CONGESTIVE HEART FAILURE ↓ Na, H O retention

2
Thiazide
complex clinical syndrome that can result from
⎯ mild CHF
any cardiac disorder that impairs the ability of
⎯ edema management
the ventricle to deliver adequate quantities of
blood to the metabolizing tissues during ⎯ S/E: hypokalemia, hyperglycemia,
normal activity or at rest hyperuricemia, hyperlipidemia
Causes: ⎯ Note: Thiazide + digoxin: increase digoxin
⎯ impaired contraction - MI, arrhythmia toxicity (due to hypokalemia)
Loop Diuretics
⎯ increased work load – HTN
Strategy: ⎯ Furosemide, Torsemide, Ethacrynic acid,
Bumetanide
⎯ ↑ contractility – inotropics
⎯ ↓ resistance – vasodilators ⎯ acute and chronic heart failure, especially
acute pulmonary edema
⎯ ↓ fluid retention - diuretics
Aldosterone Antagonists
⎯ Spironolactone, Eplerenone
A. INOTROPICS - ↑ force of contraction
1. Digoxin
DIURETIC AGENTS
⬆ contraction; ⬇ heart rate
↑ urine flow
no longer considered first-line drugs in the
inhibit Na reabsorption, water follows
treatment of heart failure (Katzung, 9th ed)
MOA: inhibits Na-K ATPase pump
Nephron Parts
low therapeutic index
Nephron: main functional unit of the kidney
DI: (+) verapamil, quinidine, amiodarone
displacement of digoxin from tissue-protein Part Reabsorption of Diuretic
binding sites and competing with digoxin for Action
renal excretion. Proximal Na+, K+, Ca2+, carbonic
S/E: Digitalis toxicity (especially if Convoluted Mg2+, glucose, anhydrase
hypokalemic); anorexia; fatigue, headache & Tubule amino acids, inhibitors
malaise; mental confusion & disorientation; (PCT) NaHCO3
alterations in visual perception (green-yellow Loop of active loop
halo on bright objects); arrhythmia atrial Henle reabsorption of diuretics
tachycardia with A-V block (most classic) Na+, K+ & Cl-
Digoxin Toxicity Management: secondary
Lidocaine or Phenytoin reabsorption of
Cholestyramine Ca2+ & Mg2+
Digoxin-specific Fab fragment antibodies
Digoxin Digitoxin Distal active thiazide
Lipid medium high Convoluted reabsorption of diuretics
solubility Tubule Na+ & Cl-
Half-life short long Ca2+
reabsorption
excretion renal hepatic
under parathyroid
hormone control
2. Inamrinone, Milrinone
inhibits phosphodiesterase ↑ cAMP ↑
Collecting Na+ reabsorption potassium-
Ca
Duct coupled to K+& sparing
inodilators
H+ secretion diuretics
S/E: hypotension, arrhythmia,
thrombocytopenia
Note: These agents should not be used in
chronic failure because they have been
shown to increase morbidity and mortality
3. Dopamine CARBONIC ANHYDRASE INHIBITORS
2-5 mcg/kg/min: renal D receptor Acetazolamide, Dorzolamide, Brinzolamide
+ -
1
5-10 mcg/kg/min: β receptor CO2 + H2O H2CO3 H + HCO3
1 + +

>10 mcg/kg/min: α receptor H exchanged for Na in the PCT

1 +
4. Dobutamine no H , no Na reabsorption diuresis
β & β agonist with some α agonist effect Indication:
⎯ glaucoma (↓aqueous humor
1 2 1
↓ intraocular P)
produces less tachycardia
⎯ acute mountain sickness
Not for chronic failure (also dopamine), due to
S/E: metabolic acidosis (loss of bicarbonate),
tolerance, lack of oral efficiacy and
hypokalemia, drowsiness, paresthesias, allergy
arrythmogenic effects)
B. Vasodilators
LOOP (HIGH-CEILING) DIURETICS
↓ PR
Furosemide, Torsemide, Bumetanide, Ethacrynic
Clinical Studies:
Acid
⎯ Nitrates + Hydralazine ⬇ mortality rates
decrease Na reabsorption by inhibiting the
among African americans + + -
⎯ Prazosin did not benefit patients. Na /K /2Cl transporter in the loop of Henle
⎯ CCBs have no value in heart failure. Uses: CHF, acute pulmonary edema, acute
Nitroprusside; Hydralazine; Prazosin; Nitrates; hypercalcemia
Nesiritide - Atrial peptide vasodilator, diuretic for S/E: ototoxicity, hypovolemia, hypomagnesemia,
Acute severe decompensated failure hypokalemia, hyperuricemia, allergy
S/E renal damage, hypotension
C. DIURETICS
 THIAZIDE DIURETICS
Hydroflumethiazide; Methyclothiazide;
Metolazone; Polythiazide; Quinethazone;
Trichlormethiazide
increase urinary excretion of Na & H O by
2
+ -
inhibiting Na -Cl symporter in the DCT
Uses: HTN, renal calcium stone formation
S/E: hypokalemia, hyponatremia,
hypomagnesemia, hypercalcemia,
hyperuricemia, hyperglycemia, hyperlipidemia,
allergy

POTASSIUM-SPARING DIURETICS
Spironolactone; Amiloride; Triamterene;
Eplerenone
inhibit Na reabsorption, K secretion at the
collecting tubule
combined with loop, thiazide diuretics to prevent K
loss
hyperaldosteronism (Conn’s syndrome), CHF
Spironolactone (aldosterone antagonist)
S/E: hyperkalemia, gynecomastia, impotence
(due to structural similarity with progesterone)

OSMOTIC DIURETICS
Mannitol, Urea
osmotic effect in PCT & thin descending limb of
loop of Henle
lowering of intracranial pressure, removal of toxins
S/E: hypovolemia, pulmonary edema;
Contraindication: CHF

D. β BLOCKERS
For many years the prevailing view was that -
blockers are contraindicated in CHF
Rationale of Use:

⎯ ⬆ circulating plasma norepinephrine levels

correlate, ⬇ survival in CHF
⎯ It appears that norepinephrine levels are more
than just markers of disease severity:
norepinephrine is actually directly toxic to
cardiac myocytes, at least in culture.
⎯ The addition of either an α- or β-blocker
confers partial protection from norepinephrine
damage. Combined α- or β-blockade (e.g
carvedilol) confers additive protection
Bisoprolol, Metoprolol, CarvedILOL

E. Angiotensin-converting enzyme inhibitors

this are now the first line agent for CHF
D/I: Potassium sparing diuretics + ACEI
 4. Ganglionic Blockers
Trimethaphan, Hexamethonium
⎯ rarely used due to side effects:
Parasympathetic blockade urinary
retention, blurring of vision
Sympathetic blockade orthostatic
hypotension, sexual dysfunction
5. Postganglionic Adrenergic Neuron Blockers
Reserpine, Guanethidine
⎯ deplete catecholamine stores in the brain
& in the peripheral adrenergic system
⎯ rarely used due to low efficacy & side
effects
B. DIURETICS
↓ Na, H 0 retention ↓ BV ↓ CO
2

C. VASODILATORS
1. Hydralazine
directly relaxes arterioles ↓ PR
hypertensive crisis (IV or IM) HPN crisis:
BP 210/150 or above
HYPERTENSION S/E: reflex tachycardia, systemic lupus
most common cardiovascular disorder erythematosus
sustained BP ≥ 130/80 (systolic/ diastolic) 2. Minoxidil
directly relaxes arteriolar smooth muscle ↓
PR
Anti-HPN Drugs decreases renal vascular resistance
A. Sympatholytics S/E: hypertrichosis
1. Centrally-Acting / α Agonist
2 3. Sodium Nitroprusside
Methyldopa, Clonidine, Guanabenz, has potent effects on both the arterial &
Guanfacine venous systems
⎯ presynaptic α agonist ↓ NE release acute hypertensive crisis (IV)
2
S/E: hypotension, cyanide toxicity
by(-) feedback
4. Diazoxide
⎯ activity of methyldopa: due to stimulation
exerts a direct action on the arterioles
of central alpha adrenoceptors by
acute hypertensive crisis (IV)
methyldopamine & methylNE
hypoglycemia due to hyperinsulinism
⎯ S/E: (prevents insulin release)
sedation, dry mouth, depression S/E: hypotension, hyperglycemia
methyldopa: false (+) Coomb’s test D. Calcium Channel Blockers
for hemolytic anemia have natriuretic effect. No need for diuretic
clonidine: rebound hypertension on for patients with HPN + Angina/diabetes
withdrawal 1. Dihydropyridines:
2. α Blockers
1 1st gen: Nifedipine
Prazosin, Terazosin, Doxazosin 2nd gen: Amlodipine, Felodipine, Isradipine,
⎯ block α ↓ vasoconstriction ↓ PR Nicardipine, Nisoldipine, Nimodipine
1 (selective in cerebral vasculature) vascular
⎯ S/E: orthostatic hypotension especially smooth muscles
st
a. vasodilation - ↓ PR
after the 1 dose 2. Non-dihydropyridines:
3. β Blockers Verapamil & Diltiazem
↓ HR, contractility ↓ CO
⎯ vascular smooth muscles & cardiac
block stimulation of renin secretion
muscles
selectivity:
⎯ vasodilation - ↓ PR
⎯ (-) inotropic / chronotropic effect - ↓ CO
Selective Non-Selective
E. ACE Inhibitors
Betaxolol Propranolol
↓ angiotensin II ↓ vasoconstriction ↓ PR
Bisoprolol Penbutolol ↓ angiotensin II ↓ aldosterone ↓ Na, H 0
Esmolol Carteolol 2

Atenolol CarvedILOL (α & β) retention ↓ blood volume ↓ CO

⬆ bradykinin level vasodilation
Acebutolol LabetALOL (α & β)
Metoprolol Timolol
Celiprolol Nadolol
Pathway: Angiotensinogen Angiotensin I
intrinsic sympathomimetic activity: Angiotensin II
⎯ Pindolol, Penbutolol, Acebutolol, Carteolol
release catecholamines USES:
maintain satisfactory HR Alone: HPN/ CHF/ MI
may also prevent bronchoconstriction (+) diuretic: HPN in black and white
S/E: hypotension, bradycardia, CHF, ACEI and/or ARBS: slow progression of
bronchospasm (asthma, COPD patients) diabetic nephropathy.

DI: (+) thiazides enhance hypotensive action,
plus reducing thiazide induced hypokalemia; (+)
Potassium supplements hyperkalemia‼
S/E:
First-dose hypotension
Dry cough (most frequent symptom)
Functional renal failure
Hyperkalaemia
Fetal injury
Urticaria and angio-oedema
Sulfhydryl group-related effects
⎯ heavy proteinuria
⎯ Neutropenia
⎯ rash
⎯ taste disturbance
⎯ ⎯ Cyanide toxicity: CN-cytochrome oxidase
F. ANGIOTENSIN II RECEPTOR BLOCKERS (ARB)
Candesartan cilexetil, Eprosartan, Irbesartan,
Losartan, Olmesartan, Telmisartan, Valsartan
block the binding of angiotensin II to the
angiotensin II receptors ⬇ TPR (afterload) and
venous tone (preload)
ISCHEMIC HEART DISEASE
form of heart disease with primary manifestations
that result from myocardial ischemia due to
atherosclerotic CAD
Coronary Artery Disease (CAD): refers to a
number of diseases other than atherosclerosis
causing a narrowing of the major epicardial
coronary artery; may present as acute MI,
unstable angina, chronic stable angina or variant
angina
Angina Pectoris: most common form of IHD;
applied to varying forms of transient chest
discomfort that are attributable to insufficient
myocardial oxygen
Types of Angina
A. Stable or Classic or Typical or Exertional
(Angina of Effort) or Atherosclerotic
Angina
most common form
exertion, emotional stress, or a heavy
meal usually precipitates chest discomfort
coronary artery obstruction due to
atherosclerotic plaque
usually relieved by rest, nitroglycerin, or
both
B. Prinzmetal’s or Vasospastic or Variant
Angina or Atypical or Rest angina
usually occurs at rest rather than with
exertion or emotional stress
due to coronary artery spasm
spasm occur at any time, even at night
C. Unstable or Crescendo or Rest Angina or
the patient experiences:
⎯ rest angina
⎯ severe new-onset angina
⎯ increasing angina
⎯ decreased response to rest or
nitroglycerin
due to advanced coronary atherosclerosis
D. Angina Decubitus
norturnal angina
Anti-anginal Drugs
A. Nitroglycerin (SL, spray, transdermal patch, oral, IV
infusion) Isosorbide dinitrate; mononitrate (SL, oral)
Pentaerythritol tetranitrate (SL); Erythritol
tetranitrate (SL, oral)
converted to nitric oxide (NO) inc. cGMP
smooth muscle relaxation vasodilation
venodilation & arterial dilation ↓ O demand
2
and overall reduction in myocardial fiber
tension
S/E: throbbing headache; Flushing; postural
hypotension; reflex tachycardia due to
increased heart rate and contractility); tolerance
“Monday Disease” industrial disease caused by
chronic exposure to organic nitrates; headache,
dizziness and tachycardia after 2 days absent.
For nitrites (not nitrates) methemoglobinemia
complex oxidative metabolism and cell
death. Methemoglobin, however, has higher
affinity to cyanide than in cytochrome oxidase.
C/I: sildenafil (PDE5 inhibitor): synergism
dangerous hypotension
B. CALCIUM CHANNEL BLOCKERS
Nifedipine, Amlodipine, Felodipine, Isradipine,
Nicardipine, Nisoldipine, Nitrendipine, Bepridil,
Diltiazem, Verapamil
DOC for Prinzmetal’s angina
Verapamil and Diltiazem (used also in
supraventricular tachycardia, pulmonary
hypertension and Raynaud’s phenomenon
MOA: blockade of L-type voltage dependent
calcium channels ⬇ contractility; ⬇ heart rate;
vasodilation
S/E: Constipation (verapamil); Nausea; Flushing;
Dizziness; heart failure; AV blockade; sinus node
depression
C. β BLOCKERS
Propranolol; Metoprolol; Atenolol; Nadolol;
Timolol; Acebutolol; Betaxolol; Bisoprolol Esmolol;
Pindolol
↓ HR, contraction ↓ O demand
2
vasoconstriction (opposing to calcium channel
blockers)
⬆ diastolic filling time ⬆ oxygen supply
prophylaxis only, not for acute attack
beneficial if combined with nitrates because the
latter causes reflex tachycardia which is
counteracted by the former
S/E: Bradycardia; arteriovenous nodal block;
decompensated congestive heart failure
DRUGS AFFECTING BLOOD
Review Coagulation Pathway
Virchow’s triad of thrombus formation:
1. venous stasis- illness, surgery, paralysis, obesity
2. vascular injury- surgery, trauma, atherosclerosis
3. hypercoagulable states- malignancy, antiphospholipid
antibodies, estrogens
A. Anticoagulants
- prevents clot formation

Strategies
↑ O delivery (supply)
2
↓ O requirement (demand)
2
↑efficiency of oxygen utilization
 3. Dipyridamole
- prevention of stroke and MI; nuclear cardiac
stress testing
- inhibits adenosine reuptake dec. platelet
Heparin Warfarin
aggregatioN
Chemistry Sulfated Coumarin
glycosaminoglycan
- inhibits phosphodiesterase inc. cGMP
vasodilation
a. unfractionated
4. Glycoprotein IIb/IIIa inhibitors
b. low-MW
- Abciximab, Eptifibatide, Tirofiban
Mechanism Activates Inhibits vitamin
- for patients undergoing percutaneous coronary
antithrombin K synthesis
intervention (angioplasty)
Uses Post-MI, Prevention of -S/E: bleed
prevention of DVT DVT and PE,
and PE Atrial fibirillation ANEMIA
Artificial heart - characterized by a decrease in hemoglobin or
valves RBCs
Route IV or SC (not IM Oral, IV 1. Iron deficiency anemia
hematoma) - characterized by hypochromic microcytic anemia
Monitoring Activated partial Prothrombin - caused by inadequate dietary intake, inadequate
thromboplastin time (expressed GI absorption, increased demand
time as INR) (eg. pregnancy), blood loss and chronic diseases
Target 1.5-2.5x control INR 2-3 - Dx: serum ferritin- earliest and most sensitive
Side-effects Bleeding, allergy, Bleeding, test; CBC, peripheral blood smear
thrombocytopenia teratogenic
Antidote Protamine sulfate Vitamin K Oral iron products: 200 mg elemental iron in 2-3 divided
(1mg/100 units) doses
Salt % elemental iron
Heparin and related agents Fe sulfate 20
1. Unfractionated heparin 60-65 mg/325 mg tablet
- MW= 5,000-30,000 daltons Fe glucontae 12
2. Low molecular weight heparins (LMWH) Fe fumarate 33
- Enoxaparin, dalteparin, tinzaparin
Polysaccharide iron complex 100
- Longer half-life
Carbonyl iron 100
- Less bleeding, routine aPTT unnecessary
3. Danaparoid Na
Parenteral iron preparations:
- Mixture of 3 sulfated glycosaminoglycans: heparin,
dermatan and chondroitin • Sodium ferric gluconate-IV
4. Fondaparinux Na • Iron dextran- IM, IV
• Iron sucrose- IV

Direct thrombin inhibitors 2. Vitamin B12-deficiency anemia

- derived from hirudin obtained from the saliva of
the medicinal leech Hirudo medicinalis - macrocytic cells
- Lepirudin, Bivalirudin, Desirudin - caused by inadequate dietary intake, decreased
- anticoagulant for patients with heparin-induced absorption (eg. pernicious anemia- lack of intrinsic
thrombocytopenia (HIT) factor)
- distinguished from folate deficiency by neurologic
B. Thrombolytics abnormalities (numbness and paresthesias)
-dissolves clot - Tx: oral, parenteral or intranasal gel
- converts plasminogen plasmin (fibrinolytic) cyanocobalamin
1. Streptokinase 3. Folate-deficiency anemia
- protein from streptococci - megaloblastic anemia
- MI, DLVT, PE - no neurologic abnormalities
- S/E: hemorrhage, allergy - Tx: oral folate 1 mg daily
2. Tissue plasminogen activators 4. Anemia in chronic kidney disease
- Alteplase, Reteplase, Streptokinase - due to deficiency of erthropoeitin
- MI, DLVT, PE - Tx: epoetin alfa, darbepoetin alfa SC, IV;
- only binds to plasminogen bound to fibrin iron supplementation
- S/E: hemorrhage

C. Antiplatelets Hyperlipidemia
-inh. platelet aggregation - elevation of one or more of the following:
-prolongs bleeding time cholesterol, phospholipids, or triglycerides
- Uses: prevention of MI, stroke - elevated LDL and reduced HDL are associated
1. Aspirin with coronary heart disease
- prevents thromboxane synthesis by inhibiting
cyclooxygenase 1. Bile acid-binding resins
- Uses: prevention of MI, stroke - cholestyramine, colestipol, colesevelam
- S/E: GI ulcer, bleeding - positively-charged ammonium polymers
2. Thienopyridines - bind to negatively-charged bile acids and
- blocks ADP receptor in the platelet cell excreted in feces, interrupts enterohepatic
membrane circulation
- Uses: prevention of MI, stroke inc. synthesis of bile acids from cholesterol
a. Clopidogrel - effects: ↓LDL ↑VLDL
-S/E: nausea, vomiting, diarrhea, hemorrahe -S/E: GI discomfort (constipation, bloating,
b. Ticlopidine flatulence)
- S/E: neutropenia dec. absorption of fat soluble vitamins
 reduced bioavailability of acidic drugs (warfarin,
nicotinic acid, paracetamol etc.)
2. Niacin/ Nicotinic Acid
- aka Vitamin B3
- blocks lipolysis in adipose tissue which reduces
circulating free fatty acids
- effects: ↓LDL ↓VLDL ↑HDL
- S/E: flushing, itching, hepatitis, hyperglycemia,
hyperuricemia
- take aspirin after and avoid alcohol and hot
drinks to prevent flushing and pruritus
3. HMG-CoA reductase inhibitors
- lovastatin, simvastatin, atorvastatin, pravastatin,
fluvastatin, rosuvastatin
- structural analogs of HMG-CoA intermediate
- inhibits 3-hydroxy-3-methylglutaryl coenzyme A
(HMG CoA) reductase interrupting the conversion
of HMG-CoA to mevalonate, the rate-limiting step
in cholesterol synthesis
- most potent total and LDL lowering agents
- effects: ↓LDL
- S/E: constipation, elevated liver enzymes,
myopathy, rhabdomyolysis
4. Fibrates
- clofibrate, gemfibrozil, fenofibrate
- increases activity of lipoprotein lipase
- effects: ↓LDL ↓VLDL ↑HDL
- S/E: GI disturbance, gallstones, myositis
5.Ezetimibe
- interferes with absorption of cholesterol in the
intestines
- effects: ↓LDL
- adjunct with statins
- S/E: GI upset
I. Arrhythmia
deviations from the normal heartbeat pattern
they include: abnormalities of impulse
formation & conduction disturbances
Vaughan Williams’ Classification of Antiarrhythmic
Drugs
Class I (Na Channel Blockers)
IA: Quinidine, Procainamide, Disopyramide
IB: Phenytoin, Lidocaine, Mexiletine, Tocainide
IC: Flecainide, Propafenone, Moricizine
Class II (β Blockers)
Propranolol, Esmolol, Acebutolol
Class III (K Channel Blockers)
Bretylium, Amiodarone, Sotalol, Ibutilide, Dofetilide
Class IV (Ca Channel Blockers)
Verapamil, Diltiazem
Others:
Adenosine
Atropine
Digoxin
Magnesium sulfate
A. Sodium Channel Blockers
all group 1 drugs reduce both phase 0 (rate of
rise/upstroke) and phase 4 sodium currents
(wavy lines) in susceptible cells.
Group 1A
⎯ ⬇ upstroke
⎯ ⬇ phase 3 potassium current (I )
K
⎯ ⬆ action potential (AP) duration
⎯ ⬆ effective refractory period (ERP)
⎯ ⬇ conduction velocity
1. Procainamide
Atrial and ventricular arrhythmias,
especially after myocardial infarction
Procainamide is a particularly useful
antiarrhythmic drug, effective in the
treatment of supraventricular, ventricular,
and digitalis-induced arrhythmias.
Increased arrhythmias, drug fever,
agranulocytosis, SLE-like syndrome
(fatigue, arthralgia, myalgia & low-grade
fever)
2. Disopyramide
Similar to procainamide but longer
duration of action
toxicity includes antimuscarinic effects
and heart failure
3. Quinidine
Similar to procainamide but toxicity
includes cinchonism (tinnitus, headache,
gastrointestinal disturbance) and
thrombocytopenia.
4. Moricizine
life-threatening arrhythmias
Not classified as IA or IB, but shows
effect as them
Group 1B
⎯ ⬇ action potential duration
+
⎯ ⬆ outward K current
⎯ Minimal ⬇ in upstroke
1. Lidocaine
DOC for digitalis-induced arrhythmia
DOC for sustained ventricular arrhythmia
after acute MI
S/E: CNS reactions (most pronounced);
sedation or excitation
2. Mexiletine
Similar to lidocaine but oral activity and
longer duration of action
For acute or chronic ventricular
arrhythmias
While it is not at present an indication for
use, there is interest in using mexiletine to
treat the congenital long QT syndrome
when an abnormality in the SCN5A gene
(LQTS 3) has been found.
3. Phenytoin
an anticonvulsant and not a true local
anesthetic
sometimes classified with the group 1B
antiarrhythmic agents because it can be
used to reverse digitalis-induced
arrhythmias
 ⎯ S/E: Thyroid abnormalities, deposits in
Also in ventricular arrhythmias in skin and cornea, pulmonary fibrosis,
children optic neuritis; Torsades de pointes;
Photosensitivity
4. Tocainide ⎯ Peripheral neuritis
structural similarity to Lidocaine
For symptomatic ventricular arrhythmias
refractory to more conventional therapy 2. Sotalol
⎯ Ventricular arrhythmias and atrial
Group IC fibrillation
⎯ No effect on action potential ⎯ Dose-related torsade de pointes; cardiac
⎯ Marked ⬇ in upstroke depression
⎯ ⬇ conduction velocity 3. Ibutilide
1. Flecainide ⎯ Treatment of acute atrial fibrillation
Refractory arrhythmias ⎯ Ibutilide is IV only
intractable supraventricular arrhythmias ⎯ Torsade de pointes
most types of atrial arrhythmias 4. Dofetilide
Now restricted to use in persistent ⎯ Treatment and prophylaxis of atrial
arrhythmias that fail to respond to fibrillation
other drugs ⎯ Torsades de pointes
Increased arrhythmias; CNS excitation Drug Uses Side effects
2. Propafenone Bretylium Refractory Arrhythmia, hypotension
supraventricular arrhythmias and life- post-MI
threatening VF
ventricular arrhythmias in the absence of Sotalol oral Torsades, bradycardia,
structural heart disease asthma
3. Moricizine Ibutilide and AF torsades
Dofetilide
Drug Uses Side effects
Class IA
Procainamide All types; AF, Hypotension, lupus
VT D.Calcium Channel Blocker
Quinidine Cinchonism (HA, reduce inward calcium current during the AP and
vertigo, tinnitus) during phase 4 (wavy lines)
GI upset, inc. digoxin Major effect: ⬇ conduction velocity is slowed in the
levels, torsades de AV node
pointes refractoriness is prolonged
Disopyramide Antimuscarinic Verapamil & Diltiazem
Class IB ⎯ AV nodal arrhythmias, especially in
Lidocaine VT/VF; IV Convulsions, allergy prophylaxis
Mexiletine Oral
⎯ 1st line agents for the suppression of
Tocainide Oral Agranulocytosis
Class IC paroxysmal supraventricular tachycardia
Flecainide Refractory VT proarrythmic stemming from AV nodal reentry
Propafenone
Moricizine ⎯ S/E: Cardiac depression; constipation,
hypotension
B. Beta-Blockers ⎯ Nifedipine and the other dihydropyridines
Cardiac membrane stabilization are not useful as antiarrhythmics
Prolong ERP
1. Propranolol
⎯ Postmyocardial infarction as Drug Uses Side
prophylaxis against sudden death effects
Verapamil AF (1st line); Hypotension
ventricular fibrillation & thyrotoxicosis
IV, oral
⎯ S/E: Bronchospasm; cardiac depression, Diltiazem Oral
atrioventricular (AV) block, hypotension
2. Esmolol D. Miscellaneous Anti-Arrhythmics
⎯ Selective B -receptor blockade 1. Adenosine
1
⎯ Given via IV only, 10-min duration. ⎯ AV node that causes marked
⎯ Used in perioperative and thyrotoxicosis hyperpolarization and conduction block
arrhythmias ⎯ endogenous product of the metabolism of
adenosine triphosphate
C. Potassium Channel Blocker ⎯ Acute nodal tachycardias
⬆ AP duration ⎯ DOC for paroxysmal supraventricular
⬆ ERP tachycardia
delaying repolarization without altering phase 0 ⎯ If asthmatic: verapamil
Class III drugs have a significant risk of ⎯ S/E: Flushing, bronchospasm, chest pain,
proarrhythmia because of the prolongation of headache
action potential and the induction of torsades de 2. Potassium ion
pointes ⎯ Digitalis toxicity and other arrhythmias if
1. Amiodarone serum K is low
⎯ Refractory arrhythmias; used off-label in ⎯ Both hypokalemia and hyperkalemia are
many arrhythmias (broad spectrum of associated with arrhythmogenesis.
therapeutic action) ⎯ Severe hyperkalemia causes cardiac
⎯ 1st choice antiarrhythmic for shock- arrest
refractory ventricular
fibrillation/ventricular tachycardia
3. Magnesium sulfate
⎯ Poorly understood, possible increase in
+ +
Na /K ATPase activity
⎯ Indications: Digitalis arrhythmias and other
arrhythmias if serum Mg is low; Torsades
de Pointes
⎯ S/E: Muscle weakness, severe
hypermagnesemia can cause respiratory
paralysis,

Drug Uses Side effects

Adenosine PSVT (1st Flushing,
line); hypotension
short duration
(15 s)
Magnesium Torsade de
sulfate point