ANTIDYSRHYTHMIC DRUGS CLASS I: SODIUM BLOCKERS

DYSRHYTHMIA (ARRHYTHMIA)  Decrease sodium influx to cardiac cells

 IA – slows conduction and prolong
 Any deviation from the normal rate or
repolarization (Quinidine,
pattern of the heartbeat
Procainamide, Disopyramide)
 CARDIAC ACTION POTENTIAL
 IB – slows conduction and shortens
 DEPOLARIZATION: entry of
repolarization (mexiletine, lidocaine)
calcium and sodium
 IC – prolongs conduction with little
o PHASE 1: sodium influx
effect on repolarization
o PHASE 2: initial
(Flecainidine)
repolarization (coincides with
sodium ion influx) COMMON SIDE EFFECTS
o PHASE 3: plateau (influx of
calcium ions) QUINIDINE – nausea, vomiting, diarrhea and
o PHASE 4: rapid abdominal pain or cramps
repolarization (extrusion of MEXILETINE – nausea, vomiting, heartburn,
potassium) tremor, dizziness, nervousness, lightheadedness
o PHASE 5: resting membrane
potential CLASS II: BETA BLOCKERS

ANTIDYSRHYTHMIC DRUGS  Decrease conduction velocity, automatically

and recovery time
 Desired action is to restore cardiac rhythm  More frequently prescribed
to normal
 Propranolol (Inderal)
 FOUR CLASSES:
 Acebutolol ( Sectral)
 Fast sodium channel blockers IA, IB,
 Esmolol (Brevibloc)
IC
 Sotalol (Betapace)
 Beta blockers
 Drugs that prolong repolarization ACEBUTOLOL (SECTRAL)
 Slow calcium channel blockers
 MECHANISM OF ACTION  Is well absorbed in the GI tract. It is
metabolized in the liver, 50%-60% of the
 Block adrenergic stimulation of the
drug is eliminated in the bile feces
heart
 It is prescribed for ventricular dysrhythmias
 Depress myocardial excitability and
as well as Angina Pectoris and Hypertension
contractility
 Onset of action: 1 hour
 Decrease conduction velocity in
 Peak time 4-6 hors
cardiac tissue
 Duration of action 10hours
 Increase recovery time
 Duration of action to treat hypertension 20-
(repolarization0 of the myocardium
24 hours
 Suppress automaticity (spontaneous  Contraindications: Contraindicated to
depolarization to initiate beats) patient with asthma
CLASS III: DRUGS THAT PROLONG
REPOLARIZATION
 Used in the emergency treatment of
ventricular dysrhythmias when other anti
dysrhythmics are ineffective
 Increases refractory period and prolong the
action potential duration
 Bretylium (Bretylol)
 Amiodarone (Cordarone)
CLASS IV: CALCIUM CHANNEL BLOCKERS
 Blocks calcium influx thereby decreasing
cardiac excitability and contractility
(negative inotropic)
 Verapamil
 Diltiazem
NURSING PROCESS OF
ANTIDYSRHYTHMICS
ASSESSMENT
 Obtain health and drug history, shortness of
breath, heart palpitations, coughing chest
pain, previous angina or dysrhythmias and
drug currently takes
 Obtain VS, ECG, cardiac enzyme results
NURSING DIAGNOSIS
 Decreased cardiac output related to
deviation from the normal rate of heartbeat
 Anxiety related to irregular heartbeat
 Risk for inactivity intolerance related to lack
of oxygen supply due to irregular heart beat
PLANNING
 After a series of nursing intervention, the
patient no longer experience abnormal sinus
rhythm
 After a series of nursing intervention, the
patient will comply with antidysrhythmic
drug regimen
NURSING INTERVENTION
 Monitor VS because hypotension can occur
 Administer drug by IV push or bolus as
ordered
 Monitor ECG for abnormal patterns and
report abnormal findings
PATIENT TEACHING
 Teach to take prescribed drugs as prescribed
because compliance is essential
 Educate the patient about side effects and
report it to the nurse/doctor
EVALUATION
 Evaluate the effectiveness of
antidysrhythmic by assessing patient’s
response to drug
 Report side effects and adverse reactions.
Drug regimen may need to be adjusted
DIURETICS
 USES
 Decrease hypertension
 Decrease edema
 FIVE CATEGORIES
 Thiazide and Thiazide-like
 Loop or high-ceiling
 Osmotic
 Carbonic anhydrase inhibitors
 Potassium-sparing
THIAZIDE OR THIAZIDE-LIKE
 Acts on the distal convoluted tubule and
promote4s sodium, chloride and water
excretion
 Causes loss of potassium, sodium and
magnesium
 Promotes CALCIUM reabsorption
(hypercalcemia)
 Affects glucose tolerance (hyperglycemia)
 Contraindicated for renal failure
 WOF: Hyperuricemia, hypokalemia and
hyperlipidemia
  Hypertension
 Peripheral edema
 THIAZIDE – can be hazardous to the
patient who is digitalized or has cancer that
causes hypercalcemia
 Can be used cautiously in patients with
Diabetes Mellitus
 It affect glucose tolerance so hyperglycemia
can also occur
 Electrolytes, glucose need to be monitor
 Pharmacokinetics
 Well absorbed from the GI tract
 Should be administered in the
morning to prevent nocturia and
sleep interruption
 Pharmacodynamics:
 Act directly on arterioles to cause
vasodilation, to lower BP
 Promotes water excretion, resulting
in a decrease vascular fluid volume
 Decrease in cardiac output and blood
pressure
 Onset occurs within 2 hours
 Peak concentration time 3 to 6 hours
 Side effects and adverse reactions:
 Electrolyte imbalance (Hypokalemia,
hypercalcemia, hypomagnesemia,
bicarbonate loss)
 Hyperglycemia
 Hyperuricemia (elevated serum uric
acid level)
 Contraindications:
 Renal failure, elevated BUN,
elevated serum creatinine
 Enhances the action of Digoxin and
digitalis toxicity can occur
 Potassium supplement are frequently
prescribed
 Potassium levels are monitored
THIAZIDE NURSING PROCESS
ASSESSMENT
 Assess VS, weight, urine output and serum
chemistry values (electrolytes, glucose, uric
acid)
 Check peripheral extremities for presence of
edema. Note: pitting edema
 Obtain drug history that may cause drug
interaction
NURSING DIAGNOSIS
 Risk for deficient fluid volume related to use
or overuse of Thiazide
 Impaired urinary elimination related to
kidney dysfunction
 Excess fluid volume related to body fluid
retention
PLANNING
 After a series of nursing intervention
patient’s blood pressure will be decreased or
return to normal value
 After a series of nursing intervention
patient’s edema will be decreased
 Patient’s serum chemistry levels will remain
within normal range
NURSING INTERVENTION
 Monitor vital signs and serum electrolytes,
especially potassium, glucose, uric acid and
cholesterol levels
 Observe for signs and symptoms of
hypokalemia e.g. muscle weakness, leg
cramps, cardiac dysrhythmias.
 Monitor patient’s weight daily. 1 gm = 1 cc
 Note urine output to determine fluid loss or
retention
LOOP OR HIGH-CEILING DIURETICS
 Act on thick ascending loop of henle
 Inhibit chloride transport of sodium into the
circulation (passive reabsorption of sodium)
  Sodium and water are lost together with
potassium, calcium and magnesium
 Affects glucose and can cause
Hyperuricemia
 Saluretic (sodium-chloride losing)
 Natriuretic (sodium losing)
o Furosemide
o Bumetanide
o Ethacrynic acid
 Also called potassium-wasting diuretics
 More potent than Thiazide for promoting
dieresis
 Less effective as hypertensive agents
 Should not be prescribed if a Thiazide could
alleviate body fluid excess
 But if furosemide alone is not effective in
removing body fluid, a Thiazide may be
added
 Pharmacokinetics:
 Rapidly absorbed by the GI tract
 High protein-bound, half life vary
from 30mins-1.5 hour
 Pharmacodynamics
 Loop diuretics have a great saluretic
(sodium-chloride losing) or
natriuretic (sodium-losing). Can
cause decrease cardiac output and
blood pressure
OSMOTIC DIURETIC
CARBONIC ANHYDRASE INHIBITORS
 Increases osmolality (concentration0 and
sodium reabsorption in the proximal tubule
and loop of henle
 Excretes sodium, chloride, potassium and
water
 Uses:
 Prevents kidney failure
 Decrease intracranial pressure
 Decrease intraocular pressure
 UREA
 MANNITOL
MANNITOL
 Potent potassium-wasting diuretic
 Dieresis occurs within 1-3 hrs
 SIDE EFFECTS:
 Fluid and electrolyte imbalance,
pulmonary edema from rapid shift of
fluids, nausea, vomiting, tachycardia
from rapid fluid loss and acidosis
 Crystallization may occur in low
temperature
 Warmed the solution to dissolve
crystallization /crystal before use for IV
infusion
 CONTRAINDICATION
 Give with extreme caution to
patient with heart disease and HF
 NURSING CONSIDERATION:
 Assess VS (BP)
 Monitor serum electrolyte,
weight, urine output for baseline
levels
 NURSING DIAGNOSIS
 Risk for deficient fluid volume
related to fluid loss with excessive
use of loop diuretics
 Risk for electrolyte imbalance
9potassium deficit related to
excessive use of loop diuretics)
 Blocks the action of carbonic anhydrase
needed to maintain the body’s acid-base
balance (hydrogen and bicarbonate ion
balance)
 Causes increased sodium, potassium and
bicarbonate excretion (metabolic acidosis)
 Used primarily to decrease IOP in open-
angle glaucoma
 Acetazolamide
 Side effects/adverse reactions:
o Fluid and electrolyte imbalance
o Metabolic acidosis
o Nausea, vomiting
o Anorexia
 o Crystallurias
o Hemolytic anemia
o Renal calculi
 Contraindications:
o First trimester of pregnancy
POTASSIUM-SPARING DIURETICS
 Weaker than Thiazide and loop diuretics
 Does not excrete potassium
 Hyperkalemia may occur if potassium
supplement is given simultaneously
 Avoid K-rich food
 Monitor K-level (3.5-5.5 meq)
o Spironolactone (Aldactone)
o Amiloride
o Triamterene
o Eplerenone
 Side effects:
o Hyperkalemia:
 Caution must be used when
giving potassium-sparring
diuretics to a patient with
poor renal function
 Kidney excretes 80%-90% of
potassium
 Urine output should be at
least 600ml/day
 Should not give with ACE
inhibitors both drug retain
potassium. Hyperkalemia
becomes severe or life-
threatening
o GI disturbances: nausea, vomiting,
anorexia, diarrhea)
o Numbness and tingling of the hands
and feet
o Other side effects: rash dizziness,
weakness, GI upset
 Aldactone (Spironolactone
o Aldosterone antagonist
o Aldosterone is a mineralocorticoid
hormone that promotes sodium
retention and potassium excretion
o Prescribed for patient with cardiac
disorders because of its potassium
retaining effect
o As a result heart rate is more regular
and possibility of myocardial fibrosis
is decreased
o The effects may take 48 hrs
o More effective when used with
potassium wasting diuretic
(hydrochlorothiazide or loop
diuretic). The combination
intensifies the diuretic effect and
prevents potassium loss
 Nursing consideration:
o Note whether patient is taking a
potassium supplement
o Assess vital signs, serum
electrolytes, weight and urinary
output for baseline levels
 Patient teaching:
o Teach patient to take Spironolactone
with or with meals to avoid nausea
o Encourage patient not to discontinue
drug without consulting health care
provider
o Caution patient to avoid exposure to
direct sunlight, because drug can
cause photosensitivity
ANTIHYPERTENSIVE
 Selected regulator of blood pressure
o Blood vessels
 Baroreceptors (aorta and carotid
sinus)
 Vasomotor center (medulla)
o Kidneys
o Catecholamines
o Hormones
 Antidiuretic hormone (ADH)
 Atrial natriuretic peptide
(ANP)
 Brain natriuretic peptide
(BNP)
 Diuretics
 Sympatholytics
 o Beta adrenergic blockers ADRENERGIC NEURON CLOCKERS
o Centrally-acting alpha2 agonist (PERIPHERALLY ACTING
o Alpha adrenergic blockers SYMPATHOLYTICS)
o Adrenergic neuron blockers
 Peripherally acting  Blocks norepinephrine
sympatholytics) o Reserpine
o Alpha1 and beta1 adrenergic  May cause vivid dreams,
blockers nightmares and suicidal
intention
BETA-ADRENERGIC BLOCKERS o Guanethidine
o Guanadrel
 Propranolol (Inderal)
 Selective beta1 blockers ALPHA1 AND BETA1 ADRENERGIC
o Acebutolol BLOCKERS
o Atenolol
o Bisoprolol  Blocks both alpha1 and beta1 receptors
o Metoprolol o Labetalol
o Carteolol
CENTRALLY-ACTING ALPHA2 AGONIST
DIRECT-ACTING ARTERIOLAR
 Decreases sympathetic response from the VASODILATOR
brainstem to the peripheral vessels
 Stimulates alpha2 receptors that deceases  Relaxes smooth muscles of blood vessels
sympathetic activity, increases vagus  Increases blood flow to brain and kidneys
activity, decreases cardiac output, decreases  Can cause edema (diuretics are given)
serum epinephrine and norepinephrine and o Hydralazine
renin release o Minoxidil
o Methydopa o Nitroprusside
o Clonidine o Diazoxide
o Guanabenz ANGIOTENSIN-CONVERTING ENZYME (ace)
o Guanfacine INHIBITORS
ALPHA-ADRENERGIC BLOCKERS  Treatment of HF and hypertension
 Blocks alpha-adrenergic receptors  Side effects: constant, irritated cough
 Helps maintain renal blood flow rate  Contraindications: pregnancy 9reduces
 Decreases VLDL and LDL and increases placental blood flow)
HDL o Captopril
 Do not affect glucose metabolism o Enalapril
o Prazosin o Lisinopril
o Terazosin o Perindopril
o Doxazosin ANGIOTENSIN II RECEPTOR BLOCKERS
(ARBs)

 Blocks angiotensin II in AT1 receptors in

tissue
 Does not cause constant irritated cough
  Contraindications: pregnancy (reduces o Nicotinic acid
placental blood flow) o Cholesterol absorption inhibitors
o Losartan o Hepatic 3-hydroxyl-3-methylglutryl-
o Valsartan coenzyme A (HMG-CoA) reductase
o Irbesartan inhibitors (statins)
o Candesartan
o Olmesartan BILE ACID SEQUESTRANT
o Telmisartan  Binds with bile acid in the intestine lowering
DIRECT RENIN INHIBITOR LDL cholesterol
o Cholestyramine (Questran)
 Binds with renin o Colestipol (colestid)
o Aliskiren
FIBRIC ACID
CALCIUM CHANNEL BLOCKERS
 Effective in reducing triglycerides and
 Blocks calcium in the heart and vascular VLDL than LDL
smooth muscles o Clofibrate
o Verapamil o Fenofibrate
o Diltiazem
o Amlodipine NICOTINIC ACID
o Nifedipine  Niacin (B2)
ANTILIPIDEMICS  Reduces VLDL and LDL

 Also known as antilipemics, CHOLESTEROL ABSORPTION INHIBITOR

antihyperlipemics, antilipidemics,  Acts on the cells in small intestine to inhibit
hypolipidemics cholesterol absorption
 LIPOPROTEINS o Ezetimide (Zetia)
o High density lipoprotein (contains
more protein than fat) STATINS
 Removes cholesterol from
 Inhibits the HMG CoA reductase in
the vessel and deliver it to the
cholesterol biosynthesis
liver for excretion in bile
 Inhibits cholesterol synthesis in the liver
o Low density lipoprotein
 Decreases cholesterol within 2 weeks
 50%-60% of cholesterol in
 Monitor liver enzymes
the blood
 Check vision (cataract may occur)
o Very low density lipoprotein
 BEST be given at NIGHT
 Carries mostly triglycerides
o Atorvastatin
and less cholesterol
o Rosuvastatin
o Chylomicrons
o Simvastatin
 Large particles that transport
o Pravastatin
fatty-acid and cholesterol to
the liver
 TYPES OF ANTILIPIDEMICS
o Bile acid sequestrants
o Fibrates (fibric acid)
CARDIAC GLYCOSIDES

DIGITALIS

 Used as early as 1220 A.D.

 Obtained from purple and white foxglove
plant
 William Withering used to alleviate
“dropsy” edema of the extremities (kidney
and cardiac insufficiency)
 Be known for treating CHF
 Increase output force of the heart
 A medicine for treating heart failure
o Inhibits NA+ K+ -ATPase cause
intracellular sodium concentration,
increase Ca+ (intracellular)
o Ca+ binds to Troponin-C which
increase contractility
 Three effects on heart muscles
1. Positive iotropic action (increases
myocardial contraction volume)
2. Negative chronotropic action (decreases
heart rate)
3. Negative dromotropic action (decreases
conduction f heart cells

CHF

 Congestive heart failure

 Heart muscle weakens and enlarges
 Looses ability to pump blood to systemic
circulation

HF

 Heart failure