Hypertension is defined as Systolic Blood

Pressure (SBP) 140 mm Hg, and / or

Diastolic Blood Pressure (DBP) 90
mmHg.
JNC VII
 Classification of Blood Pressure

BP Classification SBP mm Hg DBP mm Hg

Normal <120 and <80

Prehypertension 120139 or 8089

Stage 1
140159 or 9099
Hypertension
Stage 2
160 or 100
Hypertension

JNC VII
 Diagnostic Workup
Assess risk factors and comorbidities
Reveal identifiable causes of hypertension
Assess presence of target organ damage
Conduct history and physical examination
Obtain laboratory tests: urinalysis, blood
glucose, hematocrit and lipid panel, serum
potassium, creatinine, and calcium
Optional: urinary albumin/creatinine ratio
Obtain electrocardiogram
JNC VII
 Assess for Major Cardiovascular
Disease (CVD) Risk Factors
Hypertension
Obesity (body mass index >30 kg/m2)
Dyslipidemia
Diabetes mellitus
Cigarette smoking
Physical inactivity
Microalbuminuria, estimated GFR <60 mL/min
Age (>55 for men, >65 for women)
Family history of premature CVD (men age <55,
women age <65)
JNC VII
 Assess for Identifiable Causes of
Hypertension
Sleep apnea
Drug induced/related
Chronic kidney disease
Primary aldosteronism
Renovascular disease
Cushings syndrome or steroid therapy
Pheochromocytoma
Coarctation of aorta
Thyroid/parathyroid disease
JNC VII
 Blood Pressure Measurement
Techniques
Method Notes
In-office Two readings, 5 minutes apart, sitting in
chair.
Confirm elevated reading in contralateral
arm.
Ambulatory BP Indicated for evaluation of white coat
monitoring hypertension.
Absence of 1020 percent BP decrease
during sleep may indicate increased CVD risk
Patient self- Provides information on response to therapy.
check May help improve adherence to therapy and
is useful for evaluating white coat
hypertension. JNC VII
 Causes of Resistant
Hypertension
Improper BP measurement
Excess sodium intake
Inadequate diuretic therapy
Medication
Inadequate doses
Drug actions and interactions (e.g., nonsteroidal anti-
inflammatory drugs (NSAIDs), illicit drugs,
sympathomimetics, oral contraceptives)
Over-the-counter (OTC) drugs and herbal
supplements
Excess alcohol intake
Identifiable causes of hypertension (see reverse side)
JNC VII
 Compelling indications for
Individual Drug Classes
Compelling Indication Initial Therapy Options
Heart failure THIAZ, BB, ACEI, ARB, ALDO
ANT
Post myocardial BB, ACEI, ALDO ANT
infarction
High CVD risk THIAZ, BB, ACEI, CCB
Diabetes THIAZ, BB, ACEI, ARB, CCB
Chronic kidney disease ACEI, ARB
Recurrent stroke THIAZ, ACEI
prevention
THIAZ = thiazide diuretic, ACEI= angiotensin converting enzyme inhibitor, ARB =
angiotensin receptor blocker, BB = beta blocker, CCB = calcium channel blocker,
ALDO ANT = aldosterone antagonist

JNC VII
Strategies for Improving Adherence
to Therapy

Clinician empathy increases patient

trust, motivation, and adherence to
therapy
Physicians should consider their
patients cultural beliefs and
individual attitudes in formulating
therapy

JNC VII
 Principles of Hypertension
Treatment

Treat to BP <140/90 mmHg or BP

<130/80 mmHg in patients with
diabetes or chronic kidney disease
Majority of patients will require two
medications to reach goal

JNC VII
 Algorithm for Treatment of
Hypertension
Lifestyle Modifications

Not at Goal Blood Pressure (<140/90 mmHg)

(<130/80 mmHg for those with diabetes or chronic kidney disease)

Initial Drug Choices

Without Compelling With Compelling

Indications
Stage 1 Hypertension
(SBP 140159 or DBP 9099 mmHg)
Thiazide-type diuretics for most.
May consider ACEI, ARB, BB, CCB,
or combination.
Stage 2 Hypertension
(SBP >160 or DBP >100 mmHg)
2-drug combination for most (usually
thiazide-type diuretic and
ACEI, or ARB, or BB, or CCB)
Indications
Drug(s) for the compelling indications
Other antihypertensive drugs
(diuretics, ACEI, ARB, BB, CCB)
as needed.

Not at Goal
Blood Pressure

Optimize dosages or add additional drugs

until goal blood pressure is achieved.
Consider consultation with hypertension specialist.
JNC VII
 Principles of Lifestyle
Modification
Encourage healthy lifestyles for all individuals
Prescribe lifestyle modifications for all patients
with prehypertension and hypertension
Components of lifestyle modifications include
weight reduction, DASH eating plan, dietary
sodium reduction, aerobic physical activity,
and moderation of alcohol consumption

JNC VII
 Lifestyle Modification
Recommendations
Avg. SBP
Modification Recommendation Reduction
Range
Weight Maintain normal body weight (body mass 520 mmHg/10
reduction index 18.524.9 kg/m2) kg
Adopt a diet rich in fruits, vegetables, and
DASH eating lowfat dairy 814 mmHg
plan products with reduced content of saturated
and total fat
Dietary
Reduce dietary sodium intake to <100 mmol 28 mmHg
sodium
per day (2.4 g sodium or 6 g sodium chloride)
reduction
Aerobic Regular aerobic physical activity (e.g., brisk
49 mmHg
physical walking) at least 30 minutes per day, most
activity days of the week
*Moderation Men:
1 drink = 1/2 oz or limit
15 mL to <2
ethanol drinks*
(e.g., 12 ozper day.
beer, 5 oz wine, 1.5 oz 80-proof whiskey).
24 mmHg
of alcohol
Effects Women
are dose and and lighterDASH
time dependent. weight persons:
= Dietary limit to to Stop Hypertension.
Approaches
consumption <1 drink* per day JNC VII
 Hypertension Associated
Cardiovascular Problems/Conditions

Left Ventricular Hypertrophy (LVH)

Acute Coronary Syndromes (ACS)
Heart Failure
Diabetes & Nephropathy

JNC VII
 Definition :Left Ventricular
Hypertrophy (LVH)

Left ventricular hypertrophy is

defined as an increase in the mass
of the left ventricle, which can be
secondary to an increase in wall
thickness, an increase in cavity
size, or both.
Pathophysiology :Left Ventricular
Hypertrophy (LVH)
A consequence of hypertension
Usually presents with an increase in wall
thickness, with or without an increase in
cavity size
Increase in mass results from a chronic
increase in afterload of LV caused by the
hypertension
A significant increase in the number and /or
size of sarcomeres within each myocardial
cell is the pathologic mechanism
 Pathophysiology :Left Ventricular
Hypertrophy (LVH)
Law of Laplace:
T=Pxr/h
Circumferential wall stress (T) = Transmural distending
pressure (P) x Radius of chamber (r) Wall thickness (h)
To compensate for an increase in left ventricular pressure, wall
thickness increases to reduce wall stress

r P T

J Clin Hypertens (Greenwich).

2005;7(4):231-238.
 Pathophysiology :Left Ventricular
Hypertrophy (LVH)
Peripheral resistance

LV Wall stress

Concentric LVH Nonhemodynamic factors

Oxygen demand

Coronary flow reserve Diastolic filling

Angina Myocardial Ventricular LVEDP

pectoris infarction ectopy
Left atrial pressure
Fibrosis
Sudden
death
Systolic Atrial Diastolic
heart failure fibrillation heart failure

Obstructive epicardial
coronary artery disease
J Clin Hypertens (Greenwich). 2005;7(4):231-238.
 Diagnosis :Left Ventricular
Hypertrophy (LVH)

Although the Electrocardiogram may

reveal changes suggestive of LVH
It is much less sensitive than
Echocardiography

Echocardiography, is the preferred

test to evaluate the presence and
extent of LVH in hypertensive patients
 Signs and symptoms :Left
Ventricular
Hypertrophy (LVH)
Depend on the underlying cause
As LVH usually develops slowly, there may be no
signs or symptoms for many years or none at all
If present include:
Shortness of breath
Chest pain
Irregular heart beats
Dizziness
Fainting
 Management :Left Ventricular
Hypertrophy (LVH)
Treatment of the underlying cause
The results of meta-analyses show:
Angiotensin-converting enzyme inhibitors and
angiotensin II receptor blockers achieve
significantly better results than b-blockers
The most recently published Losartan
Intervention For Endpoint reduction in
hypertension study confirmed the superiority
of angiotensin receptor blockers against b-
blockers in a large-scale prospective trial
 Acute Coronary Syndromes
(ACS)
The term used to cover any group of
clinical symptoms compatible with acute
myocardial ischemia and covers:
Unstable Angina
Non-Q-wave Myocardial Infarction and
Q-wave Myocardial Infarction

Characterized by the common

pathophysiology of a disrupted
atherosclerotic plaque
 Global Statistics

Every year:
> 4 million patients are admitted
with unstable angina and acute MI
> 900,000 patients undergo PTCA
with or without stent
 Pathophysiology
Phase 4 Phase 4

Phase 1 Phase 2 VI VI
Phase 5

I-III IV-Va Vb-Vc

Acute Syndromes
Myocardial Infarction
Unstable angina
Ischemic sudden death

Angina
No Symptoms Pectoris
Phase 3
VI
 Myocardial Ischemia
Presentation
Silent ischemia
Exertion-induced angina
Unstable angina
Acute myocardial infarction
 Patient Evaluation
Based on the patients
History / Physical examination

ECG

Patients are categorized into 3 groups

Non-cardiac chest pain

Unstable angina

Myocardial infarction
 Patient Evaluation

History
Ischemic Symptoms Physical Exam

No ST-segment ST-segment
elevation elevation ECG

Acute
Unstable anginaNon-Q MI Q-Wave MI Reperfusion
 Management of
Acute Coronary Syndromes (ACS)
Initial Treatment of ACS

STEMI* UA/NSTEMI

Antiplatelet, anti-ischemic, Antiplatelet, anti-ischemic,

or anticoagulant therapy or anticoagulant therapy

Thrombolytics PCI or CABG PCI or CABG

Long term medical management

Braunwald E et al. Available at www.acc.org Also known as Q-wave MI
Bowen WE, Mckay RG. N Engl J Med. 2001;344:1939-1942 Also known as non-Q wave MI.
 Current Medical Management of
Unstable Angina and NSTEMI*
Acute Therapy Maintenance Therapy
Oxygen, bed rest, Antiplatelet Therapy
ECG monitoring
Beta Blockers
Nitroglycerin
Calcium Channel
Beta Blockers
Blockers
ACE Inhibitors
Lipid-lowering
Antiplatelet Therapy
Agents
Anticoagulant
ACE Inhibitors
Therapy
Braunwald E et al. Available at www.acc.org * Also known as non-Q wave MI.
 Definition of Heart Failure

HF is a complex clinical syndrome

that can result from any structural
or functional cardiac disorder that
impairs the ability of the ventricle
to fill with or eject blood.
 Incidence of Heart Failure
Approximately 5 million patients have HF in U. S.
only
Over 550,000 patients are diagnosed with HF for
the first time each year
Primary reason for 12 to 15 million office visits
and 6.5 million hospital days each year
In 2001, nearly 53,000 patients died of HF as a
primary cause (U. S.)
The incidence of HF approaches 10 per 1000
population after age 65
 Causes of Heart Failure

1. Coronary artery disease

2. Hypertension

3. Dilated cardiomyopathy
Pathophysiology of Heart Failure
Neurohormonal and Cytokine Activation in Heart Failure

Vasoconstrictors Vasodilators
Angiotensin II Prostaglandin I2
Norepinephrine Prostaglandin E2
Endothelin BNP, ANP
Vasopressin Nitric Oxide
Natriuretic peptides Proinflammatory Cytokines
ANP, CNP TNF
BNP Interleukin-6
Interferon-
Other factors
? Interleukin-1 & 2
Aldosterone Soluble ILTR 1 & 2
Growth hormone
cortisol
 Pathophysiology of Heart Failure
Effect of Sympathetic Activation in Heart Failure
CNS Sympathetic Outflow

Sympathetic Activity to
Cardiac Sympathetic Activity kidneys and vasculature

1-Receptor 2-Receptor 1-Receptor 1 - 2 - Activation of RAS

Myocyte Death Vasoconstriction

Arrhythmias Sodium Retention

Disease Progression
Pathophysiology of Heart Failure
Neurohormonal Activation In Heart Failure: Angiotensin
II Effects
Direct Vasoconstriction
Increased Myocardial Contractility
Activation Of The Sympathetic Nervous System
Increase In Vasoconstrictors (Aldosterone,
Vasopressin, Endothelin-1)
Adverse Vascular Remodelling
Increased Myocyte Growth
Vascular Smooth Muscle Growth
Increased Collagen Production
Enhanced Platelet Aggregation Leading To
Thrombogenesis
Pathophysiology of Heart Failure
Deleterious Effects of Aldosterone in Heart Failure

Aldosteron
e
 Pathophysiology of Heart Failure

ANP = atrial natriuretic peptide; BNP = B-type or brain natriuretic peptide; CNP = C-type natriuretic
peptide; RAAS = renin-angiotensin-aldosterone system, SNS = sympathetic nervous system
Pathophysiology of Heart Failure
 Stages of Heart Failure
At Risk for Heart Failure:
STAGE A High risk for developing HF
STAGE B Asymptomatic LV dysfunction

Heart Failure:
STAGE C Past or current symptoms of HF
STAGE D End-stage HF
 Medical Management of Heart
Failure
Cardiovascular Medications Useful For Treatment Of Various Stages Of Heart Failure

Drug Stage A Stage B Stage C

ACE Inhibitors

Benazepril H - -

Captopril H, DN Post MI HF

Enalapril Asymptomatic LVSD HF

Fosinopril H HF

Lisinopril Post MI HF

Moexipril H

Perindopril H, CV Risk

Quinapril H HF

Ramipril H, CV Risk Post MI Post MI

Trandolapril H Post MI Post MI

 Medical Management of Heart
Failure
Cardiovascular Medications Useful For Treatment Of Various Stages Of Heart Failure

Drug Stage A Stage B Stage C

Angiotensin Receptor Blockers

Candesartan H - HF

Eprosartan H - -

Irbesartan H, DN - -

Losartan H, DN CV Risk -

Olmesartan H - -

Telmisartan H - -

Valsartan H, DN Post MI Post MI, HF

Aldosterone Antagonists
Eplerenone H Post MI Post MI

Spironolactone H - HF
 Medical Management of Heart Failure
Cardiovascular Medications Useful For Treatment Of Various Stages Of Heart Failure
Drug Stage A Stage B Stage C
Beta Blockers
Acebutolol H - -
Atenolol H Post MI -
Betaxolol H -
Bisoprolol H HF
Carteolol H -
Carvedilol H Post MI HF, Post MI
Labetalol H -
Metoprolol Succinate H HF
Metoprolol tartrate H Post MI -
Nadolol H -
Penbutolol H -
Pindolol H -
Propranolol H Post MI -
Timolol H Post MI -
Digoxin - - HF
CV Risk indicates reduction in future cardivascular events;DN, diabetic nephropathy;H, hypertension ; HF, heart failure; Asymptomatic
LVSD, Asymptomatic left ventricular systolic dysfunction; PostMI, reduction in heart failure or other cardiac events following myocardoal
infarction.
 Medical Management of Heart Failure
Oral Diuretics Recommended For Use In The Treatment Of Fluid Retention In Chronic Heart Failure

Drug Initial Daily Dose(s) Maximum Total Dose Duration of Action

Loop Diuretics
Bumetanide 0.5 to 1.0 mg once or twice 10 mg 4 to 6 hours
Furosemide 20 to 40 mg once or twice 600 mg 6 to 8 hours
Torsemide 10 to 20 mg once 200 mg 12 to 16 hours

Thiazide Diuretics
Chlorothiazide 250 to 500 mg once or twice 1000 mg 6 to 12 hours
Chlorthalidone 12.5 to 25 mg once 100 mg 24 to 72 hours
Hydrochlorothiazide 25 mg once or twice 200 mg 6 to 12 hours
Indapamide 2.5 once 5 mg 36 hours
Metolazone 2.5 mg once 20 mg 12 to 24 hours

Potassium-sparing diretics
Amiloride 5 mg once 20 mg 24 hours
Spironolactone 12.5 to 25 mg once 50 mg* 2 to 3 days
Triamterene 50 to 75 mg twice 200 mg 7 to 9 hours

Sequential nephron blockade

Metolazone 2.5 to 10 mg once plus loop diuretic
Hydrochlorothiazide 25 to 100 mg once or twice plus loop diuretic
Chlorothiazide (IV) 500 to 1000 mg once plus loop diuretic
Surgical Management of Heart
Failure
Cardiac Transplantation
In potentially eligible patients
with refractory end-stage HF
 Hypertension & Diabetes
Hypertension is an extremely common comorbid
condition in diabetes
Affects ~2060% of patients with diabetes, depending
on obesity, ethnicity, and age
In type 2 diabetes, hypertension is often present as part
of the metabolic syndrome
In type 1 diabetes, hypertension may reflect the onset
of diabetic nephropathy
Increases risk of complications, including stroke,
coronary artery disease, peripheral vascular disease,
retinopathy, nephropathy, and neuropathy
 The Metabolic Syndrome
Definition:
The metabolic syndrome, which includes:
Diabetes or prediabetes
Abdominal obesity
Unfavorable lipid profile
Hypertension

Triples the risk of myocardial infarction or

stroke and doubles mortality from these
conditions.
Diabetes Care 2002;25:829-34
Diabetes Care 2004;27(11):2676-81
 The Metabolic Syndrome
Prothrombotic state
( fibrinogen, Triglycerides
Factor VIIa,
fibrinolytic activity) Insulin
Resistance
Hyperuricemia Small dense
Hyperinsulinemia LDL

Hypertension
Microalbuminuria HDL
cholesterol
Central
obesity Impaired Glucose Tolerance

Type 2 Diabetes
Diabetes Care 1998;21(2):310314.
Williams G, Pickup JC. Handbook of Diabetes. 2nd Edition, Blackwell Science. 1999.
 The Metabolic Syndrome and
Associated CVD Risk Factors

Hypertension

Abdominal obesity
Atherosclerosi
Hyperinsulinaemia s
Insulin Diabetes
Resistance
Hypercoagulability

Dyslipidaemia Endothelial
high TGs Dysfunction
small dense LDL
low HDL-C
 Insulin Resistance and
Atherosclerosis
Insulin resistance

Hyperinsulinemia Impaired Hypertriglyceridemia Essential

glucose Decreased HDL-C hypertension
tolerance

Clinical diabetes

Accelerated atherosclerosis
 Management of Metabolic
Syndrome
Lifestyle treatment
Weight control
Diet
Increased physical activity
(primary therapy for lowering risk factors
and reducing term risk for heart disease)
Treatment of Risk Factors

NCEP Guidelines, May 2001

 Incidence of ESRD, Hypertension and
Diabetes
Incidence Per Million Population

160
Glomerulonephritis Hypertension Diabetes
120

80

40

0
1989 1990 1991 1992 1993 1994 1995 1996 1997 1998

Year
United States Renal Data System (USRDS) 2000
Annual Data Report WWW.USRDS.ORG
Pathophysiology of Nephropathy

Function Pathology

Hyperfiltration Mesangial expression

Microalbuminaria GBM Thickening

Proteinuria Glomerulosclerosis

ESRD
 Clinical Manifestations of
Nephropathy
Seen when GFR 20 to 35% of normal
Urinary protein excretion > 4gm/day
Fluid retention
Weight gain, peripheral edema, CHF,
pulmonary edema

Uremia
Anorexia, nausea, vomiting, hiccups,
neuromuscular changes, anemia, renal
osteodystrophy
 National Kidney Foundation
Algorithm for Achieving Target BP Goals in
Hypertensive Diabetic Patients
BP still not
Blood pressure Start ACE inhibitor
at goal
>130/80 mm Hg titrate upwards
(130/80 mm Hg)

If BP still not Add Thiazide

Baseline pulse
at goal Diuretic or long-
84
(130/80 mm Hg) acting CCB*
Add low-dose If BP goal achieved, convert to fixed dose
beta blocker or combinations (ACE inhibitor + CCB or ACE
alpha/beta Baseline pulse <84 inhibitor + diuretic)
blocker
Add other subgroup of CCB
BP still not at goal (amlodipine-like agent if verapamil or
(130/80 mm Hg) diltiazem already being used and the
converse)

Refer to a
clinical hypertension specialist
*If proteinuria present
(>300 mg per day) non-DHP preferred. Bakris GL, et al. Am J Kidney Dis. 2000;36(3):646-661
 Management of Risk Factors in
Hypertension and Chronic Renal
Disease
Maximal reduction of proteinuria
Dose titration of RAS inhibitors
Therapeutic combinations
Cardiovascular risk management
Reduce CV risk factors
Manage additional risk factors
Anemia
High plasma homocysteine
Thank You