Download Hypertension

27.Eylül.2014 saat 12.00-15.00
Hastane Oryantasyon Eğitimi
Approach to the patient with
hypertensive disorders
Prof.Gülçin Kantarcı, MD
Department of
Internal Medicine and
Nephrology
OBJECTIVESHYPERTENSİON
At the end of this lecture the students
Knowledge:
1.Has a good understanding the diagnosis and the differential diagnosis of hypertensive disorders, renovascular
hypertension and ischemic renal diseases with their emergent treatment requirements and methods.
2.Has knowledge about diagnosis methods of hypertensive disorders, renovascular hypertension and ischemic renal
diseases. (Laboratory tests, screening tests, other invasive and non-invasive medical procedures)
3.Explain the pathophysiology of hypertensive disorders.
Skills:
4. Can name the possible diagnosis and make a differential diagnosis of hypertensive disorders, renovascular hypertension
and ischemic renal diseases.
5.Can use the diagnosis methods for hypertensive disorders, renovascular hypertension and ischemic renal diseases
economically and properly. (Laboratory tests, screening tests, other invasive and non-invasive medical procedures)
6.Can interpret the result of these tests correctly.
7. Can choose between emergent and non-emergent situations, and give emergent treatment for diseases.
8. Arrange the initial treatments and provide appropriate conditions until the patient is sent to specialist.
Attitudes:
9. Take preventive measures against end-organ damage of hypertension
10 Presents a worthy thought, attitude and behaviour appropriate for a physician in patient communication.
Contents
1.
2.
3.
4.
5.
6.
Hypertensive disorders
Primary Hypertension
Secondary Hypertension
Hypertensive emergencies
Treatment of hypertensive disorders
Approach to the patient with urgent ant emergent
hypertensive disorders
References
Data bases: http://accessmedicine.com
http://www.uptodate.com
1.
Current Medical Diagnosis and Treatment, Maxine A. Papadakis, Stephen J.
McPhee, Eds. Michael W. Rabow, Associate Ed. Chapter 11. Systemic Hypertension
2.
Bates' Guide to Physical Examination & History Taking 11th edition, Bickleys
LS, Szilagyi PG; Lippincott Williams and Wilkins¸
3.
Kumar and Clark's Clinical Medicine, 8th edition; Kumar & Clark, Elsevier
4.
Andreoli and Carpenter's Cecil Essentials of Medicine 8th edition, Andreoli
and Carpenter, Elsevier
5.
Symptom to Diagnosis: An Evidence-Based Guide, 2e, Scott D. C. Stern,
Adam S. Cifu, Diane Altkorn
Chapter 20. I Have a Patient with Hypertension. How Do I Determine the
Cause?
6.
CURRENT Diagnosis & Treatment: Nephrology & Hypertension
Edgar V. Lerma, Jeffrey S. Berns, Allen R. Nissenson
Chapter 43. Hypertension in High-Risk Populations
SUGGESTED READING
Goldman's Cecile Medicine 24th edition
Elsevier
Goldman L, Schafer AI
Case files Internal Medicine 5th edition
Mc Graw Hill LANGE
Toy Patlan
The Cleveland Clinic Intensive Review of
Internal Medicine 5th edition
Lippincott Williams and
Wilkins
Stoller JK, Michota FA, Mandell BF
Definition:

HT is the pressure exerted by circulating blood upon the walls
of blood vessels, and is one of the principal vital signs (arterial
pressure of the systemic circulation).

During each heartbeat, blood pressure varies between a
maximum (systolic) and a minimum (diastolic) pressure.

Correct measurement and interpretation of the blood
pressure (BP) is essential in the diagnosis and management of
hypertension.
Hypertension Guidelines

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JNC 7 2003
ESC 2007
NICE 2011
CHEP 2012
ESC 2013
JNC 8 2014
Classification of HT
Joint National Committee (JNC 7)
the average of two or more properly measure readings
at each of two or more visits after an initial screen
Normal blood pressure: systolic <120 mmHg and
diastolic <80 mmHg
Prehypertension: systolic 120-139 mmHg or diastolic
80-89 mmHg
Hypertension:
Stage 1: systolic 140-159 mmHg or diastolic 90-99
mmHg
Stage 2: systolic ≥ 160 or diastolic ≥ 100 mmHg
2007 European Societies of
Hypertension
Pathogenesis:
Abnormal cardiovascular or renal development
•
•
•
The normal cardiovascular system develops so that elasticity
of the great arteries is matched to the resistance in the
periphery to optimize large vessel pressure waves. In this way,
myocardial oxygen consumption is minimized and coronary
flow maximized.
Elevated blood pressure later in life could arise from
abnormal development of aortic elasticity or reduced
development of the microvascular network.
It has been postulated as the sequence of events in low birth
weight infants who have an increased risk of hypertension
developing in adulthood. Another hypothesis proposes that the
association between low birth weight and hypertension arises
from reduced nephron number.
Definitions based upon ambulatory and
home readings
 The
diagnosis of hypertension using ambulatory
blood pressure monitoring depends upon the time
span over which it is interpreted:



A 24-hour average above 135/85 mmHg
Daytime (awake) average above 140/90 mmHg
Nighttime (asleep) average above 125/75 mmHg
 the
definition of hypertension based upon an average
of multiple home readings is the same as for
daytime ambulatory blood pressure
epidemiology


The national health and nutrition examination survey
(NHANES) conducted from 2005 through 2008
estimated that approximately 29 to 31 percent of adults
in the United States have hypertension
One of every four deaths due to hypertension .
Turkish Health Ministry, Turkish Health Load Study, 2004



BP increases with age.
About 75% of women aged 75 years and over have
hypertension and about 64% of men aged 75 years and
over have hypertension
About 2 /3 of people > 65 have hypertension
Prevalance of HT in
Turkey
HinT, 2008
Risk Factors
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Hypertension tends to be both more common and more severe in blacks.
Hypertension in maternal, paternal or both parents
Excess sodium intake
Excess alcohol intake is associated with the development of hypertension.
Obesity and weight gain. In Turkey 25 % of whole population over weight
Over 40 years 15 %  excessive obasity
the rise in blood pressure that is commonly observed with aging
Physical inactivity
Dyslipidemia, independent of obesity
fructose may increase hypertension risk , the best data suggest that it does
not raise blood pressure or increase the incidence of hypertension.
Hypertension may be more common among those with certain personality
traits, such as hostile attitudes and time urgency/impatience , as well as
among those with depression .
Vitamin D deficiency
Etiology


Primary( essential) (85 to 95% of cases) ?
The term applied to the hypertensive patients in which
elevated blood pressure results from complex
interactions between multiple genetic and environmental
factors.
Secondary
Essential hypertension


The term applied to the 95% of hypertensive patients
in which elevated blood pressure results from
complex interactions between multiple genetic and
environmental factors.
The onset is usually between ages 25 and 50 years; it
is uncommon before age 20 years.
Essential(Primary) hypertension
The best understood endogenous and environmental
determinants of blood pressure include the
• sympathetic nervous system
• the renin-angiotensin-aldosterone system
• the pressure natriuresis
• variation in cardiovascular and renal
development
• intracellular sodium and calcium levels
Sympathetic nervous system
hyperactivity


Most apparent in younger persons with hypertension,
who may exhibit tachycardia and an elevated cardiac
output. However, correlations between plasma
catecholamines and blood pressure are poor.
Insensitivity of the baroreflexes may play a role in the
genesis of adrenergic hyperactivity, and polymorphisms in
some genes have been linked to increased blood pressure
responses to stress.
Renin–-angiotensin-Aldosterone system
activity
•
Renin, a proteolytic enzyme, is secreted by cells
surrounding glomerular afferent arterioles (JGA) in
response to a number of stimuli, including
•
reduced renal perfusion pressure
diminished intravascular volume
circulating catecholamines
increased sympathetic nervous system
activity
increased arteriolar stretch, and
hypokalemia.
•
•
•
•
Renin-angiotensin-aldosterone system
Defect in natriuresis


According to the classic Guyton
hypothesis, increased salt intake
triggers an increase in blood
pressure that in turn promotes
increased natriuresis, thereby
bringing blood pressure back
toward basal levels.
Salt has long been implicated in the
genesis of hypertension, and socalled salt-sensitive hypertension
probably arises from a defect in
this self-regulating pressure–
natriuresis feedback loop.
Intracellular sodium and
calcium


Intracellular Na+ is elevated
in primary (essential)
hypertension.
An increase in intracellular
Na+ may lead to increased
intracellular Ca2+
concentration as a result of
facilitated exchange and
might explain the increase
in vascular smooth
muscle tone that is
characteristic of established
hypertension.
Blood pressure =
cardiac output (CO) × total peripheral vascular resistance (TPR)
• In most patients, CO is normal or slightly increased,
and TPR is increased.
This pattern is typical of;
• primary hypertension
• hypertension due to pheochromocytoma
• primary aldosteronism
• renovascular disease
• renal parenchymal disease
Symptoms and Signs
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usually asymptomatic until complications develop in target
organs.
Dizziness, flushed facies, headache, fatigue, epistaxis, and
nervousness
Severe hypertension can cause severe cardiovascular,
neurologic, renal, and retinal symptoms (eg, symptomatic
coronary atherosclerosis, HF, hypertensive encephalopathy,
renal failure).
A 4th heart sound is one of the earliest signs of hypertensive
heart disease.
Secondary hypertension
• suspected in patients in whom hypertension develops
at an early age or after the age of 50 years, and
in those previously well controlled who become
refractory to treatment.
• High BP resistant to three medications is
another clue although multiple medications are
usually required to control hypertension in persons
with diabetes.
Secondary hypertension
Primary renal disease —acute and chronic, glomerular or vascular disorders.
Pheochromocytoma — About ½ of patients with pheochromocytoma have paroxysmal
hypertension, most of the rest have what appears to be essential hypertension.
Primary hyperaldosteronism —should be suspected in any patient with the triad of
hypertension, unexplained hypokalemia, and metabolic alkalosis.
Genetic causes - Glucocorticoid remediable aldosteronism, Liddle syndrome
Renovascular disease — Renovascular disease is an important correctable cause of secondary
hypertension.The frequency with which it occurs is variable.
Cushing's syndrome — Moderate diastolic hypertension is a major cause of morbidity and death in patients
with Cushing's syndrome.
Other endocrine disorders — Hypertension may be induced by both hypothyroidism, hyperthyroidism, and
hyperparathyroidism.
Sleep apnea syndrome — Disordered breathing during sleep appears to be an independent risk factor for
awake systemic hypertension.
Coarctation of the aorta — Coarctation of the aorta is one of the major causes of hypertension in young
children
Oral contraceptives —
Renovascular disease
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Atheromatos diseases (70-80%)
Fibromuscular displazia (20-25%)
Dis.Aorta Anev.
Renal arterial trombozis
Abdominal trauma
Neurofibromatosis
Takayasu arteritis
Clinical findings
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Stage III-IV hypertensive retinopathy
Abdominal brut
Renal failure
Findings of peripheral vascular dis.
Heart
- left ventricular hypertrophy.
- Aortic insufficiency may be auscultated in up to 5% of patients, and hemodynamically insignificant
aortic insufficiency can be detected by Doppler echocardiography in 10–20%.
- A presystolic (S4) gallop due to decreased compliance of the left ventricle is quite common in
patients in sinus rhythm .
Pulses
-Radial-femoral delay suggests coarctation of the aorta;
loss of peripheral pulses occurs due to atherosclerosis, less commonly aortic dissection, and rarely
Takayasu arteritis, all of which can involve the renal arteries.
Renal vascular hypertension should be
suspected
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if the documented onset is before age 20 or after age 50 years,
hypertension is resistant to three or more drugs,
if there are epigastric or renal artery bruits,
if there is atherosclerotic disease of the aorta or peripheral
arteries (15–25% of patients with symptomatic lower limb
atherosclerotic vascular disease have renal artery stenosis),
if there is an abrupt increase (> 25%) in the level of serum
creatinine after administration of ACE inhibitors, or
if episodes of pulmonary edema are associated with abrupt
surges in blood pressure.
Evaluating renovascular ht
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Renovascular doppler US
Kaptopril renogram
MR angiography
BT angiography
Renal Arteriography
suspicion is moderate to low, noninvasive angiography using magnetic
resonance (MR) or CT are reasonable approaches.
Doppler sonography may play an increasing role in detection of renal
artery stenosis,
Gadolinium, a contrast agent used in MR angiography, is
contraindicated in patients with an estimated glomerular filtration
rate (GFR) of < 30 mL/min because it might precipitate nephrogenic
systemic fibrosis in patients with advanced kidney disease
Renovascular doppler US
MR Angiography
CT Angiography
Renal Arteriography
Other causes of secondary hypertension
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
Hypertension has also been associated with
hypercalcemia, acromegaly, hyperthyroidism,
hypothyroidism, baroreceptor denervation,
compression of the rostral ventrolateral
medulla, and increased intracranial pressure.
A number of medications may cause or exacerbate
hypertension—most importantly cyclosporine,
tacrolimus, angiogenesis inhibitors, erythrocyte
stimulating agents such as erythropoietin,
decongestants, and NSAIDs; cocaine and
alcohol should also be considered.
Complications of Untreated Hypertension
HYPERTENSIVE CARDIOVASCULAR DISEASE
• Left ventricular hypertrophy is associated with
incremental cardiovascular risk in association with
heart failure (through systolic or diastolic
dysfunction), ventricular arrhythmias, myocardial
ischemia, and sudden death
• The occurrence of heart failure is reduced by
50% with antihypertensive therapy.
HYPERTENSIVE CEREBROVASCULAR
DISEASE AND DEMENTIA
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
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Hypertension is the major predisposing cause of
hemorrhagic and ischemic stroke. Cerebrovascular
complications are more closely correlated with systolic than
diastolic blood pressure.
The incidence of these complications is markedly reduced by
antihypertensive therapy.
HT is associated with a higher incidence of subsequent
dementia of both vascular and Alzheimer types.
Effective blood pressure control may reduce the risk of
development of cognitive dysfunction later in life, but once
cerebral small vessel disease is established, low blood pressure
might exacerbate this problem.
HYPERTENSIVE KIDNEY DISEASE

Chronic hypertension leads to nephrosclerosis.
Aggressive blood pressure control, to 130/80 mm Hg
or lower, slows the progression of all forms of
chronic kidney disease, especially when proteinuria
is present.
AORTIC DISSECTION
&
ATHEROSCLEROTIC COMPLICATIONS


Hypertension is a contributing factor in many patients
with dissection of the aorta.
Most of the hypertensive patients die of
complications of atherosclerosis, but
antihypertensive therapy seems to have a
lesser impact on atherosclerotic complications
compared with the other effects of treatment
outlined before.
Assess target organ damages
•Cardiovascular
■Electrocardiography
■2-Dimensional echocardiography
•Cerebrovascular
•Eyes
•Kidney function
■Estimated GFR
■Proteinuria: microalbuminuria, alb/cr
46
Drug-Induced Hypertension:
Prescription Medications
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Steroids
Estrogens
NSAIDS
Phenylpropanolamines
Cyclosporine/tacrolimus
Erythropoietin
Sibutramine
Methylphenidate
Ergotamine
•
•
•
•
•
•
Ketamine
Desflurane
Carbamazepine
Bromocryptine
Metoclopramide
Antidepressants
– Venlafaxine
• Buspirone
• Clonidine
Measurement of Blood Pressure
Office monitoring:
• Patient should be seated quietly for 5 minutes in a
chair feet on the floor, and arm supported at heart
level.
• Appropriate-sized cuff should be used to ensure
accuracy.
• At least two measurements should be made at
different times of day.
• Proper Cuff Size: 40% of circumference, 6070% of length of upper arm
• The bladder is long enough to encircle > 80%
of the arm,
Measurement of Blood Pressure
Self monitoring:
 Provides information on:
1. Response to antihypertensive therapy
2. Improving adherence with therapy
3. Evaluating white-coat HTN
 Home measurement of >135/85 mmHg is generally
considered to be hypertension.
 Home measurement devices should be checked
regularly.
Ambulatory blood pressure
monitoring
• is determined using a device worn by the patient that
takes BP measurements over a 24 to 48 hour period,
usually every 15 to 20 minutes during the daytime and
every 30 to 60 minutes during sleep. Measurements
are recorded on the device, and diurnal or nocturnal
BP pressure recordings are evaluated by computer.
The diagnosis of hypertension using ambulatory blood
pressure monitoring :
• A 24-hour average above 135/85 mmHg
• Daytime (awake) average above 140/90 mmHg
• Nighttime (asleep) average above 125/75 mmHg
According to JNC 7 guidelines,
ABPM is recommended
• Suspected WCH in patients with HT and no
target organ damage.
• Apparent drug resistance (office resistance).
• Hypotensive symptoms with antihypertensive
medication.
• Episodic HT.
• Autonomic dysfunction.
Management of Hypertensive
patients
Goals of treatment
•Reduction of cardiovascular morbidity and
mortality
•Delayed progression of proteinuric renal
disease
JNC 8
JNC 8
Nonpharmacologic theraphy
Recommended for all individuals
• Weight loss and exercise
• Smoking cessation
• Diet: Increased fruits and vegetables, decreased
salt, limited alcohol, increased potassium intake
• a reduction in salt intake of 6 g/day through the
fall in blood pressure that would occur would cause
 24% reduction in stroke
 18% reduction in coronary heart disease mortality.
Pharmacologic therapy
DIURETICS:
in uncomplicated hypertensive  thiazide diuretic (ALLHAT)
a maximum of 25 mg/day This regimen is associated with a low rate of
metabolic complications, such as hypokalemia, glucose intolerance, and
hyperuricemia)
they lower urinary calcium excretion, beneficial in patients with hypercalciuria
and recurrent calcium stones and in those with osteoporosis.
Side effects:
Hypokalemia (which increases digitalis toxicity),
hyperuricemia, glucose intolerance,
hypercholesterolemia, hypertriglyceridemia,
hypercalcemia, sexual dysfunction in men,
weakness, rash
Loop Diuretics
•
Typically only beneficial in patients with resistant HTN
and evidence of fluid overload; effective if CrCl <30
ml/min
•
MUST be dosed at least twice daily (Lasix = Lasts six
hours)
Aldosteron antagonists
Can provide as much as 25 mmHg BP reduction on
top of 4 drug regimen in resistant hypertension
Monitor SCr and K
ACEI:Major additional role for reducing BP and cardiovascular
risk and proteinuric renal disease, particularly in diabetics
Side effects:
A dry, irritating cough is the most common adverse effect,
but angioedema is the most serious and, if it affects the
oropharynx, can be fatal.
Angioedema is most common among blacks and smokers. ACE
inhibitors may increase serum K and creatinine levels,
especially in patients with chronic renal failure and those
taking K-sparing diuretics, K supplements, or NSAIDs.
ACE inhibitors are the least likely of the antihypertensives to
cause erectile dysfunction. ACE inhibitors are contraindicated
during pregnancy.
ANGIOTENSIN II RECEPTOR BLOCKERS:
These drugs block angiotensin II receptors and therefore
interfere with the renin-angiotensin system. Angiotensin II
receptor blockers and ACE inhibitors are equally effective as
antihypertensives.
B-BLOKERS:
Slow heart rate and reduce myocardial contractility, thus reducing
BP. All β-blockers are similar in antihypertensive efficacy. In
patients with diabetes, chronic peripheral arterial disease, or
COPD, a cardioselective β-blocker ( acebutolol , atenolol ,
bisoprolol , metoprolol) may be preferable, although
cardioselectivity is only relative and decreases as dose increases.
• Even cardioselective β-blockers are contraindicated in patients
with asthma or in patients with COPD with a prominent
bronchospastic component
CA CANAL BLOKER:
Recent studies confirm benefits with previous coronary disease,
however, argue that ARBs may offer greater protection (LIFE trial).
*Dihydropyridines ( nifedipine) are potent peripheral
vasodilators and reduce BP by decreasing TPR; they sometimes
cause reflexive tachycardia. Leg edema*
*The nondihydropyridines (verapamil)
slow the heart rate, decrease atrioventricular conduction, and
decrease myocardial contractility. These drugs should not be
prescribed for patients with 2nd- or 3rd-degree atrioventricular
block or with left ventricular failure . Leg edema*
ALPHA2 AGONİSTS: CENTRAL ACTİNG AGENTS
•
Mechanism: false neurotransmitters reduce sympathetic
outflow reducing sympathetic tone
•
Clonidine 0.1-0.6 mg PO BID-TID; patch
•
Methyldopa, Guanabenz, Guanfacine
•
Monitor: HR
•
Side effects often limiting: Dry mouth, orthostasis,
sedation
•
Clonidine patch can be useful in elderly patients with
labile blood pressure
ALPHA1 BLOCKERS
•
Mechanism: Inhibit peripheral post-synaptic alpha1
receptors causing vasodilation
•
Terazosin 1 – 20 mg daily
•
Doxazosin 1 – 16 mg daily
•
Cause marked orthostatic hypotension, give dose at
bedtime
•
Consider only combination theraphy
•
Can be beneficial in patients with BPH
Choice of Antihypertensive
Antihypertensives for
High-Risk Patients
When to Refer

Referral to a hypertension specialist should be considered
in cases of severe, resistant or early/late onset
hypertension or when secondary hypertension is
suggested by screening.
Hypertensive Crisis
Diastolic BP > 120 mmHg
Hypertensive emergency
Acute HT+ Target organ
damage
Hypertensive urgency
Acute HT
JNC 7
2003 ESH-ESC guidelines for the management of arterial hypertension.
NICE Agust. 2011
Approach to the patient with urgent ant emergent
hypertensive disorders
Encephalopathy, Stroke
• Headache, fatigue,vomiting
• Vision disturbance
• convulsion
Acute coronary synd, Heart failure, Pulmonary
edema
• Angina pectoris, dispnea,
• ortopnea/PND
Acute aortic dissection
• Low back pain
Hypertensive emergencies
Treatment :
■Oral agents: Difficult to control: Nifedipine,
nicardipine, clonidine, labetalol, hydralazine,kaptopril
■Intravenous agents: Nitroprusside, labetalol,
enalapril, nicardipine, fenoldopam, nitroglycerin
Situations not considered emergencies:
Thrombotic stroke, asymptomatic hypertension, CKD