HYPERTENSION

Pathophysiology and Diagnostics

Bimanesh Sutarjo MD, PhD

Jakarta
Agenda

1. Overview
2. Pathophysiology of essential hypertension
3. Pathophysiology of secondary hypertension
4. Diagnostics of Hypertension
Agenda

1. Overview
2. Pathophysiology of essential hypertension
3. Pathophysiology of secondary hypertension
4. Diagnostics of Hypertension
JNC 7 : BP Classifications
 Types of hypertension

Primary HTN: Secondary HTN:

also known as less common cause
essential HTN. of HTN ( 5%).
accounts for 95% secondary to other
cases of HTN. potentially rectifiable
no universally causes.
established cause
known.
Factors influencing hypertension

- venous return - vasoactive substances

- extracellular fluid volume - thickening of arteriolar
- myocardial contractility wall
Beevers G, Lip GYH, OBrien E. BMJ 2001;322:912-916
The Control of
Peripheral Arterial
Resistance :

An orchestra of :
Vasodilating Systems
Vasoconstricting Systems
Vascular Growth Factors

Beevers G, Lip GYH, OBrien E.

BMJ 2001;322:912-916
Agenda

1. Overview
2. Pathophysiology of essential hypertension
3. Pathophysiology of secondary hypertension
4. Diagnostics of Hypertension
 Essential Hypertension
Hemodynamic effect of hormonal, neural and renal
dysregulation of blood pressure
Pathogenesis is probably a slow and gradual
process
No single or specific cause
Initiating factors may no longer be apparent when
hypertension is developed, since they have been
normalised by the compensatory interactions
Initial phase : cardiac output
Late phase : peripheral arteriolar resistance,
cardiac output is normalised

Oparil S, Zaman A, Calhoun DA. Ann Intern Med 2003; 139 : 761-776
Factors influencing essential hypertension

Oparil S, Zaman A, Calhoun DA. Ann Intern Med 2003; 139 : 761-776
Mechanisms of essential hypertension

activity of renin-angiotensin-aldosteron

Hyperfunction of sympathetic system

Vasoactive substances - endothelial dysfunction

Insulin resistance obesity

Arteriolar hypertrophy

Renal defect to excrete sodium

Phil DFP. Br J Anaest 2004; 71-76

Renin- Angiotensin- Aldosteron System

Beevers G, Lip GYH, OBrien E. BMJ 2001;322:912-916

Tissue RA - System

- catecholamine and endothelin release

- induction of hypertrophy of smooth muscle cells,
cardiomyocytes
Beevers G, Lip GYH, OBrien E. BMJ 2001;322:912-916
 Autonomic nervous system

Primary activity of
vasomotor neurons

Angiotensin II and
endothelin increases
activity of vasomotor
neurons

Norepinephrine
potentiates renin
releasing

Beevers G, Lip GYH, OBrien E. BMJ 2001;322:912-916

 Hypertrophy of Arteriolar Wall
OBESITY STRESS Na+ RETENTION RENAL
HYPOPERFUSION

NATRIURETIC
INSULIN CATECHOLAMINES HORMON ANGIOTENSIN

PRESSURE-GROWTH
EFFECTS

INTRACELLULAR Ca2+ Na+/H+ EXCHANGE

SMOOTH MUSCLE VASCULAR WALL

CONTRACTION HYPERTROPHY

PERIPHERAL VASCULAR
RESISTANCE
Hypertrophy of Arteriolar Wall
Vikrant S. J Ind Ac Clin Med 2001;2:3
Agenda

1. Overview
2. Pathophysiology of essential hypertension
3. Pathophysiology of secondary hypertension
4. Diagnostics of Hypertension
 Secondary Hypertension

Cardiac Output Systemic Vascular

Resistance
Hypervolemia Stress
renal artery stenosis sympathetic activation
renal disease Atherosclerosis


hyperaldosteronism
hypersecretion of ADH
Renal artery disease
Increased angiotensin II
aortic coarctation
pregnancy (preeclampsia) Phaeochromcytoma
Stress


increased catecholamines
Thyroid dysfunction
sympathetic activation
Phaechromocytoma Diabetes
increased catecholamines Cerebral ischaemia

Scott Gilbert. Tuft University School of Medicine

 Causes of secondary hypertension

Renal
Renal parenchymal diseases (glomerulonephritis)
Renovascular diseases

Endocrine
Pheochromocytoma
Hypertiroidism
Primary hyperaldosteronism
Adrenocortical hyperfunction/tumour (Cushing, Conn)
Exogenous glucocorticoids
Acromegaly
Pregnancy-induced
Gavras H. J Med Sci 2009; 2(1):25-28
 Causes of secondary hypertension

Drugs
Contraceptives
Sympathomimetics
Corticosteroids
Cocaine

Cardiovascular
Coarctation of aorta

Neurogenic
Increased intracranial pressure
Acute stress

Gavras H. J Med Sci 2009; 2(1):25-28

Renal parenchymal disease

Common cause of secondary HTN (2-5%)

HTN is both cause and consequence of renal disease
Multifactorial cause for HTN including disturbances in
Na+ / water balance, vasodepressors / prostaglandins
imbalance
Renal disease from multiple etiologies.

Scott Gilbert. Tuft University School of Medicine

 Renovascular hypertension

Atherosclerosis 75-90% ( more common in older

patients)
Fibromuscular dysplasia 10-25% (more common in
young patients, especially females)
Others
Aortic / renal dissection
Takayasus arteritis
Thrombotic / cholesterol emboli
CVD
Post transplantation stenosis
Post radiation

Scott Gilbert. Tuft University School of Medicine

 Pheochromocytoma

Rare cause of HTN (0.1-1.0%)

Tumor containing chromaffin cells which secrete
catecholamines
Young-middle age with female predominance
Clinical
o Intermittent HTN, palpitations, sweating, anxiety
spells (5 Ps : Pressure, Pain, Pallor, Palpitation, Perspiration)
o May be provoked by triggers such as tyramine-
containing foods (beer, cheese, wine), pain, trauma,
drugs (clonidine,TCA,opiates)

Scott Gilbert. Tuft University School of Medicine

Agenda

1. Overview
2. Pathophysiology of essential hypertension
3. Pathophysiology of secondary hypertension
4. Diagnostics of Hypertension
Sitting comfortably
Back supported
Legs uncrossed
Upper arm bared
 Using The Right Cuff

Hypertension Diagnosis and Treatment 14th ed. November 2012. www.isci.org

 Positioning the cuff

Hypertension Diagnosis and Treatment 14th ed. November 2012. www.isci.org

 Accurate BP measurement
Who checks your patients BP?

You or Staff ?
If Staff Do they know what to listen for or do they use
automated equipment
Seated quietly for 5 minutes, arm supported at level
No caffeine, exercise or smoking for 30 min
Appropriate size cuff : encircle at least 80% arm circ.
Inflate 20-30 mmHg above loss of radial pulse
Deflate at 2mmHg per second
1st sound is SBP ; Disappearance of Korotkoff sound (phase 5)
is DBP
At least 2 measurements and take average
Confirm Elevated blood pressure within 2 months
(stage 1) shorter for stage 2 if new onset

Hypertension Diagnosis and Treatment 14th ed. November 2012. www.isci.org

Blood pressure measurement
 Patient Evaluation Objectives

(1) To assess lifestyle and identify other

cardiovascular risk factors or concomitant disorders
that may affect prognosis and guide treatment
(2) To reveal identifiable causes of high BP
(3) To assess the presence or absence of target
organ damage and CVD
 History

Angina/MI Stroke: Complications of HTN, Angina

may improve with b-blockers
Asthma, COPD: Preclude the use of b-blockers
Heart failure: ACE inhibitors indication
DM: ACE preferred
Polyuria and nocturia: Suggest renal impairment
 History-contd.

Claudication: May be aggravated by beta -blockers,

atheromatous RAS may be present
Gout: May be aggravated by diuretics
Use of NSAIDs: May cause or aggravate HTN
Family history of HTN: Important risk factor
Family history of premature death: May have been
due to HTN
 History-contd.

Family history of DM : Patient may also be Diabetic

Cigarette smoker: Aggravate HTN, independently a
risk factor for CAD and stroke
High alcohol: A cause of HTN
High salt intake: Advice low salt intake
Secondary HTN - clues in medical history

Onset : at age < 30 yrs ( Fibromuscular dysplasia) or

> 55 (atherosclerotic renal artery stenosis), sudden
onset (thrombus or cholesterol embolism).
Severity : An acute rise in BP over a previously
stable baseline, Grade II, unresponsive to treatment.
Episodic, headache and chest pain / palpitation
(pheochromocytoma, thyroid dysfunction).
Morbid obesity with history of snoring and daytime
sleepiness (sleep disorders)
 Examination

Appropriate measurement of BP in both arms

Optic fundi
Calculation of BMI ( waist circumference also may be
useful)
Auscultation for carotid, abdominal, and femoral
bruits
Palpation of the thyroid gland.
Examination-contd.

Thorough examination of the heart and lungs

Abdomen for enlarged kidneys, masses, and
abnormal aortic pulsation
Lower extremities for edema and pulses
Neurological assessment
If HTN is diagnosed

Evaluate for Cardiovascular Risk Factors

Age, Family History, Lipid profile, Obesity,
microalbuminuria, Inactivity, Smoking
Evaluate for Target Organ Damage
LVH or reduced EF, Angina, stroke, dementia,
Kidney disease, PAD, retinopathy

Think about Secondary Hypertension with any new

onset hypertension or uncontrolled hypertension
Routine Labs
EKG.
Urinalysis.
Blood glucose and hematocrit; serum
potassium, creatinine ( or estimated GFR),
and calcium.
HDL cholesterol, LDL cholesterol, and
triglycerides.
Optional tests : urinary albumin excretion.
albumin/creatinine ratio.
Secondary HTN - clues on routine labs

Increased creatinine, abnormal urinalysis

(renovascular and renal parenchymal disease)
Unexplained hypokalemia (hyperaldosteronism)
Impaired blood glucose ( hypercortisolism)
Impaired TFT (Hypo-/ hyper- thyroidism)

Ker JA. S Afr Fam Pract 2011;53(5):441-442

Secondary HTN - Screening tests

Ker JA. S Afr Fam Pract 2011;53(5):441-442

 Conclusion
Clinical Principles

A clearer understanding of the pathogenesis of hypertension

will probably lead to more highly targeted therapies and to
greater reduction in hypertension-related cardiovascular disease
morbidity that cannot be achieved with current empirical treatment

Oparil S, Zaman A, Calhoun DA. Ann Intern Med 2003; 139 : 761-776
 Conclusion
Physiologic Principles
More than 90% of cases of hypertension do not have a clear cause

Hypertension clusters in families and results from a complex interaction

of genetic and environmental factors

The hypertension-related genes identified to date, regulate salt and

water handling

Major pathophysiologic mechanisms of hypertension include activation

of the sympathetic nervous system and renin-angiotensin-aldosterone
system

Endothelial dysfunction, increased vascular reactivity, and vascular

remodeling may be causes, rather than consequences, of blood
pressure elevation; increased vascular stiffness contributes to isolated
systolic hypertension in the elderly
Oparil S, Zaman A, Calhoun DA. Ann Intern Med 2003; 139 : 761-776
Thanks for your kind attention
Questions will be well taken