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PRESENTED BY-
GUIDED BY-
• Introduction
• History
• Definitions
• Measurement
• Normal Values
• Factors Determining BP
• Regulation of BP :
• Short term regulation
• Long term regulation
• Applied Physiology
• Hypertension
• Periodontal Implications
• Hypotension
• Conclusion
Riva- Rocci (1896) Present-day Technique
Simple palpation of the pulse Early Egyptians
Stephen Hales (1677-1761)
Now, in the 21st century BP is monitored continually by
sensors worn on the patient's thumb;
Inflatable cuffs coupled to a servomechanism which
maintains suitable cuff pressure.
Strain gauges, photocells and semiconductors are
coming into use in the recording of blood pressure.
Proc. roy. Soc. Med. Volume
70 November 1977
Blood pressure is defined as the force exerted by the blood on unit area of
vessel wall.
VENOUS PRESSURE
PERIPHERAL VENOUS
PRESSURE CAPILLARY PRESSURE
FEW MORE TERMS RELATED TO BP
Recumbent
mm
of
Hg
Indirect method
Auscultatory Palpatory Oscillatory
Arterial pressure fluctuates between
a systolic level of 120 mm Hg
and a diastolic level of 80 mm Hg,
Thus a BP of 120/80 is considered as normal.
Chronic or Prolonged Elevation → Chronic Hypertension
Secondary
Hypertension
Cardio-vascular shock or Spinal shock → BP falls
Essential
Hypertension
3. DRUG INDUCED
• Amount of blood ejected per ventricle per beat
depends on-
a) Cardiac inflow
b) Contractility of the heart
c) Heart rate
CARDIAC OUTPUT :
Heart rate
(within physiological limits)
Cardiac Output
(Minute Volume)α
BP = Cardiac output X Peripheral resistance.
Not applicable to Windkessel vessels
• Chiefly Arterioles & to a small extent Capillaries.
depends on
a) Viscosity
b) Velocity
c) Elasticity
d) Lumen of vessel
PERIPHERAL RESISTANCE
R = 8ηl/π r4 =ΔP/Q
R = Peripheral resistance l = Length of the blood vessel
r = Radius of blood vessel Q = Cardiac output
ΔP = Difference in pressure in the vessel η= dynamic fluid viscosity
Hagen-Poiseulle
law
The Baro-receptor mechanism
The Chemo-receptor mechanism
The CNS Ischemic mechanism
SHORT TERM REGULATION
BARORECEPTOR MECHANISM
CHEMORECEPTOR MECHANISM
THE CNS ISCHEMIC MECHANISM
• ↓ CEREBRAL Blood flow causes
• Failure of the slowly flowing blood to
Carry CO2 away from the
VASOMOTOR CENTER
• Stimulation of Vasomotor centre
Systemic Arterial Pressure RISE
• Above threshold level such that HEART can pump blood &
CEREBRAL blood flow RESTORED
LONG TERM REGULATION
Hypertension is a persistently raised BP resulting from increased peripheral arteriolar resistance (scully & cawson)
DEFINITION
CLASSIFICATION
-ACCORDING TO ETIOLOGY
• >95%
• Underlying cause not known
Primary Hypertension
• 5 % of pts
• Consequence of disease/ abnormality
• Sodium retention
• With or without vasoconstriction
Secondary Hypertension
CLASSIFICATION-BASED ON BP MEASUREMENTS
In 2003, the National Heart, Lung and Blood Institute issued revised
guidelines for evaluation and management of hypertension
Do’s Average
value of 3 recordings
3 different appointments
Do
n’ts Diagnose by
Single Recording.
DIAGNOSIS
The Higher value is considered for the
classification among Systolic & Diastolic.
Isolated Systolic Hypertension
OBJECTIVE OF INITIAL EVALUATION OF
NEWLY DIAGNOSED…
Obtain accurate and representative measurements
Identify contributory factors/underlyingcause
Quantify cardiovascularrisk
Any complications (target organ damage)
Choice of antihypertensive therapy.
CLINICAL FEATURES
IF UNDIAGNOSED…
RISK FACTORSN
on
-mo
dif
iab
le • Age
• Sex
• Genetics
• Ethnicity
Mo
dif
iab
le • Obesity
• Salt intake
• Saturated fats
• Dietary fibers
• Alcohol
• Physical activity
• Environmental stress
MANAGEMENT
Urinalysis for blood, protein,
& glucose
Blood urea, electrolytes# &
creatinineBlood glucose
Serum total and HDL
Cholesterol
12-lead ECG (LVH, CAD)
# Hypokalaemic alkalosis may indicate Primary
Aldosteronism but is usually due to diuretic therapy.
- INVESTIGATIONS FOR ALL HYPERTENSIVES
• Cardiomegaly, Heart failure
• Coarctation of aortaChest X-ray
• To assess ’white coat’ hypertension
Ambulatory BP recording
• Detect or quantify LVHEchocardiogram
• Detect possible renal disease
Renal ultrasound /Angiography
- INVESTIGATIONS FOR SELECTED
↓ Alcohol intake
Restricting Salt intake
Appropriate life-style
(Correcting Obesity)
Eating oily fish
Regular physical exercise
Quitting smoking
↑ Consumption
of fruit/ vegetables
- NON DRUG THERAPY
ANTIHYPERTENSIVE DRUGS
ANTIHYPERTENSIVE DRUGS
• Losartan (50-100 mg)
• Valsartan (40-160 mg)
• Blocks Angiotensin II type I
Angiotensin receptor blockers
• Amlodipine (5-10 mg)
• Nifedipine (30-90 mg)
• Side effects- flushing, palpitations, Gingival Enlargement
• Used Hypertension co-exists with angina
Calcium antagonists
• Vasodilators
• α- Blockers
• Prazosin
• Hydralazine
• Minoxidil
Other Drugs
TREATMENT MODIFICATIONS
Period
on
tal pro
ced
ure • Safe if
stress minimized
Patient on
medic
ation • Consult
Physician
Info
rm the
Ph
ysic
ian • Duty of
dentist
• Degree of stress
• Length of procedure
• Complexity of treatment
TREATMENT MODIFICATIONS
Risk of providing emergency dental care must out weigh risk of possible
hypertensive complication.#
TREATMENT CONSIDERATIONS
• Analgesics for pain
• Antibiotics for infection
• Surgical I & D
Do’s
• Treatment of HT pt not on medication
• LA with adrenalin >1:1,00,000 IU
Dont’s
Important to minimize pain → providing profound local anesthesia → avoiding
an increase in endogenous epinephrine secretion. (Mealy BL, 1996 & Muzyka
bc, Glick M, 1997)
SOME PHARMACOLOGICAL ASPECTS
Epinephrine- α & βadrenergic agonist
• ↑Heart rate by direct stimulation
• α -Vasoconstriction
• Β-Vaso dilatation
• Propanolol/ Nadolol+ LA with ADRENALIN = ↑ BP
WHY NOT ADRENALIN / EPINEPHRINE
WITH LA IN HYPERTENSIVES ???...
However, The benefits of the small doses of Epinephrine used in dentistry far
outweigh the potential for hemodynamic compromise!!!
BP increases around awakening
and peaks around mid morning
(Smolensky; 1996, Raab FJ et al; 1998)
HENCE, AFTERNOON DENTAL APPOINTMENTS MAY BE
PREFERRED
Postural hypotension is
very common!!
MINIMIZED BY SLOW POSITIONAL CHANGES
Strong positive association between
increased subgingival colonization by
A.a, P.g, T. forsythia and T. denticola
and prevalent Hypertension is seen
Nausea, sedation, oral
dryness, lichenoid reaction &
GINGIVAL OVERGROWTH
DESVARIEUX ET AL (2012)
ARTERIAL HYPERTENSION DOES NOT NORMALLY
PRECLUDE PERIODONTAL SURGERY. .(LINDHE)
ASSOCIATED WITH CERTAIN ANTIHYPERTENSIVE AGENTS
GINGIVAL OVERGROWTH &
ANTIHYPERTENSIVE AGENTS
Hypertensive pt
Calcium channel blockers
Nifedipine=44%
Diltiazem = 20%
Verapamil = 4%
Safe among other CCB
Other Anti-Hypertensives
No Gingival Overgrowth
Safe
•The dihydropyridine derivative, ISRADIPINE, can replace
Nifedipine in some cases and does not induce gingival
overgrowth.
A decrease in blood pressure below the normal value is termed as Hypotension
Acute Chronic
Systemic Causes
Serious Infections
Acute Hemorrhage
Vomiting
Diarrhea
Severe Burns
Anaphylactic shock
MI
Tachycardia
WeaknessLethargyEasy fatigabilityDizziness and fainting (erect posture)Interference with neural pathway
CLINICAL FEATURES
Dizziness Bradycardia Postural hypotension
Fainting
MANAGEMENT
Thorough Case history
High salt diet High fluid intake
Vaso-vagal shock-ATROPINE 0.6mg
iv
Hypertension is highly prevalent!!
Role of periodontist can be vital.
Hence, as periodontal surgeons we should
1. Record proper History
2. Consult the physician – Discuss
3. Minimize stress
4. Periodic recall and follow-up even can help in
hypertension monitoring.
CONCLUSION
1. Davidson’s Principles and Practice of Medicine, 18th Ed.
2. Concise Medical Physiology- Choudhuri, 2nd Ed.
3. Textbook of Medical Physiology – Guyton & Hall, 9th Ed.
4. Review of Medical Physiology – William F. Ganong, 20th Ed.
5. Carranza’s Clinical Periodontology, 10th Ed.
6. Journal of periodontol, 2002, 73: 954 – 68.
7. Clinical Periodontology and Implant dentistry – Jan Lindhe, 4th Ed.
8. Periodontics-Medicine, Surgery and Implants – Rose, Mealey, Genco & Cohen.
9. Harrison’s Principles of Internal Medicine, 16th Ed.
10. Vanderheyden et al. JADA 1989: 119; 407-412
11. Perio 2000: vol 23; 136 -141