Sem 11 Cardiovascular System & Dental Considerations

7/27/2019 Sem 11 Cardiovascular System & Dental Considerations

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Cardiovascular system &

dental considerations


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ContentsIntroduction

Anatomy & physiology

Examination of CVS

Questionnare

ECG & JVP

Infective endocarditis

Rheumatic fever

Hypertension

Ischaemic heart disease

Anticoagulation therapy and dental care

Acute coronary syndromes

Congenital heart diseases

Valvular heart diseases

Cardiac Arrhythmias

Heart failure

Conclusion


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IntroductionCardiovascular 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 walksof 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.


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Anatomy & physiology


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Clinical examinationof CVS


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QuestionnareHave 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 )


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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


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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 offighting for breath

Questions regarding exertional dysapnea, orthopnea , paroxysmal nocturnal

dyspnea should be asked .


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3 distinct waves are produced

during cardiac cycle

P wavecaused by atrial

depolarization

QRS complexcaused by

ventricular depolarization

T waveresults from ventricular

repolarization

ECG


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ECG interpretationP 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


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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


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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.InvertedT 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


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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).


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Jugular venous pulseJugular 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.


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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.


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The various waves on JVP reflect the phasic pressure

changes in the right atrium.

Normal JVP has three positive waves, namely, a, c andv waves, and two negative descents namely xdescent andy descent

awave is due to right atrial contraction

Thecwave 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.

Thexdescent ('systolic collapse9) is due to atrialrelaxation and downward displacement of tricuspid

valve during systole.

a They descent ('diastolic collapse') is due to opening ofthe tricuspid valve and the rapid flow of blood into


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Causes for raised JVP

Abnormalities in wave form


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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 calledinfective endarteritis.


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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.


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EtiologyA 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)


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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.


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PATHOPHYSIOLOGY AND COMPLICATIONSThe 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

Flow from a high- to a low-pressure chamberFlow across a narrowed orifice at high velocity Fibrin and platelets then

adhere to the roughened endothelial surface and form small clusters or masses

callednonbacterial thrombotic endocarditis (NBTE)

A similar and frequently indistinguishable condition is found in somepatients with systemic lupus erythematosis and is called Libman-Sacksverrucous endocarditis


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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.


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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


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ComplicationsHeart 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.


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SIGNS AND SYMPTOMSThe 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 ofIE due to emboli and/or immunologic responses areless frequently seen since the advent of antibiotics. These include petechiae of

the palpebral conjunctiva, the buccal and palatal mucosa, and extremities.


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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.


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DUKES CRITERIAThe 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)


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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 majorcriteria, one major and three minor criteria, or five minor criteria.


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LABORATORY FINDINGSComplete 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.


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ECG may show evidence of conduction block with myocardial involvement or

infarction. Other abnormal findings may include an elevated erythrocyte sedi-

mentation 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.


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Dental considerationsAntibiotic ProphylaxisDental 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.


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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


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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


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Special SituationsPatients Already Taking AntibioticsPatients 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.


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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.


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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.


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Other ConsiderationsNo 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.


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Rheumatic feverRheumatic 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.

EtiologyRheumatic fever follows an antecedent pharyngeal infection with group A

beta hemolytic steptococci

Latent period between the pharyngeal infection and the onset of fever 1-5weeks, with average duration being 19 days.

Fewer than 2-3% of previously healthy persons develop rheumatic fever.


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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 proliferativeinflammatory lesions of the connective tissues. It mainly involves the heart,

joints and subcutaneous tissues.


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MANAGEMENT Bedrest Antistreptococcal therapyA 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.


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SalicylatesAspirin 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.


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CorticosteroidsPatients 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


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PreventionPrimary 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.


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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 of5years.Decisionto 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.


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4 Regimens: One of the following regimens may be used:

Intramuscularinjection of 1.2 millionunits ofbenzathine penicillin

G every 3 weeks (most efficient regimen).

Oral penicillinV 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 topenicillins and sulpha)


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HYPERTENSIONHypertension 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.


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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.


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EtiologyAbout 90% of patients have no identifiable cause for their disease, which is

referred to asessential, primary, or idiopathichypertension. For the remaining10% of patients, an underlying cause or condition may be identified; for these

patients, the termsecondaryhypertension 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.


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Pathophysiology and ComplicationsIn 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)


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Signs & symptomsHypertension 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 issystolic pressure.

Diastolic pressure represents the total resting resistance in the arterial system

after passage of the pulsating force produced by contraction of the left

ventricle.

The difference between diastolic and systolic pressures is calledpulse pressure.

Mean arterial pressure is roughly defined as the sum of the diastolic pressure

plus one-third the pulse pressure.

Labile hypertension is the term that was previously used to

describe a subgroup of patients with wide variability in blood

pressures


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About 15% to 20% of patients with untreated stage 1 hypertension have what

is calledwhite 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 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


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Alcohol and smoking should be avoided for 30mins beforemeasurement

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

2/3rdof the arm

Palpate radial /brachial artery

Inflate the cuff slowly to about 200-250 mm Hg or until the pulse

is no longer palpable

Assessment of blood pressure


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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.


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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


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DENTAL CONSIDERATIONSThe 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 .


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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.


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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.


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Drug interactionsSome 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 .


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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


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Burketsoral medicine 10th& 11thedition.

Essentials of medical physiology 3rdedition. Sembulingam.

Davidsonsprinciples & practice of medicine 20thedition.

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


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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.


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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).


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Coronary obstruction/Cardiac pain/Cardiac Ischemia lesion

II) Occlusion

Obstruction:Impediment.Stenosis Narrowingof blood vesslePain :Angina Pectoris Cardiac lesionsIschemia fibrosis.

Occlusion:Closed vesselPain :InfarctPain

Cardiac lesionsInfarct (necrosis).

I) Obstruction Narrowlumen

Closureof thelumen


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Risk factors


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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

women.

Studies have confirmed that individuals with parents or siblings affected bycoronary atherosclerotic heart disease have a greater risk of developing the diseaseat a younger age than do those without such a history. This risk may be as highas 5 times greater.


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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.


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DurationStable 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 lowlevels of exertion ,any

factors .

Upto 30 mins

Due to spasm and partialobstruction of coronaries.

Variants of angina


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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


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ElectrocardiographyECG 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 testingtreadmill 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.


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Dental considerations


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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 .


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MYOCARDIAL INFARCTIONSynonymscoronary 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


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MI Types


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MI - Types

Transmural

Full thickness

Superimposed thrombus in

atherosclerosis

Focal damage

Sub-endocardial

Inner 1/3 to half of ventricular

wall

Decreased circulating bloodvolume( shock, Hypotension,

Lysed thrombus)

Circumferential


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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

Signsrestlessness , acute distress

Skincool ,pale ,moist

Heart ratebradycardia later tachycardia

Investigations


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ECGuseful 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)


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Plasma enzymes1 . 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 )



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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 .


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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 highrisk 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.


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Anticoagulation therapy and dental care


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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 drugeluting stents

The most common antiplatelet drug is aspirin , which is used

chronically in low doses to prevent CVD . Aspirin irreversiblydecreases platelet aggregation and pts will take between 81-325 mg

/day

Data that address the risk of bleeding from dental extractions in pts who


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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-desamino8D- arginine vasopressin(DDAVP) can

be instituted to improve hemostatis

DDAVP isadministered parenterally at 0.3g/kg , maximum dose 20-24gwithin 1 hour of surgery

A nasal spray containing 1.5 mg DDAVP per mm can be given in a dose of

300 mg /kg


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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


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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 4872 hrs and lasts

for 3672 hrs if the drug is discontinued

The efficacy of warfarin therapy is monitored by INR and in the range of 2-

3.5 is considered as adequate .


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There is minimal indication for discontinuation of anticoagulation therapy ,

before minor oral surgical procedures when pts INR is


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3) warfarin therapy is discontinued and the patient is placed on an alternative

anticoagulation therapy

Advantagepts risk for developing thromboembolic events is minimized by

comparision with the 2ndprotocol .

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 combinationwoth oral anticoagulants until desirable INR has been achieved .

The advantage of using heparin are its short half life of 4-6 hrs and the


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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


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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 , nonST elevation MI to acute ST elevation MI (STEMI)


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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 accompanyunstable angina , STsegment elevation is the hallmark of an acute

MI


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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 )

4aadministration of vasodilator and oxygen


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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 .

Recognize the problem ( chest pain or dysapnea)Emergency management


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Discontinue dental treatment

Activate office emergency kit

Pposition . Commonly sitting or standing upright . The supine position is

rarely preferred

A-B-C ( AIRWAYBREATHINGCIRCULATION) or basic lifesupport (BLS)

Ddefinitive management

History of angina

present

Administer

vasodilators and

O2

If pain resolves consider

further dental

modifications , monitor

vital signs and

treatment


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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


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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


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Are the common heart disease among children , present in 1% of live

births

Cyanotic

transposition of great vessels , tetralogy of FallotAcyanotic

Atrial and ventricular septal defect , pantent ductus arteiosus,

soarctation of aorta ,pulmonary and aortic stenosis , mitral valve

prolapse


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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


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Mitral valve disease - mitral valve prolapse(MVP) ,

mitral regurgitation (MR) , mitral stenosis (MS )

Aortic valve diseasesAR and AS

Prosthetic heart valves currently most widely used is the bileaflettilting 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


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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


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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


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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


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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.

Th l f i l d l i i i f


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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.


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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.


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Investigations


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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


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Heart failureh d f f h d l d h


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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.


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When right-sided ventricular enlargement occurs as the result of a lung

disorder (e.g., emphysema), pulmonary hypertension is produced; this

condition is calledcorpulmonale

.


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Conclusion


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Referencesk l d th & th d


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Burketsoral medicine 10th& 11thedition




edition. Little


mathew

Referencesk l di i th & th di i


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Burketsoral medicine 10th& 11thedition.

Essentials of medical physiology 3rdedition. Sembulingam.




edition. Little


mathew


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Documents

Sem 11 Cardiovascular System & Dental Considerations