End organ damages of hypertension 2

Dr. Chinedu Ibeh(MBBS; MPH; MWACP)

 Introduction
 Hypertensive Cerebrovascular diseases
 Hypertensive Encephalopathy
 Cerebrovascular Accidents
▪ Ischaemic CVA
▪ Haemorrhagic CVA
 Hypertensive Eye Disease
 Retinopathy
 Hypertensive Heart Diseases
 LeftVentricular Hypertrophy
 Coronary Artery Disease
 Cardiac Arrhythmias and
 Congestive Heart Failure
 Hypertensive Kidney diseases
 Benign Nephelosclerosis
 Malignant Nephelosclerosis

 Hypertension is a condition in which the blood vessels have
persistently raised pressure.1
 Blood pressure is the product cardiac output and systemic vascular
resistance.1
 Hypertensive Urgency is defined as severely elevated BP with no
evidence of target organ damage.2
 Hypertensive Emergency is a condition in which elevated blood
pressure (BP) results in target organ damage.2
 End Organ damage usually refers to damage to major organs fed by the
circulatory system which can sustain damage due uncontrolled
hypertension, hypotension or hypovolemia.5
 World Hypertension Day(May 17; 2018 theme: Know your numbers).

American College of Cardiology 2017 Guideline on
Categories of BP in Adults. 6
BP Category SBP DBP
Normal <120 mmHg and <80 mmHg
Elevated 120–129 mm Hg and <80 mmHg
Stage 1 130–139 mm Hg or 80–89 mm Hg
Stage 2 ≥140 mm Hg or ≥90 mm Hg

 Factors that play a role in the pathogenesis of Hypertension:
 Genetics
 Activation of neuro-hormonal systems
▪ Sympathetic nervous system
▪ Renin-angiotensin-aldosterone system
 Obesity, Increased salt intake
 Factors involved in short term and long term regulation of BP
for adequate tissue perfusion
 Cardiac output and circulatory blood volume
 Vascular caliber , elasticity and reactivity
 Humoral mediation, Neural stimulation
.Complications are largely attributed to the
▪ remodeling of the arterial wall, including accelerated atherosclerosis

Vision Eye Institute. Hypertensive retinopathy 2017 . Available from
https://visioneyeinstitute.com.au/eyematters/hypertensive-retinopathy/. [accessed on 19/3/18]

 Hypertensive Encephalopathy
 Cerebrovascular accidents
 Haemorrhagic CVA
 Ischaemic CVA

 This is a syndrome consisting of a sudden elevation of
arterial pressure usually preceded by severe headache
and followed by convulsions, coma or a variety of
transitory cerebral phenomena.3
 Symptoms may include
 Headache
 Vomiting
 Trouble with balances
 confusion
 Onset is generally sudden
 Complications include
 Seizures

 CVA is a medical name for
stroke.
 A stroke is a sudden death
of some brain cells due to
lack of oxygen when
blood flow to a part of the
brain is impaired either by
blockage or rupture of a
blood vessel.
 World stroke day: 29/10
 Theme: 1/6 of us will suffer a
stroke in our lifetime; we all
have good reason to prevent
stroke.

 Muscular: difficulty walking, paralysis with weak muscles,
problems with coordination, stiff muscles, overactive reflexes,
or paralysis of one side of the body
 Whole body: balance disorder, fatigue, light-headedness, or
vertigo
 Visual: blurred vision, double vision, sudden visual loss, or
temporary loss of vision in one eye
 Speech: difficulty speaking, slurred speech, or speech loss
 Sensory: pins and needles or reduced sensation of touch
 Facial: muscle weakness or numbness
 Limbs: numbness or weakness
 Also common: difficulty swallowing, headache, inability to
understand, mental confusion, or rapid involuntary eye
movement

 Ischemic stroke occurs when an artery to the
brain is blocked.
 Ischemic stroke can be divided into two main
types: thrombotic and embolic.
 A thrombotic stroke occurs when diseased cerebral
arteries become blocked by blood clot within the
brain-responsible for almost 50 percent of all strokes.
 An embolic stroke is also caused by a clot within an
artery outside the brain itself.
 This results in near-immediate physical and
neurological deficits.

 Medical history to identify risk factors for
atherosclerotic and cardiac disease:
 Hypertension, Diabetes mellitus,Tobacco use
 High cholesterol, History of coronary artery disease,
coronary artery bypass, or atrial fibrillation
 In younger patients, elicit a history of the following:
 Recent trauma, Coagulopathies
 Illicit drug use (especially cocaine)
 Migraines, Oral contraceptive use
 Nausea, vomiting, headache, and a sudden change
in the patient’s level of consciousness are more
common in hemorrhagic strokes

 Hemiparesis, monoparesis, or (rarely) quadriparesis
 Hemisensory deficits
 Monocular or binocular visual loss
 Visual field deficits
 Diplopia
 Dysarthria
 Facial droop
 Ataxia
 Vertigo (rarely in isolation)
 Aphasia
 Sudden decrease in the level of consciousness
 No historical feature distinguishes ischemic from
hemorrhagic stroke,.

 Cranial nerves
 Motor function
 Sensory function
 Cerebellar function
 Gait
 Language (expressive and receptive capabilities)
 Mental status and level of consciousness

 A hemorrhagic stroke is either a
brain aneurysm burst or a weakened blood
vessel leak.
 Blood spills into or around the brain and
creates swelling and pressure, damaging cells
and tissue in the brain.
 There are two types of hemorrhagic stroke
called
 intracerebal and
 subarachnoid.

 Blood vessel inside the brain ruptures and
leaks blood into surrounding brain tissue.
 High blood pressure and aging blood vessels
are the most common causes of this type of
stroke.
 Sometimes intracerebral hemorrhagic stroke
can be caused by an arteriovenous
malformation (AVM).

 This type of stroke involves bleeding in the area
between the arachnoid membrane and the pia
mater known as the subarachnoid space.
 This type of stroke is most often caused by a
burst aneurysm.
 Other causes include:
 Artero-Venous Malformation
 Bleeding disorders
 Head injury
 Blood thinners

 Generalized symptoms, including
 nausea, vomiting, and headache, as well as an
altered level of consciousness, may indicate
increased
▪ intracranial pressure and are more common with
hemorrhagic strokes and large ischemic strokes.
 Seizures are more common occurring in 28%
of hemorrhagic stroke generally at the
 onset of the intracerebral hemorrhage or within
the first 24 hours..

 Focal symptoms of stroke include the following:
 Weakness or paresis that may affect a single extremity, one half of the body,
or all 4 extremities
 Facial droop
 Monocular or binocular blindness
 Blurred vision or visual field deficits
 Dysarthria and trouble understanding speech
 Vertigo or ataxia
 Aphasia
 Symptoms of subarachnoid hemorrhage may include the following:
 Sudden onset of severe headache
 Signs of meningismus with nuchal rigidity
 Photophobia and pain with eye movements
 Nausea and vomiting
 Syncope - Prolonged or atypical

 Time is of essence in the diagnosis of stroke.
 There is urgency to make the diagnosis and determine
whether treatment with thrombolytic medications (clot-
busting drugs) to “reverse” the stroke is a possibility.
 The time frame to intervene is narrow and may be as short
as 3 to 4 ½ hours after onset of symptoms
 AHA and ASA recommend that everybody be aware
of “FAST“ in recognizing stroke:
 Face Drooping, ArmWeakness, Speech Difficulty,Time to
Call 9-1-1(emergency line 112 for Nigeria)
 In the emergency department, doctors may perform a
more in depth and standardized neurologic
examination..

 Radiological tests including
 CT is used to look for bleeding or masses.
 CT perfusion scan done to check brain blood supply (perfusion).
 An MRI of the brain may be possibly indicated.
 Blood tests may include a
 Full blood count
 SEUCr,
 FBS,
 Blood Clotting function with international normalized ratio
(INR), prothrombin time (PT) and partial thromboplastin time
(PTT).
 An ECG may be performed to check the heart's rate and
rhythm.

 Hypertensive retinopathy is retinal
vascular damage caused by
hypertension.
 Symptoms usually do not develop until
late in the disease and include blurred
vision or visual field defects.
 Signs usually develop late in the
disease.
 Funduscopic examination shows
 arteriolar constriction,
 arteriovenous nicking,
 vascular wall changes,
 flame-shaped hemorrhages,
 cotton-wool spots,
 yellow hard exudates, and
 optic disk edema
▪ World sight day: 2nd Thursday of october(11/10)

 HHD is a term applied generally to heart
diseases that are caused by the direct or
indirect effects of elevated BP such as
 LeftVentricular Hypertrophy
 Coronary Artery Disease
 Cardiac Arrhythmias and
 Congestive Heart Failure
▪ World Heart Day: 29/09

 Left ventricular hypertrophy is the enlargement
and thickening of the walls of the left ventricle.
 Left ventricular hypertrophy is more common in
people who have uncontrolled high blood
pressure

 Left ventricular hypertrophy usually develops
gradually.
 One may experience no signs or symptoms, especially
during the early stages of the condition.
 As left ventricular hypertrophy progresses, you may
experience:
 Shortness of breath
 Fatigue
 Chest pain, often after exercising
 Sensation of rapid
 Palpitations
 Dizziness or fainting

 Develops when the major blood vessels that supply
the heart with blood, oxygen and nutrients (coronary
arteries) become damaged or diseased.
 This is due to deposition of Cholesterol-containing
deposits (plaque) in the coronary arteries.

 Chest pain (angina).
 pressure or tightness in the chest usually occurs on the
middle or left side of the chest which is generally triggered
by physical or emotional stress.
 this pain may be fleeting or sharp and felt in the neck, arm
or back.
 Shortness of breath.
 Heart attack.
 A completely blocked coronary artery may cause a heart
attack.
 The classic signs and symptoms of a heart attack include
▪ crushing pressure in the chest and
▪ pain in the shoulder or arm, sometimes with shortness of breath
and sweating.

 A cardiac arrhythmia is any abnormal heart rate or
rhythm.
 In normal adults, the heart beats regularly at a rate of 60
to 100 beats per minute, and the pulse matches the
contractions of the ventricles.
 Cardiac arrhythmias sometimes are classified according to
their origin as
 ventricular arrhythmias or
 supraventricular arrhythmias
 They also can be classified according to their effect on the heart
rate,
▪ with bradycardia indicating a heart rate of less than 60 beats per
minute and
▪ tachycardia indicating a heart rate of more than 100 beats per minute.

 Asymptomatic
 Dizziness
 Fainting
 Extreme fatigue.
 Palpitations
 Lightheadedness
 Loss of consciousness

 Congestive heart failure(CHF) is a condition in
which the heart's function as a pump is
inadequate to meet the body's needs.
 The symptoms of congestive heart failure
vary, but can include:
 Easy fatiguability
 Diminished exercise capacity,
 shortness of breath and
 swelling (edema).

 Hypertensive kidney disease is a medical
condition referring to damage to the kidney due
to chronic high blood pressure.
 HN can be divided into two types:
 benign and malignant.
 Benign nephrosclerosis is common in individuals over
the age of 60
 Malignant nephrosclerosis is uncommon and affects
1-5% of individuals with high blood pressure, that
have diastolic blood pressure passing 130 mm Hg.
▪ World kidney day(8/03); theme: kidneys & women’s health:
include, value, empower.

 Chronic high blood pressure causes damages
to kidney tissue including
 the small blood vessels, glomeruli, kidney tubules
and interstitial tissues.
 The tissue hardens and thickens which is known
as nephrosclerosis.[4]
 The narrowing of the blood vessels means less
blood is going to the tissue and so less oxygen is
reaching the tissue resulting in tissue death
(ischemia).

 Glomerular ischemia
 High blood pressure damages the endothelium which
leads to a build-up of plaques and eventual renal arteries
stenosis with consequent ischemic kidney disease leading
to a decrease in the size of the kidneys.
 Glomerular hypertension and glomerular
hyperfiltration
 An alternative mechanism of hypertensive nephropathy is
prolonged glomerular hypertension and hence glomerular
hyperfiltration. As a compensatory mechanism, the
unaffected nephrons vasodilate to increase blood flow to
the kidney and increase glomerular filtration across
undamaged glomeruli.

 Damage to the glomeruli allows proteins that are
usually too large to pass into the nephron to be
filtered.
 This leads to an elevated concentration of albumin in
the urine.
 Protein in the urine is best identified from a 24-hour
urine collection.
 Haematuria
 Definitive diagnosis requires morphological
examination.
 Common histological features include Glomerulosclerosis
which is either focally or globally and characterized by
hardening of the vessel walls..

 Thank you for your attention
 Questions and contributions

1. WHO. Q&As on hypertension. September 2015. Available from
http://www.who.int/features/qa/82/en/ [accessed on 19/3/18]
2. Bisognano JD, Batuman V. Malignant Hypertension. Medscape. Available from
https://emedicine.medscape.com/article/241640-overview [accessed on 19/3/18]
3. Finerly JA. Management of hypertensive encephalopathy. Available from
https://www.ncbi.nlm.nih.gov/pubmed/721056 [accessed on 19/3/18]
4. Internet Stroke Centre. Ischaemic Stroke. http://www.strokecenter.org/patients/about-
stroke/ischemic-stroke/ [accessed on 19/3/18]
5. Prakashkumar K. Kunar J. Biswar TK. Varshil M. Sojib BZ. End Organ Damage in
Hypertensive Geriatric Age Group: A cross sectional study. Journal of Medical Research
and Innovation. Available from https://jmri.org.in/jmri/article/view/75 [accessed on 19/3/18]
6. Whelton PK, Carey RM, Aronow WS, et al. 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.
Journal of the American College of Cardiology. Nov.2016. Available from
http://www.onlinejacc.org/content/early/2017/11/04/j.jacc.2017.11.006?_ga=2.217900830.9
42552789.1521573549-211035663.1521573549 [accessed on 19/3/18]

End organ damages of hypertension 2

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