GUIDED BY-PRESENTED BY-
•   Introduction•   History•   Definitions•   Measurement•   Normal Values•   Factors Determining BP•   Regulation of BP :...
Proc. roy. Soc. Med. Volume                                                   70 November 1977Simple palpation of the puls...
Blood pressure is defined as the force exerted by the blood on unit area of             vessel wall.
FEW MORE TERMS RELATED TO BP              Recumbent                 PERIPHERAL                   VENOUS    VENOUS        P...
mmofHg
Indirect methodAuscultatory       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 ...
Chronic or Prolonged Elevation → Chronic Hypertension                                       Secondary   Essential         ...
3. DRUG INDUCED
CARDIAC OUTPUT :    • Amount of blood ejected per ventricle per beat               depends on-                   a) Cardia...
PERIPHERAL RESISTANCE• Chiefly Arterioles & to a small extent Capillaries.         depends on              a) Viscosity   ...
SHORT TERM REGULATION  The Baro-receptor  mechanism  The Chemo-receptor  mechanism  The CNS Ischemic  mechanism
BARORECEPTOR MECHANISM
CHEMORECEPTOR MECHANISM
THE CNS ISCHEMIC MECHANISM• ↓ CEREBRAL Blood                                Systemic Arterial   • Above threshold         ...
LONG TERM REGULATION
DEFINITION      Hypertension is a persistently raised      BP resulting from increased peripheral      arteriolar resistan...
CLASSIFICATION   -ACCORDING TO ETIOLOGY• >95%                   • 5 % of pts• Underlying cause not   • Consequence of  kno...
CLASSIFICATION           -BASED ON BP MEASUREMENTSIn 2003, the National Heart, Lung and Blood Institute issued revisedguid...
The Higher value is considered for theclassification among Systolic & Diastolic.Isolated Systolic HypertensionDIAGNOSIS ...
OBJECTIVE OF INITIAL EVALUATION OFNEWLY DIAGNOSED…  Obtain accurate and representative  measurements  Identify contributor...
CLINICAL FEATURES        IF UNDIAGNOSED…
RISK FACTORS                 •                            •Non-modifiable                                 Modifiable      ...
MANAGEMENT - INVESTIGATIONS FOR ALL HYPERTENSIVESUrinalysis for           Blood urea,blood, protein,         electrolytes#...
- INVESTIGATIONS FOR SELECTED                   • Cardiomegaly, Heart failure  Chest X-ray      • Coarctation of aorta Amb...
- NON DRUG THERAPY                Appropriate life-    ↓                style             QuittingAlcohol                 ...
ANTIHYPERTENSIVE DRUGS
ANTIHYPERTENSIVE DRUGS                           • Amlodipine (5-10 mg)      •   Vasodilators • Losartan (50-100 mg)    • ...
TREATMENT MODIFICATIONS                        • Safe if                             • Consult                            ...
TREATMENT MODIFICATIONSRisk of providing emergency dental care must out weigh risk of possiblehypertensive complication.#
TREATMENT CONSIDERATIONS • Analgesics for                        • Treatment of HT   pain                                 ...
SOME PHARMACOLOGICAL ASPECTSEpinephrine- α & βadrenergic agonist• ↑Heart rate by       • Propanolol/  direct stimulation  ...
WHY NOT ADRENALIN / EPINEPHRINEWITH LA IN HYPERTENSIVES ???...However, The benefits of the small doses of Epinephrine used...
BP increases around awakening            and peaks around mid morning  (Smolensky; 1996, Raab FJ et al; 1998)HENCE, AFTERN...
Strong positive association between         increased subgingival colonization by         A.a, P.g, T. forsythia and T. de...
GINGIVAL OVERGROWTH &ANTIHYPERTENSIVE AGENTS                                 Nifedipine                                   ...
A decrease in blood pressure below the          normal value is termed as Hypotension                      Acute          ...
CLINICAL FEATURES   Dizziness   Bradycardia     Postural                             hypotension                Fainting
MANAGEMENT  Thorough Case     High salt diet    High fluid intake     history                  Vaso-vagal shock-          ...
CONCLUSIONHypertension is highly prevalent!!Role of periodontist can be vital.Hence, as periodontal surgeons we should1. R...
1.    Davidson’s Principles and Practice of Medicine, 18th Ed.2.    Concise Medical Physiology- Choudhuri, 2nd Ed.3.    Te...
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
Blood  pressure (periodontal perspective)
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Blood pressure (periodontal perspective)

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  • The main function of the circulatory system is to cater the various needs of tissues by capillary exchange between blood, plasma, interstitial fluid & tissues. The blood which is being continuously pumped by heart reaches various tissues of the bodyA pressure gradient is maintained across various parts of the circulatory system which defines the amount and speed of blood flow to particular region. This phenomenon is understood by understanding the Blood Pressure.The Blood pressure or BP is vital for the perfusion of various important organs like brain & filtration of blood in kidneys etc.LETS throw some light on the evolution of this phenomena
  • Although there can be little doubt that simple palpation of the pulse was carried out by the early Egyptians , actual measurements of the pressure in parts of the circulation really started in the middle of the eighteenth century with the experiments of Stephen Hales . It is most surprising that the common occurrence of blood spurting from torn vessels did not arouse the curiosity of physiologists long before the eighteenth century. However, it took the enquiring mind of Hales to investigate this phenomenon and to him can be attributed the discovery of blood pressure.Riva-Rocci advocated the present day technique…His technique involved compression of the arm around its whole circumference and not just one of its aspects. A rubber bag, surrounded by a cuff ofsome in expansible material, was wrapped round the whole girth of the arm and was inflated with air by means of an attached rubber bulb. The pressurein the cuff was registered by the usual mercury manometer, and was increased until the radial pulse could no longer be palpated. When the pressure was slowly released the mercury level in the manometer fell, and the reading at which the pulse reappeared was taken as the systolic blood pressure, Now, in the 1970s, blood pressure can be monitored continually by sensors worn on the patient's thumb; inflatable cuffs are coupled to a servomechanism which maintains suitable cuff pressure.Strain gauges, photocells and semiconductors are coming into use in the recording of blood pressure.
  • It is the maximum pressure exerted during systole. It undergoes considerable variations . Height of sbp indicates-extent of work done by the heart.Dbp- it is the minimum pressure exerted during diastoleand does not show considerable variations, it is the measure of total peripheral resistance. The dbp signifies extent of work done by heart against a constant load.mbp is the measure of the pressure throughout the cardiac cycle.Q.A high pulse pressure combined with bradycardia and an irregular breathing pattern is associated with increased intracranial pressure and should be reported to a physician immediately. This is known as Cushing's triad and can be seen in patients after head trauma related to intracranial hemorrhage or edema.
  • Venous Pressure: Blood from all over the body is collected in right atria. The pressure in the right atria is hence called venous pressure or much correctly central venous pressure.Peripheral Venous Pressure: Peripheral venous pressure correlates with central venous pressure of human being in recumbent positionCapillary Pressure: It is defined as the pressure in the capillaries which tends to force the fluid outward through the capillary membrane.
  • Traditionally blood pressure has been measured by using a mercury manometer in mm of Hg.
  • In this method the arterial pressure is directly measured from the systemic arteries by invasive procedures. A metallic cannula is inserted in to a suitable big artery (usually carotid). This cannula is connected to a mercury manometer through a U shaped pressure tube. The manometer is connected to a sensitive float which raises or falls according to variation in BP.however, it requires invasive surgical entry in to carotid artery and may have potential complications. Its use is limited for experimental animal studies
  • Indirect method of measuring BP is by three methods:Auscultatory MethodPalpatory Method Oscillatory Method Riva–Rocci in 1896 first described the method for measuring BP non invasively. The instrument was called as Sphygmomanometer. Later modified and subsequently improved by Von Recklinghausen
  • This is the most commonly used indirect method clinically. A sphygmomanometer and a stethoscope are used for this purpose. The patient is made to lie down on his back comfortably. The inflatable cuff of the sphygmomanometer is wrapped around the arm (preferably the left arm, as the left subclavian artery is direct branch of aorta) taking care that heart, sphygmomanometer and cuff placed on the arm are at same horizontal plane. The bell of the stethoscope is placed over the brachial artery and the pressure in the cuff is first elevated well above arterial systolic pressure. As long as this pressure is higher than systolic pressure, the brachial artery remains collapsed and no blood jets into the lower artery during any part of the pressureThen the cuff pressure is gradually reduced. Just as soon as the pressure in the cuff falls below systolic pressure, blood slips through the artery beneath the cuff during the peak of systolic pressure, and one begins to hear tapping sounds in the brachial artery in synchrony with the heartbeat. This marks the SBPThe cuff is deflated slowly till the disappearance of all sounds. Between the first appearance of the tap sounds to their disappearance, a series of sounds called Korotkoff sounds are heard. The point of disapperance of sounds marks the DBP
  • Now I shall discuss about the korotkoffs sounds…Q-Auscultatory gapThe other indirect method commonly used is…
  • In this method the pulse is simultaneously palpated on the radial artery while inflating the cuff. At certain point the pulse is lost. Inflation is continued for still sometime and now deflation is started slowly. When the pulse is again felt it is marked as SBP. But the SBP recorded by this method is a trifle lower than that obtained by Auscultatory method and only the SBP value can be determined by this method.Similar to Auscultatory method, the pressure cuff is wrapped over the brachial artery and the oscillations that are produced by pulsations are observed taking all necessary precautions. When the cuff pressure is increased and raised above the systolic pressure, the oscillations disappear, but on releasing the pressure gradually, oscillations become larger and prominent. The pressure head, at which the larger oscillations are seen, is considered as systolic pressure. The pressure at which oscillation just become small or disappears, is recorded as diastolic pressure.
  • There are many feature which affects these normal values… the conditions affecting are
  • Various condition affecting blood pressure can be PHYSIOLOGICALPATHOLOGOCALDRUG INDUCEDAmong them, physiological are,AGE: The BP is affected by age. In the young people BP is usual low and reaches the adult value of 120/80. Thereafter, both the SBP and DBP rise gradually till 40 years. From 40 years onwards the rise is steep, particularly with SBP. At 70 years of age, the BP is normally about 160/90 mm of Hg and 80 it is about 180/95 mm of Hg.Sex: Before the onset of menopause women have little lower BP than their male counterparts of same age group.After menopause, women have little higher BP than males of similar age groups.Emotion:Rage and panic raise the BP. However, in exceptional panic, there may be fainting attacks.Meals:After meals the BP is little higher.
  • Exercise: Uses a rise of SBP and fall of DBP. The mean BP remains practically unaltered or even it may show a fall. Sleep:Causes a fall of BP. However, sleep associated with nightmare dreams may cause rise of BP. Exposure to cold: increases blood pressure.Diurnal variation: of 5-10 mm of Hgis common in SBP, lets c wt are the pathological conditions…
  • Chronic or prolonged elevation of BP above normal values is called chronic hypertension. In great majority of cases the etiology cannot be found and is called essential hypertension. In a small percentage of cases, the rise of BP is due to such causes like: (i) Renal artery stenosis, (ii) Pheochromocytoma and (iii) pre-eclamptic toxemia etc. Such cases are called Secondary Hypertension2. Blood pressure falls, sometimes alarmingly, in cardio­vascular shock and spinal shock.
  • Many drugs produce alteration of Blood pressure,
  • Among these the major are the cardiac output and peripheral resistance…
  • However this law doesn’t apply to Windkessel vessels in which the BP doesn’t change.
  • It is the resistance which blood has to overcome while passing through periphery,the chief seat of peripheral resistance is the arterioles and to small extent the capillaries
  • Blood pressure is regulated according to the needs of the body by various mechanisms. These are mainly classified intoShort term regulationLong term regulation
  • The carotid sinus baroreceptors are not stimulated by pressures between 0 and 60 mm Hg, But above 60 mm Hg, they respond progressively more rapidly and reach a maximum at about 180 mm Hg. The responses of the aortic baro receptors are similar to those of the carotid receptors except that they operate, in general, at pressure levels about 30 mm Hg higher
  • It is the control of arterial pressure by the brain's vasomotor center in response to diminished brain blood flow .Despite the powerful nature of the CNS ischemic response, it does not become significant, reaching its greatest degree of stimulation at a pressure of 15 to 20 mm of Hg. It is sometimes called the "last ditch stand” pressure control mechanism.
  • 1. Non-modifiable risk factors:(a) AGE: Blood pressure rises with age in both sexes and the rise is greater in those with higher initial blood pressure.. (b) SEX: Early in life there is little evidence of a difference in blood pressure between the sexes. However, at adolescence, men display a higher average level.(c) GENETIC FACTORS: There is considerable evidence that blood pressure levels are determined in part by genetic factors, and that the inheritance is polygenic. The evidence is based on twin and family studies. Twin studies have confirmed the importance of genetic factors in hypertension. The blood pressure values of monozygotic twins are usually more strongly correlated than those of zygotic twins. (d) ETHNICITY: Population studies have consistent! revealed higher blood pressure levels in Asian and African communities than other ethnic groups  2. Modifiable risk factors:(a) OBESITY: Epidemiological observations have identified obesity as a risk factor for hypertension. The greater the weight gain, the greater the risk of high blood pressure. Data also indicate that when people with high blood pressure lose weight, their blood pressure generally decreases. (b) SALT INTAKE: There is an increasing body of evidence to the effect that a high salt intake (i.e., 7-8 g per day)increases blood pressure proportionately. Low sodium intake has been found to lower the blood pressure .Potassium supplements have been found to lower blood pressure of mild to moderate hypertensives. Other cations such as calcium, cadmium and magnesium have also been suggested as of importance in reducing blood pressure levels. (c) SATURATED FAT : Recent evidence suggests that saturated fat raises blood pressure as well as serum cholesterol.  (d) DIETARY FIBRE: Several studies indicate that the risk of CHD and hypertension is inversely related to the consumption of dietary fibre. Most fibres reduce plasma total and LDL cholesterol. (e) ALCOHOL: High alcohol intake is associated with an increased risk of high blood pressure.It appears that alcohol consumption raises systolic pressure more than the diastolic. But the finding that blood pressure returns to normal with abstinence suggests that alcohol-induced elevations may not be fixed, and do not necessarily lead to sustained blood pressure elevation. (f) HEART RATE: When groups of normotensive and untreated hypertensive subjects, matched for age and sex, are compared, the heart rate of the hypertensive group is invariably higher. This may reflect a resetting of sympathetic activity at a higher level. The role of heart variability in blood pressure needs further research to elucidate whether the relation is causal or prognostic. (g) PHYSICAL ACTIVITY: Physical activity by reducing body weight may have an indirect effect on blood pressure. (h) ENVIRONMENTAL STRESS: The term hypertensionItself implies a disorder initiated by tension or stress. Since stress is nowhere defined, the hypothesis is untestable.However, it is an accepted fact that psychosocial factors operate through mental processes, consciously or unconsciously, to produce hypertension. Virtually all studies on blood pressure and catecholamine levels in young people revealed significantly higher noradrenalin levels in hypertensives than in normotensives. This supports the contention that over activity of the sympathetic nervous system has an important part to play in the pathogenesis of hypertension. (i) SOCIO-ECONOMIC STATUS: In countries that are in post-transitional stage of economic and epidemiological change, consistently higher levels of blood pressure have been noted in lower socio-economic groups.  (j) OTHER FACTORS: The commonest present cause of secondary hypertension is oral contraception, because of the estrogen component in combined preparations. Other factors such as noise, vibration, temperature and humidity require further investigation.
  • A formal estimate of absolute cardiovascular risk may help to determine whether the likely benefits of therapy will outweigh its costs and hazards. This should take account of all the relevant risk factors and not just the blood pressure.In the hypertension optimal treatment (HOT) trial the optimum blood pressure for reduction of major cardio­vascular events was found to be 139/83 mmHg, and even lower in patients with diabetes; moreover, reducing blood pressure below this level caused no harm. Unfortunately, it seems clear that, despite best practice, the targets sug­gested by the British Hypertension Society will not be achievable in many patients. Patients taking antihypertensive therapy require follow-up, typically at 3-month intervals, to monitor blood pres­sure, minimize side-effects and reinforce lifestyle advice.
  • Appropriate lifestyle measures may obviate the need for drug therapy in patients with borderline hypertension, reduce the dose and/or the number of drugs required in patients with established hypertension, and directly reduce cardiovascular risk. Correcting obesity, reducing alcohol intake, restricting salt intake, takingregular physical exercise and increasing consumption of fruit and, vegetables can all lower blood pressure. Moreover, quitting smoking, eating oily fish and adopting a -diet that is low in saturated fat may produce further reductions in cardiovascular risk.
  • Thiazide and other diuretics:The mechanism of action of these drugs is incompletely understood, and it may take up to a month for the maximum effect to be observed. A daily dose of 2.5 mg bendroflumethiazide (bendrofluazide) or 0.5 mg cyclopenthiazide is appro­priate. More potent loop diuretics, such as furosemide (frusemide) 40 mg daily or bumetanide 1 mg daily, have few advantages over thiazides in the treatment of hypertension unless there is substantial renal impairment or they are used in conjunction with an ACE inhibitor.Beta-adrenoceptor antagonists (β-blockers):. Metoprolol (100-200 mg daily), atenolol (50-100 mg daily) and bisoprolol (5-10mg daily) are cardioselective and there­fore preferentially block the cardiac βadrenoceptors, as opposed to the α-adrenoceptors which mediate vasodi-latation and bronchodilatation. Labetalol:Labetalol (2.4 g daily in divided doses) is a combined β'and α adrenoceptor antagonist which is sometimes more effective than pure βblockers and can be used as an infusion in malignant phase hypertension.Angiotensin-converting enzyme (ACE) inhibitors:These drugs (e.g. captopril 5-75 mg twice daily, enalapril 20 mg daily, ramipril 5-10 mg daily or lisinopril 10-20 mg daily) inhibit the conversion of angiotensin I to angio-tensin II and are usually well tolerated. They should be used with particular care in patients with impaired renal function or renal artery stenosis because they can reduce the filtration pressure in the glomeruli and precipitate renal failure. Side-effects include first-dose hypotension, cough, rash, hyperkalaemia, renal dysfunction and dys-geusia (an unpleasant metallic taste). Note that electrolytes and creatinine should be checked before and 1-2 weeks after commencing therapy.
  • Angiotensin II receptor antagonists: These drugs e.g. losartan 50-100 mg daily, valsartan 40mg daily) block the angiotensin II receptor and have similar effects to ACE inhibitors; however, they do not influence bradykinin metabolism and do not therefore cause cough.Calcium antagonists:. The dihydropyridines (e.g. amlodipine 5-10 mg daily, nifedipine 30-90 mg daily) are effecTive and usually well-tolerated antihypertensive drugs that are particularly useful in the elderly. Side-effects include flushing, palpitations and fluid retention. The rate-limiting calcium antagonists (e.g. c-Ultiazem 200-300 mg daily, verapamil 240 mg daily) can be useful when hypertension coexists with angina but they may cause bradycardia. The main side-effect of verapamil is constipation. Gingival enlargement: Some of these drugs can induce gingival enlargement. Nifedipine one of the most commonly used to treat hypertension induces gingival enlargement in 20% of cases. Some antihypertensive drugs which can cause gingival enlargement are:DiltiazemFelodipineNitrendipineVerapamilNicardipine Dose dependency of these drugs for inducing the gingival enlargement is not proven in humans.Other drugs:A variety of vasodilators are used to treat hypertension. These include the (α-adrenoceptor antag­onists (α-blockers), such as prazosin (0.5-20 mg daily in divided doses), indoramin (25-100 mg twice daily) and doxazosin (1-4 mg daily), and drugs that act directly on vascular smooth muscle, such as hvdraiazine (5-100 mg 12-hourly). Side-effects include first-dose and postural hypotension, headache, tachycardia and fluid retention. Minoxidil also causes increased facial hair and is therefore unsuitable for female patients.Centrally acting drugs, such as methyldopa (initial dose 250jTig 8-hourly) and clonidine (6.05-0.1 mg 8-hourly), are effective antihypertensive drugs but cause fatigue and are usually poorly tolerated. Choice of antihypertensive drug:Trials that have compared the major classes of antihyper­tensive drug (thiazides, β-blockers, calcium antagonists, ACE inhibitors andα-blockers) have shown no consistent or important differences in outcome, efficacy, side-effects or quality of life. The choice of antihypertensive therapy is therefore usually dictated by cost, convenience, the response to treatment and freedom from side-effects. Nevertheless, comorbid conditions may have an impor­tant influence on initial drug selection.
  • The dental office can play a vital role in the detection of hypertension and maintenance care of the patient with hypertensive disease. Before the clinician refers a patient to a physician because of elevated blood pressure, readings should be taken at a minimum of two appointments, unless the measurements are extremely high (i.e., systolic pressure >180 mm Hg or diastolic pressure >100 mm Hg). The periodontal recall system is an ideal method for hypertension detection and monitoring. Periodontal procedures should not be performed until accurate blood pressure measurements and histories have been taken to identify those patients with significant hypertensive disease
  • No routine periodontal treatment should be given to a patient who is hypertensive and not under medical management. Analgesics are prescribed for pain and antibiotics for infection. Acute infections may require surgical incision and drainage, When treating hypertensive patients, the clinician should not use a local anesthetic containing an epinephrine concentration greater than 1:1,00,000, nor should a vasopressor be used to control local bleeding. In a patient with hypertensive disease, however, it is important to minimize pain by providing profound local anesthesia to avoid an increase in endogenous epinephrine secretion.(Mealy BL, 1996 &Muzykabc, Glick M, 1997) 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)Lower blood pressures occur in the afternoon. Therefore afternoon dental appointments may be preferred.However, recent evidence indicates that BP generally increases around awakening and peaks atmidmorning.[15,74,102] Lower BP levels occur in the afternoon; therefore afternoon dental appointments may be preferred.
  • BP increases around awakening and peaks around mid morning (Smolensky; 1996, Raab FJ et al; 1998)Lower blood pressures occur in the afternoon. Therefore afternoon dental appointments may be preferred.However, recent evidence indicates that BP generally increases around awakening and peaks atmidmorning.[15,74,102] Lower BP levels occur in the afternoon; therefore afternoon dental appointments may be preferred.
  • Calcium channel blockers are drugs developed for the treatment of cardiovascular conditions such as hypertension, angina pectoris, coronary arteryspasms, and cardiac arrhythmias. They inhibit calcium ion influx across the cell membrane of heart and smooth muscle cells, blocking intracellularmobilization of calcium. This induces direct dilation of the coronary arteries and arterioles, improving oxygen supply to the heart muscle; it also reduceshypertension by dilating the peripheral vasculature.These drugs are the dihydropyridine derivatives (amlodipine [Lotrel, Norvasc], felodipine [Plendil], nicardipine [Cardene], nifedipine [Adalat, Procardia]),the benzothiazine derivatives (diltiazem [Cardizem, Dilacor XR, Tiazac]), and the phenylalkylamine derivatives (verapamil [Calan, Isoptin, Verelan,Covera HS]).[38]Some of these drugs can induce gingival enlargement. Nifedipine, one of the most often used,[39,63,65,77] induces gingival enlargement in 20% ofpatients.[8] Diltiazem, felodipine, nitrendipine, and verapamil also induce gingival enlargement.[14,46] The dihydropyridine derivative, isradipine, canreplace nifedipine in some cases and does not induce gingival overgrowth.[116]Nifedipine is also used with cyclosporine in kidney transplant recipients, and the combined use of both drugs induces larger overgrowths.[13] Nifedipinegingival enlargement has been induced experimentally in rats, where it appears to be dose dependent[32]; in humans, however, this dose dependency isnot clear. One report indicates that nifedipine increases the risk of periodontal destruction in patients with diabetes mellitus type 2.[64For patients taking nifedipine, which has a reported prevalence of gingival enlargement of up to 44%, other calcium channel blockers, such as diltiazemor verapamil, may be viable alternatives.[22] Their reported prevalence of inducing gingival enlargement is 20% and 4%, respectively.[4,9,15] Also,consideration may be given to the use of another class of antihypertensive medications rather than calcium channel blockers, none of which is known toinduce gingival enlargement.
  • Clinical features:Dizziness, sweating and loss of coherenceFaintingIt may be associated with bradycardia in case of syncopeHypotension may be seen due to sudden erect posture of some elderly patients. This is called Postural Hypotension.
  • Blood pressure (periodontal perspective)

    1. 1. GUIDED BY-PRESENTED BY-
    2. 2. • 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
    3. 3. Proc. roy. Soc. Med. Volume 70 November 1977Simple palpation of the pulse Early Egyptians Stephen Hales (1677-1761)Riva- Rocci (1896) Present-day TechniqueNow, in the 21st century BP is monitored continually bysensors worn on the patients thumb;Inflatable cuffs coupled to a servomechanism whichmaintains suitable cuff pressure.Strain gauges, photocells and semiconductors arecoming into use in the recording of blood pressure.
    4. 4. Blood pressure is defined as the force exerted by the blood on unit area of vessel wall.
    5. 5. FEW MORE TERMS RELATED TO BP Recumbent PERIPHERAL VENOUS VENOUS PRESSURE CAPILLARY PRESSURE PRESSURE
    6. 6. mmofHg
    7. 7. Indirect methodAuscultatory Palpatory Oscillatory
    8. 8.  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.
    9. 9. Chronic or Prolonged Elevation → Chronic Hypertension Secondary Essential Hypertension HypertensionCardio-vascular shock or Spinal shock → BP falls
    10. 10. 3. DRUG INDUCED
    11. 11. CARDIAC OUTPUT : • Amount of blood ejected per ventricle per beat depends on- a) Cardiac inflow b) Contractility of the heart c) Heart rate Heart rate (within physiological limits) α Cardiac Output (Minute Volume) BP = Cardiac output X Peripheral resistance. Not applicable to Windkessel vessels
    12. 12. PERIPHERAL RESISTANCE• Chiefly Arterioles & to a small extent Capillaries. depends on a) Viscosity b) Velocity c) Elasticity d) Lumen of vessel Hagen- Poiseulle  R = 8ηl/π r4 =ΔP/Q lawR = Peripheral resistance l = Length of the blood vesselr = Radius of blood vessel Q = Cardiac outputΔP = Difference in pressure in the vessel η= dynamic fluid viscosity
    13. 13. SHORT TERM REGULATION The Baro-receptor mechanism The Chemo-receptor mechanism The CNS Ischemic mechanism
    14. 14. BARORECEPTOR MECHANISM
    15. 15. CHEMORECEPTOR MECHANISM
    16. 16. THE CNS ISCHEMIC MECHANISM• ↓ CEREBRAL Blood Systemic Arterial • Above threshold Pressure RISE level such that flow causes HEART can pump blood &• Failure of the slowly • Stimulation of flowing blood to Vasomotor centre Carry CO2 away from the CEREBRAL blood VASOMOTOR flow RESTORED CENTER
    17. 17. LONG TERM REGULATION
    18. 18. DEFINITION Hypertension is a persistently raised BP resulting from increased peripheral arteriolar resistance (scully & cawson)
    19. 19. CLASSIFICATION -ACCORDING TO ETIOLOGY• >95% • 5 % of pts• Underlying cause not • Consequence of known disease/ abnormality • Sodium retention • With or without vasoconstrictionPrimary SecondaryHypertension Hypertension
    20. 20. CLASSIFICATION -BASED ON BP MEASUREMENTSIn 2003, the National Heart, Lung and Blood Institute issued revisedguidelines for evaluation and management of hypertension
    21. 21. The Higher value is considered for theclassification among Systolic & Diastolic.Isolated Systolic HypertensionDIAGNOSIS Average Diagnose by Do’s Don’ts value of 3 Single recordings Recording. 3 different appointments
    22. 22. OBJECTIVE OF INITIAL EVALUATION OFNEWLY DIAGNOSED… Obtain accurate and representative measurements Identify contributory factors/underlying cause Quantify cardiovascular risk Any complications (target organ damage) Choice of antihypertensive therapy.
    23. 23. CLINICAL FEATURES IF UNDIAGNOSED…
    24. 24. RISK FACTORS • •Non-modifiable Modifiable Age Obesity • Sex • Salt intake • Genetics • Saturated fats • Ethnicity • Dietary fibers • Alcohol • Physical activity • Environmental stress
    25. 25. MANAGEMENT - INVESTIGATIONS FOR ALL HYPERTENSIVESUrinalysis for Blood urea,blood, protein, electrolytes# & Blood glucose & glucose creatinine Serum total 12-lead ECG and HDL (LVH, CAD) Cholesterol # Hypokalaemic alkalosis may indicate Primary Aldosteronism but is usually due to diuretic therapy.
    26. 26. - INVESTIGATIONS FOR SELECTED • Cardiomegaly, Heart failure Chest X-ray • Coarctation of aorta Ambulatory BP • To assess ’white coat’ recording hypertension • Detect or quantify LVHEchocardiogramRenal ultrasound • Detect possible renal /Angiography disease
    27. 27. - NON DRUG THERAPY Appropriate life- ↓ style QuittingAlcohol (Correcting smoking intake Obesity) ↑ RegularRestricting Eating oily Consumption physicalSalt intake fish of fruit/ exercise vegetables
    28. 28. ANTIHYPERTENSIVE DRUGS
    29. 29. ANTIHYPERTENSIVE DRUGS • Amlodipine (5-10 mg) • Vasodilators • Losartan (50-100 mg) • Nifedipine (30-90 mg) • α- Blockers • Valsartan (40-160 mg) • Side effects- flushing, • Prazosin • Blocks Angiotensin II palpitations, Gingival • Hydralazine type I Enlargement • Used Hypertension co- • Minoxidil exists with angina Angiotensin Calcium receptor Other Drugs antagonists blockers
    30. 30. TREATMENT MODIFICATIONS • Safe if • Consult • Duty of Inform the PhysicianPeriodontal procedure Patient on medication stress Physician dentist minimized • Degree of stress • Length of procedure • Complexity of treatment
    31. 31. TREATMENT MODIFICATIONSRisk of providing emergency dental care must out weigh risk of possiblehypertensive complication.#
    32. 32. TREATMENT CONSIDERATIONS • Analgesics for • Treatment of HT pain pt not on • Antibiotics for medication infection • LA with adrenalin • Surgical I & D >1:1,00,000 IU Do’s Dont’sImportant to minimize pain → providing profound local anesthesia → avoidingan increase in endogenous epinephrine secretion. (Mealy BL, 1996 & Muzykabc, Glick M, 1997)
    33. 33. SOME PHARMACOLOGICAL ASPECTSEpinephrine- α & βadrenergic agonist• ↑Heart rate by • Propanolol/ direct stimulation Nadolol• α -Vaso + constriction LA with• Β-Vaso dilatation ADRENALIN = ↑ BP
    34. 34. WHY NOT ADRENALIN / EPINEPHRINEWITH LA IN HYPERTENSIVES ???...However, The benefits of the small doses of Epinephrine used in dentistry faroutweigh the potential for hemodynamic compromise!!!
    35. 35. BP increases around awakening and peaks around mid morning (Smolensky; 1996, Raab FJ et al; 1998)HENCE, AFTERNOON DENTAL APPOINTMENTS MAY BEPREFERRED Postural hypotension is very common!! MINIMIZED BY SLOW POSITIONAL CHANGES
    36. 36. Strong positive association between increased subgingival colonization by A.a, P.g, T. forsythia and T. denticola and prevalent Hypertension is seen DESVARIEUX ET AL (2012) ARTERIAL HYPERTENSION DOES NOT NORMALLY PRECLUDE PERIODONTAL SURGERY. .(LINDHE) Nausea, sedation, oral dryness, lichenoid reaction & GINGIVAL OVERGROWTHASSOCIATED WITH CERTAIN ANTIHYPERTENSIVE AGENTS
    37. 37. GINGIVAL OVERGROWTH &ANTIHYPERTENSIVE AGENTS Nifedipine =44% Calcium Diltiazem = channel 20% blockersHypertensive Verapamil = Safe among pt 4% other CCB Other Anti- No Gingival Safe Hypertensives Overgrowth•The dihydropyridine derivative, ISRADIPINE, can replaceNifedipine in some cases and does not induce gingivalovergrowth.
    38. 38. A decrease in blood pressure below the normal value is termed as Hypotension Acute ChronicSystemic Causes WeaknessSerious Infections LethargyAcute Hemorrhage Easy fatigabilityVomiting Dizziness and faintingDiarrhea (erect posture) Interference with neuralSevere Burns pathwayAnaphylactic shockMITachycardia
    39. 39. CLINICAL FEATURES Dizziness Bradycardia Postural hypotension Fainting
    40. 40. MANAGEMENT Thorough Case High salt diet High fluid intake history Vaso-vagal shock- ATROPINE 0.6mg iv
    41. 41. CONCLUSIONHypertension is highly prevalent!!Role of periodontist can be vital.Hence, as periodontal surgeons we should1. Record proper History2. Consult the physician – Discuss3. Minimize stress4. Periodic recall and follow-up even can help in hypertension monitoring.
    42. 42. 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; 407-41211. Perio 2000: vol 23; 136 -141

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