General medicine for dentistry students.pptx

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?



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B

BleedingIs abnormal hemostasis apossibility?

CChair position

Can the patient tolerate a

supine chair position?



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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?



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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?



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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

Date post:	02-Jun-2018
Category:	Documents
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General medicine for dentistry students.pptx

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