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CVP pharm test 2 > Test 2 content > Flashcards

Test 2 content Flashcards

1
Q

Negative effects of angiotensin on kidneys

A

Increased glomerular pressure and fibrosis
Protein leak
Increased Na reabsorption

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2
Q

-ACE-I use benefits HF patients, prevents the following so failing heart doesn’t haven’t to work hard:

A
  • angiotensin increased in HF since low CO
  • baroreceptors send signals to kidneys or blood vessels to increase blood volume/flow
  • preload increases
  • NE released
  • endothelin-modifies blood vessels to constrict
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3
Q

Negative effects of angiotensin on heart, primarily what side?

A

LV

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4
Q

Esmolol MOA and Dosing

A

MOA: Agent is cardioselective B-adrenergic blocker

Dose: 500mcg/kg over 1min then 50mcg/kg/min with max 300mcg/kg/min (titrate every 5 min)

Esmolol has very short duration of action which is commonly desired in ICU

Lack of intrinsic sympathomimetic and membrane-stabilizing activity

KEY: If desired effect not observed bolus administration repeated before infusion rate is increased

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5
Q

Esmolol vs Labetalol Effect on Myocardial oxygen

A

Increased

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6
Q

Esmolol vs Labetalol onset of drugs?

A

Rapid

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7
Q

Labetalol has about____ the active B effects as propranolol

A

1/5

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8
Q

Esmolol vs Labetalol Duration of Effect HR

A

Esmolol: Rapid
Labetalol: Slower

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9
Q

PANS is _____activity.

A

Cholinergic

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10
Q

Beta-blocker comparision esmolol vs labetalol

A

Onset-Rapid for both
Duration of effect HR-
Esmolol (Rapid) Labetalol (slower)

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11
Q

a-adrenergic blockers

A

Vasodilator activity on the peripheral vasculature
Side effects -
o-Orthostatic hypotension (hypotension (blood pressure drop from sitting to standing is too much for patient’s body to compensate for and pt can have syncope)

o- Reflex tachycardia - compensate for severe drop in B- this drop can be sensed by brain and drive sympathetic response

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12
Q

Spironolactone is specifically an _____ ______ and is the ______ ______ ______.

A

aldosterone antagonist

Most common one

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13
Q

SANS is ______ with alpha, B receptors

A

Adrengeric (EPI NE)

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14
Q

HTN is high ____. This causes ____ in the vasculature. The goal is to _____ the vasculature.

A

BP
constriction
dilate

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15
Q

Beta blockers can be helpful because they can decrease

A

Renin

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16
Q

Esmolol Absorption, Metabolism, and Excretion:

A
  • Onset of action is seconds and duration of action up to 10-20 min after cessation
  • Metabolism occurs in erythrocytes by esterases and has metabolite (1/500 activity) eliminated in urine
  • Do not need to adjust in hepatic or renal failure
  • Useful in patients with acute myocardial infarction
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17
Q

Central factors in HTN? 4 physiologic causes of HTN?

A

1) adrenergic drive = Increased HR & CO
2) High aldosterone - Increased Na+ and Ca2+ -> increased SVR
3) Low renin: Increased Na+ and Ca2+ -> increased SVR
4) High renin -> increased AII -> increased SVR

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18
Q

Postoperative HTN Requires rapid control of BP (3 things)

A

Control bleeding at suture sites

Neurology checks (patient used to x BP, now receiving y)

Myocardial ischemia develops due to increased oxygen needs

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19
Q

Low BP → ↓ PANS → ↑ HR ↑ SANS → ↑ CO ↑ SVR goal or end result?

A

Increase BP

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20
Q

Hydralazine on HTN

A
  • Initially slower onset of 5-15min then precipitous fall in BP lasting up to 12 hours
  • Circulating half-life is about 3 hours, however effect on BP can last up to 100 hours
  • Agent has unpredictable effects on BP and is difficult to titrate
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21
Q

Labetalol Absorption, Metabolism, Excretion

A
  • Onset of action is 5-15min and lasts up to 2-12 hours after cessation
  • Extensive first pass metabolism therefore oral form is only about 20-40% bioavailable
  • Minute amount of unchanged drug excreted in urine
  • Bolus doses of 1-2mg/kg have produced precipitous drops in BP
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22
Q

Esmolol vs Labetalol Effect on SVR

A

Esmolol: None
Labetalol: decreased SVR

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23
Q

Labetalol MOA & Dosing

A

MOA: Agent is a selective alpha and non-selective B-adrenergic receptor blocker with a to B ratio of 1:7

Dose: 20mg bolus then 1-2mg/min with max 5mg/min

a-Receptor blocking is responsible for vasodilation of arterial smooth muscle and B-blocking effects the smooth muscle as well as sympathetic stimulation

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24
Q

5 classes of treatment for HTN.

A

vasodilators:

  • Calcium Channel Blockers
  • Nitrovasodilators
  • Dopamine agonists
  • ACE inhibitors

Affect CO
- Beta-Blockers (especially selective ones)

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25
Q

barorecptors sense changes in pressure and flow to _____. Baroreceptors also sense ____ rises and drops (ex: due to dehydration)- baroreceptors can also cause signal to

A

brain

acute

increase blood volume

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26
Q

Catecholamines can increase HR and cause .

A

Vasoconstriction

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27
Q

BP Tracing- Pulse Pressure

A

(SBP-DBP)

  • HR
  • BP
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28
Q

ACE inhibitors and AT-1 blockers cause ____ in SVR by?

A

decrease

reducing Angiotensin II

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29
Q

Etiology of HTN perioperative

A

Vasoconstriction (catacholamines/baroreceptor) combined with intravascular hypovolemia

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30
Q

Angiotensin inhibition for HTN 3 ways to inhibit angiotension:

A

ACEi

ARB

Parasympathetic stimulation

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31
Q

Postoperative HTN Generally lasts about _____ Higher association with _____

A

2 to 6 hours

ICU admissions and mortality

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32
Q

Nicardipine Absorption, Metabolism, and Excretion:

A
  • Onset of action is with 1-5 min and duration of action is 2-6 hours after cessation
  • Agent is about >95% bound
  • Metabolism occurs through CYP 3A4 system substrate therefore monitor for potential drug interactions
  • Cardiac sparing effect, therefore no contractility suppression
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33
Q

Rapid changes in peripheral circulation (ie high or low) are addressed via

A

signal transmission to CNS

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34
Q

Baroreceptors provide the CNS with information regarding BP changes. Most common place is

A

Carotid arteries

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35
Q

High BP → ↑PANS → ↓ HR ↓ SANS → ↓ CO ↓ SVR goal or end result?

A

decrease BP

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36
Q

Low blood volume- sends message to kidney to

A

cause water retention through ADH (but the kidney mechanisms take longer than that of catecholamines)

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37
Q

Nitroglycerin on HTN

A
  • Only effective at higher doses
  • Concern for hypotension and tachycardia
  • Compromised cerebral and renal perfusion due to preload and caridac output
  • Difficult agent to titrate (often given as bolus instead of continuously)
  • vasodilator
  • Useful in ACS
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38
Q

objectives of Anti-HTN

A

▪ Overview of therapeutic targets for HTN management
▪ Describe the CV benefits of HTN control
▪ Describe the mechanism of action of each drug class for the management of HTN
▪ Describe the mechanism of action of intravenous therapies used to manage acute HTN

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39
Q

Indications of ACE-I therapy:

A

HTN -Lower BP

HF - Management of hypertrophy

Post-MI - Prevent additional hypertrophy

DM - Prevention of nephropathy (serum creatinine reflects kidney function, which declines -protein leaks into urine)

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40
Q

Aldosterone normally causes _____

A

sodium retention

-drugs will prevent that by maintaining sodium within tubule which water follows leading to decreased tension/volume overload

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41
Q

Aldosterone has what physiological effects?

A
  • Increases Na retention -> Water retention
  • Increased vascular hypertrophy
  • Ability to mediate cardiac injury
  • Decreases release of NE
  • Monitor serum K for patients on aldosterone antagonist therapy*****
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42
Q

Class 3: Amiodarone Toxicity effects

A

Pulmonary fibrosis

Photodermatitis:

Corneal microdeposits:

Hepatic: necrosis and failure (IV and oral)

Thyroid dysfunction (hyperthyroidism/ hypothyroidism )

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43
Q

Esmolol vs Labetalol Duration of Effect HR

A

Esmolol: Rapid
Labetalol: Slower

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44
Q

Anti-Arrythmia objectives

A

▪ Overview of the classifications for antiarrhythmic agents
Describe the mechanism of action of each drug class for the management of arrhythmias
Describe the unique side effects from Amiodarone therapy
Describe the goals of therapy for antiarrhythmics

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45
Q

Therapeutic targets for HTN

A
  • Aldo blockers
  • Diuretics
  • Catecholamine inhibitors
  • vasodilators
  • ARBs
  • ACE-i
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46
Q

What are the two classes for rate control? Rhythm control?

A

Rate: Classes 2 and 4 (BBs and CCBs)

Rhythm: Classes 1 and 3 (Na channel blockers and Potassium channel blockers)

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47
Q

Low BP → ↓ PANS → ↑ HR ↑ SANS → ↑ CO ↑ SVR goal or end result?

A

increase BP

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48
Q

which non-DHP is more cardioselective for AA:

A

diltiazem Not as cardioselective as verapamil

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49
Q

MOAs of Beta Blocker AAs

A

Prevents activation of ß receptors

Decrease the phase 4 slope of pacemaker

↓SA node activation and AV node conduction

By blocking beta receptors, it can decrease the slope of the face takes more time to reach to potential

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50
Q

Perioperative HTN: Systolic BP (SBP) is what?

A

SBP 20% >perioperative reading >15min, or increase of >50% original value

Incidence is almost 50% depending on the surgery

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51
Q

abnormal systole and diastole

A

blood pools and goes to brain and clots

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52
Q

AA Suppression of IKr drugs? what class? These drugs can be ____-arrythmia

A

class 3

can be pro-arrythmia

Ibutilide -However a higher rate of conversion for atrial fibrillation or flutter
Sotalol -QT interval increases of 25-80 msec, dosage dependent
Dofetilide -Initiation of therapy via pharmaceutical monitored program

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53
Q

Acute AP drop: send message to ANS and causes

A

endogenous catecholamine production and release (EPI and NE) and in the kidneys

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54
Q

Clinical benefits of HTN management

A
  • Decreased pressure on the aortic arch
  • Improvements in patients with Sleep Apnea
  • Reduced incidence of Stroke

-Improved kidney function
Longevity (High blood pressure is detrimental to kidney function)

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55
Q

What are the 2 most common segments of the EKG?

A

ST segment

QT interval

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56
Q

Rapid changes in peripheral circulation (ie high or low) are addressed via

A

signal transmission to CNS

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57
Q

Esmolol vs Labetalol Effect on SVR

A

Esmolol: None
Labetalol: decreased SVR

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58
Q

Toxicities of lidocaine?

A

Hypotension when given in large doses (reduced contractility)

Neurologic (tremor, Nausea, slurred speech, and seizures)

Higher incidence in patients with plasma concentrations greater than 9 mcg/ml

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59
Q

Labetalol MOA & Dosing

A

MOA: Agent is a selective alpha and non-selective B-adrenergic receptor blocker with a to B ratio of 1:7

Dose: 20mg bolus then 1-2mg/min with max 5mg/min

a-Receptor blocking is responsible for vasodilation of arterial smooth muscle and B-blocking effects the smooth muscle as well as sympathetic stimulation

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60
Q

Amiodarone Complex t1/2?

A

short term 3-10 days and chronic of several weeks to months

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61
Q

Esmolol MOA and Dosing

A

MOA: Agent is cardioselective B-adrenergic blocker

Dose: 500mcg/kg over 1min then 50mcg/kg/min with max 300mcg/kg/min (titrate every 5 min)

Esmolol has very short duration of action which is commonly desired in ICU

Lack of intrinsic sympathomimetic and membrane-stabilizing activity

KEY: If desired effect not observed bolus administration repeated before infusion rate is increased

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62
Q

Rate control AA Classes?

A

2 and 4 (BBs and CCBs)

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63
Q

Vaughan Williams Classification of AAs

A

Class I: Na channel blockers
Class 2: Beta blockers - excluding sotalol that also has class III effects
Class 3: blockade of IKr (Potassium Channel Blocking)
Class 4: CCB

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64
Q

what kind of treatment do HF patients get for Anti-Arrythmia?

A

ICD, can shut off

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65
Q

Adenosine Therapeutic use and dosing

A

Conversion of PSVT or diagnostic for EKG

Dose: 6 mg IVP followed by rapid saline flush - T1/2 in bloodstream is approx 10 sec
Can administer a second dose of 12 mg if needed

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66
Q

provides the driving force for organ perfusion & depends on ____ and ____

A

Art Pressure (AP)

CO and SVR

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67
Q

Lidocaine is what class AA? When do you use it?

A

Treatment of ventricular tachycardia & fibrillation when amiodarone is unavailable

Prevention of VF after cardioversion in Acute M
I
Prophylactic use for the prevention of VF after acute MI is NOT recommended → increased mortality

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68
Q

Class 3: Amiodarone is given for how long to a patient?

A

For life

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69
Q

Esmolol vs Labetalol onset of drugs?

A

Rapid

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70
Q

Class 4 CCB Therapeutic use:

A

Acute and chronic Paroxysmal Supraventricular Tachycardia (PSVT)

Rate control for atrial fibrillation

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71
Q

Esmolol vs Labetalol Effect on Myocardial oxygen

A

Increased

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72
Q

Adenosine is ___ effective in presence of theophylline and caffeine

A

less effective

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73
Q

Perioperative HTN: Systolic BP (SBP) is what?

A

SBP 20% >perioperative reading >15min, or increase of >50% original value

Incidence is almost 50% depending on the surgery

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74
Q

Class 4: Ca2+ Channel Blockers MOA

A

Block slow cardiac Ca-channels

↓ phase 0, ↓ phase IV of (automaticity phase) nodal tissues and enhances ERP

Suppress Ca dependent tissues activation or depolarization - ↓ SA activity & ↓ AV conduction (enhance ERP, more effect)

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75
Q

Class 3: Amiodarone Toxicity effects

A

Pulmonary fibrosis (in 45% of patients) (most important & fatal): inflammatory response to Iodine, regular x-ray monitoring required. Dose realted

Photodermatitis: Blue/Grey skin pigmentation “smurf skin”

Corneal microdeposits: optic neuritis (blindness)

Hepatic: necrosis and failure (IV and oral)

Thyroid dysfunction (hyperthyroidism/ hypothyroidism ), monitor thyroid function tests prior/during treatment (prevents conversion of T4 → T3)

76
Q

Catecholamines can increase HR and cause

A

Vasoconstriction

77
Q

Perioperative, Antihypertensive treatment reduces how are the drugs given?

A

myocardial ischemia,
neurological deficits
mortality

IV push or infusion

78
Q

BP Tracing- Pulse Pressure

A

(SBP-DBP)

  • HR
  • BP
79
Q

AA Classes 1 and 3

A

(Na channel blockers and Potassium channel blockers)

80
Q

Lidocaine is metabolized where? How many metabolites?

A

Liver

2

81
Q

Class 3: Ibutilide MOA

A

Slows repolarization via blockade of rapid component of potassium current (IKr)

82
Q

Protein in urine: microalbuminurea is a consequence:

A

of poor BP management for a long period of time.

83
Q

High sodium intake: retention of water and increased ____ _____ which will keep______

A

blood volume which will keep blood pressure high. This is why low sodium intake is important in HTN

84
Q

What are the common clinical etiologies of Arrythmias?

A
  • Ischemia
  • Hypoxia
  • Excessive catecholamine exposure - Infusion of EPI, NE, or DA
  • Drug toxicity - ie digoxin
  • Overstretch of cardiac fibers - ie HF
  • Presence of scarred tissue
85
Q

Arythmiasare an abnormality in the site of origin of the

A

impulse,
rate or regularity,
or its conduction

86
Q

Are AA Class 2 BBs selective or nonselective and for which receptors?

A

Selective B1 receptor

87
Q

5 classes of treatment for HTN.

A

vasodilators:

  • Calcium Channel Blockers
  • Nitrovasodilators
  • Dopamine agonists
  • ACE inhibitors

Affect CO
- Beta-Blockers (especially selective ones)

88
Q

Digoxin MOA? involves both ____ and ____? lower dose involves? higher dose involves?

A

sensitization of baroreceptors, central vagal stimulation, and facilitation of muscarinic activity

Increased DADs and PVCs

-Involve both the SANS and PANS
Lower dose range: PANS predominate
Higher dose range: SANS predominate

89
Q

Adenosine MOA

A

Purine base adenine attached to ribose sugar (nucleoside)

Activate adenosine receptor in nodal tissues

Activate Gi protein - decrease in cAMP

Activation of K+ channels/current (inward rectifier) and suppression of Ca2+ current

Hyperpolarization and suppression Ca dependent action potentials

Suppress AV nodal conduction & increase the refractory period

Lesser effects on SA Node

90
Q

Acute AP drop: send message to ANS and causes

A

endogenous catecholamine production and release (EPI and NE) and in the kidneys

91
Q

Class 3: Amiodarone Toxicities caused by?

A

Iodine

92
Q

provides the driving force for organ perfusion & depends on ____ and ____

A

Art Pressure (AP)

CO and SVR

93
Q

Repolarization time is aka?

A

relaxation

94
Q

Digoxin dosing and admin

A

Administration both IV and oral tablets

Dose: 500 mcg IV x1 dose, then 250 mcg x2 doses total 1 mg

Monitor: level next day and at steady state (approx 5 days)

95
Q

what are cardiac depolarizations aka?

A

contractions

96
Q

Diuretics : decrease ____-> decrease ____

A

BV -> BP

97
Q

Adenosine has ____ effect in the presence of dipyridamole? Should give ____ dose if given via central line

A

increased

reduced. start at 3mg

98
Q

Class 3: K channel blockers MOA

A

Block K-channels (↓IK delayed rectifier current) slowing phase 3 (repolarization) of AP

↑APD and ERP

Lower incidence of prolonged QT-prolongation and torsades de pointes

99
Q

Therapeutic targets for HTN

A
  • Aldo blockers
  • Diuretics
  • Catecholamine inhibitors
  • vasodilators
  • ARBs
  • ACE-i
100
Q

Cardiac effects of Lidocaine?

A

Uses – always administered by IV infusion (since low F)

Blockade of activated and inactivated Na channels

Effects on cells with longer potentials (ie ventricles) in comparison to atria

101
Q

ACE inhibitors and AT-1 blockers cause ____ in SVR by?

A

decrease

reducing Angiotensin II

102
Q

Goals of Therapy

A

Rate control

Rhythm control - both it and rate have Pharmacologic and Electrical

Stroke Prevention - anticoagulation

Prevention of Sudden Cardiac Death - ICD

103
Q

Chronically, HTP causes thickening of

A

LVH- this will compromise EF.

104
Q

Arrythmias consist of cardiac depolarizations that _____ ____ ____ the prior mentioned pathways for conduction

A

Do not follow

105
Q

Low blood volume- sends message to kidney to

A

cause water retention through ADH (but the kidney mechanisms take longer than that of catecholamines)

106
Q

after the atram signal travels via _____ system and ____

A

His-Purkinje system

ventricles.

Generally in synchrony, therefore hemodynamically effective

107
Q

Pharmacologic Management for (Anti hypertensives)

A
  • Sodium Nitroprusside
  • Esmolol
  • Labetalol
  • Fenoldopam
  • Nicardipine
  • Misc(nifedipine, NTG, and hydralazine)
108
Q

What’s the least pro-arrythmia drug?

A

Amioderone

109
Q

_____ mechanisms regulate CV function are under control of receptors in the arteries and veins (ie baroreceptors)

A

Neural and hormonal (neurohormonal)

110
Q

Electrolytes are affected by AA in what ways?

A

2 most common are
Hypokalemia - Serum K less than 4 mEq/L can intensify IKr drug block
Hypocalcemia-Severe levels measured via ionized Ca

Hypomagnesemia- Serum Mg level less than 2 mg/dl

Intracellular depletion with diuretic therapy- Slow Vd during replacement phase

Repletion of electrolytes will shorten QT interval

111
Q

Chronically, HTP causes thickening of

A

LVH- this will compromise EF.

112
Q

Inhibitors of renal cation exchange can prolong effect (ie cimetidine, HCTZ, etc) of what drug?

A

Class 3: Dofetilide

113
Q

Rhythm control AA classes?

A

Classes 1 and 3 (Na channel blockers and Potassium channel blockers)

114
Q

Nicardipine MOA & Dose

A

MOA: Agent is 2nd generation dihydropyridine CCB which is particularly selective for cerebral and coronary vessels

Dose: 5mg/hr titrate to max of 15mg/hr every

5 min by 2.5mg and bolus dosing is NOT FDA approved

Primary mechanism of action on the L-type calcium channels

PO and IV formulation available, since 100 times more hydrophilic than nifedipine

115
Q

Antiarrhythmic Class 1c agents

A

Flecanide

Propafenone

116
Q

Postoperative HTN Generally lasts about _____ Higher association with _____

A

2 to 6 hours

ICU admissions and mortality

117
Q

catheter ablation is not the 1st treatment. why? when can it be a first treatment?

A

arrythmia isnt localized to one specific area.

Can be first when flutter because Arrythmia is localized

118
Q

Central factors in HTN? 4 physiologic causes of HTN?

A

stress

1) adrenergic drive = Increased HR & CO
2) High aldosterone - Increased Na+ and Ca2+ -> increased SVR
3) Low renin: Increased Na+ and Ca2+ -> increased SVR
4) High renin -> increased AII -> increased SVR

119
Q

Etiology of HTN perioperative

A

Vasoconstriction (catacholamines/baroreceptor) combined with intravascular hypovolemia

120
Q

AntiArrythmia Beta BLocker Therapeutic uses:

A

Prophylaxis in post-MI - To prevent arrhythmias

Supraventricular tachyarrhythmias (SVTs)- Atrial flutter & atrial fibrillation -Slows AV nodal conduction & reduce the ventricular response

Esmolol (IV) is used in acute SVT & intraoperative arrhythmias

121
Q

Class 4 AAs are CCB. What type of CCBs? Where does it slow conduction?

A

nonDHPs;

Slows conduction in areas more Ca dependent (ie SA and AV nodes)

122
Q

Therapeutic targets for HTN

A
  • Diuretics - Decrease volume
  • Beta-blockers- Decrease heart rate and sympathetic drive
  • Calcium channel blockers- vasodilation (decrease in SVR
    )
  • Angiotensin inhibitors -
    Vasodilation, Aldosterone inhibition, Decrease hypertrophy
123
Q

Signal transmission flows from ____ to ____ via _____

A

atria to ventricles via AV node

124
Q

Labetalol Absorption, Metabolism, Excretion

A
  • Onset of action is 5-15min and lasts up to 2-12 hours after cessation
  • Extensive first pass metabolism therefore oral form is only about 20-40% bioavailable
  • Minute amount of unchanged drug excreted in urine
  • Bolus doses of 1-2mg/kg have produced precipitous drops in BP
125
Q

Normal impulse generating cardiac contraction originates at the _____ with what bpm?

A

SA node;

60-100 bpm

126
Q

_____ mechanisms regulate CV function are under control of receptors in the arteries and veins (ie baroreceptors)

A

Neural and hormonal (neurohormonal)

127
Q

Class 3: Ibutilide Administration via IV for

A

acute conversion of atrial fibrillation or atrial flutter

128
Q

What are AA classes 2 and 4?

A

2 and 4 (BBs and CCBs)

129
Q

Nicardipine Absorption, Metabolism, and Excretion:

A
  • Onset of action is with 1-5 min and duration of action is 2-6 hours after cessation
  • Agent is about >95% bound
  • Metabolism occurs through CYP 3A4 system substrate therefore monitor for potential drug interactions
  • Cardiac sparing effect, therefore no contractility suppression
130
Q

Class 4: Ca2+ Channel Blockers - Verapamil dosing, metabolism, admin, and side effects?

A

IV administration for acute use and oral therapy for chronic

Dose: 2.5 to 5 mg IV as bolus

Extensive hepatic metabolism

Side effects: constipation, hypotension (vasodilatation), AV block

Drug interactions: CYP 3A4 inhibitor

131
Q

As a whole, beta blockers decrease SV and HR so they They help decrease _____ by working together with ACE-Inhibitors

A

decrease CO.

renin secretion

132
Q

Class 3: Amiodarone is drug of choice for ____

A

wide array of arrhythmias

133
Q

objectives of Anti-HTN

A

▪ Overview of therapeutic targets for HTN management
▪ Describe the CV benefits of HTN control
▪ Describe the mechanism of action of each drug class for the management of HTN
▪ Describe the mechanism of action of intravenous therapies used to manage acute HTN

134
Q

Net effect of amiodarone conversion from atrial fibrillation in 24 hr*

Intravenous= ?
Oral= ?
A 
Intravenous= 28%
Oral= 52%
135
Q

Angiotensin inhibition for HTN 3 ways to inhibit angiotension:

A

ACEi

ARB

Parasympathetic stimulation

136
Q

Overall, HTN will cause

A

HF

137
Q

Class 3: Dofetilide MOA

A

Acts by blockade of the rapid component of the delayed rectifier potassium current (IKr)

Increase APD & ERP

Used to maintain sinus rhythm in Atrial fibrillation

Bioavailability is 100%, initiate in hospital - QTc > 500 msec can be fatal

Renal elimination accounts for 80% unchanged

Inhibitors of renal cation exchange can prolong effect (ie cimetidine, HCTZ, etc)

138
Q

Postoperative HTN Requires rapid control of BP (3 things)

A

Control bleeding at suture sites

Neurology checks (patient used to x BP, now receiving y)

Myocardial ischemia develops due to increased oxygen needs

139
Q

Extracardiac effects of Class 3: Amiodarone

A

Hypotension, secondary to IV administration due to the diluent, polysorbate 80

Resolve hypotension by slowing the rate of infusion

140
Q

Nitroglycerin on HTN

A
  • Only effective at higher doses
  • Concern for hypotension and tachycardia
  • Compromised cerebral and renal perfusion due to preload and caridac output
  • Difficult agent to titrate (often given as bolus instead of continuously)
  • vasodilator
  • Useful in ACS
141
Q

what are the classes of Arrythmias?

A

Suprventricular

ventricular

142
Q

Non-pharmacologic methods for management

A

Ablation - catheter fries cardiac muscle to prevent Arrythmia
Implantation of ICD
Electrical cardioversion

143
Q

a-adrenergic blockers

A

Vasodilator activity on the peripheral vasculature
Side effects -
o-Orthostatic hypotension (hypotension (blood pressure drop from sitting to standing is too much for patient’s body to compensate for and pt can have syncope)

o- Reflex tachycardia - compensate for severe drop in B- this drop can be sensed by brain and drive sympathetic response

144
Q

Esmolol Absorption, Metabolism, and Excretion:

A
  • Onset of action is seconds and duration of action up to 10-20 min after cessation
  • Metabolism occurs in erythrocytes by esterases and has metabolite (1/500 activity) eliminated in urine
  • Do not need to adjust in hepatic or renal failure
  • Useful in patients with acute myocardial infarction
145
Q

Class 4: Ca2+ Channel Blockers - Diltiazem admin, dosing, side effects,

A

IV administration for acute use and oral therapy for chronic

Dose: 20 mg IVP, then infusion of 2.5 mg/hr

Not as cardioselective as verapamil

Side effects: hypotension and bradycardia

Drug interactions: CYP 3A4 inhibitor

146
Q

Acutely (IMMEDIATELY) reducing BP can be bad too because your body has been used to this

A

high pressure, and now the brain isnt going to get enough perfusion, neither is the kidneys, etc.

147
Q

8 Risk Factors of AAs

A

Electrolyte abnormalities (ie K, Mg, Ca)

ECG findings (Bradycardia, Ion channel mutations)

Female - have longer Q-T intervals by 5-10

CAD

Recent electrical cardioconversion - toward rhythm control

Overdose of QT-prolongation medications

Drug-Drug interactions

Medications -Antiarrhythmic’s and Non-antiarrhythmics

148
Q

Hydralazine on HTN

A
  • Initially slower onset of 5-15min then precipitous fall in BP lasting up to 12 hours
  • Circulating half-life is about 3 hours, however effect on BP can last up to 100 hours
  • Agent has unpredictable effects on BP and is difficult to titrate
149
Q

what are the supraventricular Arrythmias?

A

atrial and AV node

150
Q

Clinical benefits of HTN management

A
  • Decreased pressure on the aortic arch
  • Improvements in patients with Sleep Apnea
  • Reduced incidence of Stroke

-Improved kidney function
Longevity (High blood pressure is detrimental to kidney function)

151
Q

Conduction via the AV node is_____ than SA

A

slower

152
Q

Baroreceptors provide the CNS with information regarding BP changes. Most common place is

A

carotid arteries

153
Q

Net effect of conversion of Class 3: Ibutilide Atrial fibrillation ?
Dose: ?

A

within 90 minutes for 44% of patients*

1 mg over 10 minutes

Metabolism via liver and metabolite clearance via kidney

Adverse event: Torsades de pointes

Monitor QTc 4 hours after dose given

154
Q

Amiodarone Advanced Cardiac Life Support (ACLS) 1st line for ?

A

Acute VT

155
Q

Class 3: Amiodarone Cardiac Effects of what classes?

A

1, 2, 3, and 4

Chronic administration IKs
Weak Class 2 and Class 4 effects with IV administration

156
Q

As a whole, beta blockers decrease SV and HR so they? They help decrease _____ by working together with ACE-Inhibitors

A

decrease CO.

renin secretion

157
Q

Why is it important to do eye exams on patients on amiodarone?

A

see what kind of corneal microdeposits they have to prevent blindness

158
Q

Nicardipine MOA & Dose

A

MOA: Agent is 2nd generation dihydropyridine CCB which is particularly selective for cerebral and coronary vessels

Dose: 5mg/hr titrate to max of 15mg/hr every

5 min by 2.5mg and bolus dosing is NOT FDA approved

Primary mechanism of action on the L-type calcium channels

PO and IV formulation available, since 100 times more hydrophilic than nifedipine

159
Q

What kind of depolarizations are AA Class 2 BBs effective for?

A

Efficacy against ventricular ectopic depolarizations

Direct membrane effects are not fully characterized

160
Q

Therapeutic targets for HTN

A
  • Diuretics - Decrease volume
  • Beta-blockers- Decrease heart rate and sympathetic drive
  • Calcium channel blockers- vasodilation (decrease in SVR)
  • Angiotensin inhibitors -
    Vasodilation, Aldosterone inhibition, Decrease hypertrophy
161
Q

Perioperative, Antihypertensive treatment reduces? how are the drugs given?

A

myocardial ischemia,
neurological deficits
mortality

IV push or infusion

162
Q

-Absorption, metabolism, and excretion are the_____ for all catecholamines

A

same

163
Q

Isoproterenol MOA & dosing

A

MOA: Non-selective B-receptor agonist with B1= B2 activity
Dosing: 0.01 mcg/kg/min then titration
-Lowers peripheral vascular resistance
-Shortens AV nodal conduction
-Increase in CO secondary to HR rather than SV
-Useful for patients to increase HR (ie. torsades de pointes)

164
Q

High perfusion and low congestion is what class?

A

Dry-Warm

165
Q

Catecholamine Therapies for HF

A

NE-primarily B1 and alpha
Epi-Beta1=Beta2, alpha
-depends on dose
-higher dose causes beta 1(increases HR) and alpha 1(increases BP)
Dobutamine(synthetic)-beta 1 more than beta 2 activity(3:1 ratio)
-increase contractility with minor drop in BP
-can have minor alpha activity
Dopamine-beta 1 and beta 2, not beneficial for patients
-dilates renal vasculature for increase blood flow BUT negative electrophysiological response

166
Q

Phosphodiesterase (PDE) III Inhibitors MOA and drugs

A

cAMP triggers calcium increase
Rememeber milrinone as main PDE-I
-commonly combined with dobutamine(beta1)
-milrinone works inside cell while dobutamine works outside cell
Amrinone causes thrombocytopenia(low platelet levels)
-not available

167
Q

Low Perfusion and high congestion is what class?

A

Wet-Cold

168
Q

Catecholamines in general have

A

very short half life

169
Q

RV send what kind of blood to lungs? What happens if RV isnt working?

A

deoxygenated blood

-if not working, deoxygenated blood won’t be oxygenated

170
Q

Chronic HF therapies (patients ready for discharge, at home, taking the meds for years to come)

A 
ACE-I/ARBs
BB
Aldosterone antagonists
Diuretics
Digoxin
Hydralazine/Isosorbide dinitrate
171
Q

Nitroprusside is metabolized by ____ and causes _____

A

blood vessels to nitric oxide leading to cGMP and vasodilation

causes vasodilation (can decrease preload and afterload)

Tolerance generally does not develop as with NTG
Little effect on renal blood flow and myocardial oxygen demand

172
Q

Adrenergic effects of NE in HF

A

NE can act on alpha 1vasoconstriction
Epi at high dose can act on alpha 1vasoconstriction
-low dose refers to EPI PEN(0.3mg) compared to IV(1mg)
-epi works more on beta receptors and low dose will activate them
-EPI PEN used for Beta 2 to open lungs
-adrenergic effect not always advantageous so anti-adrenergic drugs used
-too much will imbalance systole/diastole

173
Q

Congestion & Perfusion are what for the classification?

A

fluid build-up & blood flow to vital organs/extremities

Grid is specific for different infusion choices for therapy
WET-diuretic needed because fluid build-up

174
Q

RV failure can lead to ____

A

pulmonary hypertension

- hypertrophy of RV
- blood vessels constrict because hungry for oxygen but there is none so constrict even more
 - therapies to dilate that vasculature exist
175
Q

Vasopressin and Acute HF

A

Vasopressin is endogenous

  • triggered when blood volume low
  • brain releases signal
  • travels to kidney to reabsorb water(V2 receptor) to increase blood volume and BP
  • V1 receptor activated causing vasoconstriction(IV infusion used for this mechanism)

When too much volume

  • vasopressin antagonists used
  • V-2 blockage prevents water reabsorption
176
Q

De-compensation and hospitalization?

A

occur in a cycle over and over

decompensation means to get worse

177
Q

2 Types of heart failure

A

Acute and chronic

178
Q

Low perfusion and low congestion is what class?

A

Dry-Cold

179
Q

Chronic-can be managed _____

A

At home with infusions

180
Q

-nitroprusside has better vasodilation capabilities than _____ but very toxic

A

Nitroglycerin

181
Q

Dopamine MOA

A

-only during high doses will dopamine affect alpha and beta receptors because secondary to NE

182
Q

High Perfusion and high congestion is what class?

A

Wet-Warm

183
Q

Chronic HF therapies

A

*Drugs listed on top reduce mortality
RAAS-renin angiotensin aldosterone system
Spironolactone-aldosterone antagonist, potassium sparing diuretic
-prevents sodium reabsorption and water follows
-K increases because Na and K not exchanged
Beta blockade helps during hyper-adronergic states
ACE inhibitor-angiodema side effect, inibite ACE1ACE2 conversion, potassium sparing diuretic
ARB(angiotensin receptor blockers)-prevents angiotensin 2 binding to receptor preventing aldosterone release, potassium sparing diuretic
Nitrate-Hydralazine-combination which reduce preload(nitrate) and afterload(hydralazine)
*Don’t worry about novel therapies

184
Q

Mechanism of Action: Cellular Level of HF drugs

A 
MYOCARDIUM
Beta agonist(dobutamine)
-acts on beta receptor
-increases cAMP
-increases inotropic effect
PDE breaks down cAMP-milrinone is PDE-I which increase cAMP

VESSEL WALL

  • Alpha agonist-phenylephrine
  • Acts on alpha receptor
  • intracellular mechanism leadings to vasoconstriction
185
Q

Sodium Nitroprusside Toxicity/Precautions:

A
  • Hypotension being most observed side effect
  • Accumulation of cyanide can lead to lactic acidosis
  • Thiocyanate is 100 times less toxic than cyanide
  • Infusion >4mcg/kg/min for >24 hours can lead to toxicity
  • Cyanide toxicity: cardiac arrest, coma, encephalopathy, and seizures
  • usually change in mental status
  • longer infusion duration, high doses, or both are problematic
186
Q

PAH Therapies

A 
PAH-pulmonary hypertension-focus on bold, main drugs used in pulmonary hypertension
LEFT side
     -All oral
     -used only chronically
RIGHT side
     -used acutely
  • nitric oxide, not nitrous oxide(laughing gas)
    - inhaled
    - increase cGMP
    - dilates pulmonary vasculature to alleviate Right heart failure
  • sildenafil(tablet)-phosphodiesterase 5 inhibitors
    - prevent breakdown of cGMP, increasing it
    - used in patients with elevated pulmonary arterial pressures
  • prostacyclins-increase cAMP
    - dilates vasculature
    - epoprostenol(IV or inhaled)

CVP pharm test 2 (1 decks)

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