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Pharm 2 > I. Anti-Hypertensive Drugs and Vasodilators > Flashcards

I. Anti-Hypertensive Drugs and Vasodilators Flashcards

1
Q

What percent of hypertensive patients suffer from “essential HTN”?

A

90%

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2
Q

Essential HTN meaning?

A

HTN that occurs without an identifiable cause; unknown etiology

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3
Q

Secondary HTN

A

HTN resulting from an underlying condition

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4
Q

Secondary HTN examples

A

Pheochromocytoma, thyroid disease, kidney disease, diabetic nephropathy, glomerular Disease, Cushing syndrome, aldosteronism, sleep apnea (not getting enough oxygen damages blood vessels making it harder for vessels to control pressure, also the nervous system release chemicals that cause htn), obesity (more blood flow leads to HTN).

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5
Q

Drugs that cause sodium and water retention, ultimately increasing BP

A
  • NSAIDs (especially in kidney and heart patients: they inhibit prostaglandins which
    Have vasodilatory effects, therefore vasoconstriction occurs and increases bp/prostaglandins help maintain renal blood flow and inhibition disrupts renal blood flow and electrolyte regulation, ultimately leading to increased BP).
  • anti diuretics
  • steroid hormones (corticosteroids: mineralocorticoids, not glucocorticoids): increase Na reabsorption in the renal tubules
  • anti hypertensives ( diuretics must be co-prescribed to blunt the sodium - water retention)
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6
Q

Drugs used to treat HTN

A
  • Direct VD
  • Beta Blockers
  • Ca Channel blockers
  • ACE-I/ARBs
  • Diuretics
  • Alpha Antagonist
  • Other VD
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7
Q

Vascular smooth muscle contraction is primarily dependent on ____.

A

Calcium

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8
Q

Describe the cascade that occurs that leads to vasoconstriction of smooth muscle (alpha-1 MOA):
(Non-ppt)

A
  1. GQ protein complex activates Phospholipase C
  2. Phospholipase C hydrolyzes PIP2 to IP3 & DAG
  3. IP3 activates the Sarcoplasmic Reticulum to cause release of Calcium
  4. Calcium causes contraction
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9
Q

___ is a second messenger that mediates smooth muscle relaxation in response to various vasoactive agents such as nitric oxide (NO). :

(Non-ppt)

A

cGMP (cyclic guanosine monophosphate)

cGMP-mediated smooth muscle vasodilators are drugs that promote vasodilation by increasing the effect of cGMP

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10
Q

What are some examples of cGMP-mediated smooth muscle vasodilators?
(Non-ppt)

A
  1. Hydralazine
  2. Nitroprusside
  3. Nitrates (angina pectoris = Nitroglycerin)
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11
Q

.cGMP-mediated smooth muscle vasodilators are used to treat:

(Non-ppt)

A
  1. HTN
  2. Heart Failure
  3. Angina Pectoris
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12
Q

Nitrates are prodrugs. They need to be converted to ____.
(Non-ppt)

A

Nitric Oxide

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13
Q

Nitric Oxide Mechanism of Action (non-ppt)

A
  1. Nitric Oxide Synthase is present in Endothelial Cells
  2. Nitric Oxide Synthase uses L-Arginine & O2 to synthesize Nitric Oxide
  3. N.O. Diffuses to adjacent SM cells in Tunica Media where it binds and activates Guanylyl Cyclase
  4. Guanylyl Cyclase converts GTP to cGMP
  5. .cGMP is a second messenger that induces relaxation in smooth muscle cells
  6. .cGMP production results in vasodilation and decrease in BP

N.O. also acts to inhibit there effects of calcium independently of cGMP, although the mechanism is not completely understood

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14
Q

Nitrates should not be given to ____.

(Non-ppt)

A

Patients taking erectile dysfunction medication (“-afil”) - PDE5I

*ED meds block Phosphodiesterase 5 (PD5) which is responsible for converting cGMP to GMP; therefore, there will be an excessive fall in BP = MI = Death.

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15
Q

Hydralazine causes vasodilation by what mechanism?
(Non-ppt)

A

Increasing production of cGMP in SM cells, thereby reducing afterload

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16
Q

Hydralazine dilates ____ more, while nitrates dilate ___ more. (Non-ppt)

A
  • arteries (Hydralazine)
  • veins (nitrates)

Therefore, causes a larger decrease in afterload, but less of a decrease in preload

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17
Q

Hydralazine is intended to treat:

A

Acute hypertensive emergencies

Es: preeclampsia or HTN in pregnancy

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18
Q

Hrydralazine & Nitrates are often prescribed to treat:

(Non ppt)

A

Chronic heart failure

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19
Q

Hydralazine can cause what side-effect?

A

Reflex tachycardia

can choose to treat with Beta blockers
AVOID in pts with CAD
Drug-Induced systemic Lupus Erythematosus
Slow Acetylators may experience Hydralazine Toxicity (break down drug too slowly)

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20
Q

Nitroprusside is used to HTN emergencies; what is its MOA?
(Non-ppt)

A
  1. Interacts with oxyhemoglobin
  2. Produces Nitric Oxide, Methemoglobin, and Cyanide
  3. NO stimulates Guanylate Cyclase in SM to produce cGMP
  4. .cGMP causes equal VD of peripheral arteries and veins
  5. Reduces both Pre-Load (vein VD) and afterload (arteries VD)

Patients are at risk for acute Cyanide poisoning: Headache, Vertigo, Confusion, Seizures, Coma, Death

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21
Q

Treatment for cyanide poisoning (non ppt)

A
  1. Hydroxocobalamin (Injectable B12)
  2. Sodium nitrite + Sodium thiosulfate
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22
Q

What are some examples of Central Anti-Adrenergics? (Non-ppt)

A
  1. Clonidine
  2. Dexmetetomidine (Precedex)
  3. Guanabenz
  4. Guanfacine

Anti-adrenergics: term that refers to drugs that oppose the effects of the SNS Alpha-2-Agonists

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23
Q

Clinical uses of peripheral vasodilators?

A
  1. HTN
  2. Controlled HoTN (aortic dissections)
  3. Facilitation of LV (by manipulating afterload and preload)
  4. Coronary VD
  5. Pulmonary HTN
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24
Q

Nitrovasodilators generate ____ intracellularly, producing vascular smooth muscle relaxation.

A

Nitric Oxide

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25
Q

The MOA of nitrovasodilators is an endogenous/exogenous process.

A

Endogenous

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26
Q

Nitric oxide is produced from ____ and ____ in the endothelium by ____ (enzyme).

A
  • Oxygen & L-Arginine
  • Nitric Oxide Synthase
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27
Q

Nitric Oxides production is dependent on ____ as a cofactor.

A

Calcium

The increase in intracellular Calcium activates endothelial Nitric Oxide Synthase (NOS); NOS then uses L-Arginine and O2 to produce Nitric Oxide; N.O. Then diffuses into Tunica Media (smooth muscle vasculature) where it activates Guanylate Cyclase to produce cGMP (& PFG, MLCP);cGMP then relaxes smooth muscle via Calcium Reuptake

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28
Q

Physiologic effects of Nitric Oxide

A
  1. Regulation of SVR and PVR
  2. Bronchodilation
  3. Decrease platelet activation, aggregation, and adhesion (anti-platelet = bleed risk)
  4. Endogenous CNS neurotransmitter mediated by N-MDA receptors
  5. Inflammation modulation
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29
Q

How does Sildenafil (Viagra) work?

A

Increases local availability of endogenous nitric oxide = increase in BF

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30
Q

NMDA receptor induces/blocks nitric oxide synthesis.

A

Induces

Ex: Ketamine blocks NMDA receptors; NMDA receptor blockage causes inhibits N.O. Production; therefore, no vasodilation occurs; therefore there is increased SVR = possible increase in BP (and increased HR)

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31
Q

Nitroglycerin is a ____ (prodrug), and must be converted to nitric oxide (active form).

A

Nitrate

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32
Q

Nitroglycerin can also cause ____, but only at HIGH doses. It is also rare because NTG is metabolized quickly.

A

Methemaglobinemia

sublingual onset = 3 min (non-ppt)
sublingual DOA = 25 min (non-ppt)

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33
Q

Nitric Oxide is rapidly inactivated by ____ and combines to form ____.

A
  • Hemoglobin
  • Methemoglobinemia

Methemoglobinemia is more rare with NTG due to its rapid metabolism; however, MetHgb TOXICTY can occur with SNP at clinically relevant doses

Nitric Oxide production is increased by Nitroglycerin (a Nitrate) and Sodium Nitroprusside (Antihypertensive, i.e. NOT technically a nitrate)

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34
Q

T/F: Hydralazine exerts its vasodilatory effects via N.O.

A

FALSE

Hydralazine is a direct systemic arterial vasodilator and exerts its effects by promoting the influx (2K in/3Na out = net negative) of Potassium; this causes hyperpolarization of the cell and muscle relaxation. True MOA is not fully understood; it is known that cGMP is increased which causes smooth muscle relaxation = vasodilation (non-ppt)

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35
Q

What drug is used to treat hypertensive emergencies such as Preeclampsia?

A

Hydralazine

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36
Q

Which drug can cause an autoimmune-like condition called “Drug Induced Systemic Lupus Erythamatosus*?

A

Hydralazine

Red “butterfly” rash on face

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37
Q

“Slow-acetylators” possess an enzyme mutation inhibiting them from breaking down certain drugs such ____, which could lead to sustained hypotension and tachycardia.

A

Hydralazine

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38
Q

Plasma half-life of IV nitroglycerin

A

3 min

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39
Q

The blue cylinder/dial on our anesthesia machines is Nitrous Oxide (N2O), which is an anesthetic and sometimes called “laughing gas.” Nitric Oxide is used for:

A
  • pulmonary vasodilation (5-20 ppm)
  • bronchodilation
  • improved V/Q matching
  • run as infusion (gas)
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40
Q

Clinical scenarios where Nitric Oxide gas may be used?

A
  • Newborn pulmonary HTN
  • Adult Respiratory Distress Syndrome (ARDS)
  • Cardiac transplant

Methemoglobinemia can still occur as NO combines with oxyhemoglobin.

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41
Q

Sodium Nitroprusside (Nipride) causes vasodilation of ____ vascular smooth muscle.

A

ARTERIAL

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42
Q

Nitroprusside interacts with Hgb, dissociating immediately to form:

A
  • MetHgb
  • CYANIDE
  • N.O.
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43
Q

Metabolism of Nitroprusside yields:

A
  • MetHgb
  • Cyanide
  • Thiocyanate
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44
Q

Clinical uses for Nitroprusside?

A
  1. Controlled Hypotension
  2. Hypertensive Emergencies (Pheochromocytoma, Thyrotoxicosis)
  3. Cardiac Disease
  4. Aortic Surgery
  5. Cardiac Surgery
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45
Q

Clinical Considerations (S/E) of administering Nitroprusside:

A
  • Cardio: hypotension, reflex tachycardia, decrease pulmonary arterial pressures
  • CNS: Increase CBF, CBV, ICP (at <30% MAP)
  • Respiratory: Attenuates HPV (via VD)
  • Other: Rebound HTN after abrupt discontinuation , Coronary Steal, Decreased platelet aggregation (>3 mcg/kg/min)
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46
Q

Which drug is photosensitive?

A

Nitroprusside

comes in amber vial, place 250cc bag in protective sleeve, then inject medication

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47
Q

Nitroprusside (Nipride) infusion dose

A

0.3 - 10 mcg/kg/min

MetHgb toxicity can occur >8 mcg/kg/min

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48
Q

Nitroprusside IVP dose

A

100 mcg

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49
Q

Maximum dose of Nitroprusside (10 mcg/kg/min) not to be administered for greater than ____.

A

10 minutes

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50
Q

At what dose of Nitroprusside do you encounter decreased platelet aggregation (bleed risk)?

A

> 3 mcg/kg/min

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51
Q

Nitroprusside clinically observed DOA (Weirich anecdotal)?

A

~2 min short-acting

great for clipping aneurysm or cannulating aorta where acute BP control is needed temporarily

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52
Q

Cyanide Toxicity is a concern with what drug?

A

Nitroprusside

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53
Q

How is cyanide eliminated in the body?

A

Hepatic elimination at rates <2 mcg/kg/min

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54
Q

Signs of cyanide toxicity

A
  • Tachyphylaxis
  • Metabolic Acidosis
  • Anaerobic Metabolism and lactate formation (inhibits aerobic respiration)
  • Increased venous PO2
  • lactate concentration >10 mmol/L (non-ppt)*
  • cyanide >40 micro moles/L (non-ppt)*
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55
Q

Treatment of Cyanide poisoning

A

1 .100% O2 despite normal SpO2
2. NaHCO3 (Sodium Bicarbonate) to correct acidosis
3. Sodium thiosulphate (200 mg/kg) over 15 min: removes CN
4. Sodium Nitrite: sequesters the cyanide (CN)

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56
Q

Thiocyanate Toxicity can occur with what drug if it is ran for extended period? How is is treated/reversed?

A
  • Nitroprusside
  • Tx: Stop SNP infusion
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57
Q

Thiocyanate Toxicity clinical signs

A
  1. Fatigue
  2. Nausea & Vomiting
  3. Hyperreflexia (muscles have increased reflex response)/muscle cramps
  4. Psychosis (disconnection from reality)
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58
Q

Thiocyanate is ____x less toxic compared to cyanide (CN)

A

100

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59
Q

Methemoglobinemia occurs with any substance that increases N.O. (Nitric Oxide, SNP, NTG); what is the required dose (IVP & Infusion) of SNP to evoke MetHgb?

A

~10 mcg/kg

> 8 mcg/kg/min

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60
Q

MetHgb clinical signs

A
  • Impaired oxygenation despite adequate CO and arterial oxygenation
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61
Q

Treatment for Methemoglobinemia

A

Methylene Blue IVP 1-2 mg/kg

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62
Q

Nitroglycerin (NTG) causes what?

A
  1. Dilation of venous capacitance vessels (more so than systemic arterial vasculature)
  2. dilates large coronary arteries
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63
Q

NTG MOA

A

NO mediated vasodilation

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64
Q

T/F: NTG is susceptible to tolerance after 48 hours.

A

FALSE

after 24 hours

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65
Q

T/F: NTG causes increased platelet aggregation

A

FALSE

Decreased platelet aggregation

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66
Q

Nitroglycerin is a good choice to decrease/increase pre-load.

A

Decrease (venous dilation occurs resulting in venous pooling in lower extremities)

NTG also dilates large coronary arteries improving blood flow/oxygen delivery to heart; this coronary dilation decreases SVR which decreases the workload of the heart, thereby decreasing oxygen consumption.

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67
Q

Nitroglycerin causes mainly ____ dilation.

A

Venous

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68
Q

NTG causes NO to be released through ____ - dependent pathway.

A

Glutathione

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69
Q

NTG causes what side effects?

A
  • Controlled HoTN
  • Cerebral VD: increased ICP, CBF & headache
  • Uterine Relaxation
  • Rare risk of MetHbg-emia
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70
Q

NTG clinical uses

A
  • Angina Pectoris
  • Acute HTN
  • ACS
  • Cardiac Failure
  • Controlled HoTN
  • Sphincter of Oddi Spasm (muscular valve surrounding the exit of the bile duct and pancreatic duct into the Duodenum, opens to allow bile juices to assist with food digestion)
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71
Q
A
  • NTG will dilate sphincter of Oddi if surgeon is trying to cannulate (ERCP procedure)
  • Opioids will constrict it
  • Glucagon 1 mg will constrict it
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72
Q

NTG infusion dose

A

0.3 - 10 mcg/kg/min

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73
Q

NTG sublingual dose

A

0.3 mg

74
Q

Nitroglycerin transdermal dose

A

0.6 mg/hr

75
Q

NTG IVP dose

A

100 mcg

76
Q

Methods of giving NTG

A
  • infusion
  • sublingual
  • transdermal
  • oral spray
  • IVP
77
Q

Other name of NTG

A

Nitrobid

78
Q

Beta 1 blockers decrease ____ formation, ultimately leading to ____.

A

-cAMP
-increased reuptake of Calcium (less Calcium = less contraction)

79
Q

B1 Blockers are what type of antagonists?

A

Competitive

80
Q

Beta blockers decrease CO via ____ & ____.

A
  • decreasing contractility (negative inotropy)
  • decreasing HR (negative chronotropy)
81
Q

Beta blocker side effects:

A
  • Bradycardia
  • AV Heart Block
  • CHF exacerbation (the maintenance of CO depends in part on sympathetic drive)
  • HoTN
  • Reduced Myocardial Oxygen Demand
82
Q

Which type of beta blocker can allow for bronchospasm and therefore should both be given to at-risk asthmatics?

A

Non-selective (e.g. propranolol)

block Beta 2 which then inhibits bronchodilation

83
Q

Atenolol, Esmolol and Metoprolol are all what type of beta blockers?

A

Beta 1 “Selective”

84
Q

Labetalol & Carvedilol (non-selective beta blockers) are what ratio alpha:beta

A

1:7

this is counterintuitive, b/c Labetalol has far greater impact on the BP (alpha) compared to HR/Contractility (Beta)

maybe affinity for alpha receptor is far greater than beta???

85
Q

ACE-I are effective against HTN caused by ____

A

Increased renin

86
Q

What do ACE-I block?

A
  1. The conversion of Angiotensin 1 to Angiotension 2
    (This ultimately blocks the release of Calcium from SR = NO VC = decreased BP)

- If not blocked, Angiotensin 2 acts on AT1 receptors
- Activates Phospholipase C
- Phospholipase C increases DAG & IP3
- DAG & IP3 INCREASE Calcium release from SR = VASOCONSTRICTION
- Also increases release of NE & inhibits its uptake

  1. Aldosterone release is blocked (Aldosterone: Na & H2O retention)
    (This results in reduced Na & water retention = decreased BP)
87
Q

Why do we not want our patients to take ACE-I prior to surgery?

A

Because it will inhibit our ability to increase BP during the procedure

Under anesthesia, sympathetic responses are diminished = unable to increase BP
ACE-I block the ability of the body to VC through RAS pathway = unable to increase BP

88
Q

If a patient takes ACE-I or ARB prior to surgery, this suggests patient will likely be profoundly hypotensive throughout the case and unable to compensate. What medications will likely be first go-to’s?

A

Tier 2 HoTN Tx:
- Calcium Chloride
250-500 mg
- Vasopressin will not be effective b/c it acts along the RAS pathway

Tier 3 HoTN Tx:
- Neo Drip
40-100 mcg IVP
.2-.5 mcg/kg/min
Tier 4 HoTN Tx:
- Epi:
10 mcg IVP
.03-.1 mcg/kg/min
- Levophed:
10 mcg IVP
.03-.1 mcg/kg/min

Hang Albumin

89
Q

ACE-I out of system in how long?

A

~24 hours

90
Q

Why can ACE-I cause coughing?

A
  • ACE converts Bradykinin to an inactive peptide.
  • If ACE is inhibited, then bradykinin will accumulate.
  • Bradykinin causes coughing
  • If pt is sensitive to cough, then they can be prescribed an ARB (Angiotensin Receptor Blocker) Therefore, ACE is allowed to convert AT1 to AT2, then the ARB blocks AT2 receptors = pathway is blocked later still decreasing BP
91
Q

Examples of ACE-I

A

“-pril”

Captopril (Captopen)
Enalapril (Vasotec)
Lisinopril (Prinivil)

92
Q

Onset comparison of ACE-I

A

Captopril:15-30 min
Enalapril: 60-120 min
Lisinopril: 60 min

93
Q

DOA comparison of ACE-I

A

Captopril: 6-10 hr
Enalapril: 18-30 hr
Lisinopril: 18-30 hr

94
Q

ACE-I contraindications

A
  1. Renal artery stenosis (Decreased RBF = risk of CRF) [BQ]
  2. Pregnancy
95
Q

ACE-I side-effects

A
  1. Diarrhea
  2. Dry cough
  3. Edema
  4. Bronchospasm
    5.Hyperkalemia
96
Q

ARBs MOA

A
  • competitively block AT2 receptors
    1. Blocks AT2 VC
    2. Blocks Aldosterone release
    3. Blocks water reuptake
97
Q

ARBs do/do not potentiate bradykinin

A

Do not

98
Q

Examples of ARBs

A

“-sartan”

-Valsartan
-Losartan
-Candesartan

99
Q

Three chemical structures of Calcium Channel Blockers

A
  1. Phenylalkylamines
  2. Dihydropyridines (DHPs)
  3. Benzothiazepines
100
Q

Calcium channels blockers MOA

A
  1. CCBs bind to receptors on voltage gated calcium ion channels to ensure channel closure
  2. Results in a reduction of intracellularly calcium
101
Q

Phenylalkylamines occlude the calcium channels in the open/closed state.

A

Open

102
Q

Phenylalkylamines act on ___ via calcium channel inhibition and cause____.

A
  • the heart
  • decreased contractility, rate, and coronary and peripheral vasodilation
103
Q

Examples of Phenylalkylamine (CCB):

A

Verapamil (Calan)

104
Q

Verapamil IVP

A

2.5-10 mg q. 15-30 min

Max = 20mg

105
Q

Verapamil clinical use:

A
  • SVT
  • Angina
  • Essential HTN
  • Symptomatic hypertrophic cardiomyopathy
106
Q

Verapamil’s active metabolite has what relative potency?

A

1/5th - 1/10th

107
Q

Verapamil half life

A

5 hours

108
Q

Verapamil should be given with caution to what patients?

A

CHF

109
Q

Verapamil two major effects

A
  1. Vasodilation
  2. Negative inotropy (decreased contractility)
  3. Negative Chronotropy (decreased rate)

RATE DRUG

110
Q

CCB: modulation of ion channel prevents calcium entry intracellularly

A

Dihydropyrimidines

111
Q

Dihydropyrimidines (DHP)are used mainly to treat ____.

A

Systemic HTN

112
Q

DHP can cause reflex increase in ____ & ____, as well as a decrease in ____.

A
  • CO
  • HR
  • afterload
113
Q

Patients on DHP (CCB) and ACE-I may develop marked and refractory ____ under GA.

A

Hypotension

114
Q

DHP (CCB) examples:

A
  • Nicardipine (Cardene)
  • Nifedipine (Procardia)
  • Amlodapine (Norvasc)
115
Q

Nicardipine half life and infusion dose:

A
  • short 1/2 life
  • 0.5-10 mcg/kg/min OR 5-10 mg/hr
116
Q

Nicardipine considerations (S/E)

A
  • Minimal myocardial depression
  • Decreased SVR
  • Coronary artery VD
  • Tocolysis
117
Q

What DHP (CCB) has not depression of SA or AV node?

A

Nifedipine

118
Q

Nifedipine treatment for:

A
  • coronary artery vasospasm 2/2 CABG
  • prevention of cerebral arterial vasospasm 2/2 SAH
119
Q

DHP (CCB) that is PO only and is prescribed for its anti-ischemic effects after MI:

A

Amlodipine

120
Q

DHP (CCB) are primarily ____ agents.

A

Anti-hypertensive

121
Q

Benzothiazepines (CCB) are primarily ____ agents.

A

Rate-controlling

Non-DHP

122
Q

Benzothiazepines MOA

A

Block Calcium influx into heart and smooth muscle and therefore decrease HR and contraction oat SA and AV nodes

123
Q

Benzothiazepine example

A

Diltiazem (Cardizem)

124
Q

Diltiazem is used to treat what EKG abnormality?

A

A-Fib (fast irregular HR)

….or other SVT

125
Q

Diltiazem IVP

A

.25 mg/kg

126
Q

Diltiazem infusion dose

A

5-15 mg/hr

127
Q

Diltiazem uses:

A
  • peripheral arterial dilation
  • Essential HTN
  • SVT
  • Angina
128
Q

If performing a neuro case or any case where increased ICP is to be avoided, what anti-hypertensive agents should be avoided and which are more appropriate?

A
  • AVOID: Nitric Oxide agents (NTG, SNP); these can cause headaches which increase ICP/CBF (plus MetHgbemia, CN poisoning, etc.)
  • Preferred: Calcium Channel Blockers have a safer profile (e.g., Nicardipine); do not dilate cerebral vessels

Nicardipine is used frequently

129
Q

Clinical considerations of Calcium Channel Blockers:

A
  1. Cautious administration in hypovolemic and patients with poor LV function
  2. Potentiation of NMB
  3. Verapamil and Diltiazem have potent LA activity
  4. Verapamil causes cardiac collapse whe administered concurrently with Datrolene
  5. May increase plasma concentration of Digoxin
130
Q

What two CCB may lower the threshold for LA toxicity ?

A
  1. Verapamil
  2. Diltiazem

NON-DHP

131
Q

Where are alpha 2 receptors located relative to neuronal synapses?

A

Presynaptic and Postsynaptic

132
Q

Major effects of Alpha 2 agonists

A
  1. Sedation
  2. Analgesia
  3. Hypotension
133
Q

Alpha 2 agonists MOA

A
  1. Inhibits adenylyl cyclase, Calcium, and Potassium Ion channels
  2. Result is reduction of cAMP = decrease in Calcium levels = decreased BP & hyperpolarization (decrease in cardiac conduction?)
134
Q

Clonidine & Precedex are centrally-acting alpha-2 agonists that bind to ____ in order to ____.

A
  • Pre-syaptic alpha 2 receptors
  • decrease NE release (via negative feedback loop) which decreases sympathetic tone.
  • decreased NE release in brain causes sedation (also benefits for ADHD pts)
135
Q

Clonidine and Precedex clinical effects:

A
  • Sympatholytic
    1. Decrease BP
    2. Decrease HR
  • Sedation
  • Anxiolysis
  • Analgesia
  • Antisialagogue
  • minimal respiratory depression
136
Q

Precedex cautions:

A
  • most providers avoid initial bolus dose (opting for infusion) IOT avoid HoTN and Bradycardia (produced by vagal stimuli)
  • abrupt discontinuation of leads to Rebound HTN
137
Q

Other uses of alpha-2 agonists

A
  1. Opioid withdrawal
  2. Adjunct to regional
  3. Analgesia
138
Q

Alpha Antagonist examples

A
  • Phentolamine (Regitine) [non-selective]
  • Phenoxybenzamine (Dibenzylene) [non-selective]
  • Prazosin (Minipress) [alpha 1 selective]
  • Terazosin (Hytrin) [alpha 1 selective]
139
Q

Alpha Antagonists are used almost exclusively for the treatment of:

A

Pheochromocytoma

block the actions of catecholamines

140
Q

Alpha 2 blockage leads to:

A

NE release and increase in HR

141
Q

Phosphodiesterase Inhibitors (PDEIs) increase levels of cAMP/cGMP and activates cardiac ____ channels/

A

Calcium

142
Q

PDEIs cause an influx of calcium into the cell which leads to ____ & ____.

A
  • increase in HR
  • increased force of contraction (inotropy)
  • increased relaxation speed (lusitropy)
143
Q

increase in cAMP = ____.

Increase in cGMP = ____.

A

Increased cAMP: increased Calcium = increased contractility (positive inotropy)

  • Increased cGMP: vasodilation (decrease in preload/afterload)
144
Q

Whenever a PDEI is given, what should be given with it?

A

Vasoconstrictor IOT to offset vasodilation effects of PDEI

145
Q

PDE 3 Inhibitors

A
  • Amrinone (Inocor)
  • Milrinone (Primacor) more common
146
Q

Amrinone is what type of drug

A

Selective PDE 3 Inhibitor

147
Q

What does Amrinone cause

A

Dose-dependent inotropy and VD

148
Q

Amrinone loading dose

A

0.5-1.5 mg/kg

149
Q

Amrinone infusion dose

A

2-10 mcg/kg/min

150
Q

Milrinone causes:

A
  • positive inotropy
  • vasodilation
151
Q

Which PDEI is used in acute LV dysfunction?

A

Milrinone

152
Q

Milirinone loading dose

A

50 mcg/kg

Hint: He made his first Mil at 50

153
Q

Infusion dose Milrinone

A

0.5 mcg/kg/min

154
Q

When is PDE 3 like Milrinone used?

A

IOT make tachycardic:
- Whenever pt has weak heart/LV dysfunction (coming of CPB, EF < 20%)
- Elicit arrhythmia (A-Fib) IOT ID abnormal paths

Isuprel and Dobutamine can also be used for similar effects

155
Q

Non-Selective PDEI

A
  • Theophylline
    ~found green/black tea
    ~Tx bronchospasm due to asthma
    ~GERD can occur due to gastroesophageal relaxation
    ~Narrow therapeutic index
  • Caffeine
  • Theobromine
156
Q

PDE 5 Inhibitors are selective for ____ in the lung and corpus cavernosum.This causes ____.

A
  • cGMP
  • pulmonary vasodilation & erections
157
Q

PDE 5 Inhibitors examples:

A
  • Sildenafil (Viagra)
  • Tadalafil (Cialis)
158
Q

Rule of 5’s initial infusion doses for vasoactive agents

A

Epi/NE/REMI: 0.05 mcg/kg/min

Neo/SNP/NTG: 0.5 mcg/kg/min

DA/Dobutamine: 5 mcg/kg/min. (DA = Dopamine)

Esmolol/Labetalol: 50 mcg/kg/min

159
Q

Hydralazine is a _____..

A

Potent systemic arterial vasodilator

160
Q

Hydralazine MOA

A

Promote efflux of Potassium which leads to hyperpolarization and muscle relaxation

Potassium (+) out of cell makes cell more negative, less able to reach action potential

161
Q

Hydralalazine can cause what side effects:

A
  • Reflex tachycardia
  • Rebound HTN
  • Used commonly in PIH?
162
Q

Hydralazine concentration

A

20 mg/cc

163
Q

Hydralazine IVP

A

5-10 mg IVP

164
Q

Hydralazine onset & DOA

A

Onset: 10-20 min

DOA: 3-8 hours

165
Q

Give Hydralazine ____ min before end of case to allow for onset IOT to thwart increased BP.

A

25-30 min

166
Q

If you give Labetalol to treat anticipated spike in BP at emergence, give it ____ min before.

A

5 min (one cycle of cuff)

167
Q

Weirich suggested emergence protocol for antihypertension:

A

30 min out: Hydralazine 5 mg (Opens Potassium Channels = VD)
K Channels stay open, K exits the cell via concentration gradient, cell loses positivity, hyperpolarizes, no action potential, no vasoconstriction.

10 min out: Labetalol 10mg (Blocking Alpha 1 = VD)

5 min out: Start Cardene gtt (Blocking Calcium Channels = VD)

168
Q

Hydralazine draw up method (Weirich)

A

3cc Saline + 1 cc Hydralazine = 5 mg/cc

169
Q

What PDEI is good for coronary and cerebral vasodilation/prevent vasospasm?

A

Papavarine

170
Q

Magnesium acts as a ____. How does it do this?

A
  • CCB
  • Stimulates production of VD
  • Reduces Prostaglandins (inflammatory markers)
  • Increases N.O.
171
Q

____ is a first line treatment for pre-eclampsia and eclampsia.

A
  • Magnesium
  • Hydralazine (non-ppt*)

Magnesium is also administered to stop premature labor = Tocolytic

172
Q

Normal pulmonary arterial pressure (PAP)

A

23-30 mmHg

173
Q

Pulmonary arterial pressure equation

A

PAP = LAP + (CO x PVR)/80

know for test

174
Q

Pulmonary HTN caused by 3 factors

A
  1. Increased LAP (left atrial pressure)
  2. Increased CO
  3. Increased PVR
175
Q

Other pulmonary vasodilators

A
  1. Inhaled NO (or iNO)
  2. PDE5 Inhibitors (Sildenafil)
  3. CCB (Diltiazem & Verapamil)
  4. PGE1: neonates with CHD to maintain PDA latency
  5. PGI2: Primary Tx for Pulmonary HTN (Prostaglandins)

not tested

176
Q

Sildenafil & Tadalafil are what type of PDEIs?

A

PDE Type 5 Inhibitors

HINT: Sildenafil (Viagra) = Type V

177
Q

What type of PDEI is Milrinone and Amrinone?

A

PDE Type 3 Inhibitor

HINT: “milli = 3 decimal places (1 milliliter = .001L)

178
Q

Caffeine, Theophylline, Theobromine, Paraxanthine are all what kind of PDEI?

A

Non-Selective PDEI

179
Q

Caffeine Fun Facts (non-ppt)

A
  • Causes increased Ca release via PDEI pathway by increasing cAMP = Increased force of contraction & Increased BP due to VC of vessels
  • Binds and blocks Adenosine receptors: causes increased neuronal activity, Increases NE, constricts vessels = Increase in HR & Alertness
    ~Adenosine causes sleepiness, decreased neuronal activity, decreased HR, VD
  • Relieves headaches due to increased Adenosine (VD causes increased CBF) = VC reduces BF & relieves headache
180
Q

What alpha antagonist put patients at increased risk of fall due to orthostatic HoTN and dizziness?

A

Terazosin

Pharm 2 (6 decks)

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