Professional Documents
Culture Documents
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Q U I N T E S S E N C E I N T E R N AT I O N A L
Key words: cardiac arrhythmia, cardiovascular disease, coronary artery disease, dental
treatment, heart failure, hypertension, medical management, thromboembolic
disorders
HYPERTENSION
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220
200
180
Systolic
Diastolic
Range
> 160
140159
160
140
120139
> 100
< 120
120
9099
8089
100
80
< 80
60
Normal
Prehypertension
Stage 1
hypertension
Stage 2
hypertension
Clinical manifestations
Primary hypertension is asymptomatic until
complications develop in target organs, particularly in the kidneys, cardiovascular system, cerebrovascular system, peripheral vascular system, and eyes. The kidneys are
major targets for the ill effects of hypertension, although this damage may be occult
until late in the progression of the disease.27
Clinically, the ultimate pathophysiologic condition is hypertensive nephrosclerosis characterized by decreased glomerular filtration
and tubular dysfunction, which can progress
to end-stage renal disease. Hypertensive
nephrosclerosis may predispose patients to
refractory hypertension, especially in African
Americans.27 Large-scale studies have also
demonstrated a linear relationship between
increasing blood pressure and cardiovascular disease.28 The risk of cardiovascular disease doubles for individuals aged 40 to 70
years with each increment of 20 mm Hg in
systolic or 10 mm Hg in diastolic blood pressure across the entire blood pressure range
from 115/75 to 185/115 mm Hg.29 Chief cardiovascular complications include arteriosclerotic and atherosclerotic changes in
coronary arteries.3033 Coronary artery disease (CAD) leads to angina pectoris and
myocardial infarction. Other cardiovascular
complications include left ventricular (LV)
hypertrophy, which progresses to cardiac
myopathy, dilation, and ultimately failure.3033
Diagnosis
The diagnosis of primary hypertension is
based on evidence of elevated systolic
and/or diastolic blood pressure in the
absence of secondary causes. The Seventh
Joint National Committee on Detection,
Evaluation, and Treatment of High Blood
Pressure (JNC 7) provides a new classification of blood pressure for adults aged 18
years or older (Fig 1).36 When systolic and
diastolic pressures fall into different categories, the higher category is used to determine treatment strategies. Patients with prehypertension are at increased risk for progression to hypertension. Those in the
130/80 to 139/89 mm Hg blood pressure
range have twice the risk of developing hypertension as those with lower values.36
The basic evaluation recommended for
patients with elevated blood pressure
includes a review of the medical history, physical examination, and laboratory studies.35,3739
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Ta b l e 1
Therapeutic goal
Pharmacologic strategies
Diuretics
1-adrenergic receptor antagonists
ACE inhibitors
Angiotensin II-receptor antagonists
Calcium-channel blocking agents
1-adrenergic receptor antagonists
2-adrenergic receptor agonists
The medical evaluation of patients with documented elevated blood pressure has three
objectives: (1) rule out identifiable causes of
high blood pressure (see above); (2) identify
cardiovascular risk factors or concomitant disorders that may affect prognosis or treatment
strategies (see below); and (3) assess the
presence or absence of target-organ damage.35 Major cardiovascular risk factors
are35,3739:
Obesity
Dyslipidemia
Diabetes mellitus
Age (> 55 years for men, > 65 years for
women)
Family history of cardiovascular disease (<
55 years for men, < 65 years for women)
Social history (cigarette smoking, alcohol
use/abuse, sedentary lifestyle)
Fewer than 5% of the patients with high
blood pressure have secondary hypertension.21 Indications for specialized diagnostic
procedures to rule out secondary hypertension are: onset of hypertension before age
30 or after age 60, diastolic blood pressure
greater than 120 mm Hg, abrupt onset of
hypertension, hypertensive retinopathy, or
refractory hypertension.3739 Renovascular
disease is the most likely etiologic factor in
younger and older patients suffering from
severe hypertension.
disease. This may be achieved by maintaining systolic blood pressure below 140 mm
Hg and diastolic pressure below 90 mm Hg.
Treatment to lower levels may be useful, particularly to prevent stroke, preserve renal
function, and prevent or slow the progression
to heart failure. While the mainstay of treatment for hypertension is pharmacologic,
adoption of a healthy lifestyle is critical for the
prevention of high blood pressure, and it is
an indispensable part of the management of
those with hypertension. Major lifestyle modifications shown to lower blood pressure
include aerobic exercising for 30 to 45 minutes, three to five times a week; weight reduction (in overweight and obese individuals);
adopting a diet rich in fruits, vegetables, and
low-fat dairy products that are rich in potassium and calcium; reduction of dietary sodium;
and moderation of alcohol consumption.35
Pharmacologic strategies include reducing volume overload, blocking adrenergic
receptors in the heart, dilating peripheral
blood vessels, and reducing sympathetic
outflow from the central nervous system
(Table 1). Clinical trial outcome data prove
that thiazide-type diuretics, 1-adrenergic
blocking agents, ACE inhibitors, angiotensin
II-receptor blocking agents, and calciumchannel blocking agents all reduce the complications of hypertension.35 Thiazide diuretics are the initial drugs of choice for most
patients with hypertension. If the initial drug
at full dose has no effect on the blood pressure or causes troublesome side-effects,
substituting a drug from a different class is
recommended. If the initial drug produces
only a partial response but is well-tolerated,
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CORONARY ARTERY
DISEASE
Aerobic metabolism (conversion of pyruvic
acid to CO2 and H2O) accounts for the majority of the energy produced in cardiac muscles. Anaerobic metabolism is used only in
extreme hypoxia. The factors that increase
the oxygen demand of the heart are: heart
rate, wall tension, and contractile state. The
faster the heart rate, the more oxygen it uses.
The larger the heart, the more oxygen is
required for its contraction. The greater the
force of myocardial contraction, the greater
the amount of oxygen consumed. If there is a
temporary deficiency of oxygen to a portion
of the myocardium, painful coronary insufficiency takes place and the patient is said to
have suffered from an attack of angina pectoris. If the deficient supply of oxygen to a
portion of the myocardium is permanent,
necrosis will develop and myocardial infarction occurs.
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Clinical manifestations
Myocardial ischemia develops either when
myocardial oxygen demand increases to a
level exceeding the capacity of the diseased
coronary arteries to deliver blood or when
coronary vasoconstriction increases coronary resistance so that flow decreases to critical levels.46 Vasoconstriction can be mediated through neural pathways; caused by
endothelial injury secondary to substances
released by aggregating platelets and cigarette smoking; or associated with exposure to
cold or exercising. The myocardial ischemia
caused by either an excessive increase in
myocardial oxygen demand or by vasoconstriction may be silent, may be accompanied
Diagnosis
Dyslipidemia. The National Cholesterol
Education Programs Adult Treatment Panel
II, sponsored by the National Institutes of
Health and endorsed by the American Heart
Association (AHA), recommends the routine
measurement of nonfasting total cholesterol
and high-density lipoprotein (HDL) every 5
years.47,48 The American College of Physicians and American Academy of Family Physicians suggest periodic cholesterol measurement in men aged 35 to 65 years and
women aged 45 to 65 years.49 The primary
goal of screening younger people is to promote lifestyle changes, which may provide
long-term benefits later in life. Total cholesterol levels below 200 mg/dL are classified as
desirable blood cholesterol; those 200 to
239 mg/dL are classified as borderline-high
blood cholesterol; and those 240 mg/dL and
above are classified as high blood cholesterol. Patients with desirable blood cholesterol levels (< 200 mg/dL) are given general
dietary and risk reduction education and
advised to have another serum cholesterol
test within 5 years. Patients with borderlinehigh blood cholesterol (200 to 239 mg/dL)
and two other CAD risk factors (hypertension,
diabetes mellitus, severe obesity, family history of CAD, and cigarette smoking) and those
with high blood cholesterol (> 240 mg/dL)
should undergo lipoprotein analysis.
LDL is considered the main risk factor for
CAD. Consequently, LDL levels serve as the
key index for clinical decision making about
cholesterol-lowering therapy. Levels of LDL of
160 mg/dL or higher are classified as highrisk LDL, and those 130 to 159 mg/dL are
classified as borderline-high-risk LDL.
Patients with high-risk LDL levels and those
with borderline-high-risk LDL who have two
other risk factors should have a complete clinical evaluation and begin cholesterol-lowering
treatment. However, LDL represents only a
proportion of the atherogenic lipoproteins
accumulated in plasma and has significant
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Surgical intervention
There are two routinely available procedures
for the surgical management of patients with
CAD: (1) percutaneous coronary intervention, such as balloon angioplasty and stent
implantation; and (2) coronary artery bypass
graft (CABG) surgery.68 The advantages of
percutaneous coronary intervention for the
treatment of ischemic heart disease include
a low level of procedure-related mortality,
short hospital stay, and early return to activity. Disadvantages include a risk of acute
coronary occlusion during angioplasty and a
significant risk of restenosis. CABG procedures carry increased risk of mortality in the
first 12 months after surgery but thereafter
appear to reduce the risk of death from CAD
for up to 5 to 10 years.
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Ta b l e 2
Therapeutic goal
Pharmacologic strategies
Lipid-lowering agents
HMG-Co-A reductase inhibitors
Nitrates
Calcium-channel blocking agents
1-adrenergic receptor antagonists
Antithrombotic agents
Anticoagulants
CARDIAC ARRHYTHMIA
The primary pacemaker of the heart is the
sinoatrial (SA) node. Under the influence of
the autonomic nervous system, the SA node
generates electric impulses at regular intervals and with a frequency of 60 to 100 beats
per minute. The impulses spread rapidly
through the atria and enter the atrioventricular (AV) node. After a brief delay at the AV
node, the impulses propagate over the HisPurkinje system as depolarization progresses
over the ventricles in an anatomically synchronous and hemodynamically effective
fashion. Interruption of this system compromises tissue oxygenation and may lead to
death.
Clinical manifestations
A disturbance in the rhythm of the heart, or
arrhythmia, may manifest as bradyarrhythmia
or bradycardia (slow rhythm) or tachyarrhythmia or tachycardia (rapid rhythm).70
Common disorders of impulse generation
are as follows:
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Diagnosis
In the investigation of arrhythmias, it is customary to take a twelve-lead ECG: three limb
leads (lead I, lead II, and lead III), three augmented limb leads (aVR, aVL, and aVF), and
six precordial leads (V1, V2, V3, V4, V5, and
V6). An ECG is a graph of voltage variants
plotted against time (Fig 2). The paper on
which the ECG is recorded is ruled in lines
spaced 1-mm apart horizontally and vertically. When the tracing is properly standardized,
each vertical space represents a voltage
change of 0.1 mv and each horizontal space
represents a time interval of 0.04 second.
Each fifth line, horizontally and vertically, is
wider than the others. The time interval
between the heavy horizontal lines is 0.2 second. The voltage change between heavy vertical lines is 0.5 mv.
The P wave of an ECG reflects atrial depolarization. The PR segment is a measure of
the time interval from the beginning of atrial
depolarization to the beginning of ventricular
depolarization. This interval is usually 0.2
second for heart rates over 60 beats per
minute. The QRS interval is the depolarization complex of the ventricular musculature.
The duration of the QRS interval is measured
from the beginning of the first wave of the
complex to the end of the last wave and normally does not exceed 0.1 second. The T
wave is the wave of ventricular repolarization.
The vast majority of arrhythmias can be diagnosed by evaluating atrial rhythm (P waves),
ventricular rhythm (QRS complex), AV conduction (the relationship between P waves
and QRS complexes), and the presence of
unusual complexes (early, late, or unusual
contour).7174 Counting the number of R-R
intervals within 16 heavy vertical lines (15
time spaces) and multiplying it by 20 determines the heart rate.
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Atrial contraction
sic cardiac electric activity. Today, most pacemakers in the United States use adaptive-rate
pacing to modify pacing rate for changing
metabolic needs.76 A single-chamber pace-
Ventricular contraction
Myocardial
repolarization
ST
segment
T
Q
PR
interval
S
QRS
interval
Nonpharmacologic management
of arrhythmias
The basic function of a pacemaker is to stimulate (or pace) the heart and to sense intrin-
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Ta b l e 3
Therapeutic goal
Pharmacologic strategies
HEART FAILURE
Cardiac muscle contraction is under the regulatory control of the autonomic nervous system. On a cellular level, the combination of a
catecholamine with its membrane-bound 1adrenergic receptor activates the enzyme
adenylate cyclase. The resultant increase in
intracellular cyclic adenosinemonophosphate (AMP) then promotes myocardial contraction by facilitating transmembrane calcium flux. In cardiac muscle, the 1-adrenergic
pathway can therefore be characterized as a
series of events that begins with the combination of a 1-agonist with a receptor and
concludes with an increase in muscle contraction. Consequently, in patients with normal heart function, the pumping actions of
the left and right sides of the heart complement each other and produce a continuous
flow of blood to the tissues. When the heart
is no longer able to pump an adequate supply of blood to meet the metabolic needs of
tissues, heart failure, a state of circulatory stasis, follows.
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failure begins with impaired ventricular function, much of what follows is caused by the
retention of salt and water.89,90
The kidneys are responsible for regulating
the balance of salt and water by conserving
both during periods of deprivation and
excreting diluted urine when water consumption is high. This activity requires an
abundant blood supply. Consequently, renal
function is dependent on an adequate cardiac output, 25% of which is apportioned to
the kidneys. Normal salt and water homeostasis is maintained by negative-feedback
mechanisms. Key among them is the reninangiotensin-aldosterone system.91,92 Renin,
released from the juxtaglomerular and macula densa cells of the kidneys, cleaves four
amino acids from circulating angiotensinogen, produced by the liver, to form angiotensin I. The ACE, which is bound to the plasma membrane of endothelial cells, cleaves
two amino acids from angiotensin I to form
angiotensin II. Angiotensin II promotes the
constriction of renal and systemic arterioles
and sodium reabsorption in the proximal
segments of the nephrons. It also stimulates
the adrenal cortex to secrete aldosterone,
which promotes the reabsorption of sodium,
in exchange for potassium, in the distal segments of the nephrons.
The contribution of aldosterone to the
retention of sodium in patients with congestive heart failure is now well established.9396
Aldosterone secretion in patients with heart
failure is regulated by several major stimuli.
These include angiotensin II and elevations in
serum potassium concentrations. Plasma corticotropin concentrations are also critically
increased, contributing to the increase in
aldosterone secretion.97 Finally, because of
reduced hepatic perfusion, decreased metabolic clearance of aldosterone by the liver can
account for significant increase in plasma
aldosterone concentrations.98 In addition to its
classic mineralocorticoid properties, aldosterone has other adverse effects that can contribute to the pathophysiology of heart failure.
These effects include coronary and renovascular remodeling (fibrosis), endothelial cell
and baroreceptor dysfunction, and inhibition
of myocardial norepinephrine uptake.99101
The persistent activation of the renin-
angiotensin-aldosterone system induces inappropriate intravascular and extravascular volume expansion; induces fibrosis of the heart,
kidneys, and other organs; and contributes to
the progressive nature of heart failure, which
leads to episodes of symptomatic heart failure
and sudden death.
Clinical manifestations
The American College of Cardiology and
AHA guidelines for the evaluation and management of heart failure state that there are
four stages of heart failure.102 Patients with
stage A heart failure are at risk of developing
heart failure because of the presence of conditions strongly associated with the development of heart failure, such as hypertension,
CAD, diabetes mellitus, history of cardiotoxic
drug therapy, alcohol abuse, history of rheumatic fever, or family history of cardiomyopathy. Patients with stage B heart failure have
structural heart disease associated with the
development of heart failure but have not
shown symptoms or signs of heart failure.
These patients have a prior myocardial infarction, LV hypertrophy or fibrosis, LV dilatation
or hypocontractility, or asymptomatic valvular
disease. Patients with stage C heart failure
have current or prior symptoms of heart failure associated with structural heart disease.
Patients with stage D heart failure have
advanced structural disease and marked
symptoms of heart failure at rest despite maximal medical therapy and required specialized interventions. Heart failure is usually a
relatively slow, progressive condition. By the
time it is recognized clinically, congestive
heart failure has become the end stage of a
sustained disproportion between the load on
the heart and the ability of the heart muscle
to handle the load. The traditional clinical
manifestations of heart failure represent
stages C and D, which manifest impairment
of either the left or right ventricle.103105
Left ventricular failure. LV failure characteristically develops in hypertension, CAD,
cardiomyopathy, and most forms of congenital heart defects. It may manifest as tachycardia, fatigue on exertion, dyspnea on mild
exercise, and intolerance to cold. Paroxysmal
nocturnal dyspnea and nocturnal cough
reflect the redistribution of excess fluid into
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Diagnosis
Clinical signs and symptoms such as exertional dyspnea, orthopnea, edema, tachycardia, pulmonary rales, and jugular vein distension have a high diagnostic specificity for
heart failure. Diagnostic sensitivity and predictive accuracy can be increased with blood
chemistry, ECG, chest radiograph, and
echocardiography.106112
Compensated heart failure. Patients who
experience dyspnea and fatigue only with
heavy muscular work and manifest no signs
of intravascular or extravascular volume
expansion have compensated heart failure.113
These patients have mild to moderate impairment of renal perfusion, and the ratio of sodium to potassium in the urine is greater than
1 because the release of natriuretic peptides
from the distended atria and ventricles stimulates sodium excretion.
Decompensated heart failure. Patients
who experience dyspnea and fatigue at rest
or during mild exertion and manifest signs of
intravascular or extravascular volume expansion have decompensated heart failure.113
Decompensation occurs because these
patients have moderate to marked reductions in renal perfusion. Plasma renin activity
increases, and the resulting increases in
angiotensin II and aldosterone production
override the action of natriuretic peptides.
Urinary sodium retention becomes nearly
complete, and the sodium-to-potassium ratio
is less than 1.
Surgical intervention
Heart transplantation is the primary surgical
treatment for patients with end-stage heart
failure, with 1-year survival of 86% and 5-year
survival of 69%.115117 Because heart transplantation is an option to only a small number of patients, classic interventions such as
revascularization procedures, valve repair, or
valve replacement have been improved and
modified to meet the special need of patients
with heart failure.118
THROMBOEMBOLIC
COMPLICATIONS OF
CARDIOVASCULAR
DISEASES
The clotting of blood involves the sequential
initiation, interaction, and completion of several stages of hemostasis. The vascular
stage is initiated by tissue injury, and the
response or outcome is vasoconstriction.
The platelet phase is initiated by adhesion
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Ta b l e 4
Therapeutic goal
Pharmacologic strategies
Reduce workload
Diuretics
ACE inhibitors
1-adrenergic receptor antagonists
Vasodilators
Cardiac glycosides
Antithrombotic agents
Anticoagulants
Clinical manifestations
Arterial thrombi contribute to transient
ischemic attacks and stroke, occlusion of coronary artery grafts, coronary artery rethrombosis after thrombolysis, myocardial infarction
and death in unstable angina, increased incidence of periprocedural myocardial infarction
in patients undergoing coronary angioplasty,
mural thrombosis after myocardial infarction,
and recurrent myocardial infarction.119121
Arterial thrombi can also contribute to systemic
embolism in patients with prosthetic heart
valves or atrial fibrillation and death in patients
CONCLUSION
Hypertension is the most common primary
diagnosis in the United States. While a blood
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pressure of 180/110 mm Hg is not an independent risk factor for cardiovascular complications during noncardiac procedures, elevated blood pressure is a reliable indicator of
CAD. Cardiac ischemia during noncardiac
procedures correlates with intra- and postoperative morbidity. Structural coronary arterial
abnormalities and their consequences are
the cause of the majority of arrhythmias leading to sudden death. Finally, hypertension
and CAD are major causes of congestive
heart failure, which has also been identified
as a further risk factor for coronary events.
The physiologic response to the trauma of
an oral/dental procedure and the administration of anesthetic agents can affect cardiac
function. Consequently, oral health care
providers must have an understanding of cardiovascular diseases. Such an obligation is
tempered only by the extent to which such
diseases relate to the dental professions
anatomic field of responsibility and the extent
to which such illnesses require modification
of dental therapy or alter prognosis. This
overview provides the framework for considering cardiac risk in association with
oral/dental procedures and for determining a
patients clinical risk profile to be used in
making treatment decisions that may influence both short- and long-term outcomes.
Ta b l e 5
Therapeutic goal
Antithrombotic agents
Anticoagulants
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