Cardiovascular Drugs

Dra. Hena W. Alcantara

The Cardiovascular System
• Heart
• Blood
• Blood Vessels
– Arteries
– Veins
– Capillaries
The Heart
Blood
Blood Vessels
Circulation
In simple terms…

• The heart is a pump.

• It pumps blood through a system of
blood vessels that has a limited
volume capacity.
• An electric conduction system
maintains regular rate and rhythm.
• Myocardial cells require oxygen.
Malfunctions
when the heart
can no longer
pump enough
blood to meet the HEART FAILURE
metabolic
demands of the
body

when blood
volume is great
compared to the
HYPERTENSION
space available
inside blood
vessels
Malfunctions
when the electrical
conduction
pathways ARRHYTHMIA
malfunction

the heart’s way of

signaling that
some of the cells ANGINA
are not getting
enough oxygen
Malfunctions

when oxygen-
starved areas of MYOCARDIAL
the heart begin INFARCTION
dying

when you broke

with someone…
Cardiovascular Drugs
Cardiovascular Drugs
• Anti-hypertensives
• Drugs for Heart Failure
• Anti-anginal and Drugs for MI
• Anti-arrhythmic Agents
Anti-Hypertensive Drugs
Physiology of BP Regulation

• Hydraulic Equation:

BP = CO x TPR
 Factors that alter the Blood Pressure Equation
Sympathetic Adrenergic
System

Blood Cardiac Total Peripheral

= x
Pressure Output Arterial Resistance
Aldosterone

vasoconstriction
Na+& H2O
Reabsorption

Heart Blood
Stroke Venous
Volume
Rate x Volume Return Rises
Pituitary
Gland Angiotensin II
Renin –
ACE
Angiotensin
System Angiotensin I
Low Blood Pressure
Low Blood Volume Kidney
Na+ depletion
Renin
Determinants of Blood
Pressure
• Cardiac Output (CO)
– volume of blood pumped out by the
heart in 1 minute
– approximately 2.2 – 3.5 L / min / m2 BSA
– determined by Stroke Volume (SV) and
Heart Rate (HR)
Determinants of Blood
Pressure
• Stroke Volume (SV)
– volume of blood pumped out by the
heart in every contraction
– determined by:
• Inotropic activity –strength of cardiac
contraction
• Venous return – cardiac preload; amount of
blood delivered to the heart from the veins;
affected by the tone of the veins
Determinants of Blood
Pressure
• Heart Rate (HR)
– speed of heart contraction
– chronotropism
• Fluid Content of the Blood
• Total Peripheral Resistance (TPR)
– resistance or pressure encountered by
the heart as it pumps out blood into the
peripheral circulation (cardiac afterload)
– determined by the arterioles
Mechanisms of BP
Regulation
• Baroreceptor Reflex Arch Mechanism
– aka: Postural Reflex Mechanism
– moment-to-moment BP regulation
• Baroreceptor – a type of sensory nerve
ending found in the walls of the atria of the
heart, the vena cava, the aortic arch, and
the carotid sinus that is stimulated by
changes in pressure

• Renin Angiotensin Aldosterone

Renin Angiotensin Aldosterone
System (RAAS)
Angiotensinogen (from the liver)
Renin

Angiotensin I (inactive)

Angiotensin Converting Enzyme (ACE)

or
Peptidyl dipeptidase
(majority found in the lungs)

Angiotensin II (active)

-direct vasoconstriction
-stimulates synthesis & release of Epi & NE
-stimulates the synthesis & release of
aldosterone
Hypertension
Hypertension
• persistent or recurrent elevation of BP
defined as having a:
– Systolic reading > 140 mmHg
– Diastolic reading > 90 mmHg
– BP > 140/90
• most common cardiovascular
disorder
Hypertension
• Systole
– the period during which the ventricles
are contracting
• Diastole
– the period during which the ventricles
are relaxed and filling with blood
Hypertension
• Essential (Primary, Idiopathic)
– hypertension with no identifiable cause
– accounts for > 90% of HTNsive cases

• Secondary
– resulting from identifiable causes
• kidney diseases
• adrenal cortical disorders
• pheochromocytoma (adrenal medulla tumor)
• coarctation of the aorta
• drugs such as steroids, sympathomimetics, contraceptives
– treat the underlying cause
– accounts for ~ 10% of HTNsive cases
 Classification of BP based on the 7 th Report of the
Joint National Committee on Detection, Evaluation
and Treatment of High Blood Pressure (JNC VII)

Classification of Blood Pressure (JNC VII)

Systolic BP, mm Hg Diastolic BP, mm
Hg

Normal <120 and <80

Prehypertension 120-139 or 80-89

Stage 1 hypertension 140-159 or 90-99

Stage 2 hypertension >160 or >100

Adapted from JNC VII

Hypertensive Emergency
• aka: Hypertensive Crisis

• rare, but life-threatening situation

• systolic pressure > 210 mm Hg

• diastolic pressure > 150 mm Hg
Risk Factors
• Family history
• Patient history
• Racial predisposition
– More common in blacks
• Obesity
• Smoking
• Stress
• High dietary intake
– Saturated fats and
sodium
• Sedentary lifestyle
• DM
• Hyperlipidemia
• Gender – males
• Age > 60
• Postmenopausal
women
Treatment Goals

• Rule out uncommon secondary causes of

hypertension
• Determine the presence and extent of
target organ damage
• Determine the presence of other CV risk
factors
• To lower BP with minimal side effects
Complications
• Cardiac effects
– Increased oxygen requirements  angina pectoris;
because of atherosclerosis  angina, MI, sudden death
• Renal effects
– Increased blood volume; renal parenchymal damage due
to atherosclerosis
• Cerebral effects
– Transient ischemic attacks, cerebral thromboses,
aneurysms with hemorrhage
• Retinal effects
– Visual defects (blurred vision, spots, blindness)
Treatment
• First line: diuretics (thiazides) and beta blockers

• Alternatives: ACE inhibitors, ARBs, alpha blockers, calcium-

channel blockers  for px who cannot tolerate first line
agents

• Monitor:
– blood pressure routinely
– observe adverse effects

• Patient Counseling:
– Importance of compliance  make px realize seriousness
of noncompliance
Anti-hypertensives
• Diuretics
• Sympathoplegics
• Vasodilators
• Calcium Channel Blockers (CCBs)
• ACE Inhibitors
• Angiotensin II Receptor Blockers
(ARBs)
Diuretics
• agents that cause urinary loss of Na +
and H2O

• Gen MOA: act on their specific sites

in the renal tubule
 Five major classes
1. Thiazides and thiazide-like
2. Loop diuretics
3. Potassium-sparing
4. Carbonic anhydrase inhibitors
5. Osmotic diuretics
Renal Tubule
Carbonic Anhydrase
Inhibitors
• MOA: inhibit carbonic anhydrase (the
enzyme that catalyzes the reaction of
CO2 and H2O leading to H+ and
HCO3-) that can lead to the spillage of
Na+ causing diuresis.

• act on the proximal convoluted tubule

(PCT)
Carbonic Anhydrase
Inhibitors
• Acetazolamide
• Brinzolamide
• Dorzolamide
Carbonic Anhydrase
Inhibitors
• limited diuretic effect (2 to 3 days)

• SE: metabolic acidosis, bone marrow

depression (sulfonamide-like toxicity),
allergic reactions (Stevens-Johnson’s
Syndrome)
Loop Diuretics
• aka: High Ceiling Diuretics

• high ceiling (most efficacious) as

compared with other diuretics

• act on the thick ascending Loop of

Henle
Loop Diuretics
• MOA: inhibit the Cl-Na-K-
cotransporter at the thick ascending
LOH

• Furosemide
• Bumetanide
• Torsemide
• Ethacrynic acid
Loop Diuretics
• for px who cannot tolerate thiazides,
have renal impairment, or
ineffectiveness of thiazides

• SE: hypovolemia, ototoxicity, increase

serum creatinine

• DI: their efficacy can be reduced by

NSAIDs
Loop Diuretics
• Side-effects
–Hypokalemia
–Bicarbonate is lost in the urine
–INCREASED calcium excretion
Hypocalcemia
–Ototoxicity
• due to the electrolyte imbalances
Thiazide Diuretics
• MOA: inhibit Na-Cl-cotransporter at
the distal convoluted tubule

• Chlorothiazide
• Hydrochlorothiazide
• Chlorthalidone
• Indapamide
Thiazide Diuretics
• first-line drug for uncomplicated
hypertension as recommended by
JNC 7

• effective initial therapy together with

beta-blockers

• also used for Nephrogenic Diabetes

Thiazide Diuretics
• SE: hypokalemia, hyponatremia,
hyperuricemia, hyperglycemia,
hyperlipidemia

• DI: their efficacy can be reduced by

NSAIDs
Thiazide
• Side effects
–Hypokalemia
–DECREASED calcium
excretion hypercalcemia
–DECREASED uric acid
secretion hyperuricemia
–Hyperglycemia
Potassium-Sparing Diuretics
• MOA: act in the collecting tubule by
inhibiting Na+ reabsorption, K+
secretion and H+ secretion

• Spironolactone
• Eprenolone
• Amiloride
• Triamterene
Potassium-Sparing Diuretics
• for patients where potassium loss is
significant and supplementation is not
feasible
• often combined with thiazides 
potentiation
– Amiloride, Spirinolactone, Triamterene
• precautions
– Avoid in px with acute renal failure; use
with caution  px with impaired renal
function
Potassium Rich Foods
TOPP PNBB’S
• T- Tomatoes
• O-Oranges
• P- Peaches
• P-potatoes
• P-Prunes
• N-Nuts
• B-Banana
• B-Broccoli
• S-Spinatch
Potassium-Sparing Diuretics
• not associated with hypokalemia

• can be given with other diuretics to

lessen the risk of hypokalemia

• SE: hyperkalemia, gynecomastia,

impotence, sterility
Osmotic Diuretics
• MOA: increase the osmotic pressure
at the proximal convoluted tubule and
Loop of Henle preventing water
reabsorption

• Mannitol
• Sorbitol
• Urea
Osmotic Diuretics
• used to induce forced diuresis
• mostly used to reduce intracranial
pressure

• SE: hypernatremia, hypovolemia

Diuretic class Major site of action Special Side effect
Diuretics Comparison (s)
1. Carbonic Proximal tubule Acidosis
anhydrase
inhibitor

2. Thiazide and Distal tubule Hyperuricemia

thiazide like Hypokalemia
3. Loop diuretics L p of Henle Hypokalemia
Ototoxicity
4. Potassium Distal tubule Hyperkalemia
sparing
5. Osmotic Glomerulus Hypovolemia &
diuretic hypotension
Diuretic class Special Uses
Diuretics Comparison
1. Carbonic Mountain sickness
anhydrase
inhibitor Meniere’s disease
2. Thiazide and Nephrolithiasis due to calcium
thiazide like stones
Hypocalcemia
3. Loop diuretics Hypercalcemia

4. Potassium CHF taking digoxin

sparing
5. Osmotic Increased ICP
diuretic
LITHIUM TOXICITY
Sympathoplegics
Sympathoplegics
• Centrally-acting
• Peripherally-acting
• Alpha-1 blockers
• Beta blockers
Centrally-Acting
Sympathoplegics
Centrally-Acting
Sympathoplegics
• MOA: act primarily within the CNS on
alpha-2 receptors to decrease
sympathetic outflow to the CVS

• Clonidine
• Methyldopa
• Guanfacine
• Guanabenz
Clonidine
• MOA: agonist at alpha-2 receptors
(leading to vasodilation)

• effective in patients with renal

impairment

• SE: transient increase in BP,

sedation/depression, rebound
hypertension on abrupt withdrawal
Methyldopa
• reduce TPR with little effect on CO
and blood flow to vital organs (such
as kidneys)

• effective for patients with renal

impairment
• used in the management of HTN in
pregnancy (pre-eclampsia,
eclampsia)
Methyldopa
• SE: sedation, depression,
hepatotoxicity (at doses >2g / day),
(+) Coomb,s Test*

* Coomb’s Test – indicator of a

possible immune-mediated hemolytic
anemia
Guanfacine, Guanabenz
• adjunctive therapy to other anti-
HTNsive drugs

• avoided unless necessary to treat

severe refractory HTN that is
unresponsive to other meds
Peripherally-Acting
Sympathoplegics
Peripherally-Acting
Sympathoplegics

• Trimethaphan
• Reserpine
• Guanethidine
• Guanadrel
Trimethaphan
• ganglionic receptor blocker

• given via IV infusion

• used in hypertensive emergencies

caused by pulmonary edema or aortic
aneurism when other agents cannot
be used
Reserpine
• plant alkaloid

• inhibits catecholamine (NE, Epi,

Dopamine, Serotonin) storage

• impairs sympathetic function because

of decreased release of
Norepinephrine (NE)
Guanethidine, Guanadrel
• inhibit the response of the adrenergic
nerve to stimulation or to indirectly-
acting sympathetic amines

• blocks the release of stored

Norepinephrine

• SE: orthostatic hypotension, impaired

male sexual function
Alpha-1 Blockers
Alpha-1 Blockers
• MOA: inhibit the alpha-1 receptors,
resulting to vasodilation of arteries
and veins

• Prazosin
• Doxazosin
• Alfazosin
• Terazosin
Alpha-1 Blockers
• alternative drugs for the management
of HTN esp among patients with BPH

• First-Dose Phenomenon:
– orthostatic hypotension
– syncope
– remedy: take the drug at bedtime, slow
increase in dose
Beta Blockers
Beta Blockers
• used for the initial therapy of HTN;
effective for patients with rapid resting
HR or concomitant IHD
• MOA
– Block stimulation of renin secretion
– Decrease contractility  decrease CO
– Decrease sympathetic output centrally
– Reduction in HR  reduced CO
– Combination of all
Beta Blockers
• SE/Precautions/Contraindications:
– can mask hypoglycemia
– CI to patients with bronchospastic
disease: COPD, Bronchial Asthma
– rebound tachycardia and HTN
– easy fatigability
– severe bradycardia and heartblock
(seen esp with concomitant use of
verapamil and diltiazem)
Beta Blockers
• Selective • Membrane Stabilizing
B – Betaxolol Activity
– Anesthetic-like effect
B – Bisoprolol
– Cannot be given as
E – Esmolol ophthalmic drops
A – Acebutolol P – Propranolol
A – Atenolol P – Pindolol
M – Metoprolol A – Acebutolol
L – Labetalol
M – Metoprolol
Beta Blockers
• Mixed alpha and • Intrinsic
beta blocking sympathomimetic
effect activity
– partial agonist effect
– not usually associated
L – Labetalol with rebound
C – Carvedilol hypertension
A – Acebutolol
B – Bisoprolol
C – Carteolol
P – Pindolol
P - Penbutolol
Nematodes (Roundworms)
Nematodes (Roundworms)
Vasodilators
Vasodilators
• second-line agents

• directly relax the peripheral vascular

smooth muscles

• not used alone  inc in plasma renin

activity, CO, HR
Vasodilators
• common SE: reflex tachycardia,
peripheral edema

• common CI: as single agents, should

be avoided in patients with Ischemic
Heart Disease (IHD)
Vasodilators
• Hydralazine
• Diazoxide
• Minoxidil
• Sodium Nitroprusside
Hydralazine
• used in the management of HTN in
pregnancy

• SE: Lupus-like side effect (drug-

induced SLE or Systemic Lupus
Erythematosus)
Diazoxide
• used in the emergency treatment of
hypertensive crisis
Minoxidil
• most effective arteriolar vasodilator

• SE: hypertrichosis, hirsutism

Sodium Nitroprusside
• metabolized in the body into nitric
oxide (NO) also called EDRF or
Endothelium-Derived Relaxing Factor

• 1st line drug for almost all types of

HTNsive emergencies
Sodium Nitroprusside
• Caution: use freshly prepared
solutions or admixtures

• protect from light

• SE: thiocyanate or cyanide toxicity,

acute psychosis, severe hypotension,
coma, death
Calcium Channel Blockers
Calcium Channel Blockers
(CCBs)
• alternative for the mgt of HTN

• MOA
– Inhibit influx of Ca through the slow
channels in vascular smooth muscle
and cause relaxation
Classification
• Dihydropyridine (DHP)
– block Ca channels in the blood vessels
– Nifedipine, Nicardipine, Felodipine,
Amlodipine

• Non-dihydropyridine (Non-DHP)
– block Ca channels both in the heart and blood
vessels
– Verapamil – heart > blood vessels
– Diltiazem – heart = blood vessels
Calcium Channel Blockers
(CCBs)
• SE:
– peripheral edema
– reflex tachycardia (DHP)
– bradycardia (Non-DHP)
– heart block (Non-DHP + Beta Blocker)
ACE Inhibitors
Angiotensin Converting Enzyme
Inhibitors
• MOA: inhibit ACE, thereby preventing the
conversion of angiotensin I into the active
form angiotensin II

• Short-acting
– Captopril
Generally, long acting ACE
• Long-acting Inhibitors are prodrugs:

– Enalapril Enalapril Enalaprilat

– Lisinopril (prodrug) (active)

– Perindopril
Angiotensin Converting Enzyme
Inhibitors
• SE:
– idiosyncratic dry cough
ACE
Bradykinin inactive
fragments
(causes cough)

– angioedema
– hyperkalemia
Angiotensin II Receptor
Blockers
Angiotensin II Receptor
Blockers (ARBs)

• direct inhibitors of angiotensin II receptors

• Losartan, Valdesartan, Candesartan

• clinical use: same as ACE Inhibitors

• Advantage over ACE inhibitors: less

associated with dry cough
1. A friend has very severe hypertension and asks
about a drug her doctor wishes to prescribe. Her
physician has explained that this drug is
associated with tachycardia and fluid retention (w/c
may be marked) and increased hair growth. Which
of the following is most likely to produce the effects
that your friend has described?
A. Captopril
B. Guanethidine
C. Minoxidil
D. Prazosin
E. Propanolol
2. A patient is admitted to the emergency
department with severe bradycardia following a
drug overdose. His family reports that he has been
depressed about his hypertension. Each of the
following can slow the heart rate EXCEPT

A. Clonidine
B. Guanethidine
C. Hydralazine
D. Propanolol
E. Reserpine
2. A patient is admitted to the emergency
department with severe bradycardia following a
drug overdose. His family reports that he has been
depressed about his hypertension. Each of the
following can slow the heart rate EXCEPT

A. Clonidine
B. Guanethidine
C. Hydralazine
D. Propanolol
E. Reserpine
2. A patient is admitted to the emergency
department with severe bradycardia following a
drug overdose. His family reports that he has been
depressed about his hypertension. Each of the
following can slow the heart rate EXCEPT

A. Clonidine
B. Guanethidine
C. Hydralazine
D. Propanolol
E. Reserpine
3. Which one of the following is characteristic of
enalapril treatment in patients with essential
hypertension?

A. Competitively blocks angiotensin II at its

receptor
B. Decreases angiotensin II concentration in the
blood
C. Decreases renin concentration in the blood
D. Increases sodium and decreases potassium in
the blood
E. Decreases sodium and increases potassium in
the urine
4. A pregnant patient is admitted to the
hematology service with moderately severe
hemolytic anemia. After a thorough workup, the
only positive finding is a history of treatment with
an antihypertensive drug since 2 months after
beginning the pregnancy. The most likely cause of
the patient’s blood disorder is
A. Atenolol
B. Captopril
C. Hydralazine
D. Methyldopa
E. Minoxidil
5. Postural hypotension is a common
adverse effect of which one of the
following types of drugs?

A. ACE inhibitors
B. Alpha receptor blockers
C. Arteriolar dilators
D. Beta-selective receptor blockers
E. Nonselective B-blockers
5. Postural hypotension is a common
adverse effect of which one of the
following types of drugs?

A. ACE inhibitors
B. Alpha receptor blockers
C. Arteriolar dilators
D. Beta-selective receptor blockers
E. Nonselective B-blockers
5. Postural hypotension is a common
adverse effect of which one of the
following types of drugs?

A. ACE inhibitors
B. Alpha receptor blockers
C. Arteriolar dilators
D. Beta-selective receptor blockers
E. Nonselective B-blockers
Congestive Heart Failure
Heart Failure
• is the failure of
the heart as a
pump
• inability of the
heart to pump
sufficient
amount of
blood to the
body
Congestive Heart Failure
• pumping ability of the heart becomes
impaired
• accompanied by congestion of body
tissues
• etiology
– acute MI, HPN, cardiomyopathies
– excessive work demands on the heart
Forms of CHF
• High-output • Low-output
– uncommon – caused by disorders
– caused by excessive that impair the
need for cardiac pumping ability of the
output heart (IHD)
– high metabolic – normal metabolic
demands demands, heart
unable to meet them
 Forms of CHF
• Right sided • Left-sided
– fatigue – exertional dyspnea
– jugular vein – paroxysmal nocturnal
distension dyspnea
– liver engorgement – cough
– blood-tinged sputum
– anorexia, GI distress
– cyanosis
– cyanosis
– pulmonary edema
– elevation in
peripheral venous
pressure
– peripheral edema
Treatment Goals
• To remove or mitigate the underlying
cause
• To relieve the symptoms and improve
pump
function by:
– Reducing metabolic demands (rest,
relaxation, pharm’l controls)
– Reduce fluid volume excess (food intake,
meds)
– Administer digitalis and other inotropic
agents
– Promote px compliance and self-regulation
through education
– Select appropriate px for cardiac transplants
Compensatory Mechanism
• Myocardial Hypertrophy
– long-term compensatory mechanism
– increase in the number of contractile
elements in myocardial cells as a means
of increasing their myocardial
performance
– ventricular remodeling
Compensatory Mechanism
• Frank-Starling Mechanism
– is the intrinsic ability of the heart to
adapt to changing volumes of inflowing
blood
– the greater the heart muscle is stretched
during filling, the greater the force of
contraction and the greater the quantity
of blood pumped into the aorta
– within physiologic limits, the heart
pumps all the blood that comes to it
without allowing excessive damming of
blood in the veins
Drugs for CHF
Drugs for CHF
• Inotropic Agents
– Cardiac glycosides
– Beta Agonists
– Phosphodiesterase Inhibitors
• Unloaders
– ACE Inhibitors & ARBs
– Beta Blockers
– Diuretics
– Vasodilators
Cardiac Glycosides
• from Digitalis species

• Digoxin, Digitoxin

• MOA: inhibit the Na-K-ATPase pump

leading to an increase in intracellular
calcium
Cardiac Glycosides
• Digoxin • Digitoxin
– ~75% Bioavailable – >90% Bioavailable
– half-life: 168 hours
– half-life: 36-40
– >90% protein bound
hours
– excreted in the bile
– 20-40% protein
bound
– excreted in the
urine
Cardiac Glycosides
- have low therapeutic indices
- toxicity can be enhanced by:
- hypokalemia
- hypomagnesemia
- hypercalcemia
Toxicity
• Cardiac Manifestations
– arrhythmias (ventricular tachycardia)
– cardiac death

• Extra-cardiac Manifestations
– GI disturbances (nausea & vomiting)
– visual disturbances (blurred vision,
alteration of color perception, haloes on
dark objects)
Management of Toxicity
• give potassium supplement

• give digitalis antibodies (FAB

fragments)

• for arrhythmias, give lidocaine or

amiodarone
Nematodes (Roundworms)
Nematodes (Roundworms)
Beta-1 Agonists
• Dopamine
• Dobutamine

• MOA: increase intracellular cAMP,

which results in the activation of
protein kinase, that leads to an
increase in intracellular calcium
Dobutamine
• given as an IV infusion

• primarily used in the management of

acute heart failure in the hospital
setting
Phosphodiesterase Inhibitors
• MOA: inhibits the enzyme
phosphodiesterase which hydrolyses
cAMP , thereby prolonging the action
of protein kinase

• Amrinone
• Milrinone
Unloaders
• ACE Inhibitors & ARBs
– preload and afterload unloaders
– vasodilating effect
– Captopril, Enalapril
• Beta Blockers
– vasodilating effect
– Carvedilol,labetalol
• Diuretics
– preload unloaders
– Spironolactone
• Vasodilators
– Hydralazine, Nitroprusside
1. Drugs that have been found to be useful in one
or more types of heart failure include all of the
following EXCEPT
A. Na+/K+ ATPase inhibitors
B. Alpha-adrenoceptor agonists
C. Beta-adrenoceptor agonists
D. ACE inhibitors
2. The mechanism of action of digitalis is
associated with

A. A decrease in calcium uptake by the

sarcoplasmic reticulum
B. An increase in ATP synthesis
C. A modification of the actin molecule
D. An increase in systolic intracellular calcium
levels
E. A block of cardiac B adrenoceptors
4. A 65-year old woman has been admitted to the
coronary care unit with a left ventricular myocardial
infarction. If this patient develops acute severe
heart failure with mark pulmonary edema, which
one of the following would be most useful?

A. Digoxin
B. Furosemide
C. Minoxidil
D. Propanolol
E. Spironolactone
6. Drugs associated with clinically useful or
physiologically important positive inotropic effects
include all of the following EXCEPT

A. Amrinone
B. Captopril
C. Digoxin
D. Dobutamine
E. Norepinphrine
7. Successful therapy of heart failure with digoxin
will result in which one of the following?

A. Decreased heart rate

B. Increased afterload
C. Increased aldosterone
D. Increased renin secretion
E. Increased sympathetic outflow to the heart
8. Which of the following has been shown to
prolong life in patients with chronic congestive
failure but has a negative inotropic effect on
cardiac contractility?

A. Carvedilol
B. Digoxin
C. Dobutamine
D. Enalapril
E. Furosemide
10. Which of the following is the drug of choice in
treating suicidal overdose of digitoxin?

A. Digoxin antibodies
B. Lidocaine
C. Magnesium
D. Phenytoin
E. Potassium
Coronary Artery Diseases
(CAD)
or
Ischemic Heart Diseases
(IHD)
Coronary Artery Diseases
Coronary Artery Diseases
• occur when the
coronary arteries
become so narrowed
by atherosclerosis
that they are unable
to deliver sufficient
blood to the heart
muscle
– Localized areas of
thickened tunica
intima associated with
accumulation of
smooth muscle cells
and lipids, principally
cholesterol
Coronary Artery Diseases
• Angina Pectoris
– episodic, reversible oxygen insufficiency
– severe chest pains generally radiating to the left
shoulder and down the inner side of the arm
– usually precipitated by physical exertion or emotional
stress

• Myocardial Ischemia
– deprivation of oxygen to a portion of the myocardium
(reversible)
• Myocardial Infarction
– severe, prolonged deprivation of oxygen to a portion
of the myocardium that leads to myocardial tissue
necrosis (reversible)
Risks Factors
• Smoking
• Hypertension
• Diabetes Mellitus
• Males >45 yo; Females >55 yo
• Dyslipidemia
• Obesity
• Family history of CAD
• Others:
– sedentary lifestyle, hx of chronic inflammation
Etiology
• Decreased blood flow
– Atherosclerosis – most common cause
– Coronary artery spasm – sustained
contraction of 1 or more coronary arteries 
Prinzmetal’s angina or MI
– Traumatic injury – that interferes with blood
flow in the heart
– Embolic events – can abruptly restrict oxygen
supply
• Increased oxygen demand
– Exertion and emotional stress  sympathetic
stimulation  increase HR
• Reduced blood oxygenation
– Reduced O2-carrying capacity (anemia)
Angina Pectoris
• chest pain

• a symptom of myocardial ischemia in

the absence of an infaction
Angina Pectoris
• Types:
– Stable Angina
• aka: Classical Angina
• develops on exertion and lasts for < 5 min
• relieved with rest or drugs
• mechanism: imbalance oxygen supply

– Unstable Angina
• can be experienced at rest, or with increasing
severity for the last 1-2 months or a new chest pain
for < 1 month
• mechanism: thrombosis
Angina Pectoris
• Types:
– Angina Decubitus
• nocturnal angina
• occurs in recumbent position

– Prinzmetal Angina
• aka: Variant Angina
• precipitated by coronary artery spasm
Drugs for Angina Pectoris
• Nitrates
• Beta Blockers
• Calcium Channel Blockers
Nitrates
• MOA: metabolized into NO in the
body, leading to peripheral
vasodilation
• examples
– amyl nitrite
– nitroglycerin
– isosorbide dinitrate (ISDN)
– isosorbide mononitrate (ISMN)
• SE:
– throbbing headache, tolerance
Nitrates
• MOA
– Decrease oxygen demand and facilitate
coronary blood flow
– converted to nitric oxide intracellularly which
activates guanylate cyclase  increase
cGMP  dephosphorylation of myosin
light chain  relaxation of vascular smooth
muscle  vasodilation
• Important SE
– HEADACHE – most common side effect
– Tolerance (“Nitrate-free interval”)
– Postural hypotension, facial flushing, reflex
tachycardia
Beta Blockers
• drug of choice for stable angina

• MOA: decreases HR & contractility 

reduce oxygen demand (rest and
during exertion)  reduce arterial BP
CCBs
• MOA
– inhibits calcium influx into vascular smooth
muscle & heart muscles  increased blood
flow  enhance oxygen supply  prevent
and reverse coronary spasm
– dilates peripheral arterioles & reduce
contractility  reduce total peripheral vascular
resistance  reduced oxygen demand
• Indications
– Stable angina not controlled by nitrates & beta
blockers; px who could not take beta blockers
– Prinzmetal’s angina (with or without nitrates)
– DOC of angina at rest
Other Agents
• Morphine
– Unstable angina with no CI; IV doses
given after 3 sublingual nitroglycerin
tabs have failed to relieve pain
• Aspirin
– Indefinite in px with stable or unstable
angina
• Heparin, Enoxaparin, Dalteparin
– Together with aspirin  hospitalized px
with unstable angina until resolved
Myocardial Infarction
Myocardial Infarction (MI)
– Results from prolonged myocardial
ischemia, precipitated in most cases by
an occlusive coronary thrombus at the
site of a pre-existing atherosclerotic
plaque
Note:
Damage on myocardial tissue
Cellular not reversible 
ischemia ismyocardial tissue dies
Tissue injury
Tissue necrosis
Myocardial Infarction (MI)
Myocardial Infarction (MI)
• persistent, severe chest pain or
pressure  “crushing”, “squeezing” or
heavy “an elephant sitting on the
chest”
Signs and Symptoms of MI
• Compared to angina
– Pain persists longer
– Not relieved by rest or nitroglycerin
– Sense of impending doom, sweating, nausea,
vomiting, difficulty in breathing; some px 
fainting and sudden death
– Extreme anxiety, restlessness, ashen pallor
• Some px:
– Mild or indigestion-like pain, manifest in
worsening CHF, loss of consciousness, acute
confusion, dyspnea, sudden drop in BP, lethal
arrhythmia
 IMMEDIATE TREATMENT FOR
MYOCARDIAL INFARCTION

M MORPHINE

OXYGEN
O
NITROGLYCERINE
N ASA
Drugs for MI
Drugs for MI
• Nitrates
• Oxygen
• Morphine
• Thrombolytic Agents
Oxygen
• for patients who have chest pain and
who may be ischemic
• improve oxygenation of myocardium
Morphine
• MOA
– causes venous pooling and reduces preload,
cardiac workload, and oxygen consumption
– IV until pain is relieved
• Indication
– DOC for MI pain and anxiety
• Precautions
– can produce orthostatic hypotension and
fainting
– monitor for hypotension & signs of resp
depression
– GI SE: nausea and vomiting; constipation
Thrombolytic Agents
• MOA:
– Lysis of thrombus clot
• The following are given IV within 12 h to
restore normal blood flow in an acute MI:
– Recombinant t-PA (recombinant tissue-type
plasminogen activator
– alteplase
– Streptokinase
– Anisoylated plasminogen streptokinase
activator complex (APSAC)
– Reteplase
– Tenecteplase
Post thrombolysis adjunctive
therapy
• Aspirin
– prevents platelet aggregation; shown to
reduce post-infarct mortality
– also: dipyridamole, ticlopidine, clopidogrel
• Heparin
– prevent re-occlusion once a coronary artery
has been opened
– not used with streptokinase  increased risk
of hemorrhage
• Warfarin
– reduce mortality, prevent recurrent MI
Post thrombolysis adjunctive
therapy
• Beta Blockers
– if administered early  reduce ischemia,
reduce potential zone of infarction, decrease
oxygen demands, preserve left ventricular
function, decrease cardiac workload
• ACE Inhibitors
– improve exercise capacity and reduce
mortality in px with CHF; aid in the prevention
of progressive ventricular remodelling
• “Statins”
– reduced mortality due to MI when used by px
to aggressively lower cholesterol
Post thrombolysis adjunctive
therapy
• Lidocaine
– used for px who develop ventricular
arrhythmia
• Calcium Channel Blockers
– decrease incidence of reinfarction in px
with non-Q-wave infarcts; not for acute
mgt.
Items 1-3. Mr. Green, 60 years old, has
severe chest pain when he attempts to carry
parcels upstairs to his apartment. The pain
rapidly disappears when he rest. A decision
is made to treat him with nitroglycerin.
2. In advising Mr. Green about the adverse effects
he may notice, you point out that nitroglycerin in
moderate doses often produces certain symptoms.
These toxicities result from all of the following
EXCEPT

A. Meningeal vasodilation
B. Reflex tachycardia
C. Hypotension
D. Methemoglobinemia
3. 2 years later, Mr. Green returns complaining
that his nitroglycerin works well when he takes it
for an acute attack but that he is having frequent
attacks now and would like something to prevent
them. Useful drugs for the prophylaxis of angina of
effort include which one of the following?

A. Amyl nitrite
B. Diltiazem
C. Sublingual isosorbide dinitrate
D. Sublingual nitroglycerin
4. The antianginal effect of propanolol may be
attributed to which one of the following?

A. Block of exercise-induced tachycardia

B. Decreased end-diastolic ventricular volume
C. Dilation of constricted coronary vessels
D. Increased cardiac force
E. Decreases heart rate
5. The major common determinant of myocardial
oxygen consumption is

A. Blood volume
B. Cardiac output
C. Diastolic blood pressure
D. Heart rate
E. Myocardial fiber tension
6. You are considering therapeutic options for a
new patient who presents with hypertension and
angina. In considering adverse effects, you note
that an adverse effect which nitroglycerin,
prazosin, and ganglion blockers have in common
is

A. Bradycardia
B. Impaired sexual function
C. Lupus erythematosus syndrome
D. Orthostatic hypotension
E. Throbbing headache
7. A patient is admitted to the emergency
department following a drug overdose. He is noted
to have severe tachycardia. He has been receiving
therapy for hypertension and angina. A drug that
often causes tachycardia is

A. Diltiazem
B. Guanethidine
C. Isosorbide dinitrate
D. Propanolol
E. Verapamil
Arrhythmias
Arrhythmias

• deviations from normal heartbeat

pattern
– abnormalities in impulse formation
– conduction disturbances
Arrhythmias
• The heart is endowed with a
specialized electrogenic system for:
– Generating rhythmical impulses to
cause rhythmical contraction of the
heart muscle
– Conducting these impulses rapidly
throughout the heart
Cardiac Conduction System
• Sinoatrial node
– Pacemaker of the heart
– 60 – 100 beats/min
– Location: posterior wall of the right atrium
near the entrance of the superior vena cava
• Atrioventricular node
– Location: posterior septal wall of the right
atrium immediately behind the tricuspid valve
– Connects the atrial and ventricular conduction
systems
Cardiac Conduction System
• Bundle of His (AV bundle)
– Delayed transmission
• Delays in transmission provide mechanical
advantage  atria complete ejection of
blood before initiating ventricular
• Purkinje system
contraction
– Supplies the ventricles
– Has large fibers that allow for rapid conduction and
almost simultaneous excitation of the entire left and
right ventricles
– Rapid rate of ejection is necessary for the swift and
efficient ejection of blood from the heart
Cardiac Conduction System
Myocardial Action Potential
• electric current generated by nerve
and muscle cells

• involve movement or flow of

electrically charged ions at the level
of the cell membrane
Myocardial Action Potential
Resting Membrane Potential
• membrane is
relatively permeable
to K+
• charges of opposite
polarity become
aligned along the
membrane
(+)  outside
(-)  inside
Depolarization
• cell membrane
suddenly becomes
selectively
permeable to
current-carrying ions
such as Na+
• Na+ enters cell 
sharp rise of
intracellular potential
to positivity while K+
migrate outside
 Repolarization
• re-establishment of
the resting potential
• slower process;
increased
permeability to K+ 
K+ ions move outward
 removes (+)
charges inside the
cell
– The Na-K pump
helps to preserve
the intracellular
Myocardial Action Potential
• Five Phases:
Phase 0: Rapid Depolarization
Phase 1: Early Rapid Repolarization
Phase 2: Plateau Phase of
Repolarization
Phase 3: Final Rapid Repolarization
Phase 4: Slow Depolarization
Myocardial Action Potential
Myocardial Action Potential
Electrocardiography (ECG)
• A recording of the electrical activity of
the heart during depolarization-
repolarization
– P wave
• SA node and atrial depolarization
– QRS complex
• Ventricular depolarization
– T wave
• Ventricular repolarization
Electrocardiography (ECG)
– Isoelectric line between P wave & Q
wave
• Depolarization of the AV node, bundle
branches, Purkinje system
– ST segment
• Absolute refractory period; part of
ventricular repolarization
– Atrial repolarization occurs during
ventricular depolarization and is hidden
in the QRS complex.
Cardiac arrhythmia may
cause the heart to
• To beat too slowly
• To beat too rapidly
• To respond to impulses originating from
sites other than the SA node
• To respond to impulses travelling along
extra pathways
CAUSES OF ARRHYTHMIA
• Abnormal automaticity
• Effect of drug
• Abnormalities in impulse conduction
Electrocardiography (ECG)
Action Potential & ECG
Classification of Arrhythmias
• By origin
– Supraventricular arrhythmia
• Stem from enhanced automaticity of the SA
node or from re-entry conduction

– Ventricular arrhythmia
• Occur when an ectopic pacemaker triggers
a ventricular contraction before the SA
node fires
Normal ECG Pattern
ECG Patterns of Arrhythmias
Anti-arrhythmic Agents
 •Quinidine
Antiarrhythmics Class IA •Procainamide
•Disopyramide

Sodium Channel Blockers •Lidocaine

•Tocainide
Class IB •Mexiletine
•Phenytoin
•Flecainide
Class IC •Propafenone
•Moricizine
•Propranolol
Beta Adrenergic Blockers Class II •Esmolol
•Acebutolol

•Amiodarone
Potassium Channel Blockers Class III •Sotalol
•Bretylium

•Verapamil
Calcium Channel Blockers Class IV •Diltiazem
CLASS 1A
• Slows phase 0 depolarization
• Prolong action potential
• Slow conduction
CLASS 1B
• Shortens phase 3 repolarization
• Decrease duration of action potential
CLASS 1C
• Markedly slow phase 0 depolarization
CLASS II
• Suppresses phase 4 depolarization
CLASS III
• Prolongs phase 3 repolarization
CLASS IV
• Slows phase 4 spontaneous
depolarization
• Shorten action potential
Miscellaneous Agents
• Adenosine
• MgSO4
TYPE OF ARRHYTHMIA
AND DRUGS
• Atrial flutter
• Class 1 – quinidine
• Class II - propranolol
• Class IV – verapamil
• Others - digoxin
• Atrial fibrillation
• 1- quinidine
• 2- propranolol
• 3- amniodarone
• 4 – anticoagulant
• AV –NODAL REENTRY
• PROPRANOLOL
• VERAPAMIL
• DIGOXIN
• ACUTE SUPRAVENTRICULAR
TACHYCARDIA
• Verapamil
• adenosine
• ACUTE VENTRICULAR TACHYCARDIA
• Lidocaine
• Sotalol
• Amniodarone
• VENTRICULAR FIBBRILLATION
• Lidocaine
• Bretylium
• Amnidarone
• epinephrine
Procainamide
• can cause SLE (Systemic Lupus
Erythematosus)
Quinidine
• drug interaction with digoxin
• can increase serum levels of digoxin
by at least 2x
Lidocaine
• anesthetic
• DOC for digitalis-induced arrhythmias
Propafenone
• for acute atrial fibrillation
Amiodarone
• iodine-containing molecule
• first-line treatment for almost all types
of Ventricular Tachycardia and Atrial
Fibrillation
Verapamil
• alternative for acute SVT
(Supraventricular Tachycardia)
Adenosine
• first-line drug for acute SVT
Drugs for Coagulation
Disorders
Clotting Mechanism
• inciting event: epithelial vascular injury
• followed by:
– migration of platelets to the site of injury
– platelet aggregation
• aka: primary hemostasis
• white thrombus
• platelet plug
• unstable clot
– deposition of fibrin over the plug
– attachment of other blood cells
• aka: secondary hemostasis
• red thrombus
• stable clot
Clotting Mechanism
• thrombus
– clot that adheres to a blood vessel wall

• embolus
– detached thrombus
Clotting Mechanism
• the coagulation process that
generates thrombin that is essential in
the formation of fibrin used in clot
formation involves coagulation
cascade
Coagulation Cascade
Drugs for Coagulation
Disorders
Anticoagulants

Anti-Platelet Drugs

Fibrinolytic Agents

Pro-coagulant Drugs
Anticoagulants
Anticoagulants
• Site of action
– synthesis of or directly against clotting factors
(II, IIa)

• Types:
– Parenteral
• Hirudin, Heparin
– Oral
• Dicumarol, Warfarin
Parenteral Anticoagulants
Hirudin
• obtained from medicinal leeches
(Hirudo medicinalis)

• used in the management of HIT

(Heparin-Induced Thrombocytopenia)

• Lepirudin – produced by recombinant

DNA technology
Heparin
• heterogeneous mixture of sulfated
mucopolysaccharides
– Regular or Unfractionated heparin
• activates antithrombin III which in turn
inactivates thrombin (IIa); Ixa, Xa, Xia
• SQ/IV
– Low MW Heparin
• Inactivates IIa and Xa
• Enoxaparin,fraxiparin,dalteparin
• SQ
Heparin
• Clinical use
– initiation of anticoagulant therapy
– mgt of MI or unstable angina
– tx & prevention of pulmonary embolism
& DVT
– anticoagulation in pregnancy (APAS)
• SE:
– hemorrhage (monitor aPTT – activated
partial thromboplastin time) 2-2.5x or
delay of 50 – 80 secs except SQ
– Thrombocytopenia
CONTRAINDICATIONS
• Hypersensitivity
• Active bleeding
• Thrombocytopenia
• Severe HPN
• Active TB
Oral Anticoagulants
• DICUMAROL
• aka: bis-hydroxycoumarin
• high incidence of GI side-effects
• PHENPROCOUMON
• INDANEDIONES ex:
anisindione,phenindione
• WARFARIN
• MOA: blocks carboxylation of X, IX,VII,II
• ONSET: 8 – 12 hrs maximum after 1 to
3days
• delay in the anticoagulant effect
• Clinical use
– Chronic anticoagulation (DVT prophylaxis,
cardiac thrombus, prosthetic heart valves)
• SE:
– Hemorrhage
• Monitor PT (Prothrombin Time) and INR
(International Normalized Ratio)
• Goal for INR = 2-3
• <2  insufficient dose
• >3  x’sive dose
• With prosthetic heart valves INR goal = 3-4
SE:
• Hemorrhagic dse of the newborn
• Teratogenic: abnormal bone formation
• Cutaneous necrosis
• Purple toe syndrome
• Alopecia, urticaria,dermatitis
Anti-Platelet Drugs
Anti-Platelet Drugs
• Thromboxane Synthesis Inhibitors
• Phosphodiesterase Inhibitors
• ADP Inhibitors
• Glycoprotein IIb/IIIa Inhibitors
Thromboxane Synthesis
Inhibitors
• Irreversibly acetylates COX- inhibition
of TXA2 synthesis, lasts for 8 – 10
days

• Aspirin
– primary prophylaxis for MI
– secondary prophylaxis for MI and stroke
Phosphodiesterase Inhibitors
• Dypiridamole
– given together with antiplatelet;
ineffective when alone
– Inc CAMP
– SE: coronary steal phenomenon
ADP Inhibitors -
Thienopyridines
• Ticlopidine
– SE: thrombocytopenia
purpura,neutropenia,
– n/v,diarrhea

• Clopidogrel
– safer than ticlopidine
Glycoprotein Inhibitors
• Abciximab
• Eptifibatide
• Tirofiban
Fibrinolytic Agents
Fibrinolytic Agents /
Thrombolytics
• MOA
– catalyse activation of plasminogen to
plasmin(serine protease)
• Use
– mgt of severe pulmonary embolism
– heart attack, acute MI,DVT
• Ex
– Streptokinase – destroy fibrin that is either
bound to clots or is in the unbound form
– Tissue plasminogen activator – binds to fibrin
bound to a clot
– Anistreplase (APSAC)
Pro-coagulant Drugs
Pro-coagulant Drugs
• Mgt of bleeding disorders
– Vitamin K
• K1 – phytonadione (in plants, useful
clinically)
• K2 – menaquinone (intestinal bacteria)
• K3 – menadione (synthetic)
• used for Vit. K deficiency; hemorrhagic
disorders in newborns
– Aminocaproic Acid
• prevents activation of plasminogen
– Tranexamic Acid (analogue)
Drugs for Dyslipidemia
Dyslipidemia
• Hypercholesterolemia (inc LDL, dec
HDL)
• Hypertriglyceridemia (inc TG, ~ inc
VLDL, chylomicrons)
• Liver
– Only organ in the body that efficiently
uses cholesterol
• Converts it to bile salts
 Cholesterol Synthesis
HMG-CoA
Reductase
HMG-CoA Mevalonate Cholesterol

Cholesterol Source
hydroxymethylglutaryl-
Coenzyme A (HMG-CoA) –Diet (exogenous)
–Endogenous
Atherosclerosis
Condition
associated with
cholesterol
deposition in
vascular smooth
muscles (arthroma)
with consequent
narrowing of the
lumen of the
affected blood
Atherosclerosis
• Could lead to…
– CAD
– Cerebrovascular disease
– Aortic disease
– Renal artery disease
Atherosclerosis
• Major Risk factors
• Minor Risk Factors
– Age (males: > 45;
– Chronic infection
females: > 55)
– Sedentary lifestyle
– Smoking
– DM • Modifiable Risk
– HPN Factors
– Dyslipidemia – By therapy
– Obesity – By lifestyle change

– Family history of
premature heart
attack
Drugs for Dyslipidemia
• HMG-CoA Reductase Inhibitors
• Nicotinic Acid
• Bile Acid Sequesterants
• Fibric Acid Derivatives
• Probucol
HMG-CoA Reductase
Inhibitors
• “-statins”

• MOA: inhibit the enzyme HMG-CoA

Reductase, thereby inhibiting the first
step (rate-limiting step) in cholesterol
synthesis

• first-line drugs for dyslipidemia

HMG-CoA Reductase
Inhibitors
• Diurnal Pattern of Cholesterol
Synthesis
– means that the biosynthesis of
cholesterol in the body occurs at night
– thus most statins are given at bedtime
(esp the short-acting ones)
HMG-CoA Reductase
Inhibitors
• Short-acting
– simvastatin
– lovastatin
– fluvastatin
• Long-acting
– atorvastatin
– rosuvastatin Long-acting statins can
be given any time of
the day.
HMG-CoA Reductase
Inhibitors
• SE:
– hepatotoxicity
– myositis
– rhabdomyolysis (muscle wasting)
Nicotinic Acid

• MOA: In adipose tissue, niacin inhibits the

lipolysis of triglycerides by hormone-
sensitive lipase, which reduces transport
of free fatty acids to the liver and
decreases hepatic triglyceride synthesis
Nicotinic Acid

• used in the management of

hypertriglyceridemia

• SE: flushing (due to percutaneous

vasodilation), myositis
Bile Acid Sequesterants
• aka: Bile Acid – Binding Resins

• MOA: Inhibit reabsorption of bile acid

• since liver must maintain a certain

amount of bile, it will synthesize bile
from endogenous cholesterol when
bile levels go low
Bile Acid Sequesterants
• Cholestyramine
• Colestipol

• SE:
– constipation
– impaired absorption of certain drugs
– may increase incidence / risk of biliary
stone formation
Fibric Acid Derivatives
• MOA: stimulate lipoprotein lipase
which decreases triglycerides

• first-line drug in hypertriglyceridemia

• Gemfibrozil
• Fenofibrate
• Clofibrate (withdrawn)
Fibric Acid Derivatives
• SE:
– myositis
– rhabdomyolysis
– increase risk of bile stone formation
– hepatobiliary cancer (Clofibrate)
Probucol
• MOA: anti-oxidant

• SE:
– increase risk of arrhythmia
– produces fetid odor
Ok, before we end our
lecture, quiz muna tayo…

Question 1:
• Which enzyme is responsible for the
conversion of Angiotensin I into the
active form Angiotensin II?
A. Renin
B. ACE
C. HMG-CoA
D. Streptokinase B
Question 2:
• A 55 y/o male patient was
diagnosed to have uncomplicated
HTN. Which of the following drugs
would most likely be given to him?
A. Thiazide diuretic + Beta Blocker
B. ACE Inhibitor
C. CCB + ACE Inhibitor
D. ACEi + ARB A
Question 3:
• From the list of anti-hypertensive
drugs below, select the one most
likely to lower blood sugar:
A. Prazosin
B. Nifedipine
C. Propranolol
D. Hydralazine
C
E. Labetalol
Question 4:
• Which of the following conditions
predisposes a patient taking digitalis
into arrhythmia?
A. hypocalcemia
B. decreased heart rate
C. hyponatremia
D. hypokalemia D
Question 5:
• All of the following mechanisms of
action correctly match a drug,
EXCEPT:

A. Quinidine: blocks Na+ channels

B. Bretylium: blocks K+ channels
C. Propranolol: blocks β-receptors
D. Procainamide: Dblocks K+ channels
Question 6:
• Which of the following adverse
effects is associated with nitrates?
A. nausea
B. throbbing headache
C. sexual dysfunction
D. anemia
B
Question 7:
• A patient experienced orthostatic
hypotension after taking the first
dose of her drug. She most likely
took:
A. Labetalol
B. Valdesartan
C. Prazosin
C
D. Digoxin
Question 8:
• Mrs. G. R. is a hypertensive patient
under therapy. After some time, she
developed Lupus-like symptoms.
Which of the ff drugs may have
cause this?
A. Hydralazine
B. Losartan
C. Furosemide A
Question 9:
• Which of the following antagonizes
the co-factor functions of Vitamin K?
A. Tranexamic acid
B. Heparin
C. Warfarin
D. Hirudin
C
Question 10:
• The following drugs for dyslipidemia
can cause rhabdomyolysis,
EXCEPT:
A. simvastatin
B. atorvastatin
C. colestipol
C
D. fenofibrate
 “The only thing greater than the
power of the mind is the courage of
the heart.”
- from the movie, A Beautiful Mind