Professional Documents
Culture Documents
Essential Hypertension
and
Hypertensive Heart
Disease
MASRUL SYAFRI
Refferences
Perhatian
Introduction
Hypertension :
Prevalence up to 1 billion individuals world
wide
7.1 million deaths per year
62 % of cerebrovascular disease and 49 %
of ischemic heart disease
Riskerdas 2013 : Indonesian prevalence ±
25%, West Sumatera 22,6%
Overall prevalence of worldwide
population 30-45%
Most common, readily identifiable, and
reversible risk factor for cardiovascular
disease
Checklist for Accurate Measurement of BP
Definition
Hypertension :
BP 140/90 mmHg or higher (for every age!)
JNC VII :
Blok 2.5
Grade of Hypertension
(latest)
ESC Guideline Arterial Hypertension
Blok 2.5
*Factors that can be changed and, if changed, may reduce CVD risk.
†Factors that are difficult to change (CKD, low socioeconomic/educational
status, obstructive sleep apnea, cannot be changed (family history, increased
age, male sex), or, if changed through the use of current intervention techniques,
may not reduce CVD risk (psychosocial stress).
CKD indicates chronic kidney disease; and CVD, cardiovascular disease.
BP Patterns Based on Office and Out-of-Office
Measurements
Office/Clinic/Healthcare Home/Nonhealthcare
Setting /ABPM Setting
Normotensive No hypertension No hypertension
Sustained
Hypertension Hypertension
hypertension
Masked
No hypertension Hypertension
hypertension
White coat
Hypertension No hypertension
hypertension
ABPM indicates ambulatory blood pressure monitoring; and BP, blood pressure.
Corresponding Values of SBP/DBP for Clinic, HBPM,
Daytime, Nighttime, and 24-Hour ABPM Measurements
Clinic HBPM Daytime Nighttime 24-Hour
ABPM ABPM ABPM
120/80 120/80 120/80 100/65 115/75
Mortality caused by
hypertension
Blok 2.5
Cardiovascular Continuum
Blok 2.5
Pathophysiology of Hypertension
Blok 2.5
Essential Hypertension
Mechanism of Essential
Hypertension
Neural Mechanism
Increased sympathetic activity
Renal Mechanism
Defect in renal sodium retention
Vascular Mechanism
Endothelial dysfunction
Vascular remodeling
Hormonal Mechanism : Renin-Angiotensin-Aldosterone
System (RAAS)
Most important mechanism in hypertension
Blok 2.5
Renal
mechanism of
hypertension
Volume-based hypertension by
retaining excessive sodium and
water due to :
Failure to regulate renal blood
flow appropriately
Ion channel defect (Na K
ATPase)
Inappropriate hormonal
regulation
Abnormality of renal pressure
natriuresis
Blok 2.5
Neurohormonal mechanism
Neurohormonal mechanism
Baroreceptor reflexes buffering moment-to-
-moment changes in BP that varies during
daily activities.
Baroreceptor detect sudden increase or
decrease of BP and causing reflex mechanism
through vagal stimulation and sympathetic
or parasympathetic activation.
Baroreceptor reflex
Blok 2.5
Neurohormonal mechanism
Blok 2.5
Vascular mechanism
Endothelial cells of vascular
vessel have expresses nitric
oxide synthase which
produce NO and possess
vasodilatation properties
Several condition (i.e
diabetes, vascular
inflammation, and
hypertension) cause
dysfunctional endothelium
characterized by impaired
release of NO and
enhanced release of
endothelium-derived
constricting,
proinflammatory,
prothrombotic, and growth
factor
Blok 2.5
Vascular mechanism
RAAS
Blok 2.5
RAAS
Blok 2.5
RAAS
Blok 2.5
Diagnostic of Essential
Hypertension
Out-clinic blood
pressure monitoring
Ambulatory BP
monitoring (ABPM)
Home BP monitoring
(HBPM
Blok 2.5
ABPM HBPM
Blok 2.5
Investigation of hypertension
Blok 2.5
Blok 2.5
Blok 2.5
Treatment of Hypertension
Strategies :
Life styles changes
Monotherapy or combination antihypertension drugs
Blok 2.5
Lifestyles changes
Blok 2.5
Blok 2.5
Blok 2.5
Complication of
hypertension
Target organ Damage
Blok 2.5
Complication of hypertension
Blok 2.5
Burden of Hypertensive
Heart Disease
Blok 2.5
Global Burden to
Hypertensive Heart Diseae
Blok 2.5
Ventricular hypertrophy
Diagnostic modality
ECG
Blok 2.5
Diagnostic modality
Chest X ray
Blok 2.5
Diagnostic modality
Echocardiography
Blok 2.5
Management
Management
Current Medication :
ACE-I / ARB
CCB
β –blocker and α-blocker
Diuretics
Future perspectives
cyclosporin
HMG CoA reductase inhibitor
Recombinant human B-type natriuretic peptide
Blok 2.5
Blok 2.5
BP Thresholds for and Goals of Pharmacological Therapy in Patients With
Hypertension According to Clinical Conditions
BP
BP Goal,
Clinical Condition(s) Threshold,
mm Hg
mm Hg
General
Clinical CVD or 10-year ASCVD risk ≥10% ≥130/80 <130/80
No clinical CVD and 10-year ASCVD risk <10% ≥140/90 <130/80
Older persons (≥65 years of age; ≥130 (SBP) <130 (SBP)
noninstitutionalized, ambulatory, community-
living adults)
Specific comorbidities
Diabetes mellitus ≥130/80 <130/80
Chronic kidney disease ≥130/80 <130/80
Chronic kidney disease after renal ≥130/80 <130/80
transplantation
Heart failure ≥130/80 <130/80
Stable ischemic heart disease ≥130/80 <130/80
Secondary stroke prevention ≥140/90 <130/80
Secondary stroke
ASCVDprevention (lacunar)
indicates ≥130/80
atherosclerotic cardiovascular <130/80
Peripheral arterial disease
disease; BP, blood pressure; CVD, ≥130/80 <130/80
cardiovascular disease; and SBP, systolic blood
pressure.
2017 ACC/AHA/AAPA/ABC/ACPM/AGS/
APhA/ASH/ASPC/NMA/PCNA
Guideline for the Prevention, Detection,
Evaluation, and Management of High
Blood Pressure in Adults
BP Measurement Definition
*Factors that can be changed and, if changed, may reduce CVD risk.
†Factors that are difficult to change (CKD, low socioeconomic/educational
status, obstructive sleep apnea, cannot be changed (family history, increased
age, male sex), or, if changed through the use of current intervention techniques,
may not reduce CVD risk (psychosocial stress).
CKD indicates chronic kidney disease; and CVD, cardiovascular disease.
2017 Hypertension Guideline
Classification of BP
Definition of High BP
Measurement of BP
Accurate Measurement of BP in the Office
27–34 cm Adult
Office BP
at goal
Yes No
Increased Office BP
CVD risk or ≥5–10 mm Hg
target organ above goal on
damage ≥3 agents
Yes No Yes No
Screen for Screen for
Screening Screening
masked uncontrolled white coat effect with
not necessary not necessary
hypertension with HBPM HBPM
(No Benefit) (No Benefit)
(Class IIb) (Class IIb)
HBPM BP HBPM BP
above goal at goal
Yes No
ABPM BP
above goal
White coat effect:
Continue titrating
Yes No Confirm with ABPM
therapy
(Class IIa)
Masked uncontrolled
Continue current
hypertension:
therapy
Intensify therapy
(Class IIa)
(Class IIb)
Colors correspond to Class of Recommendation in Table 1.
ABPM indicates ambulatory blood pressure monitoring; BP, blood
pressure; and HBPM, home blood pressure monitoring.
2017 Hypertension Guideline
Causes of Hypertension
Secondary Forms of Hypertension
Recommendations for Secondary Forms of
COR LOE
Hypertension
Screening for specific form(s) of secondary
hypertension is recommended when the
I C-EO clinical indications and physical examination
findings are present or in adults with resistant
hypertension.
If an adult with sustained hypertension screens
positive for a form of secondary hypertension,
IIb C-EO referral to a physician with expertise in that form
of hypertension may be reasonable for
diagnostic confirmation and treatment.
Screening for Secondary Hypertension
New-onset or uncontrolled hypertension in adults
Conditions
• Drug-resistant/induced hypertension
• Abrupt onset of hypertension
• Onset of hypertension at <30 y
• Exacerbation of previously controlled hypertension
• Disproportionate TOD for degree of hypertension
• Accelerated/malignant hypertension
• Onset of diastolic hypertension in older adults (age ≥65 y)
• Unprovoked or excessive hypokalemia
Yes No
Positive
screening test
Yes No
Nonpharmacological Interventions
Nonpharmacological Interventions
Patient Evaluation
Basic and Optional Laboratory Tests for Primary
Hypertension
Basic testing Fasting blood glucose*
Complete blood count
Lipid profile
Serum creatinine with eGFR*
Serum sodium, potassium, calcium*
Thyroid-stimulating hormone
Urinalysis
Electrocardiogram
Optional testing Echocardiogram
Uric acid
Urinary albumin to creatinine ratio
*May be included in a comprehensive metabolic panel.
eGFR indicates estimated glomerular filtration rate.
2017 Hypertension Guideline
Treatment of High BP
BP Treatment Threshold and the Use of CVD Risk Estimation to
Guide Drug Treatment of Hypertension
Clinical ASCVD
Nonpharmacologic
Promote optimal or estimated 10-y CVD risk
therapy
lifestyle habits ≥10%*
(Class I)
No Yes
Reassess in Reassess in
3–6 mo 1 mo
(Class I) (Class I)
1y 3–6 mo therapy
BP-lowering medication BP-lowering medication†
(Class IIa) (Class I) (Class I)
(Class I) (Class I)
Reassess in Reassess in
3–6 mo 1 mo
(Class I) (Class I)
BP goal met
No Yes
Consider
intensification of
therapy
Angina
pectoris
Yes No
Add
Add
dihydropyridine CCBs,
dihydropyridine CCBs
thiazide-type diuretics,
if needed
and/or MRAs as needed
(Class I)
(Class I)
BP goal <130/80 mm Hg
(Class I)
Albuminuria
(≥300 mg/d or ≥300 mg/g
creatinine)
Yes No
ACE inhibitor
intolerant
Yes No
Patient
qualifies for IV
thrombolysis
therapy
Yes No
And
For adults with a lacunar stroke, a target SBP goal of less than
IIb B-R 130 mm Hg may be reasonable.
Previous
diagnosed or treated
hypertension
Yes No
Restart
antihypertensive
Established Established
treatment
SBP ≥140 mm Hg or SBP <140 mm Hg and
(Class I)
DBP ≥90 mm Hg DBP <90 mm Hg
Aim for
BP <140/90 mm Hg
(Class IIb) Initiate Usefulness of starting
antihypertensive antihypertensive
treatment treatment is not
(Class I) well established
(Class IIb)
Aim for
BP <130/80 mm Hg
(Class IIb)
Other Considerations
Resistant Hypertension: Diagnosis, Evaluation, and Treatment
.
BP indicates blood pressure; CKD, chronic kidney disease; DBP, diastolic
blood pressure; eGFR, estimated glomerular filtration rate; NSAIDs,
nonsteroidal anti-inflammatory drugs; and SBP, systolic blood pressure.
Adapted with permission from Calhoun et al.
Hypertensive Crises: Emergencies and Urgencies
Yes No
Hypertensive
Markedly elevated BP
emergency
Admit to ICU
(Class I) Reinstitute/intensify oral
antihypertensive drug therapy
and arrange follow-up
Conditions:
• Aortic dissection
• Severe preeclampsia or eclampsia
• Pheochromocytoma crisis
Yes No
Reduce SBP to <140 mm Hg Reduce BP by max 25% over first h†, then
during first h* and to <120 mm Hg to 160/100–110 mm Hg over next 2–6 h,
in aortic dissection† then to normal over next 24–48 h
(Class I) (Class I)