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 Introduction
 Determinants of Arterial BP
 Functions Of Blood Pressure
 Physiological Variations In Bp
 Blood Pressure Regulation
 Applied Physiology
 Conclusion
 Arterial blood pressure is defined as the lateral
pressure exerted by the column of blood on the
wall of arteries.
 Arterial blood pressure is expressed in four
different terms:
 1. Systolic blood pressure
 2. Diastolic blood pressure
 3. Pulse pressure
 4. Mean arterial blood pressure.
 Systolic blood pressure : measures the
pressure in blood vessels when heart beats.
 Diastolic pressure : measures the pressure in
blood vessel when heart rests between beats.
 Normal value --- 120/80 mm Hg
 At risk ( pre hypertension) --- 120-139 / 80-89
mm Hg
 High – higher than 140 /90 mm Hg
 Central Factors
 Cardiac output: systolic pressure is directly
proportional to cardiac output.
 Hear t Rate : marked alteration in heart rate
effects BP by altering the cardiac output.
 Peripheral factors:
 Peripheral Resistance : Diastolic pressure is
directly proportional to peripheral resistance
 Blood Volume: BP is directly proportional to blood
volume.
 Venous Return: blood pressure is directly
proportional to venous return.
 Elasticity of blood vessels: BP is inversely
proportional to the elasticity of blood vessels.
 Velocity of Blood Flow: BP is directly proportional to
the velocity of blood flow.
 Diameter of Blood Vessels: BP is inversely
proportional to the diameter of blood vessel.
 Viscosity of Blood: BP is directly proportional to the
viscosity of blood.
 Intra-ventricular BP for ejection of blood (stroke
volume).
 Systemic arterial BP for blood flow to tissues
(tissue perfusion)
 Capillary hydrostatic BP for filtration (tissue fluid
formation).
 Systemic venous BP for blood flow back to heart
(venous return)
 Systemic arterial blood pressure
= cardiac output * total peripheral resistance
 AGE
 SBP AND DBP gradually rise with age (>30)
 SEX
 Rise in BP is more in males with age
 CIRCADIAN VARIATON ( DIURAL VARIATION)
 Lowest during sleep and highest in the mornings after
waking up.
 Increased transient during physical stress, mental stress,
emotion excitement.
 EFFECT OF GRAVITY
 When erect BP in any vessel varies in relation to the
vertical distance from the heart level.
 SHORT TERM REGULATION
 BARORECEPTOR MECHANISM / SINOAORTIC MECH
 CHEMORECEPTOR MECHANISM
 VASOMOTOR CENTER MECHANISM
 INTERMEDIATE TERM REGULATION
 STRESS RELAXATION
 FLUID SHIFT MECHANISM
 RENIN ANGIOTENSIN MECHANISM
 LONG TERM REGULATION
 RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
 The nervous regulation is rapid among all the
mechanisms involved in the regulation of
arterial blood pressure
 nervous system brings the pressure back to
normal within few minutes
 quick in action, but it operates only for a
short period and then it adapts to the new
pressure.
 Works for few seconds
 Baroreceptor mechanism
 Baroreceptors are stretch receptors located in the walls of
heart and blood vessels.
 Whenever BP increases, BR present in carotid sinus
(bifurcation of carotid artery) and arch of aorta are
stimulated.
 Inhibits the Vasomotor Center (VMC) and stimulates Vagal
nucleus.
 IX and X cranial nerves, called Buffer Nerves.
 Posture and Baroreceptors
 Change of posture lying down to sitting / standing
reduces arterial blood pressure and blood flow to
the upper parts of the body.
 Discharge of impulse decreases from
baroreceptors triggering spontaneous discharge
from VMC.
 This restores blood pressure by an increases in
heart rate and peripheral resistance.
 Chemoreceptor Mechanism
 Decrease in BP reduces blood flow to
chemoreceptors present in the carotid body and
arch of aorta.
 Reduced oxygen supply stimulates the
chemoreceptor.
 Stimulate VMC increasing the heart rate and
peripheral resistance by vaso constriction
 Increase of blood pressure.
 Vasomotor Center Mechanism
 Reduced blood flow to VMC causes its ischemia.
 Stimulate VMC causing increase in heart rate and
peripheral resistance.
 Net effect, changes the increase in BP
 Few minutes to few hours.
 Stress relaxation
 Increased BP exerts greater force on the walls of
blood vessels.
 Stretch of blood vessel causes initial contraction
of smooth muscle in its walls followed by
relaxation.
 Relaxation of the vessel wall brings down BP.
 Fluid shift mechanism
 Increased BP increases hydrostatic pressure
 This pushes fluid out of blood vessel into interstitial
space
 Loss of fluid from blood vessel reduces blood volume
 Reduced venous return and hence decrease in BP
 Renin Angiotensin Mechanism
 Reduced BP decreases blood flow to kidney.
 Causes juxta glomerular apparatus of kidney to produce
Renin.
 Renin acts on plasma substrate, angiotensinogen, to
form angiotensin I
 Angiotensin I converted to angiotensin II by
angiotensin converting enzyme (ACE) present in
lungs.
 ACE inhibitors prevent conversion of angiotensin I to
angiotensin II
 angiotensin II causes peripheral vaso constriction and
increases peripheral resistance.
 Restore the blood pressure
 Renin-Angiotensin- Aldosterone Mechanism
 Angiotensin II produced during intermediate term
regulation stimulates adrenal cortex to produce
aldosterone as a delayed effect.
 Aldosterone increases sodium reabsorption
 Water retained along with sodium
 Helps to increase fluid volume
 Increased fluid volume increase venous return
to heart and blood pressure increases
 Stimulate hypothalamus and posterior
pituitary to release anti diuretic hormone
(ADH)
 ADH helps in water retention
 Mechanism activates thirst, enhancing fluid
intake.
 Retention of salt and water increases systemic
arterial pressure
 In turn will increase hydro static pressure
facilitating formation of larger volume of
filtrate
 Increased salt and water promoting formation
of a larger volume of filtrate rich in salt is
termed PRESSURE NATRIURESIS AND DIURESIS.
 Pulmonary hypertension
 Primary Hypertension
 Secondary Hypertension
 Isolated Hypertension
 Hypotension
 Type of blood pressure affecting arteries in
lungs and right side of heart.
 Arteries and capillaries become narrowed,
blocked or destroyed.
 Thus harder for blood to flow through lungs,
raises pressure within lung arteries.
 Lower chamber of heart has to work harder,
causing heart muscle to weaken and fails.
 Pul. Arterial circulation is high flow and low
pressure sys with lower blood pressure than
systemic BP.
 Doesn’t exceed 30/15mmHg even in exercise.
 Normal value btw 3-8mmHg in pulmonary vein.
 Pulmonary hypertension is defined as a
systolic BP in the pulmonary arterial
circulation above 30mmHg.
 Types
 Pulmonary Idiopathic
 Secondary
 Idiopathic Pul. Hypertension
 Uncommon condition of unknown cause.
 Young females between 20-40years, children
around 5 years.
 Etiology
 Neurohumoral vasoconstrictor mechanism
 Unrecognized thromboemboli / amniotic fluid emboli
 Collagen vascular disease
 Ingestion of substance like bush tea, oral contraceptive,
appetite depressant agents like amniorex
 Familial occurrence
 Secondary pulmonary Hypertension
 Occurs secondary to recognized lesion in heart or lungs.
 Any age it can occur, more in above 50 years.
 Etiopathogensis
 Passive:
1) mitral stenosis
2) chronic left ventricular failure
 Hyperkinetic pulmonary hypertension
 The lethal effects of hypertension are caused mainly
in three ways:
 1. Excess workload on the heart leads to early heart
failure and coronary heart disease, often causing
death as a result of a heart attack.
 2. The high pressure frequently damages a major
blood vessel in the brain, followed by death of major
portions of the brain; this is a cerebral infarct.
Clinically it is called a “stroke.” Depending on which
part of the brain is involved, a stroke can cause
paralysis, dementia, blindness, or multiple other
serious brain disorders.
 3. High pressure almost always causes injury in the
kidneys, producing many areas of renal destruction
and, eventually, kidney failure, uremia, and death.
 It is the persistent high blood pressure.
 Clinically when systolic pressure remains
elevated above 150mmHg, and diastolic
pressure remains elevated above 90mmHg, it
is considered as hypertension.
 Types
 Primary hypertension
 Benign hypertension
 Malignant hypertension
 Secondary hypertension
 Cardiovascular hypertension
 Endocrine hypertension
 Renal hypertension
 Neurological hypertension
 Hypertension during pregnancy
 Elevated blood pressure in the absence of any
underlying diseases.
 It is increases because of increased peripheral
resistance, which occurs due to some unknown
cause.
 About 90 to 95 per cent of all people who have
hypertension are said to have “primary
hypertension,” also widely known as “essential
hypertension”
 In most patients, excess weight gain and sedentary
lifestyle appear to play a major role in causing
hypertension.
 Benign hypertension
 historical terms that are considered
misleading, as hypertension is never benign, and
consequently they have fallen out of use
 The terminology persisted in the International
Classification of Disease (ICD9), but is not included in
the current ICD10
 Malignant Hypertension
 Extremely high blood pressure that develops
rapidly
 Typically above 180/120 mmHg
 Treated as a medical emergency
 Cause
 high blood pressure is the main cause of malignant
hypertension. Missing doses of blood pressure
medications can also cause it.
 Collagen vascular disease, such as scleroderma
 Kidney disease
 Spinal cord injuries
 Tumor of the adrenal gland
 Use of certain medications, including birth control
pills and MAOIs
 Use of illegal drugs, such as cocaine
 Rare case About 1% of people who have a
history of high blood pressure develop this life-
threatening condition.
 Symptoms
 Damage happens to the kidneys or the eyes
 Blurred vision
 Chest pain (angina)
 Difficulty breathing
 Dizziness
 Numbness in the arms, legs, and face
 Severe headache
 Shortness of breath
 Malignant hypertension can cause brain swelling,
which leads to a dangerous condition called
hypertensive encephalopathy.
 Symptoms include:
 Blindness
 Changes in mental status
 Coma
 Confusion
 Drowsiness
 Headache that continues to get worse
 Nausea and vomiting
 Seizures
 Diagnosis
 A diagnosis of malignant hypertension is based on
blood pressure readings and signs of acute organ
damage.
 Recheck blood pressure and listen
to heart and lungs for abnormal sounds
 Examine eyes to check for damage to the blood
vessels of the retina and swelling of the optic nerve
 Blood And Urine Tests that may include:
 Blood urea nitrogen (BUN) and creatinine
levels, which increase in kidney damage
 Blood clotting tests
 Blood sugar (glucose) level
 Complete blood count
 Sodium and potassium levels
 Urinalysis to check for blood, protein, or
abnormal hormone levels related to kidney
problems
 Echocardiogram to check heart function and blood
flow through the heart
 Electrocardiogram (ECG) to check the heart’s
electrical function
 Chest X-ray to look at the shape and size of the heart
structures and to detect fluid in the lungs
 Treatment
 Malignant hypertension is a medical emergency,
treated in a hospital, often in an intensive care unit.
 The goal of treatment is to carefully lower blood
pressure within a matter of minutes.
 Blood pressure medicines through an IV, Once blood
pressure is at a safe level, the medications may be
switched to oral forms. If pat develops kidney failure,
need to do kidney dialysis.
 Complications
 Untreated, malignant hypertension causes death.
 Aortic dissection, which is a sudden rupture of
the main blood vessel leaving the heart
 Coma
 Fluid in the lungs, called pulmonary edema
 Heart attack
 Heart failure
 Stroke
 Sudden kidney failure
 Reno Vascular Hypertension
 condition in which high blood pressure is caused by
the kidneys' hormonal response to narrowing of
the arteries supplying the kidneys.
 When functioning properly this hormonal axis
regulates blood pressure.
 Due to low local blood flow, the kidneys mistakenly
increase blood pressure of the entire circulatory
system.
 It is a form of secondary hypertension - a form of
hypertension whose cause is identifiable.
 Signs and symptoms
 High blood pressure (early age)
 Kidney dysfunction
 Narrowing of arteries elsewhere in the body
 Pulmonary edema
 Cause
 Any narrowing/blockage of blood supply to the renal
organ (renal artery stenosis).
 As a consequence of this action the renal organs release
hormones that indicate to the body to maintain a higher
amount of sodium and water, which in turn causes blood
pressure to rise.
 Factors that may contribute are:
 Diabetes
 High cholesterol
 Advanced age
 Unilateral condition is sufficient to cause renovascular
hypertension.
 Diagnosis
 Blood test (for renal function)
 Urinary test (tests for microalbuminuria)
 Serology (to exclude systemic lupus erythematosus )
 Lipid profile
 Urinalysis (to exclude presence of red blood cells)
 Treatment
 Surgical revascularization versus medical therapy for
atherosclerosis, it is not clear if one option is better than the
other according to a 2014 cochrane review; balloon angioplasty
did show a small improvement in blood pressure.
 Surgery can include
 Percutaneous surgical revascularization
 Nephrectomy or autotransplantation
 Individual may be given beta-adrenergic blockers.
 Early therapeutic intervention is important if
ischemic nephropathy is to be prevented.
 Inpatient care is necessary for the management of
hypertensive urgencies, quick intervention is required
to prevent further damage to the kidneys.
 Pregnancy hypertension
 Few women of childbearing age have high
blood pressure, up to 11%
develop hypertension of pregnancy.
 While generally benign, it may herald three
complications of pregnancy:
 Pre- Eclampsia
 a disorder of pregnancy characterized by the onset
of high blood pressure and often a significant
amount of protein in the urine
 HELLP syndrome
 complication of pregnancy characterized
by hemolysis, elevated liver enzymes, and
a low platelet count.
 Eclampsia
 onset of seizures (convulsions) in a woman with pre-
Eclampsia
 Follow-up and control with medication is
therefore often necessary.
 Diastolic blood pressure is greater than about 90
mm hg and the systolic pressure is greater than
about 135 mm hg.
 In severe hypertension, the mean arterial
pressure can rise to 150 to 170 mm Hg, with
diastolic pressure as high as 130 mm Hg and
systolic pressure occasionally as high as 250 mm
Hg.
 At severely high pressures—mean arterial
pressures 50 per cent or more above normal—a
person can expect to live no more than a few
more years unless appropriately treated.
 Neurogenic hypertension
 Excessive secretion of norepinephrine and
epinephrine which
promotes vasoconstriction resulting from chronic
high activity of the sympathoadrenal system,
the sympathetic nervous system and the adrenal
gland.
 The specific mechanism involved is increased
release of the "stress
hormones", epinephrine (adrenaline)
and norepinephrine which increase blood output
from heart and constrict arteries
 Diastolic number less than 80mmHg and
systolic higher or equal to 130 mm Hg is
called as ISP
 Caused by underlying conditions like
 artery stiffness
 an overactive thyroid (hyperthyroidism)
 Diabetes
 Isolated systolic hypertension can lead to
serious health problems, such as:
 Stroke
 Heart disease
 Chronic kidney disease
 SYSTOLIC PRESSURE LESS THEN THAT OF 90mm
Hg
 BP below 100/60mmHg in females and less than
110/70mmHg in men.
 Ortho static hypotension, blood rushes into the
lower parts of the body when sitting down or
standing up fast.
 Causes
 Diseases
 Severe hemorrhage
 Heart diseases
 Addison’s diseases
 Drug
 Anti hypertensive drug
 Diuretics
 Vasodilators
 Treatment
 If cerebral, renal and cardiac perfusion is
maintained, hypotension itself doesn’t need any
vigorous direct treatment.
 Sympathomimetic agents used in in emergency
 Nor epinephrine
 Phenylephrine
 Blood pressure in the body is regulated
through different mechanism which helps
the body to maintain normal
physiological functions.
 Mild to severe variation in it, can alter
normal physiological function and even
damage of organs which can even lead to
death.
 Thus it is important to have regular
checkups to maintain the normal blood
pressure.
 Essentials of physiology for dental students by
K Sembulingam
 Januszewicz A,et al, Malignant hypertension:
new aspect of an old clinical entity, Pol Arch
Med Wewn.2016;126(1-2):86-93.
Blood pressure regulation

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Blood pressure regulation

  • 1.
  • 2.  Introduction  Determinants of Arterial BP  Functions Of Blood Pressure  Physiological Variations In Bp  Blood Pressure Regulation  Applied Physiology  Conclusion
  • 3.  Arterial blood pressure is defined as the lateral pressure exerted by the column of blood on the wall of arteries.  Arterial blood pressure is expressed in four different terms:  1. Systolic blood pressure  2. Diastolic blood pressure  3. Pulse pressure  4. Mean arterial blood pressure.
  • 4.  Systolic blood pressure : measures the pressure in blood vessels when heart beats.  Diastolic pressure : measures the pressure in blood vessel when heart rests between beats.  Normal value --- 120/80 mm Hg  At risk ( pre hypertension) --- 120-139 / 80-89 mm Hg  High – higher than 140 /90 mm Hg
  • 5.  Central Factors  Cardiac output: systolic pressure is directly proportional to cardiac output.  Hear t Rate : marked alteration in heart rate effects BP by altering the cardiac output.  Peripheral factors:  Peripheral Resistance : Diastolic pressure is directly proportional to peripheral resistance
  • 6.  Blood Volume: BP is directly proportional to blood volume.  Venous Return: blood pressure is directly proportional to venous return.  Elasticity of blood vessels: BP is inversely proportional to the elasticity of blood vessels.  Velocity of Blood Flow: BP is directly proportional to the velocity of blood flow.  Diameter of Blood Vessels: BP is inversely proportional to the diameter of blood vessel.  Viscosity of Blood: BP is directly proportional to the viscosity of blood.
  • 7.  Intra-ventricular BP for ejection of blood (stroke volume).  Systemic arterial BP for blood flow to tissues (tissue perfusion)  Capillary hydrostatic BP for filtration (tissue fluid formation).  Systemic venous BP for blood flow back to heart (venous return)  Systemic arterial blood pressure = cardiac output * total peripheral resistance
  • 8.  AGE  SBP AND DBP gradually rise with age (>30)  SEX  Rise in BP is more in males with age  CIRCADIAN VARIATON ( DIURAL VARIATION)  Lowest during sleep and highest in the mornings after waking up.  Increased transient during physical stress, mental stress, emotion excitement.  EFFECT OF GRAVITY  When erect BP in any vessel varies in relation to the vertical distance from the heart level.
  • 9.
  • 10.
  • 11.  SHORT TERM REGULATION  BARORECEPTOR MECHANISM / SINOAORTIC MECH  CHEMORECEPTOR MECHANISM  VASOMOTOR CENTER MECHANISM  INTERMEDIATE TERM REGULATION  STRESS RELAXATION  FLUID SHIFT MECHANISM  RENIN ANGIOTENSIN MECHANISM  LONG TERM REGULATION  RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
  • 12.  The nervous regulation is rapid among all the mechanisms involved in the regulation of arterial blood pressure  nervous system brings the pressure back to normal within few minutes  quick in action, but it operates only for a short period and then it adapts to the new pressure.
  • 13.  Works for few seconds  Baroreceptor mechanism  Baroreceptors are stretch receptors located in the walls of heart and blood vessels.  Whenever BP increases, BR present in carotid sinus (bifurcation of carotid artery) and arch of aorta are stimulated.  Inhibits the Vasomotor Center (VMC) and stimulates Vagal nucleus.  IX and X cranial nerves, called Buffer Nerves.
  • 14.
  • 15.  Posture and Baroreceptors  Change of posture lying down to sitting / standing reduces arterial blood pressure and blood flow to the upper parts of the body.  Discharge of impulse decreases from baroreceptors triggering spontaneous discharge from VMC.  This restores blood pressure by an increases in heart rate and peripheral resistance.
  • 16.  Chemoreceptor Mechanism  Decrease in BP reduces blood flow to chemoreceptors present in the carotid body and arch of aorta.  Reduced oxygen supply stimulates the chemoreceptor.  Stimulate VMC increasing the heart rate and peripheral resistance by vaso constriction  Increase of blood pressure.
  • 17.  Vasomotor Center Mechanism  Reduced blood flow to VMC causes its ischemia.  Stimulate VMC causing increase in heart rate and peripheral resistance.  Net effect, changes the increase in BP
  • 18.  Few minutes to few hours.  Stress relaxation  Increased BP exerts greater force on the walls of blood vessels.  Stretch of blood vessel causes initial contraction of smooth muscle in its walls followed by relaxation.  Relaxation of the vessel wall brings down BP.
  • 19.  Fluid shift mechanism  Increased BP increases hydrostatic pressure  This pushes fluid out of blood vessel into interstitial space  Loss of fluid from blood vessel reduces blood volume  Reduced venous return and hence decrease in BP
  • 20.  Renin Angiotensin Mechanism  Reduced BP decreases blood flow to kidney.  Causes juxta glomerular apparatus of kidney to produce Renin.  Renin acts on plasma substrate, angiotensinogen, to form angiotensin I
  • 21.  Angiotensin I converted to angiotensin II by angiotensin converting enzyme (ACE) present in lungs.  ACE inhibitors prevent conversion of angiotensin I to angiotensin II  angiotensin II causes peripheral vaso constriction and increases peripheral resistance.  Restore the blood pressure
  • 22.  Renin-Angiotensin- Aldosterone Mechanism  Angiotensin II produced during intermediate term regulation stimulates adrenal cortex to produce aldosterone as a delayed effect.  Aldosterone increases sodium reabsorption  Water retained along with sodium  Helps to increase fluid volume
  • 23.  Increased fluid volume increase venous return to heart and blood pressure increases  Stimulate hypothalamus and posterior pituitary to release anti diuretic hormone (ADH)  ADH helps in water retention  Mechanism activates thirst, enhancing fluid intake.  Retention of salt and water increases systemic arterial pressure
  • 24.  In turn will increase hydro static pressure facilitating formation of larger volume of filtrate  Increased salt and water promoting formation of a larger volume of filtrate rich in salt is termed PRESSURE NATRIURESIS AND DIURESIS.
  • 25.  Pulmonary hypertension  Primary Hypertension  Secondary Hypertension  Isolated Hypertension  Hypotension
  • 26.  Type of blood pressure affecting arteries in lungs and right side of heart.  Arteries and capillaries become narrowed, blocked or destroyed.  Thus harder for blood to flow through lungs, raises pressure within lung arteries.  Lower chamber of heart has to work harder, causing heart muscle to weaken and fails.
  • 27.  Pul. Arterial circulation is high flow and low pressure sys with lower blood pressure than systemic BP.  Doesn’t exceed 30/15mmHg even in exercise.  Normal value btw 3-8mmHg in pulmonary vein.
  • 28.  Pulmonary hypertension is defined as a systolic BP in the pulmonary arterial circulation above 30mmHg.  Types  Pulmonary Idiopathic  Secondary
  • 29.  Idiopathic Pul. Hypertension  Uncommon condition of unknown cause.  Young females between 20-40years, children around 5 years.  Etiology  Neurohumoral vasoconstrictor mechanism  Unrecognized thromboemboli / amniotic fluid emboli  Collagen vascular disease  Ingestion of substance like bush tea, oral contraceptive, appetite depressant agents like amniorex  Familial occurrence
  • 30.  Secondary pulmonary Hypertension  Occurs secondary to recognized lesion in heart or lungs.  Any age it can occur, more in above 50 years.  Etiopathogensis  Passive: 1) mitral stenosis 2) chronic left ventricular failure  Hyperkinetic pulmonary hypertension
  • 31.  The lethal effects of hypertension are caused mainly in three ways:  1. Excess workload on the heart leads to early heart failure and coronary heart disease, often causing death as a result of a heart attack.  2. The high pressure frequently damages a major blood vessel in the brain, followed by death of major portions of the brain; this is a cerebral infarct. Clinically it is called a “stroke.” Depending on which part of the brain is involved, a stroke can cause paralysis, dementia, blindness, or multiple other serious brain disorders.  3. High pressure almost always causes injury in the kidneys, producing many areas of renal destruction and, eventually, kidney failure, uremia, and death.
  • 32.  It is the persistent high blood pressure.  Clinically when systolic pressure remains elevated above 150mmHg, and diastolic pressure remains elevated above 90mmHg, it is considered as hypertension.  Types  Primary hypertension  Benign hypertension  Malignant hypertension
  • 33.  Secondary hypertension  Cardiovascular hypertension  Endocrine hypertension  Renal hypertension  Neurological hypertension  Hypertension during pregnancy
  • 34.  Elevated blood pressure in the absence of any underlying diseases.  It is increases because of increased peripheral resistance, which occurs due to some unknown cause.  About 90 to 95 per cent of all people who have hypertension are said to have “primary hypertension,” also widely known as “essential hypertension”  In most patients, excess weight gain and sedentary lifestyle appear to play a major role in causing hypertension.
  • 35.  Benign hypertension  historical terms that are considered misleading, as hypertension is never benign, and consequently they have fallen out of use  The terminology persisted in the International Classification of Disease (ICD9), but is not included in the current ICD10
  • 36.  Malignant Hypertension  Extremely high blood pressure that develops rapidly  Typically above 180/120 mmHg  Treated as a medical emergency  Cause  high blood pressure is the main cause of malignant hypertension. Missing doses of blood pressure medications can also cause it.  Collagen vascular disease, such as scleroderma
  • 37.  Kidney disease  Spinal cord injuries  Tumor of the adrenal gland  Use of certain medications, including birth control pills and MAOIs  Use of illegal drugs, such as cocaine
  • 38.  Rare case About 1% of people who have a history of high blood pressure develop this life- threatening condition.  Symptoms  Damage happens to the kidneys or the eyes  Blurred vision  Chest pain (angina)  Difficulty breathing  Dizziness  Numbness in the arms, legs, and face  Severe headache  Shortness of breath
  • 39.  Malignant hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy.  Symptoms include:  Blindness  Changes in mental status  Coma  Confusion  Drowsiness  Headache that continues to get worse  Nausea and vomiting  Seizures
  • 40.  Diagnosis  A diagnosis of malignant hypertension is based on blood pressure readings and signs of acute organ damage.  Recheck blood pressure and listen to heart and lungs for abnormal sounds  Examine eyes to check for damage to the blood vessels of the retina and swelling of the optic nerve
  • 41.  Blood And Urine Tests that may include:  Blood urea nitrogen (BUN) and creatinine levels, which increase in kidney damage  Blood clotting tests  Blood sugar (glucose) level  Complete blood count  Sodium and potassium levels  Urinalysis to check for blood, protein, or abnormal hormone levels related to kidney problems
  • 42.  Echocardiogram to check heart function and blood flow through the heart  Electrocardiogram (ECG) to check the heart’s electrical function  Chest X-ray to look at the shape and size of the heart structures and to detect fluid in the lungs
  • 43.  Treatment  Malignant hypertension is a medical emergency, treated in a hospital, often in an intensive care unit.  The goal of treatment is to carefully lower blood pressure within a matter of minutes.  Blood pressure medicines through an IV, Once blood pressure is at a safe level, the medications may be switched to oral forms. If pat develops kidney failure, need to do kidney dialysis.
  • 44.  Complications  Untreated, malignant hypertension causes death.  Aortic dissection, which is a sudden rupture of the main blood vessel leaving the heart  Coma  Fluid in the lungs, called pulmonary edema  Heart attack  Heart failure  Stroke  Sudden kidney failure
  • 45.  Reno Vascular Hypertension  condition in which high blood pressure is caused by the kidneys' hormonal response to narrowing of the arteries supplying the kidneys.  When functioning properly this hormonal axis regulates blood pressure.  Due to low local blood flow, the kidneys mistakenly increase blood pressure of the entire circulatory system.  It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.
  • 46.  Signs and symptoms  High blood pressure (early age)  Kidney dysfunction  Narrowing of arteries elsewhere in the body  Pulmonary edema
  • 47.  Cause  Any narrowing/blockage of blood supply to the renal organ (renal artery stenosis).  As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise.  Factors that may contribute are:  Diabetes  High cholesterol  Advanced age  Unilateral condition is sufficient to cause renovascular hypertension.
  • 48.  Diagnosis  Blood test (for renal function)  Urinary test (tests for microalbuminuria)  Serology (to exclude systemic lupus erythematosus )  Lipid profile  Urinalysis (to exclude presence of red blood cells)
  • 49.  Treatment  Surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 cochrane review; balloon angioplasty did show a small improvement in blood pressure.  Surgery can include  Percutaneous surgical revascularization
  • 50.  Nephrectomy or autotransplantation  Individual may be given beta-adrenergic blockers.  Early therapeutic intervention is important if ischemic nephropathy is to be prevented.  Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.
  • 51.  Pregnancy hypertension  Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy.  While generally benign, it may herald three complications of pregnancy:  Pre- Eclampsia  a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine
  • 52.  HELLP syndrome  complication of pregnancy characterized by hemolysis, elevated liver enzymes, and a low platelet count.  Eclampsia  onset of seizures (convulsions) in a woman with pre- Eclampsia  Follow-up and control with medication is therefore often necessary.
  • 53.  Diastolic blood pressure is greater than about 90 mm hg and the systolic pressure is greater than about 135 mm hg.  In severe hypertension, the mean arterial pressure can rise to 150 to 170 mm Hg, with diastolic pressure as high as 130 mm Hg and systolic pressure occasionally as high as 250 mm Hg.  At severely high pressures—mean arterial pressures 50 per cent or more above normal—a person can expect to live no more than a few more years unless appropriately treated.
  • 54.  Neurogenic hypertension  Excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from chronic high activity of the sympathoadrenal system, the sympathetic nervous system and the adrenal gland.  The specific mechanism involved is increased release of the "stress hormones", epinephrine (adrenaline) and norepinephrine which increase blood output from heart and constrict arteries
  • 55.  Diastolic number less than 80mmHg and systolic higher or equal to 130 mm Hg is called as ISP  Caused by underlying conditions like  artery stiffness  an overactive thyroid (hyperthyroidism)  Diabetes
  • 56.  Isolated systolic hypertension can lead to serious health problems, such as:  Stroke  Heart disease  Chronic kidney disease
  • 57.  SYSTOLIC PRESSURE LESS THEN THAT OF 90mm Hg  BP below 100/60mmHg in females and less than 110/70mmHg in men.  Ortho static hypotension, blood rushes into the lower parts of the body when sitting down or standing up fast.
  • 58.  Causes  Diseases  Severe hemorrhage  Heart diseases  Addison’s diseases  Drug  Anti hypertensive drug  Diuretics  Vasodilators
  • 59.  Treatment  If cerebral, renal and cardiac perfusion is maintained, hypotension itself doesn’t need any vigorous direct treatment.  Sympathomimetic agents used in in emergency  Nor epinephrine  Phenylephrine
  • 60.  Blood pressure in the body is regulated through different mechanism which helps the body to maintain normal physiological functions.  Mild to severe variation in it, can alter normal physiological function and even damage of organs which can even lead to death.  Thus it is important to have regular checkups to maintain the normal blood pressure.
  • 61.  Essentials of physiology for dental students by K Sembulingam  Januszewicz A,et al, Malignant hypertension: new aspect of an old clinical entity, Pol Arch Med Wewn.2016;126(1-2):86-93.