MEDICINE III

DR. ROY DIAMOND ARCO

TOPIC: Hypertension
DATE: Aug 20, 2022

According to the study conducted by Fitz et.al, people with BP of less than
OUTLINE PAGE 120 has less morbidity and mortality. Therefore people with BP greater
Hypertension 1 than 130 are considered hypertensive. In the Philippines, based on our
Definition 1 population hypertensive BP is >140/90 mmHg.
➢ White Coat Hypertension 2
➢ Masked Hypertension 2 Categories of BP in Adults (ACC/AHA 2017 Hypertension
Complications 2 Guidelines)
➢ Essential Hypertension 2 BP Category SBP DBP
➢ Secondary Hypertension 2 Normal <120 mmHg <80 mmHg
➢ Primary Aldosteronism 2
Elevated 120-129 mmHg <80 mmHg
➢ Renovascular Hypertension 2
Secondary Hypertension 2 Stage 1 HPN 130-139 mmHg 80-89 mmHg
➢ Clinical Clues 3 Stage 2 HPN >or equal to 140 mmHg >or equal to 90 mmHg
Approach To Patient 3
*Individuals with SBP and DBP in 2 categories should be designated to
➢ Patient Evaluation 3
the higher BP category.
➢ Blood Pressure Measurement 3
➢ Physical Exam 4 Corresponding Values of Systolic BP/ Diastolic BP for Clinic,
➢ Basic Laboratory Tests for Initial Evaluation 5 Home, Daytime, nighttime and 24-hour Ambulatory Measurements
Special Studies to Screen Secondary Hypertension 5 Clinic HBPM Daytime Nighttime 24-Hour
➢ Imaging 5 ABPM ABPM ABPM
➢ Algorithm for Management of Hypertension 5
120/80 120/80 120/80 100/65 115/75
Cardiovascular Risk Factors 5
➢ Major Risk Factors 5 130/80 130/80 130/80 110/65 125/75
➢ Target Organ Damage 5 140/90 135/85 135/85 120/70 130/80
Antihypertensive Medications 6 160/100 145/90 145/90 140/85 145/90
➢ Diuretics 6
➢ Renin Angiotensin System Antagonists 6 • ABPM>HBPM>Clinic BP
➢ Vasodilators 6 • Nighttime blood pressures are generally 10-20% lower than daytime
➢ Sympatholytics 6 blood pressures and an attenuated nighttime blood pressure “dip”
Hypertensive Heart Disease 7 maybe associated with increased cardiovascular disease risk.
Hypertensive Crises 7 • If you have a BP of 130 or more you are a “non-dipper” which is
➢ Hypertensive Emergency 7 indicates hypertension
➢ Hypertensive Urgency 7
2020 Clinical Practice Guidelines for the Management of
➢ Diagnosis and Management of Hypertensive Crises 7
Hypertension in the Philippines
➢ Parenteral Medications for Hypertensive Emergency 7
• Hypertension is defined as an office blood pressure of 140/90 mm
HYPERTENSION hg or above, typically at least twice taken on two separate days
I. Prevalence of Hypertension
Blood Pressure Classification for Adult Filipinos
II. Definition
III. Complications Category Blood pressure range
IV. Essential HPN/Primary HPN Normal BP <120/80 mm hg
V. Secondary HPN Borderline BP 120-139/80-89 mm hg
VI. Patient Education and Diagnosis Hypertension >140/90mm hg
VII. Management

DEFINITION
• From an epidemiologic perspective, there is no obvious level of
blood pressure that defines hypertension
• Clinically defined as that level of blood pressure at which the
institution of therapy reduces blood pressure-related morbidity and
mortality
• JNCB/ESC 2018/ISH: Systolic BP >140 mmHg and/or Diastolic BP
>90 mmHg
• ACC/AHA 2017: >130/80 mmHg

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WHITE COAT HYPERTENSION PRIMARY ALDOSTERONISM
• 20-25 % of patients with stage 1 office hypertension have • The presence of primary mineralocorticoid excess, primarily
“whitecoat” or isolated office hypertension in that their blood aldosterone, should be suspected in any patient with the triad of
pressure is repeatedly normal when measured at HOME hypertension, unexplained hypokalemia, and metabolic alkalosis.
• Associated with an increased risk of target organ damage • Increased aldosterone production is independent of the renin-
• increased risk for developing sustained hypertension angiotensin system
Most of hypertension associated with decreased RAAS
MASKED HYPERTENSION
• Etiology: adrenal adenoma or hyperplasia
• normal BP in the clinic but elevated BP out at home/ambulatory • Increased plasma aldosterone/plasma renin activity ratio
COMPLICATIONS
• risk factor for premature cardiovascular disease and heart failure
HEART DISEASE - most common cause of death in HPN
• hypertension is the most important risk factor for the development
of intracerebral hemorrhage
• hypertension is the most common and most important risk factor for
ischemic stroke
• second most common cause of Chronic Kidney Disease (dialysis
and kidney transplant)
taking a lot of hypertensive drug can damage kidney
• number 1 common cause of kidney transplant and dialysis is DM
CVD Risk Factors Common in Patients with Hypertension TREATMENT
Modifiable risk factors* Relatively fixed risk factors⁺ • Surgical – adrenalectomy
• Medical – spironolactone, K sparing diuretics
Current cigarette smoking, CKD
secondhand smoking RENOVASCULAR HYPERTENSION
Diabetes mellitus Family history • Blood pressure elevation due to partial or complete occlusion of one
Dyslipidemia/hypercholesterolemia Increased age or more renal arteries or their branches
Low socioeconomic/ Macrovascular Microvascular
Overweight/obesity educational status Renal Artery Stenosis “Malignant” hypertension
Physical inactivity/low fitness Male sex Atheroembolic renal disease “Hypertensive nephrosclerosis”
Obstructive sleep apnea • Abnormal heartbeat
Unhealthy diet • Atrial Fibrillation
Psychosocial stress
Thromboembolic renal disease
*Factors that can be changed and, if changed, may reduce CVD risk
⁺Factors that are difficult to change (CKD, low socioeconomic/educational Fibromuscular dysplasia
status, obstructive sleep apnea, cannot be changed (family history, • Common in females
increased age, male sex), or, if changed through the use of current • Defect in blood vessels
intervention techniques, may not reduce CVD risk (psychosocial stress).
CKD indicates chronic kidney disease; and CVD, cardiovascular disease.
ESSENTIAL / PRIMARY HYPERTENSION
• 80-95% Of hypertension
• ETIOLOGY: unknown ??
Probably caused by hyperactive sympathetic renal
aldosterone hormone
Born with ↓ kidneys
• Diagnosis by exclusion
Pathophysiology
Suspected in:
• Increase sympathetic neural activity, with enhanced beta-
adrenergic responsiveness • severe or refractory hypertension, recent loss of hypertension
control or recent onset of moderately severe hypertension
• Increased angiotensin II and mineralocorticoid excess
you already gave 4 different antihypertensive drugs, still
• Genetic factors account for approximately 30% of the variation in
increased BP
blood pressure
• extensive atherosclerotic disease
• Reduced adult nephron mass
past history of recurrent strokes
• a continuous (systolic/diastolic) abdominal bruit
SECONDARY HYPERTENSION
• Unilateral small kidney (>1 cm difference) normal kidney size is 9-
• Approximately 5% of patients have hypertension secondary to 13cm
identifiable specific causes ex: one kidney is 8, second kidney is 9.5cm – suspect a renal
• HPN develops at an early age(<25yo) or after the age of 50 years artery stenosis
• Those previously well controlled BP who become refractory to
treatment

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 SECONDARY HYPERTENSION FREQUENTLY USED MEDICATIONS AND OTHER SUBSTANCES
RENAL PARENCHYMAL Virtually all disorders of the kidney THAT MAY CAUSE ELEVATED BP
DISEASE (CKD) – different from may cause hypertension (the MC Prescribed Meds STREET DRUGS/ Natural Products
stenosis. cause of secondary HPN) • NSAIDS, COX-2 inhibitors • cocaine and cocaine withdrawal
Ex: Hypertensive Nephrosclerosis, • bupropion • ephedra alkaloids (e.g., ma-huang)
Glomerulonephritis, Kidney Failure • bromocriptine • “herbal ecstasy”
CUSHING’S SYNDROME Excess cortisol production due • buspirone • phenylpropanolamine analogs
either to excess ACTH secretion • carbamazepine • nicotine withdrawal
(from a pituitary tumor or an ectopic • ketamine • anabolic steroids
tumor) or to ACTH-independent • metoclopramide • narcotic withdrawal
adrenal production of cortisol • ergot-containing herbal products
PHEOCHROMOCYTOMA Catecholamine-secreting tumors • St. John’s wort
are located in the adrenal medulla FOOD
(pheochromocytoma) or in extra- • sodium
adrenal paraganglion tissue • Ethanol
(paraganglioma) • licorice
COARCTATION OF AORTA COA typically occurs just distal to • energy drinks
the origin of the left subclavian
artery, so the blood pressure is
lower in the legs than in the arms APPROACH TO PATIENT
PATIENT EVALUATION
1. Uncovering secondary forms of hypertension because most of the
OBSTRUCTIVE SLEEP APNEA
time, 90-95% of Hypertension is primary.
(OSA)
2. Establishment of pre-treatment baseline
Ex: people with short neck,
3. Assessing factors that may influence type of therapy because
obstructed breathing while
different medications have different side effects
sleeping causing decreased O2
4. Determining if target organ damage is present especially
and patients tend to wake up from
Cardiovascular risk
time to time (no complete deep
5. Determining presence of other risk factors
sleep)
BLOOD PRESSURE MEASUREMENT
Who Should Be Suspected of Having Secondary Hypertension and
Should Be Referred for Work-Up • When taking blood pressure for the first time, make sure to take
both sides. Whichever side is higher, you record that side. The
• With early onset of hypertension (<30yo) patient may have an occlusion due to peripheral atherosclerotic
• BP difficult to control, requiring 3 drugs or more disease which could explain the discrepancy.
• With elevated serum creatinine and/or with abnormal urinalysis
• Instruct the patient to take the BP at home. They can take the
• With high or low serum potassium
morning and evening BP. This way they can have a record which
CLINICAL CLUES OF SECONDARY HYPERTENSION you can compare the BP taken in the clinic and out of office.
Abdominal flank masses, Family POLYCYSTIC KIDNEY KEY STEPS FOR PROPER BP MEASUREMENTS
history of adult polycystic kidney – DISEASE Step 1: Properly 1. Have the patient relax, sitting in a chair (feet on
kidneys are larger than normal, you prepare the floor, back supported) for >5 min.
can palpate it patient 2. The patient should avoid caffeine, exercise, and
Delayed or absent femoral pulses; COARCTATION OF THE smoking for at least 30 min before measurement.
decreased BP in the lower AORTA 3. Ensure patient has emptied his/her bladder.
extremities 4. Neither the patient nor the observer should talk
Truncal obesity with purple striae CUSHING’S SYNDROME during the rest period or during the measurement.
Tachycardia, tremors, orthostatic PHEOCHROMOCYTOMA 5. Remove all clothing covering the location of cuff
hypotension, sweating, flushing placement.
Anemia, edema, azotemia, urinary CHRONIC KIDNEY DISEASE 6. Measurements made while the patient is sitting or
cast (RPD) lying on an examining table do not fulfill these
Pulse discrepancy TAKAYASU’S ARTERITIS criteria.
Neck mass with bruit, lid lag, tremors, THYROTOXICOSIS Step 2: 1. Use a BP measurement device that has been
exophthalmos Use proper validated, and ensure that the device is calibrated
Excessive snoring OSA technique for BP periodically.*
measurements 2. Support patient's arm (e.g., resting on a desk).
3. Position the middle of the cuff on the patient's
upper arm at the level of the right atrium (the
midpoint of the sternum).
4. Use the correct cuff size, such that the bladder
encircles 80% of the arm, and note if a larger- or
smaller-than-normal cuff size is used (Table 9).
5. Either the stethoscope diaphragm or bell may be
used for auscultatory readings (54.1-5,54.1-6).

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Step 3: 1. At the first visit, record BP in both arms. Use the
Take the proper arm that gives the higher reading for subsequent
measurements readings.
needed for 2. Separate repeated measurements by 1-2 min.
diagnosis and 3. For auscultatory determinations, use a palpated
treatment of estimate of radial pulse obliteration pressure to
elevated estimate SBP.
BP/HPN 4. Inflate the cuff 20-30 mm Hg above this level for
an auscultatory determination of the BP level.
5. For auscultatory readings, deflate the cuff
pressure 2 mm Hg per second, and listen for
Korotkoff sounds.
Step 4: Properly 1. Record SBP and DBP. If using the auscultatory
document technique, record SBP and DBP as onset of the
accurate BP first Korotkoff sound and disappearance of all
readings Korotkoff sounds, respectively, using the nearest
even number.
2. Note the time of most recent BP medication taken
before measurements.
Step 5: Average Use an average of ≥2 readings obtained on ≥2
the readings occasions to estimate the individual's level of BP.
Step 6: Provide Provide patients the SBP/DBP readings both verbally
BP readings to and in writing.
patient
PHYSICAL EXAM
• General body habitus
Is the patient obese? Does he have truncal obesity? So we
can rule out Cushing’s syndrome.
• BP on both arms
• Cardiac exam: murmurs, arrythmias, displaced apex, cardiomegaly,
pulmonary edema
Look for cardiac organ damage
• Peripheral vascular exam: carotid, femoral, abdominal pulse; JVP
• Peripheral edema
E.g., Renal failure, Heart failure
• Neurologic exam
• Fundoscopic exam
• Flank tenderness
For patients with Polycystic Kidney disease
• Thyroid
For Thyrotoxicosis
Here are your signs of elevated blood pressure: your fundoscopic exam -
the cotton wool spot, papilloedema, flame hemorrhage; you palpate the
major arteries for bruits to rule out renal artery stenosis renovascular
hypertension.

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BASIC LABORATORY TESTS FOR INITIAL EVALUATION BP THRESHOLDS FOR AND GOALS OF PHARMACOLOGIC
BASIC TESTING OPTIONAL TESTING THERAPY
FBS Echocardiogram Clinical Condition(s) BP Threshold BP Goal
CBC Uric Acid mmHg mmHg
Lipid profile Urine albumin to creatinine ratio General
Serum Creatinine Clinical CVD or 10-year ASCVD risk ≥ ≥130/80 <130/80
Serum Na, K, and Calcium 10%
TSH No clinical CVD and 10-year ASCVD risk ≥140/90 ≥140/90
Urinalysis <10%
ECG Older persons (>65 y0; non- ≥130 SBP <130 SBP
*Urine Albumin to creatinine ratio is better test for Protein finding from institutionalized, ambulatory, community-
urinalysis living adults
Specific Comorbidities
Diabetes mellitus ≥130/80 <130/80
Chronic kidney disease ≥130/80 <130/80
Chronic kidney disease post-renal ≥130/80 <130/80
transplantation
Heart failure ≥130/80 <130/80
Stable ischemic disease ≥130/80 <130/80
Secondary stroke prevention ≥140/90 <130/80
Peripheral arterial disease ≥130/80 <130/80

SPECIAL STUDIES TO SCREEN SECONDARY HYPERTENSION CARDIOVASCULAR RISK FACTORS

A. Pheochromocytoma MAJOR RISK FACTORS
• 24H urine assay for metanephrines and catecholamines • Hypertension
B. Cushing’s Syndrome • Cigarette smoking
• Overnight dexamethasone suppression test • Obesity (BMI ≥30)
• 24h Urine Cortisol • Physical inactivity
C. Primary aldosteronism – PA:PRA • Dyslipidemia
D. Renovascular HPN- Renal angiogram • Diabetes mellitus
• Microalbuminuria or estimated GFR < 60 mL/min/1.73 m2
IMAGING • Age (>55 yo for men, >65 yo for women)
• X-RAY: Check for cardiomegaly/cardiac damage
• CT scan: Adrenal mass TARGET ORGAN DAMAGE
• Aortogram: to map out the artery • Heart
• Renal angiogram: For renal artery stenosis Left ventricular hypertrophy
Angina or prior myocardial infarction
ALGORITHM FOR THE MANAGEMENT OF HYPERTENSION Prior coronary revascularization
Heart failure
• Brain
Stroke
• Chronic Kidney disease
• Peripheral arterial disease
• Retinopathy

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 ANTI HYPERTENSIVE MEDICATIONS ARB
Diuretics Thiazides • Provide selective blockade of AT1 receptors
Loop Diuretics • Less cough
Aldosterone antagonist • Drugs ending in “tan” – Example: Losartan, Candesartan,
Renin Angiotensin System ACE inhibitors Valsartan, etc.
Antagonists ARB blockers • More or less, same side effects with ACEI
Renin inhibitors • ACEI and ARBs
Good for patients with heart failure because lesser
Sympatholytics B blockers cardiovascular death
Central alpha 2 agonist The heart size will decrease, lesser proteinuria (for patients
Combined alpha and bet blockers with CKD)
Vasodilators Ca channel blockers
Direct Renin Inhibitors (Aliskerin)
Direct vasodil (hydralazine, minoxidil)
• Block the RAAS system at its origin without increasing bradykinin
PHARMACOLOGIC THERAPY: DIURETICS • Heart failure, chronic kidney disease (decreased albumin)
• Newest drugs among blockers of RAAS, Longer acting
Thiazides Diuretics
• Inhibit the Na+/Cl- pump in the distal convoluted tubule So patients with heart failure, large heart, ACEI ang drug of choice.In
• Increased incidence of metabolic side effects (hypokalemia, insulin chronic kidney disease, we also found out na muless ang proteinuria, so
resistance, increased cholesterol) we give ACEI or ARB inhibitors even in patient who is nonhypertensive
• Side effect: Sodium is excreted, you will diuresis, the effect is because of its secondary effect of decreasing albumin.
Potassium is also excreted so there will be hypokalemia thus The side effect of ACEI and ARB is hyperkalemia. If we give the patient
decreasing cholesterol. ACEI and ARB, we check for potassium after 2 weeks if mag
• After 2 weeks of medication, check for electrolytes hyperkalemia.
In patients with kidney failure (those dili mu ihi ang patients),
VASODILATORS
it will be useless.
CALCIUM CHANNELS
Loop Diuretics • Antiarrhythmic, antianginal, and antiHPN because they block the
• Block Na+K2+Cl- transport in the thick ascending loop of Henle, opening of voltage-gated (L-type) Ca2+ channels in cardiac
where a large portion of the filtered sodium is reabsorbed myocytes and vascular smooth muscle cells
• Stronger diuretics, watch out for hypotension (side effect) • Reduces intracellular calcium and blunts vasoconstriction
Even a dose of 20 mg of Furosemide, the patient will always Dihydropyridines: amlodipine (Norvasc), nifedipine
urinate so there will be a drop in blood pressure. Nondihydropyridines: diltiazem, verapamil
• Ascending LOH – major absorption site of sodium, 80-90%) ‣ Side effects of flushing, headache, and edema
• Distal tubule – 20% sodium absorption We usually pair calcium channels with diuretics to lessen the edema.

Aldosterone antagonist (spironolactone) CENTRAL SYMPATHOLYTICS

• These are drugs that attack your aldosterone.
• Effect: absorbs your potassium so there will be an increase in
potassium (compared to other diuretics)
BLOCKERS OF THE RENIN-ANGIOTENSIN SYSTEM
ACEI
• Decrease the production of angiotensin II, increase bradykinin
levels, and reduce sympathetic nervous system
• Causes vasoconstriction of the endothelial system so the side effect
is cough.
• Drugs ending with “pril” – Captopril, Enalipril, Lisinopril – are your
ACEI.
• 10-20% will experience coughing
“good cough”/dry cough (due to the bradykinin)
The problem is there are other patient who will have difficulty
coughing so they invented drugs that target the AT1 receptor
to lessen the cough (ARBs)
• Lower blood pressure by stimulating alpha adrenergic receptors in
the central nervous system, thus reducing efferent peripheral
sympathetic outflow
• Decreased sympathetic drive -> decreased heart rate, cardiac
output, and peripheral vascular resistance
• EX: Clonidine (sublingual) and methyldopa (for pregnant, frequently
used in OB)
BETA BLOCKERS
• central acting drugs
• Lower blood pressure by decreasing cardiac output, due to a
reduction of heart rate and contractility
• Central nervous system effect
NON-SELECTIVE: Propanolol
CARDIOSELECTIVE: Metoprolol, atenolol, acebutolol,
bisoprolol
‣ Inhibits B1>B2 at lower doses
• All β-blockers can precipitate heart block, and they can aggravate
preexisting asthma
• SE: fatigue, nasal congestion, ED
• COMBINED ALPHA AND BETA BLOCKER: Carvedilol
BETA BLOCKERS SLIDE
Propanolol - More on tachycardia, thyrotoxicosis
CARDIOSELECTIVE: Metoprolol, atenolol, acebutolol, bisoprolol
- All beta blockers, can cause heart block. If you have patients with
problems with rhythm, be careful, basin ma precipitate ang heart
block if you use beta blockers.
- SE: fatigue, nasal congestion, erectile dysfunction

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COMBINED ALPHA AND BETA BLOCKER DIAGNOSIS AND MANAGEMENT OF A HYPERTENSIVE CRISIS
- Cardevilol
(Short story about Marcos death; Marcos died of Chronic kidney disease
secondary to glucose nephritis, he died of hypertensive nephrosclerosis,
no ARB/ CCB during the 1960’s-1970’s)
PRIMARY DRUG OF CHOICE
AHA/ ACC For initiation of antihypertensive drug therapy, first
line agents include thiazide diuretics, CCBs, and
AC inhibitors or ARBs
PHIL CPG 2020 Among persons with uncomplicated hypertension,
angiotensin converting enzyme (AC) inhibitors or
angiotensin- receptor blockers (ARBs), calcium
channel blockers, thiazide/ thiazide- like diuretics
are all suitable first- line antihypertensive drugs,
either as monotherapy or combination.
Later-line alternatives/ secondary drugs:
• Beta blockers
• Alpha blockers
• Alpha 1/ beta blockers (eg. Carvedilol)
• Vasodilating beta- blockers (eg. Nebivolol)
• Central alpha 2/ - adrenergic agonists (eg. Clonidine)
• Direct vasodilators (eg. Hydralazine)
• Loop diuretics (eg. Furosemide)
• Aldosterone antagonists (eg. Spironolactone) 1st step – check for target organ damage
• Peripherally acting adrenergic antagonists Hypertensive emergency reduce the bp within 24-48 hr, while in
hypertensive urgency: day.
HYPERTENSIVE HEART DISEASE
• A term applied generally to heart diseases, such as LVH, coronary PARENTERAL MEDICATIONS FOR HYPERTENSIVE EMERGENCY
artery disease, cardiac arrhythmias, and CHF, that are caused by the Antihypertensive Agent Intravenous Dose
direct or indirect effects of elevated BP Nitroprusside Initial 03 (ug/kg)/min; usual 2-4 (ug/kg)/min;
• LVH - a marker of increased risk of cardiovascular morbidity and maximum 10 (ug/kg>/min for 10 min
mortality Nicardipine Initial 5 mg/h; titrate by 2.5 mg/h at 5-15 min
Should be treated aggressively intervals; max 15 mg/h
Labetalol 2 mg/min up to 300 mg or 20 mg over 2 min, then
HYPERTENSIVE CRISES
40-80 mg at 10-min intervals up to 300 mg total
HYPERTENSIVE EMERGENCIES
Enalaprilat Usual 0.625-1.25 mg over 5 min every 6-8 h;
• An acute, often sever, elevation in blood pressure, accompanied by maximum 5 mg/ dose
rapidly progressive target organ dysfunction
Esmolol Initial 80-500 ug/kg over 1 min, then
Hypertensive encephalopathy, ICH, acute ischemic stroke,
50-300 (ug/kg)/min
acute MI, acute LV failure with pulmonary edema, unstable
Phentolamine 5-15 mg bolus
angina pectoris, dissecting aortic aneurysm, acute renal
failure, and eclampsia Nitroglycerin Initial 5 ug/min, then titrate by 5 ug/min at
• Life threatening and require immediate treatment, usually with 3-5-min intervals; if no response is seen at
parenteral medications in a monitored setting 20 ug/min, incremental increases of
10-20 ug/min may be used
HYPERTENSIVE URGENCY Hydralazine 10-50 ma at 30-min intervals
• Severe asymptomatic HPN, markedly elevated BP
• Blood pressure is severely elevated ( > 180 SBP or > 120 DBP), but SUMMARY
there is no associated organ damage • Hypertension is associated with a heavy burden of
• Common in clinical practice, especially among patients with known cardiovascular, renal, and cerebrovascular disease
hypertension who are not fully adherent to their medications • Your 1st line drugs: thiazide diuretics, ACEi, ARB, and CCB
• May or may not experience or more of these symptoms: • Hypertensive emergency are life threatening and require
Severe headache immediate tx
Shortness of breath • Based on the latest guidelines: BP Goal is < 130/80
Nosebleeds
Severe anxiety

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