CMED 214 | Trans 019

Pharmacology: Antihypertensive Drugs

Dr. Christian James A. Amil | December 5, 2022

OUTLINE normal for adults is less than 120 mmHg systolic and less
1. Hypertension 4. Sympathetic nervous system than 80 mmHg diastolic. Take note of the qualifier “and” and “less
A. Causes 5. Inhibitors of Angiotensin
B. Primary vs Secondary
than”.
6. JNC 8: Hypertension Treatment
C. Urgency vs Emergency if new patient comes to clinic and gets 140/100 BP, is that
D. Guidelines 2017 ACC/AHA already stage 1? NO. It should base on 2 careful readings on at
E. When to start pharma
treatment? least 2 occasions.
2. Basic Pharmacology of
Antihypertensive Agents Computation: BP= CO x PVR
3. Diuretics
C. Hypertensive Urgency vs Hypertensive Emergency
I. HYPERTENSION 1. Hypertensive Emergency
• Most common cardiovascular disease • Severe elevations in BP (>180/120 mmHg) associated with
• 60-80% of both men and women will develop hypertension by evidence of new or worsening target organ damage
age 80 Target organ damage = hypertensive encephalopathy, ICH,
• Usually asymptomatic until overt end-organ damage is acute ischemic stroke, acute MI, acute LV failure with pulmonary
imminent or has already occurred edema, unstable angina, dissecting aortic aneurysm, acute
• The diagnosis of hypertension depends on measurement of renal failure, eclampsia.
blood pressure and not on symptoms reported by the patient Treatment:

A. Causes of Hypertension • Admission to an intensive care unit is recommended for

1. Genetic Predisposition continuous monitoring of BP and target organ damage and for
2. Environmental Risk Factors parenteral administration of an appropriate agent.
o Overweight and Obesity : or coronary care unit, if available
o Sodium and Potassium Intake
o Sedentary lifestyle 2. Hypertensive Urgency
o Alcohol • Severe elevations in BP (>180/120 mmHg) associated
B. Primary vs Secondary Hypertension WITHOUT acute or impending change in target organ
1. Primary Hypertension damage or dysfunction.
• No specific cause of the hypertension could be found • Usually, these patients have withdrawn from or noncompliant
• Also referred to as essential hypertension with antihypertensive therapy and do not have clinical or
: This is the common form that we see from our tito/tita. laboratory evidence of target organ damage.
3. Secondary Hypertension Treatment:
• Hypertension due to a specific etiology (e.g. due to Cushing’s • Reinstitution/intensification of antihypertensive drug therapy
disease, pheochromocytoma) o counsel the patient to comply with medicine. If did not
occurs if you have underlying condition that causes you to yet receive any medicate, give anti-hypertensive drug.
manifest with increased blood pressure. Examples are Cushing’s Which one will you choose?
disease, pheochromocytoma, hyperthyroidism (very common). o Treatment of anxiety, if applicable
• NO INDICATION FOR:
o Referral to ER
o Immediate BP reduction in the ER
example is Catapres
o Confinement
you should have indication for admission

Table 1: Categories of Blood Pressure in Adults

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D. Insights from the 2017 ACC/AHA Guidelines on

Hypertension
A. Historical features Favoring Hypertension Cause

B. Frequency Used Medications and Other Substance that may cause Elevated BP

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C. Checklist of Accurate Measurement of BP

D. Procedure for Use of Home Blood Pressure Monitor (HBPM)

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Table 3: Selection Criteria for BP Cuff Size for Measurement of BP

in Adults

Table 2: CVD Factors Common in Patients with Hypertension

E. Best Proven Nonpharmacological Intervention for Prevention and Treatment Hypertension

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• Effective in lowering blood pressure by 10–15 mm Hg in most

patients
• Often provide adequate treatment for mild or moderate essential
hypertension.
especially if patient is compliant.

Table 4: Basic and Optional Laboratory Tests for Primary

Hypertension
E. When to Start Pharmacologic Treatment?
• According to JNC Guidelines 8:
o In the general population, pharmacologic treatment should
be initiated when blood pressure is 150/90 mm Hg or
higher in adults 60 years and older, or 140/90 mm Hg or
higher in adults younger than 60 years.
o In patients with hypertension and diabetes, pharmacologic
treatment should be initiated when blood pressure is
140/90 mm Hg or higher, regardless of age.
o Initial antihypertensive treatment should include a thiazide Figure 1: Types of Diuretics and Part of Nephron they Act on
diuretic, calcium channel blocker, ACE inhibitor, or ARB in
the general nonblack population or a thiazide diuretic or A. Thiazide Diuretics
calcium channel blocker in the general black population. one of first-line treatment for hypertension. There are four
o If the target blood pressure is not reached within one month
after initiating therapy, the dosage of the initial medication groups: Thiazide diuretics, ACE inhibitor, Calcium channel
should be increased, or a second medication should be blockers, and ARBs. Why 4? Because they are known to reduce
added. mortality due to hypertension and heart disease. Not just lower BP
but reduce mortality or chance of dying due to hypertension.
II. BASIC PHARMACOLOGY OF ANTIHYPERTENSIVE AGENTS
• Diuretics • Inhibit NaCl transport by blocking the Na+/Cl- transporter,
o Lower blood pressure by depleting the body of predominantly in the PCT (Proximal convoluted tubule)
sodium and reducing blood volume and perhaps by • Enhance Ca2+ absorption
other mechanisms • Rarely causes hypercalcemia, but may mask hypocalcemia due
• Sympathoplegic Agents to other causes (e.g. in hyperparathyroidism, carcinoma,
o Lower blood pressure by reducing peripheral sarcoidosis)
vascular resistance, inhibiting cardiac function, and • Sometimes useful in the prevention of calcium-containing kidney
increasing venous pooling in capacitance vessels. stones caused by hypercalciuria and modestly reduce the risk of
(The latter two effects reduce cardiac output.) osteoporotic fractures.
• Direct Vasodilator
• these are off-label uses.
o Reduce blood pressure by relaxing vascular
smooth muscle, thus dilating resistance vessels • Prototype drug: Hydrochlorothiazide (HCTZ)
and—to varying degrees—increasing capacitance • you will usually see this with other antihypertensive
as well medications because the effect is only modest.
• Agents that Block Production/Action of Angiotensin
o Reduce blood pressure by peripheral vascular
• Others: Chlorthalidone (only thiazide diuretic that can be given
parenterally)
resistance and (potentially) blood volume
INDICATIONS:
III. DIURETICS • Hypertension
• Lower blood pressure primarily by depleting body sodium • Heart failure
stores • Nephrolithiasis due to idiopathic hypercalciuria
where sodium goes, water follows. • Nephrogenic diabetes insipidus
• Reduce blood pressure by reducing blood volume and cardiac TOXICITY:
output • Hyperchloremic metabolic acidosis

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what is the acid base disorder associated with thiazide diuretics? • May slow the progression of albuminuria in diabetic patients and
Hyperchloremic metabolic acidosis may reduce myocardial perfusion defects after myocardial
• Impaired carbohydrate tolerance infarction.
o Hyperglycemia in patients who are overtly diabetic or mildly
abnormal glucose tolerance tests. Usually seen at higher 3. AMILORIDE
doses of HCTZ (>50 mg/d). Due to both impaired • Direct inhibitors of Na+ influx in the CCT
pancreatic release of insulin and diminished tissue • Used in Liddle’s syndrome nephrogenic diabetes insipidus
utilization of glucose. • LIDDLE’S SYNDROME
• Hyperlipidemia
o rare autosomal dominant disorder that results in activation
o 5–15% increase in total serum cholesterol and low density
lipoproteins (LDLs). of sodium channels in the cortical collecting ducts, causing
• Hyponatremia increased sodium reabsorption and potassium secretion
• Impaired uric acid metabolism and gout by the kidneys
avoid for patients with known gout. Be mindful of these, especially IV. DRUGS THAT ALTERS SYMPATHETIC NERVOUS SYSTEM
in prescription writing.
FUNCTION
B. Potassium-Sparing Diuretics
The cardiovascular system is also regulated by the nervous
why are these important? the most common problem with
system especially the vascular tone and the heart rate.
diuretics is hypokalemia (potassium wasting). How does
hypokalemia manifest? Weakness, muscle paralysis. • All of the agents that lower blood pressure by altering
sympathetic function can elicit compensatory effects through
• Prevent K+ secretion by antagonizing the effects of aldosterone
mechanisms that are not dependent on adrenergic nerves.
in collecting tubules
• The antihypertensive effect of any of these agents used alone
• Most useful in states of mineralocorticoid excess or may be limited by retention of sodium by the kidney and
hyperaldosteronism (also called aldosteronism), due either to expansion of blood volume
primary hypersecretion (Conn’s syndrome, ectopic
• Thus, sympathoplegic antihypertensive drugs are most effective
adrenocorticotropic hormone production) or secondary
when used concomitantly with a diuretic
hyperaldosteronism (evoked by heart failure, hepatic cirrhosis,
• CENTRALLY ACTING SYMPATHOPLEGICS: Clonidine,
nephrotic syndrome, or other conditions associated with
Methyldopa
diminished effective intravascular volume)
• ADRENERGIC NEURON-BLOCKING AGENTS:
MOA: Guanethidine, Reserpine
• Antagonism of mineralocorticoid (aldosterone receptors): • ADRENORECEPTOR ANTAGONISTS: Beta-blockers, Alpha1
Spironolactone, Eplerenone Blockers
remember Spironolactone because this is the most important These drugs are not considered first line agents for hypertension
potassium-sparing diuretic. because they have no evidence to lower mortality.
• Inhibition of Na+ influx channels in the luminal membrane:
A. Centrally Acting Sympathoplegic Drugs
Amiloride, triamterene • Reduce sympathetic outflow from vasomotor centers in the brain
• Others: Ularitide, Nesiritide (IV form only) stem but allow these centers to retain or even increase their
TOXICITY sensitivity to baroreceptor control
• Hyperkalemia • E.g. Methyldopa, Clonidine
do not give this medication if the patient is receiving potassium 1. METHYLDOPA
supplement • Analog of L-dopa and is converted to α-methyldopamine and α-
• Hyperchloremic metabolic acidosis methylnorepinephrine antihypertensive
• Gynecomastia – adverse effect of Spironolactone
• Action appears to be due to stimulation of central α
• Acute renal failure (in triamterene with indomethacin) o Kidney
stones (triamterene) adrenoceptors by α-ethylnorepinephrine or α-methyldopamine
• Lowers blood pressure chiefly by reducing peripheral vascular
1. SPIRONOLACTONE resistance, with a variable reduction in heart rate and cardiac
2. Competitive antagonist to aldosterone
output
3. Binds with high affinity and potently inhibits the androgen
receptor, which is an important source of side effects in males It acts as a vasodilator
(gynecomastia and decreased libido) • used primarily for hypertension during pregnancy
can improve survival in patient with Heart Failure (Category B drug)
• Oral Given for eclampsia and pre-eclampsia
2. EPLERENONE • Most common adverse effect: Sedation
• Spironolactone analog with much greater selectivity for the
• Other AEs: Lactation (with prolactin secretion); positive Coomb’s
mineralocorticoid receptor.
test (for autoimmune hemolytic anemia)
• Less active on androgen and progesterone receptors than
2. CLONIDINE
spironolactone, and therefore, eplerenone has considerably
• Commonly used sublingually in hypertensive urgency
fewer adverse effects.

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• Reduction of cardiac output due to decreased heart rate and with asthma and COPD, that would be a problem. So you have to
relaxation give cardio selective beta- blockers such as metoprolol, atenolol, and
• Capacitance vessels, as well as a reduction in peripheral nebivolol. Cardio selective blockers blocks more of beta 1 rather than
vascular resistance beta 2 receptors.
• Should not be given to patients who are at risk for mental 1. PROPRANOLOL
depression and should be withdrawn if depression occurs during Prototype beta blocker
therapy
• the first β blocker shown to be effective in hypertension and
• Concomitant treatment with tricyclic antidepressants may block
ischemic heart disease
the antihypertensive effect of clonidine.
• Largely replaced by cardio selective β blockers such as
• Withdrawal of clonidine after protracted use, particularly with
metoprolol and atenolol.
high dosages (more than 1 mg/d), can result in life-threatening
hypertensive crisis mediated by increased sympathetic nervous Propranolol is used to control hypertension in episodes of
activity. thyroid storm. Propranolol can inhibit the peripheral conversion of T3
to T4.
: Reasons why Clonidine should not be used in hypertension
urgency: 2. METOPROLOL, ATENOLOL
• Cardio selective beta blockers: although cardioselectivity is not
o You might induce a rapid lowering of blood pressure that
complete, metoprolol causes less bronchial constriction than
will also cause adverse effects.
propranolol
o Clonidine is known for rebound hypertension. You don’t
• relatively short half-life; Atenolol is reported to be less effective
want those unstable fluctuations. Better if you just give an
than metoprolol in preventing the complications of hypertension
antihypertensive among the 4 first line agents.
o If you are using it for a long period of time and you suddenly : But as a group, beta blockers are avoided in patients with
stop it, you will manifest withdrawal. asthma or COPD even if its cardio selective, because the cardio
selectivity is not 100%, so there might still be instances of
B. Adrenergic Neuron-Blocking Agents bronchoconstriction. In most cases, we give cardio selective beta
• Lower blood pressure by preventing normal physiologic release
blockers for hypertension.
of norepinephrine from postganglionic sympathetic neurons.
: Metoprolol is not a first line agent for hypertension because
1. GUANETHIDINE it does not reduce mortality.
• Rarely used. produces all of the toxicities expected from
“pharmacologic sympathectomy,” including marked postural 3. LABETALOL, CARVEDILOL, NEBIVOLOL
hypotension, diarrhea, and impaired ejaculation Very toxic • Have both β-blocking and vasodilating effects
that’s why this is not available. NEBIVOLOL
• has highly selective β1-blocking effects, while the l-isomer
2. RESERPINE causes vasodilation; vasodilating effect may be due to an
• Alkaloid extracted from the roots of an Indian plant, Rauwolfia increase in endothelial release of nitric oxide via induction of
serpentine; produces sedation, lassitude, nightmares, and endothelial nitric oxide synthase
severe mental depression. most cardio selective beta blocker with a vasodilation effect.
An alkaloid Available as a 2.5 mg tablet or 5 mg tablet
C. Beta-Adrenoreceptor-Blocking Agents (Beta-blockers) CARVEDILOL
• “-olol” • reduces mortality in patients with heart failure and is therefore
• Effects of Beta receptors particularly useful in patients with both heart failure and
o Beta 1 = located in myocardium hypertension
o Beta 2 = lungs/airways Noncardioselective
• Occupy β receptors and competitively reduce receptor The recommendation is that even if the patient has asthma or
occupancy by catecholamine and other β agonists COPD, it might still be recommended to give carvedilol if that patient
is also a survivor of MI or if that patient also has heart failure, but you
Lowers blood pressure by lowering heart rate have to be aware of the risk for bronchoconstriction
• Should not be discontinued abruptly; some patients experience LABETALOL
a withdrawal syndrome, manifested by nervousness, • useful in treating the hypertension of pheochromocytoma and
tachycardia, increased intensity of angina, and increase of blood hypertensive emergencies (given as IV bolus)
pressure. • Parenteral
there are two groups of beta blockers: cardio selective and non- ESMOLOL
cardio selective beta blockers • β1-selective blocker that is rapidly metabolized
Issue with noncardio selective beta-blocker (propranolol): you will • via hydrolysis by red blood cell esterase’s
be able to block the beta receptor in the heart lowering heart rate and • short half-life (9–10 minutes) and is administered by intravenous
bp. Since it is non-cardio selective, you will also be blocking beta 2 infusion (parenteral)
which is located in the airways. You will have bronchoconstriction. rapid onset of action
So you are lowering bp but inducing bronchoconstriction. In patients

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• used for management of intraoperative and postoperative 1. HYDRALAZINE

hypertension, and sometimes for hypertensive emergencies, • Dilates arterioles; usually given in pregnant women with pre-
particularly when hypertension is associated with tachycardia or eclampsia/eclampsia via IV route (parenteral).
when there is concern about toxicity such as aggravation of 2. MINOXIDIL
severe heart failure. • Very efficacious orally active vasodilator.
D. Alpha1-Adrenireceptor -Blocking Agents • The effect results from the opening of potassium channels in
: Alpha blockers are anti-hypertensive drug because they block smooth muscle membranes by minoxidil sulfate, the active
the alpha 1 receptor in the arterioles which promotes vasodilation metabolite
with less reflex tachycardia. • Used topically as hair grower (male pattern baldness/
androgenic alopecia)
: This is a potent antihypertensive to the point that they will cause
orthostatic hypotension (BP lowers when you rise). : Minoxidil was not formulated as a hair grower. It was formulated
as a vasodilator, but they noticed that patients who are taking
: Because we have many agents that can also reduce mortality
minoxidil were reporting increased hair growth. Drug companies
due to heart disease the clinical use of alpha blockers has been
realized that this is a better indication because during that time there
limited to the treatment of benign prostatic hyperplasia (benign
was no effective treatment that can promote hair growth for
enlargement of prostate of males >50 years old). In BPH, it constricts
androgenic alopecia.
the urethra so the patient manifest with lower urinary tract symptoms:
frequency, nocturia, dribbling. It is used for this purpose because : applied as a scalp lotion
when you give alpha blockers, they also relax the smooth muscle in 3. SODIUM NITROPRUSSIDE
the prostate gland promoting easier passage of urine which thereby • Powerful parenterally administered vasodilator that is used in
relieve the lower urinary tract symptoms experienced by patients with treating hypertensive emergencies as well as severe heart
BPH. But take note that they do not decrease the size of the prostate failure
gland. It is mainly for symptomatic improvement. • Rapidly lowers blood pressure; effects disappear within 1–10
: Prasozin, Terasozin, and Doxazosin are older alpha blockers. minutes after discontinuation
Older because the antihypertensive effect is really strong, so you • Solution is sensitive to light; given via infusion pump
have to give it by dose titration. Start it by giving the lowest dose, • FENOLDOPAM
then after a week you up titrate, and so on. • Peripheral arteriolar dilator used for hypertensive emergencies
: The newer drugs such as Tamsulosin and Alfuzosin can be and postoperative hypertension
given straightforward, 400 mcg once a day at bedtime. • It acts primarily as an agonist of dopamine D1 receptors,
resulting in dilation of peripheral arteries and natriuresis
: We give this once a day at bedtime to prevent falls due to
orthostatic hypotension. 4. FENOLDOPAM
• Peripheral arteriolar dilator used for hypertensive emergencies
1. PRASOZIN, TERASOZIN, DOXAZOSIN
and postoperative hypertension
• Selective blocking of α1 receptors in arterioles and venules
produce less reflex tachycardia when lowering blood pressure • It acts primarily as an agonist of dopamine D1 receptors,
than do nonselective α antagonists such as phentolamine resulting in dilation of peripheral arteries and natriuresis
• Alpha1-receptor selectivity allows norepinephrine to exert One of the newer antihypertensive and vasodilator.
unopposed negative feedback (mediated by presynaptic α2
5. CALCIUM CHANNEL BLOCKERS
receptors) on its own release • One of the important groups within the vasodilators would be the
• used primarily in men with concurrent hypertension and benign calcium channel blockers. One of the groups of first line agent
prostatic hyperplasia. for hypertension.
2. PHENTOLAMINE, PHENOXYBENZAMINE • Reduce PVR and BP, on top of antianginal and antiarrhythmic
• Non-selective; used in the diagnosis and treatment of effects
pheochromocytoma • Reduces BP by inhibiting calcium influx into smooth muscle cells
• Precursors of all alpha blockers that we know nowadays. This of the arteries and the arterioles so the result is vasodilation
is not available. Some calcium channel blockers also has a direct cardiac
E. Vasodilators depressive effect. These are non-dihydropyridine.
There are two groups of calcium channel blockers:
Dihydropyridines and non-dihydropyridines
DIHYDROPRIDINES
• more selective as vasodilators and have less cardiac depressant
• Amlodipine (5mg and 10 mg tablet, felodipine, isradipine,
nicardipine, nifedipine, nisoldipine
Commonly encountered
Considered as a first line treatment for hypertension

Figure 2: Mechanism of Action of Vasodilators

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NON-HYDROPRIDINES TOXICITY:
• Verapamil (greatest depressant effect on the heart) • Diltiazem • Severe hypotension (in hypovolemic patients)- an extension of
excellent antiarrhythmic agents because they also have a therapeutic effect
depressant effect on the heart • Acute renal failure (in px with bilateral renal artery stenosis)
V. INHIBITORS OF ANGIOTENSIN • Dry cough, angioedema (secondary to bradykinin and
• ACE Inhibitors substance P) – the most common clinical concern
• ARBs • Most clinicians try to avoid ACE inhibitors in patients with pre-
existing respiratory conditions like COPD or asthma
• Hyperkalemia (if given with potassium supplements or K-
sparing diuretics)
B. Angiotensin Receptor Blocking Agents (ARBs)
• Blockers of the angiotensin II type 1 (AT1) receptor
Blocks the vasoconstrictive effect of Angio II.
Beneficial among patients with CKD or those who are at risk for
CKD. Similar to ACEi, they also have a protective effect on the
kidneys and these are not associated with dry cough
• No effect on bradykinin metabolism; more selective blockers of
angiotensin effects than ACE inhibitors
• Potential for more complete inhibition of angiotensin action
compared with ACE inhibitors
• Provide benefits similar to those of ACE inhibitors in patients
with heart failure and chronic kidney disease
• ACE inhibitors and angiotensin receptor blockers or aliskiren,
which had once been considered useful for more complete
Figure 3: Sites of action of drugs that interfere with the renin-angiotensin-
inhibition of the renin-angiotensin system, are not recommended
aldosterone system. ACE, angiotensin-converting enzyme; ARBs,
angiotensin receptor blockers due to toxicity
• e.g. Losartan, valsartan, azilsartan, candesartan,
Angiotensinogen is converted to angiotensin 1 which will then be
converted to angiotensin II by ACE. Angiotensin II is a very potent eprosartan, irbesartan, olmesartan, and telmisartan
vasoconstrictor. It will cause vasoconstriction thereby increasing • “-sartan”
peripheral resistance with increased sodium and water retention all : Some of these drugs are available in combination with other
of which increase blood pressure. drugs. For example, there is a combination with hydrochorothiazide,
If we are going to treat hypertension from the RAAS, we can opt withamlodipine.
to inhibit the conversion of angio I to angio II, that’s why there are : Do not give ACE inhibitors and ARBs together because we don’t
ACE inhibitors, so that there is less angio II that is formed. want a complete inhibition of the RAAS. Remember that RAAS is
Alternatively, you can block the receptors of angio II so that it will not there to respond in cases of emergency such as bleeding.
exert the vasoconstricting effect. For that, you can give Angiotensin VI. JNC 8: HYPERTENSION TREATMENT ALGORITHM
II receptor Blocker (ARB). If you want to prevent the sodium and
water retention, there are potassium sparing diuretics.
A. Angiotensin-Converting Enzyme (ACE) Inhibitors
• Inhibit the converting enzyme peptidyl dipeptidase that
hydrolyzes angiotensin I to angiotensin II and (under the name
plasma kininase) inactivates bradykinin, a potent vasodilator
that works at least in part by stimulating release of nitric oxide
and prostacyclin
• Useful in treating patients with chronic kidney disease
because they diminish proteinuria and stabilize renal function
(even in the absence of lowering of blood pressure) – renal
protective effect of ACE inhibitors, therefore it does not destroy
the kidney.
• Useful in the treatment of heart failure and as treatment
after myocardial infarction
• Evidence suggest ACEi reduce the incidence of diabetes in
patients with high cardiovascular risk
• e.g. Captopril, enalapril, benazepril, fosinopril, moexipril,
perindopril, quinapril, ramipril, trandolapril
Figure 4: JNC 8: Algorithm
• “-pril”

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This gives you a framework on how to think when treating a o Metoprolol

patient with hypertension. o Bisoprolol
For example, you have an adult patient with hypertension, the first o Betaxolol
line treatment is still lifestyle intervention. If you think it is necessary o Acebutolol
to give a drug, which is most of the time the case, you might want to Take note that the cardio selectivity is no 100%, so use with
consider giving antihypertensive medication.
caution.
Here in the algorithm, the first question is “Does the patient have
diabetes or CKD?” If yes, <140/90 is you BP goal (refer to appendix
B). If there is no diabetes or CKD depending on the age, for example
if the patient is 60 and above, the goal should be <150/90. If the
patient is <60 years old, the BP goal is <140/90. For Filipinos, we are
non-blacks (refer to appendix B).
For every follow up, you have to assess if patient is responding
to treatment. The common interval for follow up is 1 month, but you
have the option to ask to patient to return in 2 weeks if you want a
closer monitoring. If you ask the patient to return within 1 week, you
might not see the full effects of the medicine. For every follow up, you
have to assess the patient if you have to adjust the dose or to add Figure 6: Compelling Indications and Treatment of Choice
another medication or a third medication.
These are the common indications or the common combination of
So you have three strategies. 1) To start one drug, titrate to
drugs depending on the indication. For example, most patients with
maximum dose, and when you already maxed it out, that’s the time
heart failure will be treated with ACEi or and ARB (take note that it is
you add a second drug. 2) Start one drug, for example Losartan 50,
“or” and not an “and”, you don’t give them concomitantly), with a beta-
then I will add a second drug before achieving maximum dose of the
blocker because it improves mortality, plus a diuretic, plus
first drug. So I will not wait to exhaust Losartan 100 mg, you can add
spironolactone because this drug may also improve mortality and
a second agent right away. 3) Begin 2 drugs at the same time, either
decrease the congestion due to the heart failure. (Read on the rest
as a separate pill or in fixed dose combination.
of the combinations). You don’t give all of this at the same time,
A. Hypertension Treatment especially if the patient is just newly diagnosed.
Beta-1 Selective Beta-Blockers
• Possibly safer in patients with COPD, asthma, diabetes, and
peripheral vascular disease:

Diuretics and spironolactone can be given together. Usually it is furosemide. It is a powerful diuretic to reduce congestion, because most of
these patient may also have a right-sided heart failure. Because of it, it may lead to pleural effusion, edema in the legs, so you need a powerful
diuretic for that.
DRUG CLASS AND AGENT OF CHOICE FOR TREATMENT OF HYPERTENSION

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PS: READ KATZUNG BASIC CLINICAL PHARMACOLOGY 14TH EDITION

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