epinephrine, angiotensin II, vasopressin
24
Q
Alpha 2 receptor agonist
A
Clonidine
Dexmedetomidine
25
## Footnote
**MOA of Clonidine compared to Dexmedetomidine**
Mechanism of action
**Clonidine**
* Selective partial α2 agonist
* **220:1 (α2: α1 activity) --\>** reason for **potent BP management**
* The **decreased sympathetic output from the central nervous system to peripheral tissues peripheral ----\> vasodilation,** decreased systemic blood pressure, heart rate and cardiac output
**Dexmedetomidine**
* Selective partial α2 agonist
* **1,600:1 α2 to α1 activity --\>** reason for more **sedation**
* **_alpha 2 receptors are in the locus coeruleus of brain stem_**
26
If you have a patient that is bradycardic and is on clonidine what should you do?
take clonidine off. it may cause a decrease in HR and CO
27
## Footnote
**alpha 2 receptor agonist**
**Adverse SE**
**CAUTIONS?**
**big deal with Clonidine**
* sedation
* Fever --\> case report; really high close to 40 C . It starts within hours to dex then a day
* temporal, if dex is taken off usually it subsides
* ***CAUTION:***
* **_REBOUND HYPERTENSION --\> BIG DEAL WITH CLONIDINE_**
* Abrupt dc can result in rebound hypertension **_8-36_** hours after last dose
* most likely to occur in pts taking **\>- 1.2 mg/day**
28
What can **rebound clonidine discontinuation** cause?
* **_tachycardia but predominantly hypertension_**
* **Beta 1 selective** blockers can only control the HR but not the unopposed alpha-receptor
* Beta adrenergic blockade may **worsen hypertension** due to unopposed alpha receptors
* T**ricyclic antidepressant**s may exaggerate the **hypertensive** response
29
How do you **manage** rebound hypertension with abrupt d/c of clonidine?
* Reinitiating clonidine
* Initiate vasodilators
* β- adrenergic blockade with concurrent α blockade [HR and BP control!!]
* Gradually taper (e.g., 7 days or longer)
30
MOA of ACE Inhibitor
prevents ACE then we will prevent angiotensin I conversion to angiotensin II
31
## Footnote
**Samples of Ace inhibitors**
**_C_**aptopril
**_L_**isinopril
**_E_**nalapril
**_R_**amipril
32
## Footnote
**ACE with the shortest half-life?**
## Footnote
**Captopril**
33
ACE with the **longest half-life?**
**Ramipril**
(9-18)
34
## Footnote
**ACE with active metabolites**
**If someone has renal metabolism issues what can happen?**
* **Enalapril**
* **Ramipril**
**---\> may have prolonged hypotension**
35
## Footnote
**ACE SE**
* **Hypotension**
* **Hyperkalemia**
* **Acute Renal Failure _[hold ACE]_**
* **Cough**
* **Angio edema**
36
Can you give **ACE to pregnant** women?
## Footnote
**NOOOOO!!!**
37
## Footnote
**Significant Drug Interactions with**
**ACE**
## Footnote
**Potassium Supplements**
**Potassium-sparing diuretics**
**\* remember that ACE causes hyperkalemia; check a BMP!**
38
## Footnote
**ARB SE**
**NO COUGH**
Adverse effects
**ARB**
* Hypotension
* Hyperkalemia
* Acute renal failure
* Angioedema
**Significant drug interactions**
– Potassium supplements
– Potassium-sparing diuretics
**_• Contraindications – Pregnancy_**
39
## Footnote
**MOA of Calcium Channel Blockers**
**w/c are potent vasodilators?**
**w/c have negative inotropic and chronotropic activity**
* Inhibits calcium influx through voltage-sensitive L-type calcium channels in vascular smooth muscle
* Arterial specific with little effect on venous circulation
* **_Dihydropyridines are potent vasodilators and may increase heart rate_**
* **Non-dihydropyridine are less potent vasodilators** and have **_negative inotropic and chronotropic activity_**
40
your patient has **post-op afib** and **tachyarrhythmia**
**w/c CCB will you use?**
**Verapamil**
**Diltiazem**
41
Your patient has **bradycardia** which **CCB** are **safe to give?**
* **Nifedipine**
* **Nicardipine**
* **Clevidipine**
--\> ALSO VERY POTENT VASODILATOR
--\> Nicardipine and Clevidipine --\> has the greatest **coronary artery dilation**
42
Uses for **Verapamil/ Diltiazem**
## Footnote
– Supraventricular **tachydysrhythmias [off pressors]**
– Vasospastic angina pectoris
– Hypertension
43
Nifedipine
XL :CONSIDERATION
IMMEDIATE RELEASE: CONSIDERATION
XL: Nearly impossible to titrate!
**_IR: MI, STROKE -- so potent!_**
44
Whats should you consider from the **anesthesia standpoint**
in **using CCB**
**how about other drugs such as Dig, BB, Amio?**
**Additive negative inotropy and peripheral vasodilation**
* Particular caution in patients with left ventricular hypertrophy or hypovolemia
**Digoxin, β-blockers, amiodarone**
* Increased risk for atrioventricular block
45
## Footnote
**CCB SE**
**DIHYDROPYRIDINE**
**REFLEX TACHYCARDIA**
46
**CCB SE**
Non- Dihydropyridine
## Footnote
**Bradycardia!**
47
What is the **definition** of **Hypertensive Urgency**
**Hypertensive urgency Systolic blood pressure**
**_(SBP) ≥ 180 mm Hg_** and/or **_diastolic blood pressure (DBP) ≥ 110_** mm Hg ***_without evidence of target organ damage_***
48
Definition of **Hypertensive Emergency**
**Hypertensive Emergency**
Abrupt significant elevation of **BP (often SBP \>200 mm Hg and/or DBP \>120 mm Hg) with *_concurrent target organ dysfunction_***
49
Common **Causes of Hypertensive Crisis**
* **Intoxication**
* **Withdrawal Syndrome**
* Spinal Cord Disorders
* Pregnancy
50
How do you manage **Hypertensive Urgency?**
time parameter?
ICU admission?
* **Lower BP over 24-48 h** using oral medications
* • Usually **involves restarting home medications**
* _No need for ICU admission_
51
How is **Hypertensive Emergency** managed?
**Specific blood pressure targets may not be the same for all patients**
## Footnote
* _Chronic hypertensive patients can tolerate high blood pressure_
* **Lower blood pressure in a controlled fashion** to avoid sudden decreases
52
How do you control **Acute Aortic Dissection?**
WHAT IS THE **GOAL?**
within what **time p**arameter?
**Acute aortic dissection**
Progression of dissection is dependent on arterial BP and force of left ventricular contraction
* **QUICK REDUCTION!** Control HR and contractility to decrease stress on the aorta
* **Goal HR \<60 bpm** as soon as possible **(within 5-10 min)**
* **Goal SBP \<100-120** mm Hg as soon as possible **(within 5-10 min)**
53
Management of **Acute Ischemic Stroke**
**what is the equation?**
if your ICP is high what will be the CPP?
\* THE HIGHER ICP THE LOWER THE CPP so you have drive-up your MAP
– Hypertension after a stroke is the body’s way to maintain cerebral perfusion pressure (CPP)
* CPP=MAP–ICP
* (ICP = intracranial pressure)
54
If a person has an ischemic stroke and is a candidate for **TPA** what are your considerations?
what is the **SBP/DBP** goal?
How much should you reduce your map?
Treat blood pressure for specific scenarios
## Footnote
* Thrombolytic therapy is needed **(goal SBP \<185 mm Hg and DBP \< 100 mm Hg to decrease bleeding risk)**
* The occurrence of other target organ damage
* SBP \>220 mm Hg and/or DBP \>120 mm Hg
* Goal reduction in **MAP 15-20% over 24 h**
55
Management of **Intracerebral Hemorrhage**
**SBP goal and time**
Elevated BP associated with hematoma expansion, neurological deterioration, and death
## Footnote
* **SBP \<140-160 mm Hg (within 5-10 min)** in patients without elevations in ICP shown to be safe and possibly linked with improved functional recovery
* Unclear if aggressive BP targets are safe in some patients
* SBP \>220 mm Hg, patients with large hematomas, elevations in ICP [prob need to be more aggressive]
56
Management of Hypertensive Emergency
57
Long-acting medication for Hypertensive Emergency
**Hydralazine**
increase CO
reduction of afterload
58
**very good preload reducer** [hypertensive emergency drug]
oftentimes used for people that have **CHF exacerbation** and absolutely overloaded.
may get **tachyphylaxis**
**Nitroglycerin**
little bit to maybe no effect on afterload
not as potent as Nitroprusside
59
B1 selective medication that is e**asy to titrate** because of fast onset and **shorter duration** [Hypertensive Emergency]
**Esmolol**
--\> slowing the rate to give more time to fill
60
Management of **Hypertensive Emergency**
Metoprolol IV Push
Labetalol can be given with boluses but does not last very long --\> hypertension again within 15 mins, afterload **[NON SPECIFIC BETA BLOCKER]**
61
Only IV ACE Inhibitor
**Enalaprilat**
LONG DURATION
**\*mona forgets this exist**
62
Why do we use **Phentolamine?**
**The antidote** for **extravasation** of pressors [potent vasoconstriction, from a drug that has alpha 1 activity]
-- causes local vasodilation
63
Nitroprusside
what should we **absolutely be worried about?**
**dose and time of infusion where you may see toxicity?**
Cyanide accumulation!
* Toxicity **associated with infusions \>72 h or doses \>3 mcg/kg/min**
* If **not controlled by 10 mcg/kg/min after 10 min, discontinue infusion**
64
What are the **signs of Cyanide Toxicity?**
**what is the TX?**
**Signs of cyanide toxicity**
## Footnote
**a**(acidosis) (**b**)bradycardia **c**onfusion/**c**olvusion, **d**esaturation
**Treat cyanide toxicity with _sodium thiocyanate_**
65
will Nitroprusside increase ICP?
**YES! IT WILL INCREASE ICP**
it will also cause **CORONARY STEAL!**
66
A drug that you may use with **Pregnant** ladies with **hypertensive emergency**
***Hydralazine***
but realize that you may have prolonged effects **[prolonged hypertension]**
also **reflex tachycardia!!!**
67
Hypertensive Emergency Drug that is useful for **ischemia and hemorrhagic stroke**
**Nicardipine**
* Reflex tachycardia is a risk
* Large amount of volume administered with infusion
* **Useful for ischemia and hemorrhagic stroke**
68
Hypertensive Medication that is a **lipid infusion** and you may not be suitable for patients that have an **allergy to egg**
**- how is this drug metabolized?**
**Clevidipine**
* Lipid infusion that provides 2 kcal/mL
* **Caution for use in patients with allergy to soy or eggs**
* Useful for **ischemia and hemorrhagic stroke**
* Needs dedicated IV line
* **Metabolized by plasma esterases**
69
Hypertensive Emergency
DOC for patients that has c**oronary ischemia/infarction, acute left ventricular failure, pulmonary edema**
* “vasospasm prophylaxis” after CABG in certain centers
**NITROGLYCERIN**
## Footnote
* Tachyphylaxis is common
* Adverse effects **_include flushing, headache, erythema_**
* ***_Dilates veins more than arteries_***
* **Can be used for coronary ischemia/infarction, acute left ventricular failure, pulmonary edema**
* _“vasospasm prophylaxis”_ after CABG in certain centers
70
Hypertensive Emergency medications that are **contraindicated in decompensated HF**
1. Drug that is metabolized by plasma esterases
**Esmolol**
* **_Contraindicated in decompensated heart failure_**
* Should **be used with an arterial vasodilator for management of BP** with aortic dissection (_start esmolol before nitroprusside to due later onset of esmolol comparativel_y)
* **Metabolism is via plasma esterases**
* Useful if **tachyarrhythmia** present
* Useful for coronary ischemia/infarction
**Metoprolol**
* **Contraindicated in decompensated heart failure**
* Should be used with an arterial vasodilator for management of BP with aortic dissection (**start metoprolol before nitroprusside to due later onset of metoprolol comparatively**)
* Useful if **tachyarrhythmia** present
* Useful for coronary ischemia/infarction
71
**ABSOLUTELY AVOID IN PREGNANCY**
but maybe used for Acute left ventricular failure
**Enalaprilat**
* _Contraindicated in pregnancy_
* _Risk of prolonged hypotension due to the long duration of action_
* Useful for acute left ventricular failure
72
**Fenoldopam**
caution with patients that have what?
* Reflex tachycardia is a risk
* **Caution in patients with glaucoma** (can increase intraocular pressure)
* May cause hypokalemia and **flushing**
* **May increase ICP**
* Mixed to no difference in data involving improvement of renal function
73
**Management of Hypertensive Emergency in Pregnancy**
medication to **decrease seizure**
when do you **consider hypertensive management?**
**SBP/DBP consistent?**
which **hypertensive medication will you use?**
**Pregnancy**
## Footnote
* _**Deliver**y of baby is treatment for **severe preeclampsi**_**a**
* **Magnesium** can be given to **decrease risk for seizures**
* Consider antihypertensives for consistent **SBP \> 160 mm Hg and/or DBP \>110 mm Hg**
* **_Labetalol (preferred) and hydralazine can be used_**
74
ABSOLUTELY **CONTRAINDICATED** WITH THE MANAGEMENT OF **PHEOCHROMOCYTOMA**
**BETA 1 SELECTIVE BETA BLOCKERS**
* β-blockers contraindicated unless α-receptors blocked
* Choice should include control of heart rate and blood pressure
75
Hypertensive management for **cocaine-induced hypertensive emergency**
Benzodiazepines are useful to control tachycardia and hypertension
* Diazepam 5-10 mg IV or lorazepam 2-4 mg IV
* Phentolamine 1 mg with repeat doses every 5 min prn
Other agents to consider:
* Nitroglycerin, nicardipine, clevidipine, nitroprusside, fenoldopam
* Verapamil and diltiazem may decrease coronary vasospasm associated with cocaine;
labetalol may not treat coronary vasospasm
* **_Use β-blockers only if α-antagonists present (due to coronary vasoconstriction) – conflicting data with labetalol_**
