HYPERTENSION
Dr Guta Feyisa (MD)
DEFINITION OF HYPERTENSION
 Hypertension (high blood pressure) is when the pressure
in your blood vessels is too high (140/90 mmHg or
higher). WHO
 Hypertension is major contributor to cardiovascular
diseases and complications
 Etiology is unknown in 80–95% of pts (“essential
hypertension”).
DEFINITION
 Always consider a secondary correctable form of
hypertension, especially in pts aged ≤30 or those who
become hypertensive after 55.
 Isolated systolic hypertension (systolic ≥140, diastolic
<90) most common in elderly pts, due to reduced
vascular compliance.
BP CATEGORIZATION
RECOMMENDATION FOR OFFICE BP
MEASUREMENT
HOW TO MEASURE BP
WHITE COAT AND MASKED
HYPERTENSION
 The use of office and out-of-office (home or ambulatory)
BP measurements identifies individuals with white coat
hypertension and masked hypertension.
 White coat hypertension is elevated BP only in the
office (nonelevated ambulatory or home BP)
 Masked hypertension is nonelevated BP in the office
but elevated BP out of the office (ambulatory or home)
 About 10%–30% of subjects attending clinics due to
high BP have white coat hypertension and 10%–15%
have masked hypertension.
SECONDARY HYPERTENSION
 Secondary hypertension is high blood pressure that
results from an identifiable and often treatable
underlying medical condition.
 Unlike primary (essential) hypertension, which has no
clear cause, secondary hypertension is a symptom of
another disease or disorder.
CAUSES OF SECONDARY HTN
Renal Artery Stenosis (Renovascular Hypertension)
 Due to either atherosclerosis (older men) or fibro
muscular dysplasia (young women).
 Presents with recent onset of hypertension, refractory to
usual antihypertensive therapy.
 Abdominal bruit is present in 50% of cases;
 Hypokalemia due to activation of the renin-angiotensin-
aldosterone system may be present.
Renal Parenchymal Disease
 Elevated serum creatinine and/or abnormal urinalysis,
containing protein, cells, or casts.
Coarctation of Aorta
 Presents in children or young adults (including 35% of pts
with Turner syndrome)
 Constriction is usually present in aorta at origin of left
subclavian artery.
 Examination shows diminished, delayed femoral pulsations;
systolic murmur loudest at left infrascapular region.
 CXR shows indentation of the aorta at the level of the
coarctation and rib notching (due to development of
collateral arterial flow).
 Doppler echocardiography identifies region of constriction
and measures associated pressure gradient.
Pheochromocytoma
 A catecholamine-secreting tumor, typically of the adrenal medulla or
extraadrenal paraganglion tissue.
 Presents as paroxysmal or sustained hypertension in young to middle-
aged pts.
 Sudden episodes of headache, palpitations, and profuse diaphoresis are
common.
 Associated findings include chronic weight loss, orthostatic
hypotension, and impaired glucose tolerance.
 Pheochromocytomas may be localized to the bladder wall and may
present with micturition-associated symptoms of catecholamine excess.
 Diagnosis is suggested by elevated plasma metanephrine level or
urinary catecholamine metabolites in a 24-h urine collection; the tumor
is then localized by CT or MRI.
Hyperaldosteronism
 Usually due to aldosterone-secreting adenoma or bilateral
adrenal hyperplasia
 A cause of refractory hypertension that should be suspected
when hypokalemia is present in a hypertensive pt off diuretics
 Other Causes are: Oral contraceptive usage, obstructive sleep
apnea ,Cushing’s and adrenogenital syndromes, thyroid
disease , hypercalcemia (e.g., hyperparathyroidism), and
acromegaly.
 In pts with systolic hypertension and wide pulse pressure,
consider thyrotoxicosis, aortic regurgitation , and systemic AV
fistula.
APPROACH TO THE PATIENT
History:
 Most pts are asymptomatic. So that is called silent killer
 Severe hypertension may lead to headache, dizziness, or
blurred vision.
 Clues to specific forms of secondary hypertension:
 Use of medications (e.g., birth control pills, glucocorticoids,
decongestants, erythropoietin, NSAIDs, cyclosporine);
 paroxysms of headache, sweating, or tachycardia
(pheochromocytoma)
 history of renal disease or abdominal trauma (renal
hypertension);
 daytime somnolence and snoring (sleep apnea).
Physical examination:
 Measure bp with appropriate-sized cuff (large cuff for
large arm).
 Measure bp in both arms as well as a leg (to evaluate for
aortic coarctation).
 Signs of hypertension include retinal arteriolar changes
(narrowing/nicking);
 left ventricular lift, loud A2 , S4 .
 Clues to secondary forms of hypertension include
cushingoid appearance, thyromegaly, abdominal bruit
(renal artery stenosis), delayed femoral pulses
(coarctation of aorta).
Laboratory Workup
 Screening tests for secondary hypertension: Should be
carried out on all pts with documented hypertension:
 RFT, Serum electrolyte, U/A, CXR, ECG
 blood tests including CBC, glucose, lipid levels,
calcium, uric acid;
 TSH if thyroid disease suspected.
 Abdominal U/S
 Other hormonal analysis
TREATMENT
Non-pharmacologic(life style modification) and
pharmacologic management
 Life style modification principles
 Salt restriction
 Healthy diet
 Healthy drinks
 Moderation of alcohol consumption
 Weight reduction
 Smoking cessation
 Regular physical activity
 Reduce stress and induce mindfulness
DRUG THERAPY OF ESSENTIAL HYPERTENSION
 2017 Hypertension Guidelines recommend initiating
antihypertensive drug therapy for primary prevention
when systolic BP ≥140 mmHg or diastolic BP ≥90
mmHg
 Note that if 10-year atherosclerotic event risk is ≥10%,
or if pt has had prior cardiovascular event, initiate drug
treatment for systolic BP ≥130 or diastolic BP ≥80.
 Goal is to control hypertension with minimal side
effects.
 A combination of medications with complementary
actions is often required.
 First-line agents include diuretics, ACE inhibitors,
angiotensin receptor antagonists, calcium channel
antagonists, and sometimes beta blockers.
 On-treatment blood pressure goal is <140/90 and if
comorbidity like CKD, CAD, CHF, Stroke, metabolic
syndrome exist goal is <130/80.
COMPLICATIONS
Cardiovascular Complications
 Coronary artery disease
 Heart attack (MI)
 Heart failure
 Left ventricular hypertrophy
 Aneurysms
Neurological Complications
 Stroke: Ischemic or hemorrhagic due to vessel damage
or rupture
 Transient ischemic attacks (TIAs): Mini-strokes with
temporary symptoms
 Vascular dementia: Chronic reduced cerebral perfusion
Renal Complications
 Chronic kidney disease (CKD): Damage to renal
vasculature impairs filtration
 End-stage renal disease (ESRD): May require dialysis
or transplant
Ophthalmologic Complications
 Hypertensive retinopathy: Damage to retinal vessels,
leading to vision loss
 Optic neuropathy: Rare but serious consequence of
severe hypertension
Metabolic and Other Complications
 Metabolic syndrome: Hypertension is a core component
 Sexual dysfunction: Erectile dysfunction in men,
reduced libido in women
 Peripheral artery disease (PAD): Reduced blood flow
to limbs
HYPERTENSIVE CRISIS: A MEDICAL EMERGENCY
 A hypertensive crisis is a sudden and severe elevation
in blood pressure,
 typically defined as ≥180/120 mmHg.
 It requires immediate attention to prevent life-
threatening organ damage.
 Classified as hypertensive urgency or emergency
Type Definition Urgency
Hypertensive Urgency
BP ≥180/120 mmHg
without signs of acute
organ damage
Urgent but not emergent
Hypertensive
Emergency
BP ≥180/120 mmHg
with evidence of acute
target organ damage
Immediate emergency
Symptoms of Hypertensive Emergency
 Severe headache
 Chest pain
 Shortness of breath
 Blurred vision
 Confusion or altered mental status
 Nausea/vomiting
 Seizures
 Stroke-like symptoms (e.g., facial droop, weakness,
speech difficulty)
Target Organs at Risk
 Brain: Stroke, encephalopathy
 Heart: Myocardial infarction, heart failure
 Kidneys: Acute kidney injury
 Eyes: Retinopathy, vision loss
 Aorta: Dissection
Management Approach
 Emergency: Immediate hospitalization and IV
antihypertensives (e.g., labetalol, nitroprusside)
 Urgency: Oral antihypertensives and close outpatient
follow-up
 Goal: Gradual BP reduction to avoid ischemia (e.g.,
reduce MAP by no more than 25% in first hour)
THANK YOU!

HYPERTENSION.pptx for internal medicine attachment

  • 1.
  • 2.
    DEFINITION OF HYPERTENSION Hypertension (high blood pressure) is when the pressure in your blood vessels is too high (140/90 mmHg or higher). WHO  Hypertension is major contributor to cardiovascular diseases and complications  Etiology is unknown in 80–95% of pts (“essential hypertension”).
  • 3.
    DEFINITION  Always considera secondary correctable form of hypertension, especially in pts aged ≤30 or those who become hypertensive after 55.  Isolated systolic hypertension (systolic ≥140, diastolic <90) most common in elderly pts, due to reduced vascular compliance.
  • 4.
  • 5.
  • 6.
  • 7.
    WHITE COAT ANDMASKED HYPERTENSION  The use of office and out-of-office (home or ambulatory) BP measurements identifies individuals with white coat hypertension and masked hypertension.  White coat hypertension is elevated BP only in the office (nonelevated ambulatory or home BP)  Masked hypertension is nonelevated BP in the office but elevated BP out of the office (ambulatory or home)  About 10%–30% of subjects attending clinics due to high BP have white coat hypertension and 10%–15% have masked hypertension.
  • 8.
    SECONDARY HYPERTENSION  Secondaryhypertension is high blood pressure that results from an identifiable and often treatable underlying medical condition.  Unlike primary (essential) hypertension, which has no clear cause, secondary hypertension is a symptom of another disease or disorder.
  • 9.
    CAUSES OF SECONDARYHTN Renal Artery Stenosis (Renovascular Hypertension)  Due to either atherosclerosis (older men) or fibro muscular dysplasia (young women).  Presents with recent onset of hypertension, refractory to usual antihypertensive therapy.  Abdominal bruit is present in 50% of cases;  Hypokalemia due to activation of the renin-angiotensin- aldosterone system may be present. Renal Parenchymal Disease  Elevated serum creatinine and/or abnormal urinalysis, containing protein, cells, or casts.
  • 10.
    Coarctation of Aorta Presents in children or young adults (including 35% of pts with Turner syndrome)  Constriction is usually present in aorta at origin of left subclavian artery.  Examination shows diminished, delayed femoral pulsations; systolic murmur loudest at left infrascapular region.  CXR shows indentation of the aorta at the level of the coarctation and rib notching (due to development of collateral arterial flow).  Doppler echocardiography identifies region of constriction and measures associated pressure gradient.
  • 11.
    Pheochromocytoma  A catecholamine-secretingtumor, typically of the adrenal medulla or extraadrenal paraganglion tissue.  Presents as paroxysmal or sustained hypertension in young to middle- aged pts.  Sudden episodes of headache, palpitations, and profuse diaphoresis are common.  Associated findings include chronic weight loss, orthostatic hypotension, and impaired glucose tolerance.  Pheochromocytomas may be localized to the bladder wall and may present with micturition-associated symptoms of catecholamine excess.  Diagnosis is suggested by elevated plasma metanephrine level or urinary catecholamine metabolites in a 24-h urine collection; the tumor is then localized by CT or MRI.
  • 12.
    Hyperaldosteronism  Usually dueto aldosterone-secreting adenoma or bilateral adrenal hyperplasia  A cause of refractory hypertension that should be suspected when hypokalemia is present in a hypertensive pt off diuretics  Other Causes are: Oral contraceptive usage, obstructive sleep apnea ,Cushing’s and adrenogenital syndromes, thyroid disease , hypercalcemia (e.g., hyperparathyroidism), and acromegaly.  In pts with systolic hypertension and wide pulse pressure, consider thyrotoxicosis, aortic regurgitation , and systemic AV fistula.
  • 13.
    APPROACH TO THEPATIENT History:  Most pts are asymptomatic. So that is called silent killer  Severe hypertension may lead to headache, dizziness, or blurred vision.  Clues to specific forms of secondary hypertension:  Use of medications (e.g., birth control pills, glucocorticoids, decongestants, erythropoietin, NSAIDs, cyclosporine);  paroxysms of headache, sweating, or tachycardia (pheochromocytoma)  history of renal disease or abdominal trauma (renal hypertension);  daytime somnolence and snoring (sleep apnea).
  • 14.
    Physical examination:  Measurebp with appropriate-sized cuff (large cuff for large arm).  Measure bp in both arms as well as a leg (to evaluate for aortic coarctation).  Signs of hypertension include retinal arteriolar changes (narrowing/nicking);  left ventricular lift, loud A2 , S4 .  Clues to secondary forms of hypertension include cushingoid appearance, thyromegaly, abdominal bruit (renal artery stenosis), delayed femoral pulses (coarctation of aorta).
  • 15.
    Laboratory Workup  Screeningtests for secondary hypertension: Should be carried out on all pts with documented hypertension:  RFT, Serum electrolyte, U/A, CXR, ECG  blood tests including CBC, glucose, lipid levels, calcium, uric acid;  TSH if thyroid disease suspected.  Abdominal U/S  Other hormonal analysis
  • 16.
    TREATMENT Non-pharmacologic(life style modification)and pharmacologic management  Life style modification principles  Salt restriction  Healthy diet  Healthy drinks  Moderation of alcohol consumption  Weight reduction  Smoking cessation  Regular physical activity  Reduce stress and induce mindfulness
  • 17.
    DRUG THERAPY OFESSENTIAL HYPERTENSION  2017 Hypertension Guidelines recommend initiating antihypertensive drug therapy for primary prevention when systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg  Note that if 10-year atherosclerotic event risk is ≥10%, or if pt has had prior cardiovascular event, initiate drug treatment for systolic BP ≥130 or diastolic BP ≥80.  Goal is to control hypertension with minimal side effects.
  • 18.
     A combinationof medications with complementary actions is often required.  First-line agents include diuretics, ACE inhibitors, angiotensin receptor antagonists, calcium channel antagonists, and sometimes beta blockers.  On-treatment blood pressure goal is <140/90 and if comorbidity like CKD, CAD, CHF, Stroke, metabolic syndrome exist goal is <130/80.
  • 19.
    COMPLICATIONS Cardiovascular Complications  Coronaryartery disease  Heart attack (MI)  Heart failure  Left ventricular hypertrophy  Aneurysms
  • 20.
    Neurological Complications  Stroke:Ischemic or hemorrhagic due to vessel damage or rupture  Transient ischemic attacks (TIAs): Mini-strokes with temporary symptoms  Vascular dementia: Chronic reduced cerebral perfusion
  • 21.
    Renal Complications  Chronickidney disease (CKD): Damage to renal vasculature impairs filtration  End-stage renal disease (ESRD): May require dialysis or transplant Ophthalmologic Complications  Hypertensive retinopathy: Damage to retinal vessels, leading to vision loss  Optic neuropathy: Rare but serious consequence of severe hypertension
  • 22.
    Metabolic and OtherComplications  Metabolic syndrome: Hypertension is a core component  Sexual dysfunction: Erectile dysfunction in men, reduced libido in women  Peripheral artery disease (PAD): Reduced blood flow to limbs
  • 23.
    HYPERTENSIVE CRISIS: AMEDICAL EMERGENCY  A hypertensive crisis is a sudden and severe elevation in blood pressure,  typically defined as ≥180/120 mmHg.  It requires immediate attention to prevent life- threatening organ damage.  Classified as hypertensive urgency or emergency
  • 24.
    Type Definition Urgency HypertensiveUrgency BP ≥180/120 mmHg without signs of acute organ damage Urgent but not emergent Hypertensive Emergency BP ≥180/120 mmHg with evidence of acute target organ damage Immediate emergency
  • 25.
    Symptoms of HypertensiveEmergency  Severe headache  Chest pain  Shortness of breath  Blurred vision  Confusion or altered mental status  Nausea/vomiting  Seizures  Stroke-like symptoms (e.g., facial droop, weakness, speech difficulty)
  • 26.
    Target Organs atRisk  Brain: Stroke, encephalopathy  Heart: Myocardial infarction, heart failure  Kidneys: Acute kidney injury  Eyes: Retinopathy, vision loss  Aorta: Dissection
  • 27.
    Management Approach  Emergency:Immediate hospitalization and IV antihypertensives (e.g., labetalol, nitroprusside)  Urgency: Oral antihypertensives and close outpatient follow-up  Goal: Gradual BP reduction to avoid ischemia (e.g., reduce MAP by no more than 25% in first hour)
  • 28.