HYPERTENSION

Fadillah Maricar
CLOSED
CIRCUIT
Hypertension ( HTN) is rise pressure intravascular or
intracavitary
Hypertonia : rise in
muscular tonus

Arterial Hypertension

Pulmonary Hypertension
 ARTERIAL HYPERTENSION

At least two BP determination performed at

5 minute interval suggest for increased BP level

Primary/ Essential HTN : elevation in BP without an

identified cause

Secondary HTN : elevation in BP with an exact cause

 It’s account for 5 -10% of total cases
 RISK FACTORS
• Age

• Gender

• Alcoholic, smoking and DM

• Excessive dietary intake of Sodium

• Obesity

• Family history

• Sedentary life style

• Stress
ETIOLOGY
( for Secondary HTN )

• Congenital narrowing of aorta

• Renal disease

• Endocrine disorders like Cushing’s syndrome

• Neurological disorder like brain tumors and head injury

• Sleep apnea

• Medication like oral contraceptive pills, NSAID and cocaine

• Cirrhosis of liver
 PATOPHYSIOLOGY
Symphatet Activities
ic Nervous of
System Endocrine
Activity System

BP
Activities
Activities
of Vascular
of Renal
Endotheliu
System
m
Symphatet ↑ HR and Cardiac Contraction  Vasoconstriction in Peripheral
ic Nervous Arterioles  Promotes release Renin from kidney
System ↑ Cardiac Output and Systemic Vascular Resistence
Activity
BP = CO x SVR

Activities Vascular endothelium is a single cell layer that lines the blood
of Vascular vessel
Endotheliu
m
It produces vasoactive substance and growth factors (nitric acid,
endothelin) which were potent vasoconstrictor to increase BP
level
Activities of Renal System
Activities of Endocrine
System

When Angiotensin II is
stimulated in adrenal
cortex, it will secrete
aldosterone  stimulate
kidney to retain sodium
and water
PATHOLOGY
CLINICAL FEATURES

• Sometimes the high BP does not cause any symptoms  so that is

known as silent killer disease

• In some patients the symptom were : severe headache, blurred vision,

dizziness, nausea, vomiting, fatigue, confusion, epistaxis, chest pain,
shortness of breath, irregular heart beat, papilledema
 Anamnesis and Physical
Examination
↑ density of pulse
Medical
↑ pulse rate (in case complicating history
with acute of DM
and/or chronic heart failure)
Dilation of left border of heart dullness
Mild decreased 1st heart sound, 2nd sound aortic closure is accentuated
Complete blood count
Faint systolic murmur in heart apex
DIAGNO
Hepatomegaly and inferior extremity oedema ( in case complicating with
Chest X- Ray
STIC chronic heart failure )

EVALUA
ECG
TION
> 140/90 for Clinic BP; > 130/80 for Ambulatory BP
MANAGEMENT

Life style
1. Weight Reduction modification
2. DASH diet (Dietary Approach to Stop Hypertension)
3. Dietary Sodium reduction
4. Reduce alcohol
5. Exercise
6. Stress management
Pharmacological
Therapy
……… PHARMACOLOGICAL THERAPY
……… PHARMACOLOGICAL THERAPY
 HYPERTENSIVE CRISIS
= Sudden increase of BP (systolic > 180 mmHg; diastolic > 120 mmHg)

• Lack of end organ damage

• Anxiety, cardialgia, angina pectoris, headache, dizziness
Hypertensi • Intensify oral anti hypertensive
ve • BP ⇩ in 24 hrs
Urgencies

• There is end organ damage

• Hypertensive encephalopathy, intracranial hemorrhage, NHS, Acute Pulmonary Oedema, Acute Myocardial
Hypertensi Infarction, Adrenergic Crisis, Acute Aortic Dissection, Eclampsia
ve • Start intra venous anti hypertensive
Emergenci • BP ⇩ in 1 hr
es
 PULMONARY HYPERTENSION

• Pulmonary Artery Hypertension (PAH)

• Mean Pulmonary Artery Pressure (mPAP) > 20 mmHg

• mPAP = PAWP + ( CO x PVR )

• Therefore mPAP can be elevated in states of :

 PAWP elevation : left sided heart failure

 CO elevation : hyperdynamic state, exercise

 PVR elevation : left sided heart failure

Cl
as
si
fic
ati
on
CLINICAL FEATURES
Because the earliest symptom of patient with PAH are manifest
with exercise, PAH can have insidious presentation, but usually
includes dyspnea on exertion
• Fatigue with shortness of breath
• Lower extremity oedema, complaint of abdominal distention or early
satiety secondary to venous congestion ( if right ventricular failure
had occured) )
• Angina (reflecting demand ischemia due to RVH)
• Syncope or near syncope ( if cardiac output becomes fixed and
eventually falled)
• Orthopnea or paroxysmal nocturnal dyspnea ( sign of Left heart
Failure )
PHYSICAL EXAMINATION
Bedside cardiovascular findings reliably reflect the
severity of the PH and right heart failure if the
examination is done carefully

• Low BP but often tolerated ( ≈ warm shock )

• ⇧ resting HR without another explanation  sign of decompensated RV failure
• ⇧ JVP
• Parasternal RV heave
• ‘palpable’ P2
• Murmurs of Tricuspid Regurgitation and Pulmonic Regurgitation
• Hepatomegaly, ascites, and lower extremity oedema (sign of Right Heart Failure)
• Clubbing finger ( in Eissenmenger’s and Hypoxic lung disease
 2) Pulmonary
function
test
3) Lung
Enlargement scintigraph
RVH
of the main
pulmonary Atrial y
artery and its fibrillation
Reactive major and absence 4) Contrast
policythemi branches of right axis enhanced
a Right
deviation 
susp of chest CT
ventricular
pulmonary
hypertrophy 5) Cardiac MRI
venous HT
or dilation
6) PET
Scanning
Wor
k up
char
t
 An ignorant doctor is
the aide de camp of death
----- Avicenna ----

“ Therefore in medicine
we ought to know
the causes of sickness
and health “