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CV PHARM...Master Drug List > General > Flashcards

General Flashcards

1
Q

Acetylcholine

A
  1. vasodilation (***through NO, not direct innervation)
  2. decreased HR
  3. decreased AV node conduction
  4. decreased force of atrial contraction (negative inotropic effect)
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2
Q

Adenosine

A

adenosine receptor agonist

used to terminate acute PSVT by blocking AV node

administered rapidly IV

chest tightness common
transient asystole
flushing
PSVT can recur

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3
Q

Aliskerin

A

Nonpeptide inhibitor of renin (involved in generation of AI from angiotensinogen).

deccreased AII levels.

  • An effective antihypertensive agent that induces significant dose-dependent decrease in BP.
  • As effective as ACEI and ARBs in decreasing BP.

Used with other antihypertensive agents such as ACEI or ARB and with a diuretic such as HCTZ.
– Not used as monotherapy

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4
Q

Amiloride

A

K-sparing

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5
Q

Amiodarone

A 
Class III antiarrythmic
potassium channel blocker
(w/ class I, II, IV activity)

effects look very scary on ECG

used for atrial and ventricular arrhythmias

QT prolongation w/ many other things

IV has replaced lidocaine as drug of choice in resucitation

PULMONARY FIBROSIS!!!
Many other problems

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6
Q

Amlodipine [Norvasc]

A

arterial vasodilation!

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7
Q

Atenolol [Tenormin]

A

50-100-fold more selective in blocking β1-adrenergic receptors

“Cardioselective agents”

cardioselective, NOT lipid soluble

2nd generation BB

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8
Q

Atorvastatin [Lipitor]

A

…

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9
Q

Atropine

A

ALTERS HR!
Low levels…decrease HR (b/c block presynaptic M1 receptors so inc. ACh initially)

Atropine flush…

Indications:
POST MI!! (to prevent severe bradycardia)

Abolishes reflex vagal cardiac slowing or asystole

Prevents or abolishes bradycardia from…

Facilitates AV conduction

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10
Q

Betaxolol

A

Third Generation
Beta-1 selective blocker w/ additional actions
Ca entry blockade

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11
Q

Bisoprolol [Zebeta]

A

CHF treatment

Long-acting drug (take once a day

significantly decreases all case mortality

glaucoma eyedrops

2nd generation BB

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12
Q

Candesartan [Atacand]

A

.

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13
Q

Captopril [Capoten]

A

increased synthesis of vasodilatory prostaglandins in vascular and renal endothelium

(Delays/ prevents progression of kidney disease in type I diabetics!!!)

renoprotective

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14
Q

Carvedilol [Coreg]

A

CHF treatment

non-selective β + α1-receptor antagonist

By blocking α1-AR, CO maintained with increased fall in peripheral resistance.

  • Antioxidant; binds and scavenges ROS
  • Protects membranes from lipid peroxidation. Prevents LDL oxidation and decreases LDL uptake into coronary blood vessels.
  • Primarily used for CHF & HTN; decreased mortality and morbidity in pts w/ mild to moderate CHF
  • PO; extensively protein bound; hepatic (2D6) metabolism

MSA, a1 antagonist, Ca entry blockade, antioxidant

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15
Q

Cholestyramine [Questran]

A

.

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16
Q

Clonidine [Catapres]

A

anti-HTN

analgesic for neuropathic pain (b/c releases endogenous opiates)

ADHD

a2
direct acting agonist

Side effects:

  • -Rebound HTN!!! if drug suddenly stopped
  • -dry mouth
  • -sedation
  • -bradyarrhythmias
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17
Q

Colestipol

A

.

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18
Q

Digoxin [Lanoxin]

A

..

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19
Q

Diltiazem [Cardiazem]

A

minimal arterial vasodilation

Negative chronotropic and inotropic effects
(especialy verapamil!)

intermediate in selectivity b/w verapamil and dihydropyridines in its selectivity for vascular Ca channels…

antiarrhythmic and anitanginal
(coronary vessel dilations!)

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20
Q

Dobutamine [Dobutrex]

A

b1
direct acting agonist

Increases HR and CO

Mainly Beta receptors

Increases:
CO, SV, Urine output
(Not HR)

good for afterload and inotropy in CHF

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21
Q

Dopamine [DA]

A

Low doses: D receptors

High Doses:

  • -Increases HR and CO (beta receptors)
  • -Increases BP (alpha receptors)

IV
(very short half-life)

Monitored by urinary output

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22
Q

Enalapril [Vasotec]

A

prodrug converted to enalaprilat

Potent
IV for HTN emergencies

NOT renoprotective

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23
Q

Encainide [Enkaid]

A

Class Ic antiarrhytmic

Na channel blockers

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24
Q

Ephedrine [Pretz-D]

A

Increases BP
Increases HR and CO

mixed-acting sympathomimetic
(alpha AND beta)

orally active
eliminated in urine

indications:
hypotension (esp. of analgesia)

increases:

  • -HR
  • -CO
  • -variable increase in TPR

Side effects:
angina (b/c increased work load)
ventricular dysfunction
fatal arrhythmias

herbal products containing ephedra alkaloids

Precursor of illicit amphetamine and meth!!!

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25
Q

Epinephrine [E]

A

Vasoconstrictor locally

Increases HR and CO

Mainly Beta receptors

Increases:

  • -HR
  • -SV
  • -CO
  • -arrhythmias
  • -Coronary Blood flow
  • -Systolic arteriole pressure
  • -Mean arterial pressure
  • -Mean pulmonary blood pressure

Widens Pulse pressure!!
(ESPECIALLY low dose given subcutaneously)

*at low doses, may DECREASE BP
(so on time curve, pressure goes up initially, but as drug concentration declines the pressure goes below normal!)

SA node and AV node
(not really ventricular tissue)

Vasodilation:
–skeletal muscle

Vasoconstriction:

  • -cutaneous
  • -renal (so incr renin secretion & dec BF)

Increases:

  • -pulmonary pressures (arteries and veins)
  • -Coronary BF

IV, inhaled, IM, subcutaneous (allergies)
NOT oral

side effects:
Cerebral hemorrhage (esp w/ non-selective BB)

Ventricular arrhythmias

Angina

Indications:
emergency relief of anaphylaxis

vasoconstrictor w/ local anasthetics

Restoring cardiac rhythm in pts w/ cardiac arrest

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26
Q

Ezetimibe [Zetia]

A

.

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27
Q

Fenofibrate [Tricor]

A

renal clearance

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28
Q

Gemfibrozil [Lopid]

A

.

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29
Q

Flecanide

A

Class Ic antiarrhythmic
potent and long-acting

CAST trial
DELAYED pro-arrhythmic side effects

Only life-threatening arrhythmias typically treated

Contraindicated in STRUCTURAL HEART DISEASE!!!

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30
Q

Furosemide [Lasix]

A

.

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31
Q

Hydrochlorothiazide

A

.

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32
Q

Ibutilide

A

Pure Class III antiarrhythmic

IV only

acute termination of a fib or atrail flutter

side effects: torsades/transient assystole

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33
Q

Labetolol [Normodyne]

A

non-selective beta + a1 antagonist

given IV for HTN emergencies

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34
Q

Lidocaine

A

Class Ib antiarrhythmic
Na channel blocker

binds to open and inactivated Na channels
RAPID!
especially good b/c no effect on normal HR, but good for tach

NOT effective for atrial arrhythmias

IV (b/c hepatic metab.)

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35
Q

Lisinopril

A

a lysine derivative of enalaprilat; renoprotective

36
Q

Losartan [Cozaar]

A

prodrug
–One metabolite, EXP 3174, has increased potency as an AT1 receptor antagonist.

• Competitive antagonist of thromboxane A2
receptor; attenuates platelet aggregation.

  • Unique in that it increases uric acid urinary excretion (Uricosuric). HTN gout treatment!!
  • Inhibits CYP activity.

Short half-life
ARB that increases excretion of uric acid
ARB metabolized by CYP3A4

Side effects:
Hypotension
• In hypovolemic and/or Na-depleted patients.

Hyperkalemia
• Especially in renal insufficiency, or in patients using K-sparing diuretics or K supplements.

Hepatic dysfunction
• Reported with Losartan and Valsartan.

Fetotoxicity
• Like ACE inhibitors should not be given to pregnant
women.

37
Q

Lovastatin

A

.

38
Q

Methyldopa [Aldomet]

A

.Centrally acting alpha-2a adrenergic agonist

agonists of postsynaptic a2-adrenoreceptors in rostral ventrolateral medulla (RVLM)

decreases sympathetic outflow from RVLM to heart and vessels

decrease in PVR and HR

converted into alpha-methyl NE
(dopamine–>NE, but w/ methyl group, it is a false transmitter)

a2a agonist in RVLM

decreases sympathetic tone, reduction in BP due to decrease in TPR

obsolete

pre-eclampsia

Side effects:
sedation, sleep disturbances, erectile sexual dysfunction

Na/H2O retention

lactation due to increased prolactin secretion

Side effects:

  • -sedation
  • -Positive coombs test
  • -prodrug converted to a-methyl-NE
39
Q

Metolazone [Zaroxyline]

A

thiazide-like diuretic

CHF

40
Q

Metoprolol [Lopressor]

A

CHF treatment

50-100-fold more selective in blocking β1-adrenergic receptors

“Cardioselective agents”

some MSA, cardioselective, lipid soluble

41
Q

Milrinone [Primacor]

A

HF

42
Q

Minoxidil

A

oral

open K channels–>hyperpolarization of VSM

Relaxes ARTERIOLE smooth muscle by opening K+-ATPase channels
(dilates arteries, NOT veins)

Causes reflex tachycardia and strong renin release!! (so take w/ BB and diuretics long-term)

Causes Hirsutism (increases hair…)

Rogaine!…male-pattern baldness

43
Q

N-3 Fatty Acids [Fish Oil]

A

..

44
Q

Nadolol [generic, Corgard]

A

First generation BB

45
Q

Nebivolol [Bystolic]

A

drugs w/ NO mediated vasodilation

Highly β1 selective; devoid of ISA, membrane stabilizing activities, and α1 blocking activities.

  • Has antioxidant activity/neutral to favorable effects on both carb and lipid metabolism.
  • decreased BP by decreasing HR and peripheral vascular resistance.
  • Significantly increases stroke volume, maintains CO and systemic blood flow.

Used in HTN but NOT CHF

• Drug of choice for HTN with metabolic syndrome!!!

46
Q

Nesiritide [Natrecor]

A

BNP

CHF

47
Q

Nicardipine [Cardene]

A

.

48
Q

Nicotinic Acid – vitamin B3

A

.

49
Q

Nifedipine [Procardia XL]

A

arterial vasodilation!

Coronary vasodilation
Reduced afterload (arterial)

short acting!!
great for relaxing coronaries
not used for HTN b/c reflexively activate SNS, increasing HR

50
Q

Nimodipine

A

.

51
Q

Nitroglycerin [Tridil, Ismo]

A

organic nitrate ester reductase
–>NO–>GC–>cGMP–>PKG–>SM relaxation

Decreases demand and increases supply!

increase NO
–vasodilates–>
decreases afterload

–venodilates–>
decreases preload
(so decreases contractility via Frank-Starling)

decreased preload
coronary vasodilation
(prevents or reverses vasospasm)

BP: unchanged/slight decrease
HR: unchanged or slight increase
Pulmonary vascular resistance: decreased
CO: reduced (slightly)

mucosal
--sublingual
--nasal sprays
oral
transdermal
paste
IV
High doses...
--extreme vasodilation
....hypotension
....reflexive increase in HR and contractility
(worsens angina!!!)

transient headache
(meningeal arteries dilated until tolerance)

rash

Drug interaction
–Sildenafil (Viagra) [Type 5 PDE inhibitors]
(increases cGMP by decreasing metabolism)

Rapidly metabolized (short-lived)

ok and beneficial for exertional angina
–can take it when they need it

challenge for otherstolerance

(avoided by “nitrate free” interval each day… i.e. remove patch at night)

anginal rebound
Do Not suddenly interrupt IV nitroglycerin in unstable angina…overlap w/ oral or patch form
(coronary vasospasm has been observed after abrupt stop)

coronary vasodilation
reduced preload (venous)
reduced afterload (arterial)
52
Q

Nitroprusside [Nipride]

A

Pro-drug that’s broken down into NO
–>increase in cGMP–> muscle relaxation

active in arterioles AND mainly veins!!!
Awesome for HF treatment!

Decreases CO in normal pts

Increases CO in pts w/ Left ventricular HF b/c decreases afterload (along w/ preload)

Very short half-life, given w/ pump

53
Q

Norepinephrine [NE]

A

Increases BP

Mainly alpha receptors

Increases:

  • -SV
  • -arrhythmias
  • -coronary blood flow
  • -Systolic arteriole pressure
  • -diastolic arteriole pressure
  • -mean arteriole pressure
  • -Mean pulmonary pressure
54
Q

Penbutolol [Levatol]

A

First generation BB

55
Q

Phenoxybenzamine

A

a1>a2
noncompetitive (covalent)
LONG-LASTING

alpha1 and alpha 2 antagonist

a2 antagonism can inc. presynaptic NE release…increase CO…tempering BP lowering action

indications:
sympathetic excess secondary to pheochromocytoma, Raynaud’s phenomenon, frostbite, acrocyanosis

slow onset (several hours)
long duration (3-4 days)
side effects:
sinus-tach
nasal congestion
drowsiness, fatigue, weakness...
tachycardia...cardiac arrhythmias
56
Q

Phentolamine [Regitine]

A

a1=a2

short-acting
competitive antagonist
alpha1 and alpha 2 receptors

DOSE DEPENDENCY!!!!
small dose…greater effect on a2 receptors–> increase in CV force b/c increase release of NE (positive inotropic effect dominates…inc BP

Large dose…greater effect on a1 receptors–> vasodilation and reduction BP

Indications: pheochromocytoma and hypertensive emergency

**postural hypotension

reflex tachycardia that precipitates cardiac arrhythmias (these efffects severely limit use for essential HTN)

57
Q

Phenylephrine

A

a1»»»»>a2
direct acting agonist

Increases BP

Alpha receptors

systemic arteriole vasoconstriction–>

  • -increased systolic and diastolic pressures
  • -REFLEXIVE decrease in HR and CO

IV, IM, SC

control of hypotension, especially associated w/ regional or spinal anesthesia

adverse effects:
angina
anxiety
hallucinations/psychosis
HTN...
58
Q

Pindolol [Visken]

A

does not inhibit decrease renin release

High ISA, some MSA, no cardioselectivity, lipid soluble

Non-selective drugs with partial agonist activity.
Decrease CO and HR less than other

59
Q

Pravastatin [Pravachol]

A

.

60
Q

Prazosin [Minipress]

A 
a-1>>>>>>>>a-2
Most prominent (of A-blockers) first dose hypotension

antihypertensive

(Monotherapy not recommended w/ any a1 blockers)

61
Q

Procaineamide

A

Class Ia antiarrhythmic
Na channel blockers

drug-induced lupus!!!

hepatic acetylation and renal excretion

IV

acute control of atrial and vent arrhythmias/ short term treatment

62
Q

Propafenone [Rhythmol]

A

Class Ic antiarrhythmic

BB activity

63
Q

Propranolol [Inderal]

A

decrease HR and contractility–> Decrease CO

inhibit renin release (EXCEPT Pindolol)

Decrease central sympathetic outflow (except for those w/ low lipid solubility)

Decrease release of peripheral NE by inhibiting presynaptic beta adrenergic

Especially useful in pts w/ high renin level HTN

w/ chronic use…
decrease CO and peripheral resistance and arterial pressure

1st and 2nd generation BBs:
High renin HTN
(young and caucasian)

Non-selective BB that produces resting bradycardia and decrease HR during exercise –> hypotension

membrane stabilizing activity: antiarrhythmic

produces bronchospasm; contraindicated in asthmatics

slow withdrawal of drug to prevent reflex tachycardia

MSA, lipid soluble

64
Q

Ramipril

A

prodrug, activated by deesterification

Long half-life
given once daily

65
Q

Ranolazine [Renexa]

A

novel metabolic modulator
MOA: unknown
partial fatty acid oxidase inhibitor–> increases glucose oxidation–> increased O2 utilization efficiency in heart

No effect on HR or BP

Indications: chronic stable angina

in combination w/:

  • -amlodapine,
  • -BBs, or
  • -Nitrates

will not relieve acute anginal attacks

Pregnancy category C

Expensive w/ only marginal benefit
Contraindication: use w/ cyp3A inhibitors
hepatic impairment

66
Q

Reserpine

A 
Inhibits VMAT (uptake 2)
Depletes NE and 5-HT from neurons

Decreased sympathetic tone reduces TPR, CO, renin release, BP

oral
mild to moderate HTN

Side effects:
CNS effects (sedation and mental depression)
gastric and duodenal ulcers
Shouldn’t be used in pts w/ Hx of depression

67
Q

Simvastatin [Zocor]

A

.

68
Q

Sodium Nitroprusside

A

.

69
Q

Sotalol [Betapace]

A

Class III
K channel blocker
w/ nonselective BB activity

contraindications:
long QT
renal insufficiency
asthma/copd
...
70
Q

Spironolactone [Aldactone]

A

.

71
Q

Terazosin [Hytrin]

A

a-1»»»>a-2

treatment of symptoms of BPH, urinating and bladder emptying problems, etc.

Also lower BP

Treatment of choice for older men w/ HTN and prostate problems

72
Q

Trimethaphan

A

competition w/ ACh

Side effects:
Postural hypotension
tachycardia
arrhythmias
Blurred/double vision
asthma (secondary to histamine release)
Dry mouth, constipation, paralytic ileus, N/V
urinary retention
impotence
drowsiness, seizures, hallucinations,
73
Q

Verapamil [Calan]

A

minimal arterial vasodilation

Negative chronotropic and inotropic effects
(especialy verapamil!)

More selective for heart, less selective for vessels
–not as effective vasodilating

Used as antiarrhythmic and antianginal rather than anti-HTN

***coronary artery dilators!!!! so help w/ angina!

74
Q

alpha-blockers

A

first dose orthostatic hypotension

sinus-tach (angina, palpitations), syncope, vertigo (b.c a2 receptors blocked…inc NE release)

In HTN:

advantages:
- -improve lipid profile and insulin resistance
- -good in physically active pts
- -relieve urinary symptoms in BPH pts

  • *Prototypical pts:
  • -elderly pts w/ BPH and normal CV function
  • -young physically active pts
  • -African American pts w/ no success w/ other drugs

disadvantages:

  • -not good as monotherapy
  • -increased incidence of HF

Caution:
–First dose Orthostatic HTN

decreased TPR and BP

relieve symptoms of BPH by relaxing muscles of bladder and prostate

Increase HDL
Lower LDL
beneficial effect on insulin resistance

First dose orthostatic hypotension common w/ short-acting drug
**i.e. prazosin

dizziness, vertigo, drowziness, palpitations

75
Q

Beta-blockers

A 
Best class for treatment of angina
Decreases:
--HR (in exercise)
--contractility (in exercise)
--afterload

Does NOT decrease:

  • -preload
  • -coronary vasospasm
Rationale for combining w/ nitrates:
Reduces:
--LVEDP
--LV volume
--dilates coronary arteries

BBs prevent reflex tachycardia and positive inotropic effect

rationale for combining w/ DHPs

  • -prevent coronary vasospasm
  • -reduce systemic vascular resistance

BBs prevent reflex tachycardia and positive inotropic effect

Reduced HR
Decreased contractility
Reduced afterload (arterial)
–indirect effect due to decreased renin release and some blockage of sympathetic outflow

In HTN:
Advantages:
--secondary protection in CAD
--useful in HTN pts w/....
.......tachycardia
.......high CO
.......high renin
.......hyperthyroidism
.......migraine
.......glaucoma
.......stage fright
--Bisoprolol=standard treatment w/ ACEI and diuretics (34% mortality benefit)

Disadvantages:

  • -less effective in elderly and AA
  • -multiple side effects and contraindications (especially 1st and 2nd generation BBs)
  • -Should not be discontinued abruptly

BBs do not cause H20 and salt retention
–so can be administered w/out diuretic

But has additive antihypertensive effect when administered w/ diuretic

preferred in HTN of pts w/:
MI
ischemic heart disease
HF
hyperthyroidism
migraines

treatment for:
Sinus and AV arrhythmias
open angle glaucoma
anxiety

Side effects:
Cold extremities

Bradycardia

Bronchospasm (avoid ALL drugs w/ asthma; permitted w/ COPD)

CNS side effects

Metabolic

Drug withdrawal syndrome

fatigue, decreased exercise tolerance, impotence

In diabetes…
Hypoglycemia
–b2 adrenoceptors stimulate glycogenolysis and gluconeogenesis and glucagon release
–b-blockers may mask tachycardia which is warning sign for insulin induced

BB toxicity:
Symptoms:
--bradycardia
--hypotension
--arrhythmias
--hypothermia
--hypoglycemia
--seizures
76
Q

Ganglionic blockers

A

antagonists of NICOTINIC cholinergic receptors
(ionotropic receptors)

compete w/ ACh for ganglionic nicotinic receptor sites OR block ion channel

initial EPSP is blocked, ganglionic transmission inhibited

77
Q

Sympathomimetics

A

.

78
Q

Anticholinergics

A

.

79
Q

ACEIs

A

In HTN:
Advantages:
–Good for all degrees of HTN
–especially good in pts w/ high renin levels
(young people and caucasians)
–increase efficacy of diuretics
–thiazide + ACEI good even in low-renin HTN
–initial drug used for HTN in DIABETICS (followed by CCB added on)
–may preserve renal function in non-DN
–initial anti-HTN in pts prone to HF

Disadvantages:
–hyperkalemia

block ACE conversion of Ang I to Ang II

block ACE degredation of bradykinins, ect.

Hypotensive effects result from inhibiting the action of angiotensin II (AII) and stimulating action on the Kallikerin-kinin system.

decrease aldosterone secretion some

Production of renin and AI is increased
– Accumulating AI is directed down alternative metabolic routes,
resulting in increased production of vasodilator peptides as to Ang1-7,
which are believed to be protective (in HF?)

ACEI increases renal blood flow via vasodilation of afferent and efferent arterioles
increase RBF occurs w/out increase in
GFR: thus filtration fraction is decreasedDecrease TPR and BP in HTN states
dilates arteries and veins

baroreceptors remain in tact
postural Hypotension not a problem

AntiHTN when:
Na retention OR
high renin

HF!

SIDE EFFECTS
1. Hypotension in hypovolemic and/or Na+
-depleted patients
– Precipitous first-dose hypotension unless dose is gradually increased.

  1. Hyperkalemia (especially with renal insufficiency, or in pts receiving K-sparing diuretics or K supplements).
  2. Dry cough (most common),angioneurotic edema or angiodema; both related to bradykinin actions.
    – Bradykinin activates stretch receptors in the trachea, which might causes dry cough in ~10-15% of patients receiving ACEI.
  3. Angioedema: (fluid and red blotches in face) infrequent but potentially fatal.
    – Reported with all ACEIs.
  4. Fetotoxicity: contraindicated in the 2nd and 3rd trimesters of pregnancy.
80
Q

ARBs

A

MOA
1. Selectively block AT II type 1 receptors, which are responsible for all of the vascular, renal and central effects of AII.

  1. Cause vasodilation and increase Na and H20 excretion. Thus, they decrease TPR, plasma volume, CO, and BP.
  2. Have no effect on bradykinin, therefore they are THE substitute when ACEI cause cough.
  3. Do not block the action of AII on AT2 receptors, which are thought to be protective.
81
Q

Class I antiarrhythmics

A

.

82
Q

Class II antiarrhytmics

A

.

83
Q

Class III antiarrhythmics

A

.

84
Q

Class IV antiarrhythmics

A

.

85
Q

Non-DHP CCBs

A

direct effects predominate

decrease:

  • -HR
  • -contractility
  • -AV conduction rate

–> reduces demand and prevents/ reverses vasospasm

Don’t combine with Beta Blockers!!

bradycardia
asystole
AV block

**contraindicated in HF!

pregnancy category C

Coronary vasodilation
Reduced HR
Decreased Contractile force
Reduced afterload (arterial)

86
Q

DHP CCBs

A

more potent vasodilators–>reflex cardiac stimulation

direct and indirect effects balanced

Reduces demand by reducing afterload
increases supply by coronary vasodilation

Combine w/ Beta Blockers!!!

excessive vasodilation…

peripheral edema (b/c increased precapillary dilation)

paradoxical exacerbation of angina
(dilated skeletal muscle vessels stealing all supply from coronary vessels…decreased supply)

In HTN:
Advantages:
–HTN and CAD treatment
–more powerful and preferred for treatment of HTN than non-dyhydropyridines (unless short-acting)
–Very effective in elderly and AA w/ low-renin HTN
–safe for diabetics

Disadvantages:

  • -not as trusted as ACEIs, diuretics, and BBs
  • -may increase risk of CAD or HF

Decrease BP and SVR in arterioles AND venules)

Do NOT cause large baroreceptor-mediated sympathetic discharge, so very little change in HR!!!

(EXCEPT short-acting DHP (i.e. nifedipine) do reflexively increase HR by sympathetic activation)

–Low renin HTN!!!
(elderly and AA)

–older pts w/ systolic HTN

–Many studies show no survival benefit

Side effects:
Peripheral ankle edema
Hypotension
Constipation
Reflex tachycardia (shorter-acting drugs)
87
Q

CCBs

A

Highly effective agents for relief in exertional and vasospastic angina

In CAD…fail to prevent reinfarctions or CHD death
Impaired LV function…increases mortality
BBs are better

In HTN…higher rates of MI, HF (immediate release)
less CV events (slow-release)

CV PHARM...Master Drug List (1 decks)

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