Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                
Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 58

‘Amang’ Rodriguez Memorial Medical Center

Sumulong Highway, Marikina City

Department of Internal Medicine

Hypertension
LOUIJE P. MOMBAEL
ARMMC - POST GRADUATE INTERN
OBJECTIVES:

To present a case with increased blood pressure

To discuss the different classification of high blood


pressure

To discuss the non-pharmacological and


pharmacological management of high blood pressure
GENERAL DATA:
M.D.

50 year old

Male

Filipino

Born on February 14, 1960 at San Mateo, Rizal

Roman Catholic

Currently residing at San Mateo, Rizal


CHIEF COMPLAINT:

“Sobrang pananakit ng aking ulo at


may pananakit din ng aking
dibdib”
HISTORY OF PRESENT ILLNESS:
Patient is a known case of Hypertension Stage II
for 2 years
• Sudden onset of headache at the right fronto-occipital region, described as throbbing pain, with
painscale of 5-6/10.
• No other symptoms noted like: fever, dizziness, nausea/vomiting, cough/colds, chest pain, DOB/SOB.
1 DAY • Took 1 dose of Biogesic 500mg, which claims mild relief of symptom. No consult done
PTC
• Still with headache with increased in severity with painscale of 8-9 and now accompanied with sudden
onset of chest pain at left side described as dull, non-radiating with painscale of 7/10.
• No other symptoms noted like: fever, dizziness, nausea/vomiting, cough/colds, DOB/SOB.
FEW HOURS • No medications taken.
PTC

Persistence of
the symptoms CONSULT
PAST MEDICAL HISTORY:
Hypertension (HTN) for 2 years
 Amlodipine / Olmesartan 5mg / 20mg OD (NON-COMPLIANT)

Denies diabetes, bronchial asthma, tuberculosis, thyroid


problems, cancer.

Denies any previous surgeries or hospitalization

No known allergies to food or drugs

No recent adult vaccines given


FAMILY MEDICAL HISTORY:
Mother: 80 y/o, alive with HTN.

Father: died of MI at age of 60.

Brother: alive with HTN at age 49.


Sister: alive with hypothyroidism at age 45.

Denies other heredo-familial disorder such as diabetes, asthma, tuberculosis,


cerebral vascular disease, or cancer.
PERSONAL AND SOCIAL HISTORY:
Smokes 5 sticks per day
x 20 years (5 pack
years). Drinks 2-3 cups of
2-3 bottles of beer caffeinated beverages
during occasions.
He prefers pork,
chicken and fish.
Denies illicit drug use.
He also eat fruits &
vegetables everyday
Sedentary lifestyle.
REVIEW OF SYSTEMS
General: CVS:
​(-) chills​​ (-) tremors​​ (-) dizziness​​ ​(-) malaise (-) orthopnea​​ (-) palpitation (-) syncope (-) edema (-) easy fatigability
(-) weakness​​ (-) weight loss ​ (-) fatigue ​ 
GIT:
Integumentary: ​(-) abdominal enlargement​ (-) anorexia​ (-) constipation (-) diarrhea ​(-) dysphagia​​
(​ -) dryness​​ (-) itchiness (-) jaundice​ (-) pigmentation ​(-) hematoma​​ (-) (-) flatulence ​(-) hematemesis​ (-) hematochezia ​(-) melena​​ (-) nausea​
sweating (-) sore (-) lesions/rashes
(-) steatorrhea​ (-) vomiting (-) decrease appetite

Head and Neck:
GUT:
​(-) head injury ​(-) lymphadenopathy​ (-) mass
​(-) discharge ​(-) dysuria (-) flank/suprapubic pain (-) frequency (-) hematuria
​(-) incontinence​ (-) nocturia​ (-) oliguria (-) passage of stone
Eyes:
(-) polyuria (-) urinary incontinence
​(-) diplopia​​ (-) Blurring of vision (-) photophobia
​(-) lacrimation​ (-) Diplopia (-) eye redness
Musculoskeletal:
​(-) atrophy (-) back pain​​ (-) bone deformation (-) joint pain (-) muscle pain
Ears: (-) weakness
​(-) hearing loss ​(-) tinnitus
​ Neurological:
Nose and Sinuses: (-) memory loss​​ (-) seizures​ (-) syncope (-) tremors​​ (-) hallucinations (-) LOC
​(-) disturbance in smell (-) epistaxis (-) obstruction​ (-) pain
​ Endocrine:
Mouth: ​(-) abnormal growth​​ (-) easy fatigability​​ (-) goiter​​​(-) insomnia
​(-) disturbance of taste ​(-) sore throat (-) heat/cold intolerance (-) polydipsia ​(-) polyphagia​ (-) polyuria
​  
Respiratory: Hematological:
​(-) dyspnea ​ ​(-) easy bruisability ​(-) easy fatigability​​ (-) pallor
PHYSICAL EXAMINATION
GENERAL SURVEY:
The patient is awake, conscious and coherent, well groomed, alert and calm, no slurring
of speech, and cooperative. He is well nourished, with large body built and good posture,
ambulatory.
Patient is afebrile and not in cardiac or respiratory distress.

VITAL SIGNS:
BP = 190/120 mmHg PR = 98 BPM Weight = 78 kgs BMI = 27.97 kg/m2
T = 37.4 °C RR = 20 CPM Height = 167 cm (OBESE I)

INTEGUMENTARY:
The skin is brown, thick, smooth, moist, warm to touch with good skin turgor and
mobility. No abnormal pigmentations, ecchymoses, rashes and edema noted.
Nails are clean, pinkish in color, no clubbing and no nail plate abnormalities noted.
Capillary refill <3 sec.
Cont… PHYSICAL EXAMINATION
Nose is symmetrical. No flaring of ala nasi. Vestibule
HEENT:
is patent, mucosa is pinkish, with no secretions and
no bleeding. Nasal septum is at the midline.
No tenderness and clouding of Paranasal sinuses
upon Trans illumination.
The cranium is normocephalic, symmetrical and has no
deformities. No tenderness and no masses. Temporal arteries
not visible but palpable with strong pulsations. Face is
symmetrical, no abnormal facies seen.

Lips are pinkish, dry, no lesions. Buccal mucosa is


pinkish, moist, no lesion, no swelling. Tongue not
atrophied or hypertrophied and is not deviated.
No sign of exophthalmos and enophthalmos. Anicteric sclerae, Patient is noted to have dentures. Palate is pinkish,
Pink palpebral conjunctiva. Pupils are equal, round, and about intact, no lesions. Uvula is at midline, pink, no lesion
2-3mm upon constriction, reactive to direct and consensual and located at midline. Tonsils are not swollen.
reflex. Full visual fields, upon fundoscopic examination red
reflex present, no papilledema or AV nicking noted.

External ears are symmetrical, no deformities, no lesion and no


Neck is symmetrical, has well developed muscles and
tenderness. External auditory canal is patent, walls are pinkish, has no deviation. Trachea is in the midline. No
no discharges. Intact tympanic membrane. Rinne test: air > lymphadenopathy, No mass noted.
bone conduction bilaterally, Weber test: midline
Cont.. PHYSICAL EXAMINATION
RESPIRATORY:
Symmetrical chest expansion, no retractions, clear breath sounds

CARDIOVASCULAR:
Adynamic precordium, Apex beat is at the left 5th ICS-MCL, no heaves, lift, nor thrills, normal rate
regular rhythm, no murmur

DRE:
GASTROINTESTINAL:
No skin tags, No palpable mass, No
Flabby, normoactive bowel sounds, soft, non-tender, no palpable mass, tympanitic on all quadrants tenderness, No blood on the examining
finger noted.

EXTREMITIES:
Grossly normal extremities, no edema, no cyanosis, full and equal pulses.

GENITOURINARY:
Normal looking external genitalia, no lesions.
Cont.. PHYSICAL EXAMINATION
Mental Status: conscious, coherent

Cerebrum:
NEUROLOGIC

Speech is normal and with appropriate content. Well oriented to time, place and
person. He was able to follow simple and complex commands and do simple
calculation. Has an intact immediate, recent and remote memory. He was able to
recognize objects and distinguished its appropriate function.

Cerebellum:
Patient was able to perform finger to nose test with no arm dysmetria noted.
Negative for dysdiadochokinesia, he was able to alternately do pronation and
supination. No dysmetria of lower extremities, he was able to perform heel to shin
test smoothly at both sides.
Cont.. PHYSICAL EXAMINATION
Cranial Nerves:

CN 8 - The patient was able to repeat words whispered to her


CN 1 - no anosmia and able to localized sound. Sounds are equally heard on both
ears with normal neurosensory hearing and no conductive
hearing loss.
CN 2 – Pupils are 2-3 mm in diameter, equally reactive to
NEUROLOGIC

light, VA: 20/100 OU, but 20/20 OU w/ corrective glasses,


[+] ROR, no papilledema or AV nicking noted. CN 9, 10 - Gag reflex was present bilaterally, uvula is at the
midline and no hoarseness was noted.

CN 3, 4, 6 - no limitation of EOM

CN 11 - No fasciculations, tremors or atrophy noted. Patient


was able to shrug her shoulders symmetrically, flex her head,
CN 5 – Able to distinguish sharp from blunt object. He rotate head and bend laterally against resistance
was able to contract his temporals and master muscle by
clenching his teeth. (+) corneal reflex.

CN 7 - Well delineated with normal facial creases, no CN 12 - Tongue is in the midline, symmetrical when protruded.
change in sense of taste, no facial asymmetry, able to No fasciculation or involuntary movement observed.
smile, frown, blow cheeks, and close his eyes.
Cont.. PHYSICAL EXAMINATION
Motor: No fasciculation, atrophy, and no involuntary movements. Muscles
are normotonic, 5/5 both upper and lower extremities

Sensory: 100% on both UE & LE


NEUROLOGIC

Deep Tendon Reflexes: Biceps, triceps, ankle, and knee reflexes are (2+)

Pathologic Reflexes: No Babinski

Meningeal Signs: No nuchal rigidity, Kernig’s or Brudzinski’s sign


SALIENTFEATURES
SALIENT FEATURES
Subjective: • ROS:
(-) sweating Objective:
• 50 year old (-) blurring of vision
• Male (-) diplopia • BP = 190/120 mmHg
​(-) dyspnea
• Hypertension Stage II for 2 years (-) orthopnea​​ • BMI = 27.97 kg/m2 (Obese I)
(non-compliant to medications) (-) palpitation
• Headache @ right fronto-occipital (-) syncope • No facial asymmetry
region, throbbing on character, PS: (-) edema
8-9/10. (-) easy fatigability • No tongue deviation
• Chest pain @ left side described as
dull, non-radiating, PS: 7/10. • Apex beat @ Left 5th ICS-MCL
• No other symptoms noted like:
fever, dizziness, nausea, vomiting, • No bipedal edema
cough, colds, DOB/SOB.
• Full and equal pulses
• (+) Family History: Hypertension/MI
• Smoker: 5 sticks per day for 20 • Neurological examination is
years (5 pack years). unremarkable
• Alcoholic drinker (2-3 bottles of
beer per occasion).
DIFFERENTIAL DIAGNOSIS
MIGRAINE HEADACHE
Rule in:
 Hypertension Stage II for 2 years (non-
Rule out:
compliant to medications)
 Female
 Headache @ right fronto-occipital region,
throbbing on character, PS: 8-9/10.  Recurrent episodic attacks (at least 5)
 Smoker: 5 sticks per day for 20 years (5 pack
years).  (-) Nausea & Vomiting
 Alcoholic drinker (2-3 bottles of beer per
occasion).  (-) Sensitivity to light and sound
 Sedentary lifestyle
 Drinks 2-3 cups of caffeinated beverages
daily.

-RULE OUT-
Cont… DIFFERENTIAL DIAGNOSIS
MYOCARDIAL INFARCTION
Rule in : Rule out :

50 year old  (-) Pain radiating in one or both arms, back, neck, jaw or stomach.
Male  (-) Shortness of breath
Hypertension Stage II for 2 years (non-compliant to
medications)  (-) Sweating
Headache (RARE)  (-) Nausea
Chest pain at left side described as throbbing with PS: 7/10.
 (-) Lightheadedness.
(+) Family History: Hypertension/MI
Smoker: 5 sticks per day for 20 years (5 pack years).
Alcoholic drinker (2-3 bottles of beer per occasion).
***Can be also ruled out by ECG and serial biomarkers
Sedentary lifestyle
Drinks 2-3 cups of caffeinated beverages daily. such as creatine kinase MB isoenzyme (CK-MB), aspartate
BP = 190/120 mmHg aminotransferase (AST), and lactate dehydrogenase (LD)
BMI = 27.97 kg/m2 (Obese I)

-RULE OUT-
Cont… DIFFERENTIAL DIAGNOSIS
SUBARACHNOID HEMORRHAGE (SAH)
Rule in: Rule out:
 50 year old
 (-) Dizziness
 Hypertension Stage II for 2 years (non-
 (-) Orbital pain
compliant to medications)
 (-) Diplopia
 Headache at the right fronto-occipital
region, throbbing on character, PS: 8-9/10.  (-) Visual loss

 Chest pain  (-) Seizures

 Smoker: 5 sticks per day for 20 years (5  (-) Ptosis

pack years).  (-) Focal neurologic findings

 BP = 190/120 mmHg *** Non-contrast CT followed by CT angiography (CTA) of the brain can rule
out SAH with greater than 99% sensitivity.

-RULE OUT-
Cont… DIFFERENTIAL DIAGNOSIS
HYPERTENSIVE URGENCY
 50 year old  Smoker: 5 sticks per day for 20 years
 Male (5 pack years).
 Hypertension Stage II for 2 years  Alcoholic drinker (2-3 bottles of
(non-compliant to medications) beer per occasion).
-RULE IN-

 Headache at the right fronto-  Sedentary lifestyle


occipital region, throbbing on  Drinks 2-3 cups of caffeinated
character, PS: 8-9/10. beverages daily.
 Chest pain at left side described as  BP = 190/120 mmHg
squeezing, non-radiating, PS: 7/10.  BMI = 27.97 kg/m2 (Obese I)
 (+) Family History: Hypertension  Physical / Neurological Examination
is unremarkable
IMPRESSION:

HYPERTENSIVE URGENCY r/o CVD-BLEED

HYPERTENSION STAGE II – UNCONTROLLED

OBESE I
DISCUSSION

HYPERTENSION
PREVALENCE

 An estimated 1.13 billion people


worldwide have hypertension,  Hypertension is a major cause of
most (two-thirds) living in low- premature death worldwide.
and middle-income countries.  One of the global targets for
 In 2015, 1 in 4 men and 1 in 5 noncommunicable diseases is to
women had hypertension.  reduce the prevalence of
 Fewer than 1 in 5 people with hypertension by 25% by 2025
hypertension have the problem (baseline 2010).
under control. 
PREVALENCE
 National Health and Nutrition Examination Highest in non-Hispanic black
Surveys (NHANES) data from 2011 to 2014 and
blood pressure thresholds from the 2017  Males (58.6%)
American College of Cardiology/American  Females (56.0%).
Heart Association (ACC/AHA) guideline
 Hypertension among US adults was
Incidence increases with age in
estimated to be 46.0%; people of all ancestries and both
 BP thresholds from the 7th Joint National sexes.
Committee (JNC 7) guideline.  Men > in women before 65 y/o.
 Estimated at 31.9%.  Women > in men from 65 y/o.
 NHANES data from 2013 to 2016, the AHA Lifetime risk is 90% for both men and
report
 Estimated 116.4 million adults (age ≥20
women who were normotensive at
years) with high BP in the US. 55 y/o and survive to 80 years.
According to the latest WHO data published
in 2018

• Hypertension Deaths in Philippines reached 14,488 or 2.38% of total


deaths.
• The age adjusted Death Rate is 23.44 per 100,000 of population ranks
Philippines #25 in the world.
Asian management of hypertension: Current status, home blood
pressure, and specific concerns in Philippines (a country report)

• Incidence of cardiovascular diseases (CVD) in the Philippines based on


the Philippine Heart Association survey among hospital‐based
population showed hypertension as the highest (38.6%)
• Latest data on prevalence of hypertension were 28% equal for males
and females
• 9% were unaware.
• Treatment rate was 56%
• Compliance was 57%
• BP control rate was 20%.
BP AND CVD RISK
• Many adult patients with hypertension
have other CVD risk factors.
• Among U.S. adults with hypertension
between 2009 and 2012:
 15.5% were current smokers
 49.5% were obese
 63.2% had hypercholesterolemia
 27.2% had DM
 15.8% had chronic kidney disease
 eGFR <60 mL/min/1.73 m2
and/or
 Urine albumin : creatinine >300 mg/g
• Hypertension is one of the • It is often associated with additional
leading causes of the global cardiovascular disease risk factors
burden of disease. • The risk of cardiovascular disease
• Hypertension doubles the risk of increases with the total burden of
risk factors.
cardiovascular diseases:
 Coronary heart disease (CHD) • Although antihypertensive therapy
reduces the risks of cardiovascular
 Congestive heart failure (CHF)
and renal disease, large segments of
 Ischemic and hemorrhagic stroke the hypertensive population are
 Renal failure either untreated or inadequately
 Peripheral arterial disease treated.
CLASSIFICATION OF BLOOD PRESSURE

• Individuals with SBP and DBP in 2


categories should be designated
to the higher BP category.
• BP indicates blood pressure
based on an average of >2 careful
readings obtained on >2
occasions.
CONDITIONS WITH VARIATION IN BP

Variation Description
Office BP > 3 drugs at optimal doses (including a diuretic)
Resistant Hypertension OR
Office BP < 130/80 mmHg but requires 4 drugs
Fall in SBP > 20 mmHg or in DBP > 10 mmHg within 3 minutes of assuming
Orthostatic Hypotension
upright posture from supine position.
HYPERTENSIVE CRISIS
MARKEDLY ELEVATED BP
HYPERTENSIVE HYPERTENSIVE
URGENCY EMERGENCY

BLOOD SBP > 180 mmHg SBP > 180 mmHg


and/or and/or
PRESSURE
DBP > 120 mmHg DBP > 120 mmHg

TARGET ORGAN
None Present
DAMAGE

Reinstitute or intensify Admit to ICU and


oral antihypertensive manage based on the
MANAGEMENT drug therapy & arrange presence of compelling
close follow-up conditions
CAUSES OF HYPERTENSION
Genetic Predisposition

• Hypertension is a complex polygenic • Multiple single nucleotide


disorder in which many genes or gene polymorphisms influencing control of
combinations influence BP BP since completion of the Human
• Monogenic forms of hypertension: Genome Project in 2003,the associated
 Glucocorticoid remediable aldosteronism variants have only small effects.
 Liddle’s syndrome • The presence of a high number of
 Gordon’s syndrome
small-effect alleles associated with
 Others in which single-gene mutations fully
explain the pathophysiology of hypertension higher BP results in a more rapid
 Rare increase in BP with age
CAUSES OF HYPERTENSION
Environmental Risk Factors
• Diet-related factors associated with high BP include:
 Overweight
 Obesity
 Excess intake of sodium
 Insufficient intake of potassium, calcium, magnesium, protein (especially
from vegetables), fiber, and fish fats.
 Poor diet
• Physical inactivity
• Excess intake of alcohol
CAUSES OF HYPERTENSION
Secondary Forms of Hypertension
CAUSES OF HYPERTENSION
Secondary Forms of Hypertension
CAUSES OF HYPERTENSION
Secondary Forms of Hypertension
CAUSES OF HYPERTENSION
Secondary Forms of Hypertension
Pathophysiology of Hypertension
MECHANISMS OF HYPERTENSION
INTRAVASCULAR VOLUME
• Sodium is predominant extracellular ion • Initial elevation of blood pressure 
and is a primary determinant of the ECF vascular volume expansion  increase of
volume. cardiac output  over time  peripheral
resistance increases  cardiac output
• NaCl intake exceeds the capacity of the reverts toward normal.
kidney to excrete sodium, vascular volume
may initially expand and cardiac output • Salt can activate a number of neural,
may increase. endocrine or paracrine, and vascular
mechanisms  potential to increase arterial
• Vascular beds have the capacity to pressure.
autoregulate blood flow, and if constant
• Arterial pressure increases in response to
blood flow is to be maintained in the face
high NaCl intake  urinary sodium excretion
of increased arterial pressure, resistance increases & sodium balance is maintained.
within that bed must increase
MECHANISMS OF HYPERTENSION
INTRAVASCULAR VOLUME AUTONOMIC NERVOUS SYSTEM
• “Pressure-Natriuresis” • Adrenergic reflexes  modulate
phenomenon  indirect increase blood pressure over the short term
in the glomerular filtration rate  • Adrenergic function + hormonal
decreased absorbing capacity of and volume-related factors  long
the renal tubules  hormonal term regulation of arterial pressure.
factors such as ANF.
• Norepinephrine, epinephrine, and
• Impaired capacity to excrete dopamine all play important roles
sodium  greater increases in in tonic and phasic cardiovascular
arterial pressure  achieve regulation.
natriuresis and sodium balance.
MECHANISMS OF HYPERTENSION
RENIN – ANGIOTENSIN – ALDOSTERONE
• Contributes to the regulation of arterial pressure Angiotensin II
primarily via the vasoconstrictor properties of a potent pressor
angiotensin II and the sodium-retaining properties of substance, the
aldosterone. primary tropic
• Renin is an aspartyl protease that is synthesized as an factor for the
enzymatically inactive precursor, prorenin. Most renin secretion of
in the circulation is synthesized in the renal afferent aldosterone
renal arteriole. (adrenal zona
• Renin secretion: glomerulosa)
 Decreased NaCl transport in the distal portion of the thick
ascending limb of the loop of Henle that adjoins the
potent mitogen
corresponding afferent arteriole (macula densa) that stimulates
 Decreased pressure or stretch within the renal afferent vascular smooth
arteriole (baroreceptor mechanism) muscle cell and
 Sympathetic nervous system stimulation of renin-secreting
myocyte growth.
cells via β1 adrenoreceptors
MECHANISMS OF HYPERTENSION
VASCULAR MECHANISMS
• Vascular radius and compliance of resistance • Apoptosis, low-grade inflammation, and
arteries are important determinants of arterial
pressure.
vascular fibrosis also contribute to
remodeling.
• Resistance to flow varies inversely with R^4, and
small decrease in lumen size  increase resistance. • Lumen diameter also is related to
• Hypertension  structural, mechanical, or elasticity of the vessel.
functional changes  reduce the lumen diameter
of small arteries and arterioles. • Vessels with a high degree of elasticity
• Remodeling refers to geometric alterations in the can accommodate an increase of volume
vessel wall without a change in vessel volume. with relatively little change in pressure
• Hypertrophic or eutrophic vascular remodeling  • Whereas in a semirigid vascular system,
decreased lumen size  increased peripheral a small increment in volume induces a
resistance.
relatively large increment of pressure.
PATHOLOGIC CONSEQUENCES OF HYPERTENSION
HEART BRAIN
• Heart disease is the most common • Stroke is the second most frequent cause of death in
the world
cause of death in hypertensive patients.
• 5 million deaths each year, with an additional 15
• Hypertensive heart disease is the result million persons having non-fatal strokes.
of structural and functional adaptations • Elevated blood pressure is the strongest risk factor
leading to: for stroke.
 Left ventricular hypertrophy • Approximately 85% of strokes are due to infarction,
and the 15% are due to either intracerebral or
 CHF subarachnoid hemorrhage.
 Abnormalities of blood flow due to • Incidence of stroke rises progressively with
atherosclerotic coronary artery disease increasing BP levels, particularly systolic BP in
and microvascular disease individuals >65 y/o.
 Cardiac arrhythmias. • Treatment of hypertension decreases the incidence
of both ischemic and hemorrhagic strokes.
PATHOLOGIC CONSEQUENCES OF HYPERTENSION

KIDNEY PERIPHERAL ARTERIES


• Kidney is both target and cause of hypertension. • Blood vessels are a target organ for atherosclerotic
disease secondary to long-standing elevated BP.
• Primary renal disease is the most common etiology
of secondary hypertension. • Hypertensive patients, vascular disease is a major
contributor to stroke, heart disease, and renal failure.
• Mechanisms of kidney-related hypertension include
• Hypertensive patients with arterial disease of the lower
a diminished capacity to excrete sodium, excessive
extremities are at increased risk for future cardiovascular
renin secretion in relation to volume status, and disease.
sympathetic nervous system overactivity.
• ABI is a useful approach for evaluating PAD and is
• Conversely, hypertension is a risk factor for renal defined as the ratio of noninvasively assessed ankle to
injury and ESRD. brachial (arm) systolic BP.
• Renal risk appears to be more closely related to • ABI of <0.90 is considered diagnostic of PAD and is
systolic than to diastolic blood pressure associated with >50% stenosis in at least one major
• Black men are at greater risk than white men for lower limb vessel.
developing ESRD at every level of blood pressure. • ABI of <0.80 is associated with elevated BP, particularly
systolic blood pressure.
HISTORY PHYSICAL EXAMINATION

LABORATORY TESTING

MEASUREMENT OF BP
End…

You might also like