Summarization of the Drugs in Cardiovascular Disease

Instruction: Supply the needed information that is asked

Classification of CV dse Drugs Mechanism of Action Side effects

 Diuretics a. Carbonic Anhydrase  CAIs inhibit Metabolic acidosis,
Inhibitors the activity anorexia, hematuria,
 Are chemical of the photosensitivity
derivatives of enzyme (similar
sulfonamide carbonic chemical derivatives
antibiotics anhydrase as sulfonamides),
Examples: This enzyme is melena, hypokalemia,
+Acetazolamide(Diamox) found in the kidneys, drowsiness,
eyes, & other parts paresthesias, urticaria,
+Methazolamide(Neptazane)
of the body diabetic patients
Precautions w/ (elevated blood
certain types of eye glucose/glycosuria)
diseases
 CAIs reduce the
formation of H+
& bicarbonate
Reduces H+ ion
b. Loop Diuretics concentration in
 Edema renal tubules
management: Increased
heart failure,  CNS: dizziness,
excretion of
hepatic failure, headache, tinnitus
bicarbonate, sodium,
renal disease, (toxic
water, & potassium
heart levels/administered too
Resorption of
failure resulting from water is decreased quickly),
diastolic dysfunction Urine volume is blurred vision
 Hypertension increased  GI: nausea, vomiting,
control diarrhea
 Increase renal  Decreases BP  Metabolic:
excretion of Act directly on the hypokalemia (most
calcium in ascending limb of important clinically),
patients w/ the loop of Henle to hyperglycemia
hypercalcemia inhibit chloride &  Electrolyte loss &
Examples: sodium resorption dehydration
+Furosemide (Lasix Activate renal
+Bumetanide (Bumex) prostaglandins
+Torsemide (Demedex)  Dilation of
blood vessels &
reduced
c. Osmotic Diuretics peripheral
 Treatment: vascular
oliguric phase of  Convulsions
resistance (osmotic effect),
ARF, promote makes it easier for
excretion of thrombophlebitis,
the heart to contract pulmonary
toxic & release its
substances, congestion (fluid from
contents tissues to vascular),
reduce intracranial  Treats heart
pressure, cerebral headaches, chest
failure pains, tachycardia,
edema relieves
 Not indicated for blurred vision, chills,
workload on the fever
peripheral
 edema heart
Example:
Mannitol (Osmitrol)
 CNS: dizziness,
headache
d. Potassium-  GI: cramps,
Sparing Diuretics  Increases nausea, vomiting,
 known as osmotic pressure diarrhea
aldosterone- of the glomerular  Other: urinary
inhibiting filtrate: frequency,
diuretics b/c Pulls water into weakness,
they block the renal tubules hyperkalemia
aldosterone from the
receptors surrounding tissues
Examples:  Inhibit tubular
+Amiloride (Midamor) resorption of water
+Spironolactone (Aldactone) & solutes thus  CNS: dizziness,
+Triamterene (Dyrenium) producing headache, blurred
Rapid diuresis vision
e. Thiazide &
 GI: anorexia,
Thiazide-Like
nausea, vomiting,
Diuretics  Works in diarrhea
 hepatic cirrhosis collecting ducts  GU: impotence
Hypertension (1 of & distal  Integumentary:
the most convoluted urticaria,
prescribed group tubules photosensitivity
of drugs) Interfere w/ (sulfonamide
 Edematous sodium-potassium derivative)
states exchange Metabolic:
 Diabetes Competitively bind hypokalemia,
insipidus to aldosterone glycosuria,
 Adjunct drugs in receptors hyperglycemia
treatment of Block resorption of
heart failure sodium & water
usually induced by
aldosterone

 Inhibit tubular
resorption of
sodium, chloride,
& potassium ions
 Water, sodium, &
chloride are
excreted
 Potassium is also
excreted to a
lesser extent
Dilate the arterioles
by direct relaxation
2. Hypertension a. Alpha 2 agonists  When activated,  Hypotension,
 Use in Chronic HTN; alpha 2 receptors drowsiness, dry
HTN urgencies; inhibit the mouth, headache,
Treatment of pain release of impaired
like ADHD ; and norepinephrine ejaculation
Withdrawal like from  Rebound HTN with
 Opiates and Nicotine presynaptic neurons
Example:
Clonidine (Catapress)
b. Alpha 1 blockers (...sin)
 Use in HTN, urinary
retention, and
Raynaud’s disease
Examples:
+Doxazosin (cardura)-
HTN/BPH
+Terazosin (hytrin)-HTN/BPH
+Prazosin (minipress)-HTN
+Tamsulosin (flomax)-BPH
c. Beta blockers (selective
and non-selective)
2 Types
c1. Non-selective beta
blockers (...old)
 HTN, angina, post
MI, congestive HF
(CHF)
 - Atrial fibrillation,
tachycardia
 - Some eye drops for
glaucoma
 - Hyperthyroidism,
migraine
prophylaxis,
essential tremor,
stage
 Fright
C2. Cardioselective beta 1-
blockers (...olol)
 Same as non-
selective
uses….possibly less
effective for stage
 fright and migraine
Alpha 1, Beta 1, and Beta 2
blockers
- Carvedilol: CHF
- Labetalol: hypertensive
emergencies
abrupt withdrawal
 Taper over 2-4 days
 Orthostatic
hypertension
(>10%)
 block alpha 1  Reflex tachycardia,
receptors fluid retention
 HTN: lowers bp  Dizziness, lack of
though energy, drowsiness,
vasodilation nasal congestion,
 BPH: relax headache,
smooth muscle of decreased libido
bladder neck and
prostate to
improve urine
flow
 Block beta1 and  Sexual impairment
beta2 receptors  Hypotension, Acute
 Negative HF, fatigue,
inotrope: bradycardia (beta1)
decrease force of  Peripheral
heart contraction vasoconstriction
 Negative (beta2)
chronotrope:  Bronchoconstriction
decrease HR (beta2)
 Hypoglycemia
(beta2)
 Masking
hypoglycemia
(beta1 and beta2)
NOTE: Do not stop
suddenly!
 Selectively block
beta1 receptors  Same as beta1 side
effects
 Less potential for
beta2 side effects
NOTE: Do not stop
suddenly!
- Adverse Effects
- Same as SEs as non-
selective beta blockers
- Same as SEs as alpha 1
blocker

d. Angiotensin Converting
Enzyme Inhibitors--converts
Angiotensin I to angiotensin

ACE inhibitors (...pril)

 use in Chronic HTN;  Enzyme breaks  Hypotension
Hypertensive down bradykinin  Hyperkalemia
urgencies; CHF; and (elevated
Diabetes potassium)
 Bradykinin-related
(polypeptide)--
natural vasodilator
- Dry hacky cough
- Non-allergic rash
- Angioedema
NOTE: Contraindicated in
pregnancy
e. Angiotensin-2 Receptor
Blockers  Inhibit  Same SE as ACE-I
angiotensin-2 but less likely to
Angiotensin-2 Receptor receptors (blocks cause cough, rash,
Blockers receptor instead angioedema
 Similar to ACE-Is of enzyme
 Alternative to ACE-I
in people with
bradykinin-related
side effects

f. Direct Renin Inhibitor

(...ren)  Inhibits renin  Hypotension
 Use in HTN  Thus inhibits  Less bradykinin side
conversion of effects that with
angiotensinogen ACE-Is
to angiotensin 1  Hyperkalemia (very
e. Calcium Channel Blockers rare)
(mostly ...pine)  Inhibits Ca++
 - HTN entrance into  Vasodilation:
 - Angina muscles flushing, edema,
 - Verapamil and surrounding HA, reflex
diltiazem: above vessels tachycardia
uses plus atrial  Constipation
fibrillation and  Gingival
tachycardia enlargement
 Verapamil and
diltiazem: similar to
beta-blockers
3.Anti- arrythmics CLASS 1- SODIUM CHANNEL
BLOCKERS
 Depress phase 0
depolarization  
(conduction velocity) in fast
response cells and can
decrease automaticity
+Quinidine  block voltage  prolongs QT
-primary use = treat gated sodium interval- ↑risk for
reentry arrhythmias channels torsades
involving myocytes or  binds  hypotension due to
Purkinje cells (that use fast preferentially to α-adrenergic
sodium channel for AP) open state of blockade -high
-variety supraventricular channel (tau = incidence diarrhea
& ventricular 3sec) (30-50%)
tachyarrhythmias  selectivity for:  cinchonism
cells at higher HR, (headache,
cells at less dizziness, tinnitus)
negative RMP at high dose
 interacts w/
digoxin (↑digoxin
serum level)
 block voltage
gated sodium
channels  ANA positive (60-
 binds 70%)
+PROCAINAMIDE
preferentially to  Lupus-like
(Procan)
open state of Syndrome (20-50%)
channel (tau =
3sec)
selectivity for: cells at
higher HR, cells at less
negative RMP

 No effect on AP;
minimal in normal
cells
 blocks voltage  CNS effects:
+ LIDOCAINE(Xylocaine)
gated sodium seizures (very rapid
 acute suppression
channels administration) &
ventric. Arrhythmias
 binds drowsiness,
 must be given
preferentially to dysarthria &
parentally b/c
inactivated state dysesthesia (more
extensive first pass
of channel (tau = gradual increase in
effect (IV bolus or
0.1sec, falls off serum levels)
infusion- modified
b/w beats)  depression cardiac
w/ liver dz & HF)
 selectivity for: function
 local anesthetic
ventric cells (over
atrial), cells w/
fast rate, cells w/
less neg RMP
  Minimal effects on
AP; marked effects
on conduction in  proarrhythmic: esp
normal cells in presence of
+ FLECAINIDE(Tambocor)  blocks voltage severe heart dz
 variety gated sodium  depression of LV
supraventricular channels function
tachycardias  binds pref to
 life-threatening open state (tau =
ventricular 11sec)
arrhythmias  selectivity for
cells at high HR
but greater
depression at
normal rates than
CLASS 2 -β-ADRENERGIC 1A or 1B  impotence,
BLOCKERS: block β- exacerbation of
adrenergic influences on asthma, CV effects
conducting system (bradycardia, AV
+PROPRANOLOL(Inderol) block, CHF)
______________________  blockade of β-  CNS effects:
+METOPROLOL adrenergic sedation, sleep
 chronic ventricular receptors (β1 in alterations -use w/
arrhythmias myocardium) caution in diabetics
 control ventricular  propranolol =
rate in Afib or non-selective
Aflutter  metoprolol = β1
 PSVT, symptomatic selective
sinus tachycardia
 catecholamine-
related ventric
arrhythmias

CLASS 3-POTASSIUM  potentially lethal

CHANNEL BLOCKER: pulmonary fibrosis
 hyperthyroidism or
prolong duration of AP
hypothyroidism
increase refractory
 hypotension, AV
period  prolongs AP block, arrhythmias
+AMIODARONE duration & (2%)
 FDA: only for life- refractory period  blue gray
threatening  blocks sodium discoloration
ventricular channel (phase 0)  corneal deposits 
arrhythmias  blocks calcium blurred vision
channels (phase  photosensitivity, GI
refractory to all
2) disturbances
other forms
 therapy  mech for  C: pulmonary dz or
 powerful inhibitor antiarrhythmic hyperthyroidism,
of pacemaker effect unclear  additive effect w/
automaticity other drugs
increasing QT
 long term oral use:
interval, ↑ effect of
Afib & atrial
warfarin & digoxin
flutter; SVT; life-
threatening
(sustained) Vtach  noniodinated  fewer side effects
 IV use: Vfib, form of but lower efficacy
sustained Vtach Amiodarone

+DRONEDARONE  K channel  dose-dependent

-
 Afib & Aflutter blocker, non- Torsades de
selective β- pointes (don’t
blocker circumvent like
+SOTALOL
 ventricular & atrial Amiodarone does)
arrhythmias
 K channel
blocker, Na
channel activator
-dose-dependent
Torsades de pointes
+IBUTILIDE (don’t circumvent like
 Afib & Aflutter
Amiodarone does)

CLASS -4 CALCIUM
 blocks voltage
CHANNEL BLOCKERS gated L-type
(CCB):depresses slow calcium channels
response AP in AV and SA (non-
nodes dyhydropyridines
, have effects at
+ VERAPAMIL AV & SA node)
(Isoptin, Calan)  cardiac depression
 hypotension
DILTIAZEM  constipation (most
 control of common)
 acts through A1
ventricular rate in adenosine
Aflutter & Afib receptors to
 PSVT due to activate
reentry involving potassium
AV node channels
 inhibits effects of
CLASS-5-OTHER increased Camp

+ALDENOSINE
 transient facial
(Adenocard) flushing, dyspnea or
 muscarinic
 acute conversion chest pressure,
blockade
 of PSVT due to cardiac depression,
reentry involving AV block
AV node (highly  constipation,
effective)  stimulates peripheral edema,
cardiac dizziness
 IV bolus (effects
transient- max 10- contractility via
20sec) block of Na/K-
+ATORPINE ATPase  
 sinus bradycardia amount of
(e.g., acute MI) intracellular  hot as a hare, dry as
Ca2+ a bone, red as a
beet, blind as a bat,
mad as a hatter

+ DIGOXIN
(Lanoxin)
 one of most
 control of
prevalent adverse
ventricular rate in
drug reactions
Afib & Aflutter encountered
(digitalis
intoxication):
arrhyth-mias any
type, GI & neuro
disturbances
 interaction w/
quinidine,
amiodarone, CCB,
& captopril
4.Heart Failure 1. Inotropic drugs:
a. Cardiac glycosides

+Digoxin
+Digitoxin
+Ouabain
b. Sympathomimetics
+ Dobutamine
 used inotropic agent
other than digitalis
MOA:
It ↑ CO, therefore urinary
output, and stroke volume
with affecting HR, TPR or BP.
• Tolerance may develop on
repeated use.
• As it ↑ BP it should be
avoided in patients with
history of HT.
+Dopamine
c. Phosphodiesterase lll
Inhibitors
 +Amrinone
2. Diurectic
a. High ceiling diuretics
+Furosemide
+Butamirate
b. Thiazide like diuretics
+Hydrochlorothiazide
+Metolazone
+Xipamide

3. Aldosterone antagonist
+Spironolactone
+Eplerenone
4. Inhibitors of Renin-
Angiotensin system
a. ACE-inhibitors
+Enalapril
+Ramipril
b. Angiotensin (AT receptor)
antagonists:
+Losartan
5. Vasodilators
a. Venodilators
+Glyceryl trinitrate
b. Arteriolar dilator
+Hydralazine
c. Arteriolar + Venodilator
+Sod. Nitroprusside
6. β-Adrenergic blockers
+Metoprolol
+Bisoprolol
+Carvedilol
7. Others
a. Metabolic
cardioprotectives:
+ Trimetazidine
b. Calcium sensitizers
+ Levosimendan
c. Levocarnitine

5.Ischemic Heart Disease

a. Anti- anginals
b. Atherosclerosi
s drugs
c. Coronary
Heart Disease