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8/10/2019 General medicine for dentistry students.pptx
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Dr Haidar F.
Al-Rubaee
GENERAL MEDICINE FOR
DENTISTRY STUDENTS
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One can ask himself a question that is why a dentis t should
study principles of general medicine.
This is required because:
Certain diseases might present with oral or dental symptoms & signs
e.g. buccal hyperpigmentation in addisonsdisease, mouth ulcers inrheumatological diseases
Certain diseases can be precipitated or aggravated by oral hygiene &
dental care e.g. dental caries and risk of subacute infective
endocarditis
Certain dental procedure or medications can affect the health status
of patients with certain medical illnesses e.g. use of non-steroidal
anti-inflammatory agents in patients with asthma or peptic ulcer.
Patients with high risk medical conditions might become at a greater
risk of increasing morbidity and mortality if they undergo dental
procedure or treatment.
GENERAL OBJECTIVES
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Your recommendedtextbook
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PHYSICAL EVALUATION
& RISK ASSESSMENT
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Dentistr y today is far different from what was practiced only a
decade or two ago, not only in techniques & procedures but
also in the types of patients seen.
as a result of advances in medical science, people are living
longer and are receiving medical treatment for disorders thatwere fatal only few years ago.
Like heart valve replacement, coronary intervention, organ
transplantation, etc.
The key to successful dental management of a medically
compromised patient is a thorough evaluation andassessment of risk to determine whether a patient can safely
tolerate a planned procedure.
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Dentist is no longer
treatingteeth in patients,
but ratherpatients who
have teeth.
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Increased risk
Decreased risk
Risk??
Medicalcondition
SeverityStability
Control
Functionalcapacity
Emotional status
Dental
procedure:Invasiveness
Length of procedure
Blood loss
Vasoconstrictor use
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Physician referral & consultation
Clinical laboratory tests
Physical examination
Medical history
ELEMENTS OF THE PROCESS OF
EVALUATION & RISK ASSESSMENT
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Once collection of the patients health data (history, clinical
examination, laboratory results, consultations) is complete, the
data must be assessed to determine whether the patient can
safely undergo dental treatment and what, if any, modifications
in the delivery of dental care are required.
One widely used method of expressing medical risk is the
American Society of Anesthesiologists
(ASA) Physical Classification System This system was originally developed to classify patients
according to their risk for general anesthesia, however it has
been adapted for outpatient medical and dental use for all types
of surgical and non surgical procedures, regardless the of
anesthesia used.
The implication of ASA physical classification score is that as the
classification level (ASA II-I V) increases, so does the risk.
RISK ASSESSMENT
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ASA I Normal healthy patient
ASA II
Patient with mild systemic disease that does not interfere with
daily activity, or patient with a significant health risk factor (e.g.smoking, alcohol abuse, morbid obesity)
ASA III
Patient with moderate to severe systemic disease thatis not incapacitating but that may alter daily activity
ASA IV
Patient with severe systemic disease that isincapacitating and is a constant threat to life.
AMERICAN SOCIETY OF ANESTHESIOLOGISTS
(ASA) PHYSICAL CLASSIFICATION SYSTEM
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Although it is generally helpful to classify patients according
to the ASA system, the practical usefulness of this system is
limited in that it does not provide specific information about
how treatment may need to be modified, thus further
consideration my be necessary. This can be done by considering the ABCs of risk assessment.
ABC OF RISK ASSESSMENT
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A
AntibioticsWill the patient needantibiotics, prophylacticallyor therapeutically?
Anesthesia Are any potential problems orconcerns associated with theuse of local anesthetics or withvasoconstrictors found in thelocal anesthetic?
AnxietyWill the patient need a sedative
or anxiolytic?
AllergyIs the patient allergic to anythingthat the dentist may prescribe orwith which she or he may comeinto contact in the dental office?
ABC OF RISK ASSESSMENT
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B
BleedingIs abnormal hemostasis apossibility?
CChair position
Can the patient tolerate a
supine chair position?
ABC OF RISK ASSESSMENT
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D
DrugsHave any potential druginteractions, adverseeffects, or allergies beenassociated with any of thedrugs taken by the patientor with drugs that thedentist may prescribe?
Devices
Does the patient haveprosthetic or therapeuticdevices such as prostheticheart valves, prostheticjoint, pacemaker, or AVfistula that may requiresconsideration?
ABC OF RISK ASSESSMENT
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E
EquipmentHave any potentialproblems or concerns beenassociated with the use ofdental equipment such asX-ray, ultrasonic cleaner,electro surgery, or oxygen?
Emergencies
Can any medicalemergencies beencountered with thispatient?
ABC OF RISK ASSESSMENT
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On the basis of risk assessment, modifications may need to
made in the delivery of dental treatment, these can be divided
into:
Pre-operative modifications
Intra-operative modifications
Post-operative modifications
Examples are given in the next slides
TREATMENT MODIFICATIONS
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Pre-operative modifications
Prophylactic antibiotics given prior tocertain dental procedures in a patient atrisk for bacterial endocarditis
Determination of the international
normalized ratio (INR) prior to surgery in apatient taking warfarin
Ensuring food intake prior to dental
treatment in diabetic patient on insulin ororal hypoglycemic agents
Prescribing an anxiolytic drug for ananxious patient with stable angina
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Intra-operative modifications
Limiting the amount of vasoconstrictor in apatient who takes a non-selective beta blocker
Administering Nitrous oxide/oxygen to ananxious patient with poorly controlled
hypertension
Using an upright chair position for a patientwith heart failure
Avoiding use of electrosurgery in a patient witha pacemaker
Avoiding elective radiographs in a pregnantpatient .
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Post-operative
modificationsUse of extra local measures for
hemostasis in a patient takingwarfarin
Prescribing antibiotics for a
poorly controlled diabeticfollowing surgery
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GENERAL STRESS REDUCTION PROTOCOL
Open communication about fears/concerns
Short appointments
Short acting benzodiazepines, night before appointment, and/or 1 hr beforeappointment
Pre-operative sedation
Intraoperative use of N2O/O2
Profound local anesthesia; topical, use prior to injection
Adequate post-operative pain control
Patient contacted n evening of the procedure
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CARDIOLOGY
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SYMPTOMS OF HEART DISEASE
Chest pain
Dyspnea
Palpitations
Syncope
Fatigue
Peripheral oedema.
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Differentiatingpo
ints
Site
Radiation.
Character.
Provocation
Onset
Associated
features
CHEST PAIN
Chest pain is a common
presentation of cardiac disease but
can also be a manifestation of
anxiety or disease of the lungs or
musculoskeletal or gastrointestinal
systems.
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PAIN-STANDARD QUESTIONING
Site Onset Character
RadiationAssociatedsymptoms
Timing(duration,
course, pattern)
Exacerbatingand relieving
factorsSeverity
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Central
Cardiac
Ischaemic heart disease
(infarction or angina) Pericarditis/myocarditis
Mitral valve prolapse
Aortic aneurysm/dissection
Non-cardiac
Pulmonary embolism Oesophageal disease
Mediastinitis
Costochondritis (Tietze'sdisease)
Trauma (soft tissue, rib)
Peripheral
Pulmonary
Infarction
Pneumonia
Pneumothorax
Lung cancer
Mesothelioma
Non-pulmonaryHerpes zoster
Trauma (ribs/muscular)
CAUSES OF CHEST PAIN
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Site &
radiation of
ischemic
chest pain
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SPECIFIC FEATURES OF CHEST PAIN
Angina
Retrosternal dull ache or discomfort
Ill localized
Crushing, heaviness, like a tight band
Worse with physical or emotionalexertion, cold weather and after eating
Relieved by rest and nitrates
Not affected by respiration or movement
Sometimes associated with SOB
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MyocardialInfarction
The pain is similar to that of anginabut it is:
More severe
More persistent
Associated with nausea, vomiting &sweating
Associated with Feeling ofimpending death
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Pericarditis
Constant retrosternal
Worse on inspiration (pleuritic)
Relieved slightly by sittingforward
Not related to physical oremotional exertion
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AORTIC DISSECTION
Site
Often first felt between shoulder blades and/or behind the sternum
Onset
Usually sudden
Nature
Very severe pain, often described as 'tearing'
Relieved
By nothing, tends to persist; patients often restless with pain
Accompanied
By pallor, sweating, hypertension, asymmetric pulses, unexpectedbradycardia, early diastolic murmur, syncope, focal neurological
symptoms and signs
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Esophagealspasm
Often mistake for MI or angina
A severe retrosternal burning chest pain
Onset often after eating or drinking
May be associated with dysphagia
May have history of dyspepsia May be relieved by GTN (needs more time
than that required for angina ---20 min Vs 2-3 min.
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Esophagitis
Retresternal burningpain (heart burn)
Relieved by antacids
Onset after eating
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Pleuritic(respiratory pain)
Sharp pain, worse on inspiration &coughing
Not central, may be localized to one sideof the chest
No radiation
No relief with GTN
Associated with breathlessness, cyanosise.g. respiratory symptoms or signs.
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Musculoskeletalpain
Localized to particularspot on the chest
Worsened by movementand respiration
Tender to palpation
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BREATHLESSNESS, SHORTNESS OF
BREATH, DYSPNEA
Breathlessness (dyspnoea) is an awareness of
increased drive to breathe and is normal on exercise.
It is pathological if it occurs at a significantly lower
threshold than expected. Breathlessness is a non-specific symptom and may
be caused by cardiac, respiratory, neuromuscular
and metabolic conditions, or by toxins or anxiety.
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ORTHOPNEA
Orthopnoea is dyspnoea on lying flat and is a sign of
advanced heart failure.
Lying flat increases venous return to the heart and in patients
with a failing left ventricle may precipitate pulmonary venous
congestion and pulmonary oedema.
The severity can be graded by the number of pillows the patient
uses before feeling comfortable ('three-pillow orthopnoea').
Paroxysmal nocturnal dyspnoea is sudden
breathlessness which wakes the patient from sleepchoking or gasping for air
It has a similar mechanism to orthopnoea and is caused by the
gradual accumulation of alveolar fluid during sleep.
Patients may sit on the edge of the bed and open windows in an
attempt to relieve their distress.
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CAUSES OF DYSPNEA
Left ventricular failure
(pulmonary congestion)Pulmonary embolism
Any respiratory disease Anxiety
Dyspnea
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DESCRIPTIONS OF ARRHYTHMIAS
'Heart misses a beat'
Heart 'jumps' or 'flutters'entricular or atrial
extrasystoles
Heart 'jumping about' or 'racing' Associated breathlessness May be unnoticed
Atrial fibrillation
Heart racing or fluttering
Associated polyuriaupraventricular
tachycardia
Heart racing or fluttering
Associated breathlessness
May present as syncope rather than as palpitation
Ventricular
tachycardiaVentricular
tachycardia
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SYNCOPE
Cardiovascular disorders produce dizziness and syncope by
transient hypotension, resulting in abrupt cerebral
hypoperfusion.
Recovery is usually rapid, unlike with other common causes of
syncope (e.g. s troke, epilepsy, overdose).
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POSTURAL HYPOTENSION
Syncope on standing upright reflects inadequate baroreceptor-
mediated vasoconstriction.
It is common in the elderly.
Abrupt reductions in blood pressure and cerebral perfusion
cause the patient to fall to the ground, whereupon thecondition corrects itself.
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VASOVAGAL SYNCOPE
This is caused by autonomic overactivity, usually provoked by
emotional or painful stimuli, less commonly by coughing or
micturition.
Only rarely are syncopal attacks so f requent as to be
significantly disabling ('malignant' vasovagal syndrome).
Vasodilatation and inappropriate slowing of the pulse combine
to reduce blood pressure and cerebral perfusion.
Recovery is rapid if the patient lies down.
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CAROTID SINUS SYNCOPE
Exaggerated vagal discharge following external stimulation of
the carotid sinus (e.g. from shaving, or a tight shi rt collar)
causes reflex vasodilatation and slowing of the pulse.
These may combine to reduce blood pressure and cerebral
perfusion in some elderly patients, caus ing loss ofconsciousness.
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VALVULAR OBSTRUCTION
Fixed valvular obstruction in aortic stenosis
may prevent a normal rise in cardiac output
during exertion, such that the physiological
vasodilatation that occurs in exercisingmuscle produces an abrupt reduction in blood
pressure and cerebral perfusion, resulting in
syncope.
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ISCHEMIC HEARTDISEASES
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Atherosclerosis is a progressive inflammatory disorder of the
arterial wall that is characterized by focal lipid-rich deposits
of atheroma that remain clinically silent until they become
large enough to impair tissue perfusion, or until ulceration
and disruption of the lesion result in thrombotic occlusion or
distal embolization of the vessel.
These mechanisms are common to the entire vascular tree,
and the clinical manifestations of atherosclerosis depend
upon the site of the lesion and the vulnerability of the organ
supplied.
PATHOPHYSIOLOGY
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Atherosclerosis can affect anyartery in the body
In the heart
Angina
MI
suddendeath
In the brain
stroke
transientischaemicattack
In the limbs
claudication
critical limbischaemia
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Age and sex
Premenopausal women have lower rates of disease than men, although this sexdifference disappears after the menopause.
Family history
A 'positive' family history is present when clinical problems in first-degree relativesoccur at relatively young age, such as < 50 years for men and < 55 years forwomen.
Smoking
There is a strong consistent and dose-linked relationship between cigarette
smoking and ischaemic heart disease, especially in younger (< 70 years)individuals.
Hypertension
The incidence of atherosclerosis increases as BP rises, and this excess risk isrelated to both systolic and diastolic BP as well as pulse pressure. Antihypertensive
therapy reduces cardiovascular mortality, stroke and heart failure.
RISK FACTORS
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Hypercholesterolaemia
Risk rises with increasing serum cholesterol concentrations.
Lowering serum total and LDL cholesterol concentrations reduces the risk ofcardiovascular events, including death, MI, stroke and coronary revascularisation.
Diabetes mellitus
This is a potent risk factor for all forms of atherosclerosis and is often associatedwith diffuse disease that is difficult to treat.
Haemostatic factors
Platelet activation and high levels of fibrinogen are associated with an increasedrisk of coronary thrombosis. Antiphospholipid antibodies are associated withrecurrent arterial thromboses
Physical activity
Physical inactivity roughly doubles the risk of coronary heart disease and is amajor risk factor for stroke
RISK FACTORS
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Obesity
Obesity, particularly if central or truncal, is an independent risk factor, although it isoften associated with other adverse factors such as hypertension, diabetes mellitusand physical inactivity.
AlcoholAlcohol consumption is associated with reduced rates of coronary artery disease.
Excess alcohol consumption is associated with hypertension and cerebrovasculardisease.
Other dietary factors
Diets deficient in fresh fruit, vegetables and polyunsaturated fatty acids areassociated with an increased risk of cardiovascular disease.
Personality ?????
Social deprivation
RISK FACTORS
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ISCHAEMIC HEARTDISEASE
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Stable angina
Ischaemia due to fixed atheromatous stenosis of one or morecoronary arteries
Unstable angina Ischaemia caused by dynamic obstruction of a coronary artery due
to plaque rupture or erosion with superimposed thrombosis
Myocardial infarction
Myocardial necrosis caused by acute occlusion of a coronary arterydue to plaque rupture or erosion with superimposed thrombosis
Sudden death
Ventricular arrhythmia, asystole or massive MI
CORONARY HEART DISEASE: CLINICAL
MANIFESTATIONS AND PATHOLOGY
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Angina pectoris is the symptom complex caused by transient
myocardial ischaemia
It may occur whenever there is an imbalance between
myocardial oxygen supply and demand
Coronary atheroma is by far the most common cause ofangina, although the symptom may be a manifestation of
other forms of heart disease, par ticularly aortic valve disease
and hypertrophic cardiomyopathy.
STABLE ANGINA
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Oxygen demand: cardiac work
Heart rateBP
Myocardial contractility
Left ventricular hypertrophy
Valve disease, e.g. aortic stenosis
Oxygen supply: coronaryblood flow
Duration of diastole
Coronary perfusion pressure (aorticdiastolic minus coronary sinus orright atrial diastolic pressure)
Coronary vasomotor tone
OxygenationHaemoglobin
Oxygen saturation
FACTORS INFLUENCING MYOCARDIAL
OXYGEN SUPPLY AND DEMAND
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Physical exertion
Cold exposure
Heavy meals
Intense emotion
Common
Lying flat (decubitus angina)Vivid dreams (nocturnal angina)ncommon
ACTIVITIES PRECIPITATING ANGINA
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The history is by far the most important factor in making the
diagnosis
Stable angina is characterised by central chest pain, discomfort
or breathlessness that is precipitated by exertion or other forms
of stress , and is promptly relieved by rest Physical examination is frequently unremarkable but should
include a careful search for:
evidence of valve disease (particularly aortic),
important risk factors (e.g. hypertension, diabetes mellitus),
left ventricular dysfunction (cardiomegaly, gallop rhythm),
other manifestations of arterial disease (carotid bruits, peripheral
vascular disease) and
unrelated conditions that may exacerbate angina (anaemia,
thyrotoxicosis).
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Resting ECG
The ECG may show evidence of previous MI but is often normal,even in patients with severe coronary artery disease.
Occasionally, there is T-wave flattening or inversion in some leads,
providing non-specific evidence of myocardial ischaemia ordamage.
Exercise ECG
An exercise tolerance test (ETT) is usually performed using a
standard treadmill or bicycle ergometer protocol while monitoringthe patient's ECG, BP and general condition.
Planar or down-sloping ST segment depression of 1 mm isindicative of ischaemia
Up-sloping ST depression is less specific and often occurs in normalindividuals.
INVESTIGATIONS
INVESTIGATIONS OTHER FORMS OF
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INVESTIGATIONS-OTHER FORMS OF
STRESS TESTING
Myocardial perfusion scanning.
This may be helpful in the evaluation of patients with anequivocal or uninterpretable exercise test and those who
are unable to exerciseIt entails obtaining scintiscans of the myocardium at
rest and during stress (either exercise testing orpharmacological stress, such as a controlled infusion ofdobutamine) after the administration of an intravenousradioactive isotope, such as 99technetium tetrofosmin.
Stress echocardiography
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Coronary arteriography
This provides detailed anatomicalinformation about the extent andnature of coronary artery disease, andis usually performed with a view to
coronary artery bypass graft (CABG)surgery or percutaneous coronaryintervention (PCI).
INVESTIGATION
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The management of angina pectoris involves:
a careful assessment of the likely extent and severity of ar terial
disease
the identification and control of risk factors such as smoking,
hypertension and hyperlipidaemia
the use of measures to control symptoms
the identification of high-risk patients for treatment to improve life
expectancy.
MANAGEMENT: GENERAL MEASURES
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Do not smoke
Aim for ideal body weight
Take regular exercise (exercise up to, but not beyond, the point ofchest discomfort is beneficial and may promote collateral vessels)
Avoid severe unaccustomed exertion, and vigorous exercise after aheavy meal or in very cold weather
Take sublingual nitrate before undertaking exertion that mayinduce angina
ADVICE TO PATIENTS WITH STABLE
ANGINA
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Antiplatelet therapy
Low-dose (75 mg) aspirin reduces the risk of adverseevents such as MI and should be prescribed for all
patients with coronary artery disease indefinitelyClopidogrel (75 mg daily) is an equally effective
antiplatelet agent that can be prescribed if aspirincauses troublesome dyspepsia or other side-effects.
Anti-anginal drug treatment
Four groups of drug are used to help relieve or preventthe symptoms of angina: nitrates, -blockers, calciumantagonists, and potassium channel activators
DRUG THERAPY
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Nitrates
These drugs act directly on vascular smooth muscle to produce venous and arteriolardilatation.
Their beneficial effects are due to a reduction in myocardial oxygen demand (lower preloadand afterload) and an increase in myocardial oxygen supply (coronary vasodilatation).
Beta-blockers
These lower myocardial oxygen demand by reducing heart rate, BP and myocardialcontractility,
but they may provoke bronchospasm in patients with asthma.
Calcium channel antagonists
These drugs inhibit the slow inward current caused by the entry of extracellular calciumthrough the cell membrane of excitable cells, particularly cardiac and arteriolar smoothmuscle, and lower myocardial oxygen demand by reducing BP and myocardial contractility.
Potassium channel activators
These have arterial and venous dilating properties but do not exhibit the tolerance seen withnitrates. (Nicorandil )
ANTI-ANGINAL DRUG TREATMENT
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Percutaneous coronary intervention (PCI)
This is performed by passing a fine guidewire across a coronary stenosis underradiographic control and using it to position a balloon which is then inflated todilate the stenosis
A coronary stent is a piece of coated metallic 'scaffolding' that can be deployed on
a balloon and used to maximise and maintain dilatation of a stenosed vessel. It is mainly used in single or two-vessel disease.
Stenoses in bypass grafts can be dilated, as well as those in the native coronaryarteries.
Coronary artery bypass grafting (CABG)
The internal mammary arteries, radial arteries or reversed segments of thepatient's own saphenous vein can be used to bypass coronary artery stenoses
This usually involves major surgery under cardiopulmonary bypass, but in somecases, grafts can be applied to the beating heart: 'off-pump' surgery.
CABG improves survival in symptomatic patients with left main stem stenosis orthree-vessel coronary disease (i.e. involving LAD, CX and right coronary arteries) or
two-vessel disease involving the proximal LAD coronary artery.
INVASIVE TREATMENT
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Acute coronary syndrome is a term that encompasses both
unstable angina and MI
Unstable angina is characterised by new-onset or rapidly
worsening angina (crescendo angina), ang ina on minimal
exertion or angina at res t in the absence of myocardial
damage
In contrast, MI occurs when symptoms occur at rest and there
is evidence of myocardial necrosis, as demonstrated by an
elevation in cardiac troponin or creatine kinase-MB isoenzyme
ACUTE CORONARY SYNDROME
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Unstable angina refers to:
New onset angina
Rapidly worsening angina (crescendo angina)
Angina on minimal exertion
Angina at rest It may present de novo or against a background of chronic
stable angina
UNSTABLE ANGINA
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High risk Low risk
Clinical Post-infarct angina
Recurrent pain at rest
Heart failure
No history of MI
Rapid resolution of
symptoms
ECG Arrhythmia
ST depression
Transient ST elevation
Persistent deep T-wave
inversion
Minor or no ECG changes
Biochemistry Troponin T > 0.1 g/l Troponin T < 0.1 g/l
UNSTABLE ANGINA: RISK STRATIFICATION
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ECG
May show ST/T wave changes including ST depression, transient ST
elevation and T wave inversion
Serial measurements of biochemical markers of myocardial
damage e,g, troponin
INVESTIGATIONS
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The initial treatment should include:
bed rest
antiplatelet therapy (aspirin 300 mg followed by 75-325 mg daily
long-term and clopidogrel 300 mg followed by 75 mg daily for 12months,
anticoagulant therapy (e.g. unfractionated or fractionated heparin)
-blocker (e.g. atenolol 50-100 mg dai ly or metoprolol 50-100 mg 12-
hourly).
calcium antagonist(Nifedipine with B Blockers, or diltiazem if alone)
If pain persists or recurs, infusions of intravenous nitrates or
buccal nitrates may help, but such patients should also be
considered for early revascularisation
Coronary angiography should be cons idered with a view to
revascularisation in all patients at moderate or high risk,
including those who fai l to settle on medical therapy, those
with extensive ECG changes, those with an elevated plasma
troponin and those with severe pre -existing stable angina.
TREATMENT
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The term 'myocardial infarction' should be used when there is
evidence of myocardial necrosis in a clinical setting consis tent
with myocardial ischaemia, in which case any one of the following
meets the diagnosis for MI:
Detection of rise and/or fal l of cardiac biomarkers (preferably
troponin), with at least one value above the 99th percentile of theupper reference limit, together with at least one of the following:
Symptoms of ischaemia
ECG changes indicative of new ischaemia (new ST-T changes or new lef t
bundle branch block)
Development of pathological Q waves
Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
Sudden unexpected cardiac death, involving cardiac arrest, often
with symptoms suggestive of myocardial ischaemia
Pathological findings of an acute MI
UNIVERSAL DEFINITION OF MYOCARDIAL
INFARCTION
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MI
STEMI
NSTEMISTEMI = ST Elevation MI
NSTEMI= Non ST Elevation MI
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Symptoms
Prolonged cardiac pain:
chest, throat, arms,
epigastrium or back
Anxiety and fear of
impending death
Nausea and vomiting
Breathlessness
Collapse/syncope
Physical signs
Signs of sympathetic activation:pallor, sweating, tachycardia
Signs of vagal activation:vomiting, bradycardia
Signs of impaired myocardial
function Hypotension, oliguria, cold
peripheries
Narrow pulse pressure
Raised JVP
Third heart sound
Quiet f irst heart sound
Diffuse apical impulse
Lung crepitations
Signs of t issue damage: fever
Signs of complications: e.g.mitral regurgitation, pericardit is
CLINICAL FEATURES OF ACUTE
CORONARY SYNDROMES
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ECG
The earliest ECG change is usually ST elevation; later on there isdiminution in the size of the R wave, and in transmural (fullthickness) infarction a Q wave begins to develop.
One explanation for the Q wave is that the myocardial infarctacts as an 'electrical window', transmitting the changes ofpotential from within the ventricular cavity and allowing the ECGto 'see' the reciprocal R wave from the other walls of theventricle
In contrast to transmural lesions, partial thickness orsubendocardial infarction causes ST/T wave changes without Qwaves or prominent ST elevation; this is often accompanied bysome loss of the R waves in the leads facing the infarct and isalso known as non-Q wave or non-ST elevation myocardialinfarction
INVESTIGATION
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STEMI
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Plasma biochemical markers
MI causes a detectable rise in the plasma concentration of enzymes andproteins that are normally concentrated within cardiac cells
The biochemical markers that are most widely used in the detection of MI are
creatine kinase (CK), a more sensitive and cardiospecific isoform of thisenzyme (CK-MB), and the cardiospecific proteins, troponins T and I.
The troponins are also released, to a minor degree, in unstable angina withminimal myocardial damage
CK starts to rise at 4-6 hours, peaks at about 12 hours and falls to normalwithin 48-72 hours
CK is also present in skeletal muscle, and a modest rise in CK (but not CK-MB)may sometimes be due to an intramuscular injection, vigorous physical exerciseor, in old people particularly, a fall. Defibrillation causes significant release ofCK but not CK-MB or troponins
The most sensitive markers of myocardial cell damage are the cardiactroponins T and I, which are released within 4-6 hours and remain elevated forup to 2 weeks.
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Other blood tests
A leucocytosis is usual, reaching a peak on the first day.
The erythrocyte sedimentation rate (ESR) becomes raised and may remain sofor several days.
C-reactive protein (CRP) is also elevated in acute MI.Chest X-ray
This may demonstrate pulmonary oedema that is not evident on clinicalexamination
The heart size is often normal but there may be cardiomegaly due to pre-existing myocardial damage.
Echocardiography
This can be performed at the bedside and is a very useful technique forassessing left and right ventricular function and for detecting importantcomplications such as mural thrombus, cardiac rupture, ventricular septaldefect, mitral regurgitation and pericardial effusion.
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COMMON ARRHY THMIAS IN ACUTE MYOCARDIAL INFARCTION
Ventricular fibrillation
Ventricular tachycardia
Accelerated idioventricular rhythm
Ventricular ectopics
Atrial fibrillation
Atrial tachycardia
Sinus bradycardia (particularly after inferior MI)
Heart block
Ischemia
Acute circulatory failure
Pericarditis
COMPLICATIONS OF INFARCTION
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EARLY MANAGEMENT OF ACUTE
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Immediate measures
High-flow oxygen
I.v. access
ECG monitoring
12-lead ECGI.v. analgesia (opiates) and antiemetic
Aspirin 300 mg
Reperfusion
Primary PCI or thrombolysis (streptokinase, alteplase)
Detect and manage acute complications
Arrhythmias
Ischaemia
Heart failur
EARLY MANAGEMENT OF ACUTE
MYOCARDIAL INFARCTION
LATE MANAGEMENT OF MYOCARDIAL
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Lifestyle modification
Stop smoking
Regular exercise
Diet (weight control, lipid-lowering)
Secondary prevention drug therapy
Antiplatelet therapy (aspirin and/or clopidogrel)
-blocker
ACE inhibitor
Statin
Additional therapy for control of diabetes and hypertension
LATE MANAGEMENT OF MYOCARDIAL
INFARCTION