Cardiovascular system & dental considerations

Contents
Introduction Anatomy & physiology Ischaemic heart disease Anticoagulation therapy and dental care Acute coronary syndromes Congenital heart diseases

Examination of CVS
Questionnare ECG & JVP Infective endocarditis Rheumatic fever Hypertension

Valvular heart diseases

Cardiac Arrhythmias Heart failure Conclusion

Introduction
Cardiovascular diseases (CVD) are very common in India , though more frequent and severe in the later stages of life, can also affect young

individuals.
They have high mortality rate and the associated morbidity affects all walks of life impacting the quality of life . A thorough knowledge of CVD is necessary because of its implications in dentistry and also the initial measures to be taken by the dentists in case of

certain emergency conditions can be life saving.

Anatomy & physiology

Clinical examination of CVS

Questionnare
Have you experienced chest pain or shortness of breath The quality of chest discomfort should be determined by asking the patient to describe the nature of the episode and the usual radiation pattern associated with it .

An unpleasant sensation , squeezing , pressing ,strangling , constricting ,

bursting and burning . Clenching of the fist in front of the chest while describing the sensation is a very strong indication of an ischemic origin of the pain (Levine sign )

Where does the pain ,hurt or radiate Anginal pain is usually substernal , across both sides of the chest . Pain may radiate to various regions. Common sites of radiation of ischemic chest pain include the neck and jaw , the upper epigastric region (stomach ) , intracapsular

( between shoulder blades ), to the left arm .

If the pain or discomfort is localized , the origin is not usually ischemic

Have you experienced swollen ankles or shortness of breath Bilateral swelling of the legs ,is a common feature of chronic CVDs Shortness of breath is a major symptom of CVDs . Dyspnea may vary in severity from an uncomfortable awareness of breathing to a frightening sensation of

fighting for breath

Questions regarding exertional dysapnea, orthopnea , paroxysmal nocturnal dyspnea should be asked .

How long do your anginal episode lasts If the episode or discomfort ,normally ceases within 2-10 mins by taking rest Chest pain lasting with a brief duration commonly points to a noncardiac origin such as musculoskeletal pain , hiatal hernia

Chest pain of hours suggest MI , dissecting aortic aneurysm .

Questions regarding last anginal episodes , precipitating factors and frequency

should be put forth.

Further questions regarding hospitalisation , surgeries and drug history ,over the counter medications.

ECG
3 distinct waves are produced during cardiac cycle P wave caused by atrial depolarization QRS complex caused by ventricular depolarization T wave results from ventricular repolarization

ECG interpretation
P waves are absent in atrial fibrillation and before ventricular premature beats. Normally, all P waves are followed by QRS complexes but in third degree A-V block, P waves do not bear any relation to QRS complexes. Morphology and duration of P waves are important to determine left and

right atrial hypertrophy.

A tall P wave >2.5 mm in amplitude (P pulmonale) seen in right atrial enlargement. A wide P wave >0.1 seconds (P mitrale) seen in left atrial enlargement

The P-R interval (normally 0.12-0.20 seconds) reflects intra-atrial, AV nodal and His-Purkinje conduction. It is the interval between the beginning of P wave and the beginning of QRS complex. The QRS complex, has a normal duration of 0,04-0.10 seconds. Abnormal Q

waves are present in myocardial infarction.

Wide and bizarre QRS complexes are seen in ventricular ectopics, ventricular tachycardia and supraventricular tachycardia with aberrant conduction. Increase in the height of QRS complexes indicates right or left ventricular hypertrophy

ST segment elevation or depression is seen in ischaemic heart disease, cardiomyopathies, myocarditis and conduction blocks. Some drugs like digitalis can also produce ST segment depression. T waves represent ventricular repolarisation.

Inverted T waves are frequently seen in cases with ischaemic heart disease,
bundle branch blocks, atrial fibrillation with rapid ventricular rate and in PS VT due to relative coronary insufficiency. QT interval is abnormal in hypokalemia and hypocalcaemia

Electrocardiography is useful in the following situations: Effects of drugs (digitalis). Hypothermia, pericarditis. Myocardial ischaemia and infarction. Cardiac arrhythmias. Conduction defects. Chamber hypertrophy.

Electrolyte abnormalities (hypokalemia, hyperkalemia, hypocalcaemia,

hypercalcaemia).

Jugular venous pulse

Jugular venous pulse is the oscillating top of a height of venous blood in the internal jugular vein which faithfully reflects the pressure and haemodynamic changes in the right side of heart in all phases of the cardiac cycle. Jugular venous pressure is expressed as the vertical distance in centimetres

between the top of the venous column and the sternal angle, regardless of the
body position. Normally, it is less than 3 cm. By convention, jugular venous pressure is measured from the sternal angle with the patient reclining at 45.

Central venous pressure can be accurately estimated from the jugular venous pressure. For this, the sternal angle is taken as the reference point The centre of the right atrium lies 5 cm below the sternal angle, regardless of body position. The central venous pressure is calculated as 5+jugular venous

pressure in centimetres (e.g. if jugular venous pressure is 6 cm. the central

venous pressure = 5 + 6= 11 cm of blood). Jugular venous pressure reflects the central venous pressure and also the mean right atrial pressure.

The various waves on JVP reflect the phasic pressure changes in the right atrium. Normal JVP has three positive waves, namely, a, c and v waves, and two negative descents namely x descent and y descent a wave is due to right atrial contraction The c wave is due to bulging of the tricuspid valve into the right atrium and impact of the adjacent carotid artery during ventricular systole. v wave is due to passive right atrial filling during ventricular systole. The x descent ('systolic collapse9) is due to atrial relaxation and downward displacement of tricuspid valve during systole. a The y descent ('diastolic collapse') is due to opening of the tricuspid valve and the rapid flow of blood into

Causes for raised JVP

Abnormalities in wave form

Infective endocarditis & subacute bacterial endocarditis

Infective endocarditis (IE) is a microbial infection of the endothelial surface of the heart or heart valves that most often occurs in proximity to congenital or acquired cardiac defects.

A clinically and pathologically similar infection that may occur in the

endothelial lining of an artery, usually adjacent to a vascular defect (e.g., coarctation of the aorta) or a prosthetic device (e.g., arteriovenous [AV] shunt), is called infective endarteritis.

Previously, IE was classified as acute and subacute, to reflect the rapidity of onset and duration of symptoms prior to diagnosis. It has now largely been replaced by a classification that is based on the causative microorganism (e.g., streptococcal endocarditis, staphylococcal

endocarditis, candidal endocarditis) and the type of valve that is infected (e.g.,
native valve endocarditis [NVE], prosthetic valve endocarditis [PVE]). IE is also classified according to the source of infection, that is, whether community acquired or hospital acquired, or whether the patient is an intravenous drug user.

Etiology
A total of 80% to 90% of cases of identified IE are due to Viridans streptococci (alpha-hemolytic streptococci)and staphylococci. This variation depends on the type of valve infected (i.e., native or prosthetic), whether the infection is community acquired or hospital acquired (nosocomial).

The species that most commonly cause endocarditis are Streptococcus sanguis,
Streptococcus oralis (mitis), Streptococcus salivarius, Streptococcus mutans, and Gemella morbillorum formerly called Streptococcus morbillorum). Group D streptococci, which include Streptococcus bovis and the enterococci (Enterococcus faecalis)

Other microbial agents that less commonly cause IE include the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella),

Pseudomonas aeruginosa, Corynebacterium, pseudodiphtheriticum, Listeria

monocytogenes, Bacteroides fragilis, and fungi.

PATHOPHYSIOLOGY AND COMPLICATIONS

The sequence of events leading to infection usually begins with injury or damage to an endothelial surface, most often of a cardiac valve leaflet. Although IE can occur on normal endothelium, most cases begin writh a damaged surface, usually in proximity to an anatomic defect or prosthesis. Endothelial damage can result

from any one of a variety of events, including the following:

A high-velocity jet striking endothelium

similar frequently indistinguishable A Flow fromand a highto a low-pressure chamber condition is found in some patients with systemic lupus erythematosis and is called Libman-Sacks Flow acrossendocarditis a narrowed orifice at high velocity Fibrin and platelets then verrucous
adhere to the roughened endothelial surface and form small clusters or masses

called nonbacterial thrombotic endocarditis (NBTE)

With the occurrence of a transient bacteremia, however, bacteria can be seeded

into and adhere to the mass. Additional platelets and fibrin are then deposited onto the surface of the mass, which serves to sequester and protect the bacteria that undergo rapid multiplication within the protection of the vegetative mass. Once established, the metabolic activity and cellular division of the bacteria are

reduced, which decreases the effectiveness of antibiotics.

Bacteria are slowly and continually released from the vegetations and shed into the bloodstream, resulting in a continuous bacteremia; fragments of the friable vegetations break off and embolize. A variety of host immune responses to bacteria may occur. This sequence of events results in the clinical manifestations of IE.

The clinical outcome of IE depends upon several factors, including the following: Local destructive effects of intracardiac (valvular) lesions Embolization of vegetative fragments to distant sites, resulting in infarction or

infection
Hematogenous seeding of remote sites during continuous bacteremia Antibody response to the infecting organism with subsequent tissue injury caused by deposition of preformed immune complexes or

antibody/complement interaction with antigens deposited in tissues

Complications
Heart failure that results from severe valvular dysfunction. This most commonly occurs as a problem with aortic valve involvement followed by mitral and then tricuspid valve infection. Embolization of vegetation fragments leads to complications in up to 35% of

cases of IE, with stroke being the most common.

SIGNS AND SYMPTOMS

The classic findings of IE include fever, heart murmur, and positive blood culture, although the clinical presentation may be varied. In many cases of IE that have been reported due to dentally induced bacteremia, the interval between the dental appointment and the diagnosis of IE has been

much longer than 2 weeks (sometimes months) unlikely that the initiating
bacteremia was associated with dental treatment. Peripheral manifestations of IE due to emboli and/or immunologic responses are less frequently seen since the advent of antibiotics. These include petechiae of the palpebral conjunctiva, the buccal and palatal mucosa, and extremities.

Osler's nodes (small, tender, subcutaneous nodules that develop in the pulp of the digits), Janeway lesions (small, erythematous or hemorrhagic, macular contender lesions on the palms and soles), splinter hemorrhages in the nail beds, and Roth spots, retinal hemorrhages with pale centers)

Other signs include splenomegaly and clubbing of the digits.

DUKES CRITERIA
The Duke criteria were developed and later modified to facilitate the definitive diagnosis of IE. This set of diagnostic criteria assesses the presence or absence of major and minor criteria. MAJOR CRITERIA

Positive blood cultures

Evidence of endocardial involvement (e.g., positive echocardiography, presence of new valvular regurgitation)

MINOR CRITERIA Predisposing heart condition or IV drug use Fever Vascular phenomena Immunologic phenomena Microbiologic evidence other than positive blood culture Definitive diagnosis of IE requires the presence of two major criteria, one major and three minor criteria, or five minor criteria.

LABORATORY FINDINGS
Complete blood count with differential, electrolytes, renal function tests, urinalysis, chest x-ray, and electrocardiogram (ECG). Patients with IE frequently have a normocytic, normochromic anemia that tends to worsen as the disease progresses. The white blood cell count may or may not be elevated.

Urinalysis often reveals microscopic hematuria and proteinuria. Chest x-ray

may be abnormal with evidence of heart failure.

ECG may show evidence of conduction block with myocardial involvement or infarction. Other abnormal findings may include an elevated erythrocyte sedimentation rate, increased immune globulins, circulating immune complexes, and positive rheumatoid factor.

Echocardiography is used to confirm the presence of vegetation in patients

suspected of having IE; it has become a cornerstone in the diagnostic process.

Dental considerations
Antibiotic Prophylaxis Dental treatment has long been implicated as a significant cause of IE. It was most often due to a bacteremia that resulted from an invasive dental procedure, and that through the administration of antibiotics prior to those procedures, IE

could be prevented.

CURRENT AMERICAN HEART ASSOCIATION RECOMMENDATIONS (2007) AHA cites the following reasons for revision of the previous recommendations: IE is much more likely to result from frequent exposure to random bacteremia associated with daily activities than from bacteremia caused by a dental procedure

Prophylaxis may prevent an exceedingly small number, if any, of cases of IE

in individuals who undergo a dental procedure

 The risk of antibiotic-associated adverse events exceeds the benefit, if any,

from prophylactic antibiotic therapy Maintenance of optimal oral health and hygiene may reduce the incidence of

bacteremia from daily activities and is more important than prophylactic

antibiotics for reducing the risk of IE resulting from a dental procedure

Special Situations
Patients Already Taking Antibiotics Patients who are already taking penicillin or amoxicillin for eradication of an

infection (e.g., sinus infection) or for long-term secondary prevention of

rheumatic fever are likely to have viridans group streptococci that are relatively resistant to penicillin or amoxicillin.

Clindamycin, azithromycin, or clarithromycin should be selected for prophylaxis

if treatment is immediately necessary. Because of cross resistance with cephalosporins, this class of antibiotics should be avoided. An alternative approach is to wait for at least 10 days after completion of antibiotic therapy before administering prophylactic antibiotics. In this case, the usual regimen can

be used.

Patients Who Undergo Cardiac Surgery. It is recommended that a preoperative dental evaluation be performed and necessary dental treatment provided whenever possible prior to cardiac valve surgery or replacement or repair of congenital heart disease.

Prolonged Dental Appointment. The length of a dental appointment in relation to the effective plasma concentration of an administered antibiotic is not addressed in these recommendations.

With amoxicillin, which has a half-life of approximately 80 minutes, the average peak plasma concentration of 4 (mg/mL is reached about 2 hours after oral administration of a 250-mg dose. Most of the penicillin-sensitive viridans group streptococci have an MIC requirement of 0.2 mg/mL. Thus, a 2-g dose of

amoxicillin would produce an acceptable MIC for at least 6 hours. If a

procedure lasts longer than 6 hours, it may be prudent to administer an additional 2-g dose.

Other Considerations No evidence suggests that coronary artery bypass graft surgery is associated with long-term risk for infection; thus, antibiotic prophylaxis is not recommended for these individuals. Patients who have had a heart transplant

are at increased risk for acquired valvular dysfunction, especially during

episodes of rejection. Endocarditis that occurs in this instance is associated with a high risk of adverse outcome; therefore, patients with mechanical or tissue prosthetic valves will often be taking long-term anticoagulant medication (e.g., warfarin) to prevent valve-associated thrombosis. These patients are at risk for excessive bleeding during and after surgical procedures.

Rheumatic fever
Rheumatic fever is an inflammatory disease occurring as a delayed sequale to pharyngeal infection with group A Streptococci. It primarily involves the heart, joints, central nervous system skin and subcutaneous tissues. Etiology

Rheumatic fever follows an antecedent pharyngeal infection with group A

beta hemolytic steptococci Latent period between the pharyngeal infection and the onset of fever 1-5 weeks, with average duration being 19 days. Fewer than 2-3% of previously healthy persons develop rheumatic fever.

Streptococcus-induced autoimmunity is believed to be the mechanism resulting in rheumatic process.

Several Streptococcal antigens have demonstrated cross reactivity with cardiac

and other tissues.

Acute rheumatic fever is characterised by exudative and proliferative inflammatory lesions of the connective tissues. It mainly involves the heart, joints and subcutaneous tissues.

Major manifestations Carditis Polyarthritis Chorea Erythema marginatum Subcutaneous nodules

Minor manifestations Fever Arthralgia Previous rheumatic fever or rheumatic heart disease Raised ESR Positive CRP Prolonged PR interval

Two major manifestations or one major and two minor manifestations indicate a high probability, with one supporting evidence of preceding streptococcal infection

MANAGEMENT

Bedrest Antistreptococcal therapy A course of antibiotic should be given to eradicate the streptococci, even if the throat culture is negative. One of the following regimens may be used:

a. Single injection of benzathine penicillin 1.2 million units intramuscularly.

b. Daily injection of procaine penicillin 6,00,000 units intramuscularly for 10

days.
c. Oral erythromycin 20-40 mg/kg/day in three divided doses, in patients who are sensitive to penicillin.

Salicylates Aspirin is effective in providing symptomatic relief. Aspirin is started at doses of 60 mg/kg/day in 6 divided doses. Dose is increased gradually until the drug produces either a clinical improvement or systemic

toxicity (tinnitus, headache or hyperpnoea). This dose might go up to 120

mg/kg/day or a maximum of 8 g/day.

Corticosteroids Patients who have severe carditis manifested by congestive heart failure not responding to aspirin.

Patients with severe arthritis whose symptoms and signs are not adequately
suppressed by aspirin. Prednisolone is given orally at a dose of 60-120 mg/day in four divided doses until the ESR is normal. It is then gradually tailed off over a period of 2 weeks. 4 To prevent a 'post-steroid rebound' an 'overlap course of aspirin may be added

when the steroid is being tapered off.

Aspirin is then continued for an additional 2-3 weeks

Prevention
Primary prevention can be summarised as accurate diagnosis and treatment of group A streptococcal pharyngeal infection. An outbreak of rheumatic fever in a closed population is best treated by mass penicillin prophylaxis.

Rheumatic fever prophylaxis should be given to all patients who have

experienced a documented attack of rheumatic fever.

Duration of prophylaxis is controversial. Broad outlines are: Those under the age of 18 years should receive continuous prophylaxis. Those who are over 18 years who develop rheumatic fever without carditis should receive prophylaxis for a minimum period of 5 years.

Decision to continue prophylaxis beyond 5 years in the second group depends on

many variables like age of tbe patient, relative risk of acquiring infection, socioeconomic state, presence of rheumatic heart disease, etc.

4 Regimens: One of the following regimens may be used: Intramuscular injection of 1.2 million units of benzathine penicillin G every 3 weeks (most efficient regimen). Oral penicillin V 250 mg twice a day. Sulphadiazine 1 g/day orally as a single dose (in those allergic to penicillins). Erythromycin 250 mg twice a day orally (in those allergic to penicillins and sulpha)

Regulation of BP

HYPERTENSION
Hypertension is an abnormal elevation in arterial pressure that can be fatal if sustained and untreated. People with hypertension may not display symptoms for many years but eventually can experience symptomatic damage to several target organs, :ncluding kidneys, heart, brain, and eyes. In adults, a sustained

systolic blood pressure of 140 mm Hg or greater and/or a sustained diastolic

blood pressure of 90 mm Hg or greater is defined as hypertension.

The dental patient with hypertension poses several potentially significant management considerations. These include identification of disease,

monitoring stress and anxiety reduction,

prevention of drug interactions, and

awareness and management of drug adverse effects.

Etiology
About 90% of patients have no identifiable cause for their disease, which is referred to as essential, primary, or idiopathic hypertension. For the remaining 10% of patients, an underlying cause or condition may be identified; for these patients, the term secondary hypertension is applied. The most common cause of secondary hypertension is renal parenchymal disease,

followed by renovascular disease and various adrenal disorders (a

pheochromocytoma of the adrenal medulla). Lifestyle can play an important role in the severity and progression of hypertension; obesity, excessive alcohol intake, excessive dietary sodium, and physical inactivity are significant contributing factors.

Pathophysiology and Complications

In sustained essential hypertension, the basic underlying defect is a failure in the regulation of vascular resistance. The pulsating force is modified by the degree of elasticity of the walls of larger arteries and the resistance of the arteriolar bed. Control of vascular resistance is

multifactorial, and abnormalities may exist in one or more areas. Mechanisms of

control include neural reflexes and ongoing maintenance of sympathetic vasomotor tone; neurotransmitters such as norepinephrine, extracellular fluid, and sodium stores; the renin-angiotensin-aldosterone pressor system; and locally active hormones and substances such as prostaglandins, kinins, adenosine, and hydrogen ions (H)

Physiologic factors may have an effect on blood pressure. Increased viscosity of the blood (e.g., polycythemia) may cause an elevation in blood pressure that results from an increase in resistance to flow. A decrease in blood volume or tissue fluid volume (e.g., anemia, hemorrhage) reduces blood pressure. Conversely,

an increase in blood volume or tissue fluid volume (e.g., sodium/fluid retention)

increases blood pressure. Increases in cardiac output associated with exercise, fever, and thyrotoxicosis also may increase blood pressure. The higher the blood pressure, the greater the chances of heart attack, heart failure, stroke, and kidney disease. For every 20 mm Hg systolic and 10 mm Hg diastolic increase in blood pressure, a doubling of mortality from ischemic heart disease and stroke occurs.

Signs & symptoms

Hypertension may remain an asymptomatic disease for many years, with the only sign being elevated blood pressure. Blood pressure is measured with the use of a sphygmomanometer. Pressure at the peak of ventricular contraction is systolic pressure.

Diastolic pressure represents the total resting resistance in the arterial system
after passage of the pulsating force ventricle. The difference between diastolic and systolic pressures is called pulse pressure. Labile hypertension is the term that was previously used to Mean arterial pressure is roughly definedwith as the sum of the diastolic pressure describe a subgroup of patients wide variability in blood pressures plus one-third the pulse pressure. produced by contraction of the left

About 15% to 20% of patients with untreated stage 1 hypertension have what is called white coat hypertension, which is defined as persistently elevated blood pressure only in the presence of a health care worker but not elsewhere. Before the age of 50, hypertension is typically characterized by an elevation in

both diastolic and systolic pressures. Isolated diastolic hypertension, defined as a

systolic pressure <140 and a diastolic pressure >90, is uncommon and is most often found in younger adults. Isolated systolic hypertension is defined as a systolic pressure >140 and a diastolic blood pressure <90; it is generally found in older patients and

constitutes an important risk factor for cardiovascular disease.

Assessment of blood pressure

Alcohol and smoking should be avoided for 30mins before measurement Allow the patient to rest Place the sphygmomanometer cuff on right upper arm with about 3 cm of skin visible at the ante-cubital fossa , should encircle atleast 2/3rd of the arm Palpate radial /brachial artery Inflate the cuff slowly to about 200-250 mm Hg or until the pulse is no longer palpable

Deflate cuff slowly while listening with the stethoscope over the brachial artery over the skin Record the systolic pressure as and when the first tapping sound appears ( korotkoff sounds )

Deflate cuff further until the tapping sounds become muffled i.e diastolic
pressure and then disappear.

The "ideal" cuff should have a bladder length that is 80% and a width that is at least 40% of arm circumference (a length-to-width ratio of 2:1). The recommended cuff sizes are: For arm circumference of 22 to 26 cm, the cuff should be "small adult" size:

12X22 cm
27 to 34 cm, "adult" size: 16X30 cm 35 to 44 cm, "large adult" size: 16X36 cm 45 to 52 cm, "adult thigh" size: 16X42 cm

Laboratory Findings
The INC 7 recommends that patients who have sustained hypertension should be screened through routine laboratory tests, including 12-lead electrocardiogram, urinalysis, blood glucose, hematocrit, and a serum potassium, creatinine, calcium, and lipid profile.

Additional tests should be ordered if clinical and laboratory findings suggest the
presence of an underlying cause for hypertension.

DENTAL CONSIDERATIONS
The first task of the dentist is to identify patients with hypertension, both diagnosed and undiagnosed. A medical history, including the diagnosis of hypertension, how it is being treated, identification of antihypertensive drugs, compliance of the patient, the presence of symptoms associated with

hypertension, and the level of stability of the disease, should be obtained.

Patients receiving treatment for complications of hypertensive disease, such as congestive heart failure, cerebrovascular disease, MI, renal disease, peripheral vascular disease, and diabetes mellitus should be identified .

Blood pressure measurements should be routinely performed for all new patients and at recall appointments. When a patient with upper level stage 2 blood pressure is treated, consideration should be given to leaving the blood pressure cuff on the patient's arm and periodically checking pressure during the

appointment.
The primary concern when one is providing dental treatment for a patient with hypertension is that during the course of treatment, the patient might experience an acute elevation in blood pressure that could lead to a serious outcome such as stroke or MI.

This acute elevation in blood pressure could result from the release of endogenous catecholamines in response to stress and anxiety, from injection of exogenous catecholamines in the form of vasoconstrictors in the local anesthetic, or from absorption of a vasoconstrictor from the gingival retraction cord.

Other concerns include potential drug interactions between the patient's

antihypertensive medications and the drugs prescribed and oral adverse effects that might be caused by antihypertensive medications.

Drug interactions Some NSAIDS ( indomethacin , ibuprofen , naproxen ) can reduce the efficacy of antihypertensive agents. Sodium based analgesics should be avoided

Systemic corticosteroids may raise the BP and antihypertensive treatment may

have to be adjusted .

Because some antihypertensive agents tend to produce orthostatic hypotension, sudden changes in chair position during dental treatment should be avoided. After patients have had time to adjust to the change in posture, they should be physically supported while slowly getting out of the chair and should have

obtained good balance and stability. If they complain of dizziness or

lightheadedness, they should sit back down until they recover equilibrium.

References Burkets oral medicine 10th & 11th edition. Essentials of medical physiology 3rd edition. Sembulingam. Davidsons principles & practice of medicine 20th edition. Current medical diagnosis & treatment. Lange 2004 Dental management of medically compromised patients. 7th edition. Little Medicine prep manual for undergraduates 3rd edition George mathew

Ischemic Heart Disease

Is an inflammatory disease affecting the large and medium sized arteries of heart resulting in inadequate or decreased coronary blood flow . Symptomatic coronary atherosclerotic heart disease is referred to as coronary heart disease.

Atherosclerosis & hypertension are the major contributory factors .

Atherosclerosis is the thickening of the intimal layer of the arterial wall caused ne accumulation of lipid plaques. The atherosclerotic process results in a narrowed arterial lumen with dimmer blood flow and oxygen supply.

In the later stages , the atherosclerotic plaque ruptures and exposes the arterial blood to the plaque contents and stimulates the formation of haemostatic plug . This occlusive thrombus may cause myocardial infaction. Atherosclerosis is the most common underlying cause of not only coronary an

disease (angina and myocardial infarction [MI]) but : cerebrovascular disease

(stroke) and peripheral artery disease (intermittent claudication).

Coronary obstruction/Cardiac pain/Cardiac Ischemia lesion

Obstruction: Impediment. Stenosis Narrowing of blood vessle I) Obstruction II) Occlusion Occlusion: Closed vessel Narrow lumen Pain : Infarct Pain Cardiac lesions Infarct (necrosis). Pain : Angina Pectoris Cardiac lesions Ischemia fibrosis.

Closure of the lumen

Risk factors
Male gender, older age, a family history of cardiovascular disease, hyperlipidemia, hypertension, cigarette smoking, physical inactivity, obesity, insulin resistance and diabetes mellitus, mental stress, and depression. In addition to these conventional risk factors, markers of inflammation such as C-

reactive protein, homocysteine, fibrinogen, and lipoprotein(a) have been found

to be associated with atherosclerosis. Between the ages of 35 and 44 years, the risk is 5 times greater for men than for Studies have confirmed that individuals with parents or siblings affected by coronary women. atherosclerotic heart disease have a greater risk of developing the disease at a younger age than do those without such a history. This risk may be as high as 5 times greater.

ANGINA PECTORIS
Defined as a temporary inability of the coronary arteries to supply the

myocardium with sufficient amount of circulated blood

Due to imbalance between myocardium oxygen requirement and oxygen supply. Angina is a Latin word describing a spasmodic , cramp like ,choking feeling or suffocation & pectoris meaning chest.

Variants of angina
Duration Stable Chronic , classic , exertional 1-15mins Due to obstruction of coronaries by atheroma.

Variant angina

prinzmetal or atypical or vasopastic

at rest or Odd times such as night Variable

due to Spasm of coronaries.

Unstable

Preinfarction ,crescendo

At rest or very low levels of exertion ,any factors . Upto 30 mins

Due to spasm and partial obstruction of coronaries.

The atypical attack of classic angina usually follows physical exertion or emotion stress . The patient is seized with a viselike crushing pain in the substernal region . The pain radiates characteristically to the left shoulder and down the arm to the

4th and 5th finger tips , but it may radiate to other areas , including the neck
region and even the jaws . Jaw pain has been reported to occur in the absence of precordial or substernal pain . This crushing pain lasts a few seconds to minutes, seldom longer .

Diagnosis
Electrocardiography ECG is normal in these pts at rest and in between attacks . Evidence, is demonstration of reversible ST segment depression or

elevation ,with or without T wave inversion during attack of pain .

Exercise testing treadmill testing or bicycle ergometry . Myocardial perfusion scanning using radioactive thallium Echocardiography Coronary arteriography , provides detailed information about the extent and

site of coronary artery stenosis.

Dental considerations
Acute anginal attack may occur as a result of the stress associated with dental services , particularly extractions . It is speculated that because of the over lapping of the 5th cranial nerve , 3rd cervical nerve and 1st thoracic nerve cardiac pain may be transmitted to the jaw

and interpreted as dental pain .

Anginal jaw pain is characterized by its extreme severity , its onset associated with exertion and its disappearance with rest .these characteristics serve to differentiate it from the usual pain of dental origin .

MYOCARDIAL INFARCTION
Synonyms coronary occlusion and heart attack .

MI is a clinical syndrome caused by a deficient coronary arterial blood supply to

a region of myocardium that results in cellular death and necrosis . The

syndrome is usually characterized by severe and prolonged substernal pain

similar to , but more intense and of longer duration than , that of angina pectoris Anginal attack lasting longer than 30mins is considered by definition to be a MI

MI - Types

Transmural Full thickness

Superimposed thrombus in atherosclerosis Focal damage

Sub-endocardial Inner 1/3 to half of ventricular wall Decreased circulating blood volume( shock, Hypotension, Lysed thrombus) Circumferential

Symptoms Pain severe & intolerable , prolonged 30 mins , crushing , choking , retrosternal , radiates to left arm , hand epigastrium shoulders neck and jaws Nausea and vomiting weakness , dizziness palpitations ,cold perspiration

Signs restlessness , acute distress

Skin cool ,pale ,moist

Heart rate bradycardia later tachycardia

Investigations
ECG useful in conforming the diagnosis ST segment elevation Appearance of pathologic Q waves i.e initial negative deflections .

Detectable by changes in S-T segment of ECG Myocardial infarction (MI) is diagnosed by high

levels of creatine phosphate (CPK) & lactate

dehydrogenase (LDH)

Plasma enzymes 1 . Creatine kinase (CK) More specific and starts to rise at 4-6 hrs , reaches peak 12 hrs , falls back to normal in 48-72 hrs 2. aspartate aminotransferase (AST)

Lactate dehydrogenase (LDH)

Myoglobin

Troponins (I and T )

Dental considerations

Prevention

Identification of the at-risk patient permits modification in dental care that , in

most instances will prevent the development of chest pain Elimination of stress ( emotional and physical ) is primary preventive measure .

Dental considerations
Several considerations need to be addressed when treating dental patients with CAD . The primary concern is to prevent ischemia or infraction The use of pulse oximeter to determine the level of oxygenation and the availability of an automatic external defibrillator are also advantageous .

The determination of vital signs prior to dental care is an important

preventive measure .

Studies have indicated the influence of circadian variation on the triggering of acute coronary events , occur between 6 am and noon . It has been proposed that sympathetic nervous system activation and an increased coagulative state may be precipitating factors

Therefore , dental care for high risk pts might ideally be provided in the late
morning or the early afternoon . Consultation with the patients primary physicians or cardiologists prior to dental therapy is recommended.

Anticoagulation therapy and dental care Patients with CAD may require the use of aspirin or other antiplatelet drug , such as clopidogrel . The combination of acetylsalicylic acid and clopidogrel is usually continued for a minimum period of 4 weeks after stent placement

and 3-6 months after drug eluting stents

The most common antiplatelet drug is aspirin , which is used chronically in low doses to prevent CVD . Aspirin irreversibly decreases platelet aggregation and pts will take between 81-325 mg /day

Data that address the risk of bleeding from dental extractions in pts who
use antiplatelet agents are limited although a bleeding time test is often recommended to evaluate the qualitative defect in platelets If emergency surgery needs to be performed and there is concern about

aspirin therapy , 1-desamino 8 D- arginine vasopressin(DDAVP) can

be instituted to improve hemostatis DDAVP isadministered parenterally at 0.3g/kg , maximum dose 20-24g within 1 hour of surgery A nasal spray containing 1.5 mg DDAVP per mm can be given in a dose of

300 mg /kg

Studies suggest that there is no need to discontinue or alter anticoagulation therapy prior to routine oral surgical procedures for patients taking antiplatelet medications other than aspirin There seems to be a consensus that the risk to the patient ( thromboembolism)

if these drugs are discontinued , which far exceeds the problem of prolonged
bleeding

The most commonly used antithrombin medications are the dicumarols ( e.g.warfarin) , which inhibit the biosynthesis of vitamin K dependent coagulation proteins ( factors II, prothrombin , VII ,IX and X) The full therapeutic effect of warfarin is reached after 48 72 hrs and lasts

for 36 72 hrs if the drug is discontinued

The efficacy of warfarin therapy is monitored by INR and in the range of 23.5 is considered as adequate .

There is minimal indication for discontinuation of anticoagulation therapy , before minor oral surgical procedures when pts INR is <3.5

Thus , the minimal increase of intraoral bleeding can be stopped with local
measures and the potentially devastating consequenses of thromboembolic events are prevented . 3 different protocols can be used to treat patients with marked elevation in INR .

1) warfarinn is continued with a change in the dose .

2) warfarin therapy is discontinued for 2-3 days prior to surgery

3) warfarin therapy is discontinued and the patient is placed on an alternative anticoagulation therapy Advantage pts risk for developing thromboembolic events is minimized by comparision with the 2nd protocol .

Unfractionated heparin is used for bridging the warfarin free period and
vitamin K is administrated . Heparin is continued , approximately to about 6hrs before surgery and is reinstituted after surgery with in combination woth oral anticoagulants until desirable INR has been achieved .

The advantage of using heparin are its short half life of 4-6 hrs and the availability of antidote , protamine sulfate . Patient can also self administer a subcutaneous injection of low molecular

weight heparin on an outpatient basis.

Recent guidelines from AHA suggests that there is no requirement of antibiotic prophylaxis for dental procedures in pts after coronary stent placement , unless the pt presents with an acute odontogenic pain . risk of bleeding in highly invasive dental procedures is small and bleeding

is relatively easy to manage , antiplatelet therapy should never be

discontinued for elective dental procedures.

Acute coronary syndromes

The sudden rupture of an atherosclerotic plaque ,with ensuing intracoronary thrombus formation that acutely reduces coronary blood flow , causes ACS ACSs represent a continuous spectrum of disease ranging from unstable angina , non ST elevation MI to acute ST elevation MI (STEMI)

The diagnosis of an ACS is usually made on the basis of clinical data .the patients history suggests a change in anginal pattern at rest Acutely ,the ECG is important to risk stratify the patient and to

make decisions regarding treatment

Resting ST segment depression or T wave inversions in the distribution of an epicardial coronary artery often accompany unstable angina , ST segment elevation is the hallmark of an acute MI

Step -1 termination of the dental procedure Step 2 : P (position ) the anginal patient is consciuos and usually apprehensive . The pt is allowed to position themselves in the most comfortable manner . Commonly sitting or standing upright . The supine

position is rarely preferred .

Step 3 :A-B-C ( AIRWAY BREATHING CIRCULATION) or basic life support (BLS) Step -4 : D (definitive care ) 4a administration of vasodilator and oxygen

If the patient experiences an anginal attack while in the dental chair , a nitroglycerine tablet should be placed immediately under the tongue or the patient should inhale amyl nitrate . These medications are not useful in patients known to be having a myocardial infraction.

In patients with known anginal pectoris , either classic or variant ,

relatively short acting antianginal drugs such as sublingual isosorbide nitrate tablets are recommended prophylactically before initiating dental therapy or a particularly stressful phase of dental therapy .

Emergency management

Recognize the problem ( chest pain or dysapnea)

Discontinue dental treatment Activate office emergency kit P position . Commonly sitting or standing upright . The supine position is rarely preferred A-B-C ( AIRWAY BREATHING CIRCULATION) or basic life support (BLS) D definitive management History of angina present Administer vasodilators and O2 If pain resolves consider further dental modifications , monitor vital signs and treatment

In the dental office , the use of nitrolingual spray is preferred to the sublingual tablets because of the relative insability of the tablets One or two metered sprays are recommended intially with no more than 3 metered doses within a 15 min period , whereas sublingual nitoglycerine

tablets are recommended at 0.3 0.6 mg every 5 mins as needed with no more
than 3 tablets every 15 mins

Nitroglycerine normally reduces or eliminates anginal discomfort dramatically within 2 4 mins ,commonly seen side effects are fullness or pounding in the head,flushing,tachycardia and possible hypotension . Represents a contraindication to nitroglycerine administration

Congenital heart diseases Are the common heart disease among children , present in 1% of live births Cyanotic transposition of great vessels , tetralogy of Fallot

Acyanotic
Atrial and ventricular septal defect , pantent ductus arteiosus,

soarctation of aorta ,pulmonary

prolapse

and aortic stenosis , mitral valve

Oral manifestations associated with congenital heart diseases

Delayed eruption of both dentitions Positional anomalies with permanent teeth Enamel hypoplasia Teeth have bluish white skimmed milk appearance Greater incidence of caries and periodontal diseases .

Dental considerations
Antimicrobial prophylaxis Dental bacteria may cause cerebral abscess Bleeding tendencies due to platelet dysfunction and excessive fibrinolytic activity .

Gingival retraction cord containing epinephrine

Valvular heart disease

Mitral valve disease - mitral valve prolapse(MVP) , mitral regurgitation (MR) , mitral stenosis (MS ) Aortic valve diseases AR and AS Prosthetic heart valves currently most widely used is the bileaflet

tilting disk valves

Bioprosthetic valves - heterografts made from porcine or bovine tisssue or the homografts from preserved human aortic valves. Patients with mechanical valves are on chronic anticoagulation therapy and are at an increased risk of IE

DENTAL CONSIDERATIONS
According to AHA 2007 , antimicrobial prophylaxis is now recommended only for people defined as being in higher risk for a poor outcome Prophylaxis is recommended because endothelialization of prosthetic material occurs within 6 months after the procedure.

Pacemakers
These are small implanted electronic devices that stimulates the heart to beat and pace the heart rate when it is too slow Bipolar , implanted transvenously in the subclavian or cephalic vein and typically located in right ventricle .

Dental apparatus with no known effect on cardiac pacemakers

Electric toothbrushes Electronic apex locators Piezoelectric ultrasonic scalers Dental apparatus with likely effects on cardiac pacemakers

Electronic dental analgesia units

Electrosurgical units MRI units TENS units Ultrasonic instruments

Cardiac Arrhythmias

Refers to any variation in the normal heartbeat, and includes disturbances of rhythm, rate, or the conduction pattern of the heart. Cardiac arrhythmias are present in a significant percentage of the population, many of whom will seek

dental treatment. Most arrhythmias are of little concern to the patient or die
dentist; however, some can produce symptoms, and a few may be life threatening.

The normal pattern of sequential depolarization consists of (1) sinoatrial (SA) node (2) atrioventricular (AV) node (3) bundle of His (4) right and left bundle branches (5) subendocardial Purkinje network.

Normal cardiac function depends on cellular automaticity (impulse forrnation), conductivity, excitability, and contractiiity. Disorders in automaticity and conductivity form the basis of the vast majority of cardiac arrhythmias. Disorders of conductivity (block or delay) paradoxically may lead to rapid

cardiac rhythm.

Investigations
The electrocardiogram (ECG) is the primary tool used in the identification and diagnosis of cardiac arrhythmias. Additional tests that may be used include exercise or stress testing, long-term or ambulatory ECG (Holter) recording, baroreceptor reflex sensitivity testing, body surface mapping, and

upright tilt-table testing. Electrode catheter techniques allow for

intracavitary recordings of the specialized conducting systems, which aid greatly in the diagnosis of arrhythmias.20

Drugs in arrhythmias

Dental considerations

Heart failure
HF represents the end stage of many of the cardiovascular diseases. The American College of Cardiology/ American Heart Association 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult1 defines HF as a complex clinical syndrome that may result from any

structural or functional cardiac disorder that impairs the ability of the

ventricle to fill with or eject blood. Patients with untreated or poorly managed HF are at high risk during dental treatment for complications such

as cardiac arrest, cerebrovascular accident, and myocardial infarction.

When right-sided ventricular enlargement occurs as the result of a lung . (e.g., emphysema), pulmonary hypertension is produced; this disorder condition is called corpulmonale

Conclusion

References Burkets oral medicine 10th & 11th edition Davidsons principles & practice of medicine 20th edition. Current medical diagnosis & treatment. Lange 2004 Dental management of medically compromised patients. 7th edition. Little Medicine prep manual for undergraduates 3rd edition George mathew

References Burkets oral medicine 10th & 11th edition. Essentials of medical physiology 3rd edition. Sembulingam. Davidsons principles & practice of medicine 20th edition. Current medical diagnosis & treatment. Lange 2004 Dental management of medically compromised patients. 7th edition. Little Medicine prep manual for undergraduates 3rd edition George mathew