CORONARY ARTERY DISEASE- CAD

OR
ISCHAEMIC HEART DISEASE - IHD

Dr: KAEM SHIR ALI

CORONARY ARTERY ANATOMY
 ISCHEMIC HEART DISEASE ( IHD)

Ischemic heart disease (IHD) is a condition in

which there is an inadequate supply of blood
and oxygen to a portion of the myocardium, it
typically occurs when there is an imbalance
between myocardial oxygen supply and
demand.
 EPIDEMIOLOGY

 Ischemic heart disease (IHD) : Most

common cause of cardiovascular morbidity
and mortality.
 Atherosclerosis and thrombosis are the
most important pathogenetic mechanisms.
 Peak incidence of symptomatic IHD is age
50 – 60 ( men ) and 60 – 70 (women ).
M>F
 ETIOLOGY

1. Decreased coronary blood flow due to obstruction such as:

• Atheroma.
• Spasm of coronary artery.
• Thrombosis.
• Embolism.
• Coronary arteritis
2. Increased myocardial oxygen requirement:
• Increased cardiac output: thyrotoxicosis.
• Myocardial hypertrophy: hypertension, aortic stenosis.
3. Decreased flow of oxygenated blood:
• Anemia.
RISK FACTORS
 ISCHEMIC HEART DISEASE ( IHD)

Ischemic Heart Disease ( IHD)

1- Angina 2 – Acute coronary syndrome (ACS)
whenever there is imbalance between myocardial
oxygen supply and demand the most common cause.
Is atherosclerosis however angina may also develop
in aortic stenosis and hypertrophic cardiomyopathy
even there is no coronary atheroma.
 ANGINA PECTORIS
 Is a clinical syndrome (rather than a disease).
 Characterized by paroxysmal chest pain due to
transient myocardial ischemia.
 Occur whenever there is imbalance between
myocardial oxygen supply and demand.
 The most common cause. Is atherosclerosis.
 However angina may also develop in aortic
stenosis and hypertrophic cardiomyopathy even
there is no coronary atheroma.
 ANGINA SYMPTOMS INCLUDE

 Chest pain or discomfort : It is a central usually

felt as: Pressure, Heaviness, Tightening, crushing
chest pain ,Squeezing.
Fatigue
 Anxiety
Sweating
Dizziness
 Nausea
Shortness of breath.
 SIGNS

 There are usually no physical signs. But

evidence of contributory or concomitant
diseases may be found.
 Occasionally there is fourth heart sound.
 Patients should be examined for anaemia,
obesity, diabetes, thyroid and peripheral
vascular disease.
 STABLE ANGINA
• Atherosclerotic coronary artery disease.
• Occurs when the heart has to work harder than
normal, during exercise.
• Typical : retrosternal chest pain, tightness or
discomfort, pain may be in the epigastric or
interscapularly.
• radiating to left (± right ) shoulder ̸ arm ̸ neck ̸ jaw .
• Drief duration , lasting < 10 – 15 min.
• Associated with diaphoresis , nausea , anxiety,
dyspnoea and faintness.
• Typically relieved by rest and nitrates.
 STABLE ANGINA PECTORIS

• Presentation: Typically: a man >50yrs or

lady >60yrs , with a crescendo-
decrescendo chest discomfort, lasting 2-5
min, radiating to Lt shoulder, arm neck ,
• Precipitating factors : exertion, emotion,
meal, cold exposure
• Relieving factors: rest, nitroglycerin S/L
CAUSES OF ANGINA PECTORIS
IHD probably has multiple causes.
 Coronary atheroma is the commonest cause.
Other causes and factors:
 Factors which increase myocardial oxygen
requirement and which add to the ventricular
preload such as exercise, anaemia,
hyperthyroidism.
 Those which increase after-load such as
hypertension, aortic stenosis or HOCM.
OTHER CAUSES AND FACTORS CONTN
 Increased tension of the ventricular wall as occurs
in dilatation or hypertrophy may reduce coronary
artery flow.
 Tachycardia increases cardiac work and often
brings pain.
 Strong correlation have been shown between
angina and cigarette smoking.
 Other contributing factors may be lack of exercise,
alcohol, environment (eg. climate, soft water) and
psychological factors.
 CLASSIFICATION
The Canadian classification of Angina is commonly employed to
stratify patients in term of severity. Anginal symptoms are
precipitated by
• Class I: Strenuous activity

• Class II : Moderate activity, such as walking more than one flight of

stairs
• Class III : Mild activity, such as walking less than one flight of stairs

• Class IV : Any activity, Symptoms may also occur at rest.

 The severity of angina is not directly proportional to the degree of

angiographic stenosis of diseased coronary arteries.

 More severe angina does correlate with an increased short- term risk

of death or nonfatal MI.

 ELECTROCARDIOGRAPHY
 A normal rest Electrocardiogram (ECG) does not
exclude the presence of coronary artery disease(CAD).
 The following ECG abnormalities increase the likelihood

of a cardiac etiology in patient with stable angina.

 Pathologic Q waves ( > 0.4 mV and greater than 25% of
the corresponding R wave) consistent with a prior MI.
 Resting ST is normal–and exercise ECG 1 mm ST
segment depression is suggestive of MI.
 T – wave flat or inversion

 LV hypertrophy (LVH)
INVESTIGATIONS
 FBC and ESR excludes atheromatous causes (eg
anaemia, polycythemia, giant cell arteritis).
INVESTIGATIONS CONTN
 Scanning. Myocardial perfusion scanning using
radioactive thallium may be helpful in conjunction with
exercise testing.
 Echocardiography or radionuclide bloodpool scanning
provide information about ventricular function, which
may be relevant in making a decision about coronary
arteriography.
 Coronary arteriography provides detailed information
about extent and site of coronary artery stenosis.
DIFFERENTIAL DIAGNOSES

 Pericarditis.
 Myocarditis.
 Aortic dissection.
 Massive pulmonary embolism.
 Pleurisy.
 Oesophagitis + spasms.
 MANAGEMENT

 Control of symptoms starts with explanation on how they

are caused and advise. Angina remits spontaneously in
1/3 of the patients.
 Optimise weight and fitness.
 Avoid risk factors: hypercholesterolaemia,(Targets: T chol
<5.17mmol/l , LDL < 2.58mmol/l , HDL> 1.03mmol/l)
 smoking and high BP are the three principle. Obesity,
alcohol and contraceptive pills are the other risks.
 Other factors: but not avoidable:- age, male sex, family
history, personality (type-A), Diabetes mellitus, socio-
economic class, environment.
.
MANAGEMENT CONTINUED
Drugs
 Glyceryl trinitrate (GTN) Start with 0.5mg glyceryl
trinitrate SL or spray (0.4mg intra oral puff) PRN up
to ½ h. the best use of GTN is prophylactically
before exercise known as liable to produce pain.
GTN can be given percutaneously as a paste or
plasters or as a slow-releasebuccal tablet. GTN is
virtually ineffective when swallowed, but other
nitrates such as isorbide dinitrate can be given by
mouth.
Nitrates- systemic venodilators, dilate coronary
vessels, also increase collateral flow. SL
nitroglycerin 0.4 – 0.6mg to relieve angina. If no
relieve repeat 2nd or 3rd dose at 5min intervals. Long
acting nitrates also have a role
MANAGEMENT CONTINUED
 Isosorbide dinitrate 5-40mg/6h orally (slow
release: 20-60mg/24h PO, more frequent doses
easily cause tolerance). Other forms-adhesive
nitrate skin patches and buccal absorption.
 -blokers: they are important and effective way of
preventing angina. It helps to reduce myocardial
oxygen demand esp. during exercise, largely by
reducing the heart rate for a given level of exercise
and reducing the heart rate response to anxiety,
(Remember CI asthma, LVF, and bradycadia).
MANAGEMENT CONTINUED
 Calcium channel blockers/antagonists: these
restrict slow channel Ca2+ entry in cells so
reducing Ca2+ release from sarcoplasmic
reticulum with 3 good effects:
1. Reduced myocardial oxygen consumption;
2. Dilatation of coronary arteries;
3. Peripheral vasodilatation.
4. Decrease myocardial contractility and decrease
BP.
MANAGEMENT CONTINUED

Examples;
 Nifedipine- 10-20mg/8h, Nifedipine slow
release 20mg/12h. Remember the side
effects including: flushes, headache, ankle
swelling not responding to diuretics, gum
hyperplasia, reflex tachycardia may be a
problem where -blokers cannot be used.
Use diltiazem here eg 60mg/8h orally max
160mg/8h less if elderly.
SURGERY
 Two principle indications.
1. Coronary artery bypass grafting (CABG) is indicated
if drugs fail to control angina or are not tolerated.
2. Surgery for symptoms; mortality is only reduced in
left main stem and possibly triple vessel disease.
(stenosis in all the three CAs)
 Mortality is <2% but operator variable. 70% get total
relief and 20% improvement of symptoms but pain
returns to 50% in 5 years.
 Asprin 75-300mg/24h orally reduce risk of graft
closure. An alternative is percutaneous transluminal
angioplasty.
PROGNOSIS
 0.5-4%/year end with sudden death, MI and LVF
depending on number of affected vessels. It is
doubled if there is left ventricular dysfunction.
 Overall more than 50% of the patients with angina
will live for 5 years and 33% for 10 years from the
time of diagnosis.
 Spontaneous recovery, which may prove
temporary, may occur in as many as 33%, a fact
which is useful to remember when talking to
patients about the disease.
 Prognosis is worse in patients who have had
multiple cardiac infarcts or who have cardiac
failure.
CORONARY ARTERIOGRAPHY
 Indications:
 Chronic stable angina with severe symptoms due
for revascularization
 Diagnostic difficulties to r/o IHD

 Pt with possible or known angina who have

survived a cardiac arrest
 Pt judged to be at high risk of coronary events

 Others
PRINZMENTAL (VARIANT) ANGINA
 This is angina occurring at rest due to coronary artery
spasm unrelated to exercise.
Focal spasm of epicardial coronary artery?
hypercontractility of vascular smooth muscles due to
vasoconstrictor mitogens, leucotrienes or serotonin, or
manifestations of vasospastic disorder in relation to
migraine etc
 typically occurs between midnight and 8 AM ,
awakening patients from sleep and the pain is usually
more severe and more prolonged than classical angina.
 It tend to involve right coronary artery.
 ECG shows ST segment elevation.
PRESENTATION
 Thecoronary arteries can spasm as result of:
 Exposure to cold

 Emotional stress
 Medicines that tighten or narrow blood vessels

 Smoking

 cocaine use

Younger age most common in female.

Normal cardiac examination in absence of
ischemia.
 ECG-transient ST segment elevation with rest
pain
PRESENTATION
 Exercise testing is of limited value.
 Coronary angiography-transient coronary
vasospasm
 Ergonovine ,acetylcholine,other
vasoconstrictor medications and
hyperventilation have been used to provoke
and demonstrate focal coronary stenosis.
TREATMENT
Nitrates and CCB main Treatment
 CCB-effective in preventing coronary spasm,
give maximum tolerated doses.
 SL NG-abolishes angina promptly
 Prazocin – of value in some patients.
 ASA may worsen ischemic episodes in some
patients.
 Good prognosis, 5yr LTS 90-95%
SYNDROME X
 Coronary micro-vascular disease that effects
the heart’s smallest Coronary arteries.
 Typical symptoms of angina but normal
angiogram.
 May show definite signs of ischemia with
exercise testing .
DECUBITUS ANGINA

This is angina that occurs when the patient lies

down. It usually occurs in association with
impaired left ventricular functions. Patient with this
symptoms usually has severe coronary artery
disease.
Risk factor inquiry, inquiry of disease in other
arteries.
NOCTURNAL ANGINA

This is the angina awakes the patient from sleep. It

may be provoked by vivid dreams. It may occur
due to critical coronary artery obstruction or
coronary spasm.
ASYMPTOMATIC [SILENT] ISCHEMIA

Asymptomatic but exhibit ST segment

changes during activity on ambulatory ECG
monitoring.
Some of these pts have high pain thresholds,
high level of endorphins, or may be diabetics
with autonomic neuropathy
Have positive exercise tests
 End of Sessions ???
ACUTE CORONARY SYNDROME(ACS)

ACS divided into ST – segment elevation ACS or

ST – segment elevation MI (STEMI) and non - ST
– segment elevation ACS which includes both
non - ST – segment elevation MI (NSTEMI) and
unstable angina (UA).
PATHOPHYSIOLOGY
 UA/ NSTEMI

UNSTABLE ANGINA & NON ST

SEGMENT ELEVATION
MYOCARDIAL INFARCTION
 DEFINITIONS
 UA- angina pectoris or equivalent with at
least 1 of the following:
i. Occurs at rest or with minimal exertion,
lasting >10min
ii. Severe and of new onset i.e. within 4-6wks
iii. Occurs with a crescendo i.e. more severe,
prolonged or frequent
 NSTEMI- features of UA +elevated cardiac
biomarkers
PRESENTATION
 Typical chest pain severe enough to be
considered painful.
 ON Exam: like in pts with stable angina but may
be unremarkable, if large area of ischemia-
diaphoresis, pale cool skin, tachycardia, 3 rd or 4th
HS, basilar rales.
INVESTIGATIONS
 ECG- ST segment depression, flattening and/ or
T wave inversion in 30-50%
 Cardiac biomarkers: CK-MB and troponins
elevated in NSTEMI.
ANTITHROMBOTIC THERAPY
 Aspirin preferred in pts with suspected ACS
 Clopidogrel been shown to reduce risk of MI
compared with aspirin alone though with incr in
bleeding risk
 Combination of ASA + clopidogrel
 GP2b/3a in pts due for PCI
 UFH or LMWH in addition to above. LMWH
enoxaparin is superior to UFH
ANTI- ISCHEMIC THERAPY
 To promote relief & prevent recurrence of
symptoms
 Nitrates – SL or buccal spray. If no improvement
iv nitroglycerin titrated to relieve symptoms or
until systolic BP < 100mmHg. Topical or oral
nitrates can be used once sx have resolved
 Beta blockers- initially iv followed by oral

 CCB- non- dihydropyridines (Diltiazem )

TREATMENT OF UNSTABLE ANGINA
 Isosorbide dinitrate 2-10mg/h IVI .
 Morphine 1-5mg IV every 5-30 min if
symptoms persist despite IV nitroglycerin + -
blockers
 EI + Statins for long term primary prevention
 Monitor pulse and BP. Approximately 15%
die in 1 year if untreated, so prompt
angioplasty should be considered. If pain is
uncontrolled, emergency angiography and
bypass grafting or angioplasty is needed.
ELECTROCARDIOGRAPHY NSTEMI

 ST segment depression ≥ 0.5mm in two contiguous

leads.
 T – wave inversion ≥ 1 mm in two contiguous
leads with prominent R wave or R/S ratio > 1.
 Symmetric T – wave inversion of > 2 mm across
the precordium are fairly specific for myocardial
ischemia .
 Nonspecific ST segment changes or T – wave
inversions.
MYOCARDIAL INFARCTION (MI)

Definition
 MI is a term to describe irreversible cellular
injury and necrosis of heart muscle occurring
as a result of a critical imbalance between
coronary blood supply and myocardial
demand.
 The necrosis may be confined to the sub-
endocardial region or may affect the full thickness
of the myorcardium (intramural infarction).
DEFINITION OF STEMI
 STEMI diagnosed on basis of:
 ST elevation ≥ 1mm,present in two or more
contiguous limbs leads. Or
 2 mm in two contiguous precordial leads for men
or 1.5 mm in two precordial leads for women.
 The presence of a new LBBB in the setting of
acute symptoms suggests occlusion of the
proximal left anterior descending(LAD).
CAUSES/RISK FACTOR OF MI
 Hyperlipidaemia, defined as serum cholesterol
and or triglyceride levels above the ninety-fifth
percentile for the control population.
 Systemic hypertension. 
 Smoking. 
 Diabetes mellitus especially with plasma lipid
abnormality.  
 Lack of physical activity. 
 Emotional stress.
SYMPTOMS OF MI (HISTORY)
 Pain: The cardinal symptom is pain, usually of
greater severity and duration (>30mins) than in
angina, but similar in nature.
 The pain is most often described as a tightness,
heaviness or constriction in the chest. At its’
worst the pain is one of the most severe which
can be experienced and the patient’s expression
and pallor may vividly convey the seriousness of
the situation.
 Painless (‘silent’) infarcts are quite common
especially in the elderly and DM.
SYMPTOMS OF MI CONTINUED
Breathlessness, syncope, nausea, vomiting,
sweating, and extreme tiredness are common.
 Breathlessness may be the only symptom in some
patients.
 Syncope may occur and the blood pressure falls
particularly if the patient is upright or from the
development of a serious arrhythmia or heart blockade.
 Nausea and vomiting are particularly common in the
more severe cases. It may also result from drugs given
for pan relief like morphine.
SIGNS (PHYSICAL EXAMINATION)
 Patients with small MIs particularly sub-
endocardial may not have any detectable
abnormality on physical examination.
 Anxious and restless.
 Distress with obvious discomfort, cold,
clammy, tachycardia. BP may be up or
down. May be cyanosed and have mild
pyrexia (<38.50C).
SIGNS (PHYSICAL EXAMINATION)
 Normal BP+ PR within 1st hr but can have
.Sympathetic over activity : tachycardia
,hypertension.
.Parasympathetic over activity: bradycardia
and hypotension
 Also features of complications eg LVF,
dyspnoea, crepitations, confusion and oliguria.
 Auscultation findings vary with the extent of
damage and the underlying heart pathology.
PRESENTATION
 Other symptoms of ventricular dysfunction
3rd /4th HS
Decreased intensity of 1st HS
Paradoxical splitting of 2nd HS
 Systemic murmur if mitral valve dysfunction or
VSD develops
 Pericardial friction rub present/absent.
 Temperature elevation
COMPLICATIONS OF MI
 Acute circulatory failure (cardiogenic shock) as
a consequence of LVF, papillary muscle
disfunction, rupture of portion of the ventricular
septum.
 Arrhythmias and heart block; more than 90% of
patients develop ventricular premature beats in the
first 72 hours after MI. Various types of heart
blocks (2nd degree, complete HB may follow,
LBBB, RBBB and Bilateral BBB).
COMPLICATIONS OF MI
 Acute ventricular septal defect (VSD)
 Pericarditis as a consequence of the infarct. Pain
is worse or only appears on inspiration with a
pericardial rub.
 Pulmonary embolism.
  Lower extremity venous thrombosis (DVT).
  Systemic arterial embolization.
  Ventricular aneurysm occurs late and presents as
intractable LVF, arrhythmias or embolization.
  Rupture of the heart.
COMPLICATIONS OF MI
 Dresseler’s syndrome (post-MI syndrome);
develops 2-10 weeks after an MI or surgery. It is
thought that myocardial necrosis stimulates the
formation of autoantibodies against heart muscle.
Features fever, chest pain, pleural and pericardial
rub + effusion from serositis, cardiac tamponade
may complicate the picture therefore avoid
anticoagulants. Treatment use steroids and anti-
inflammatory agents.
COMPLICATIONS OF MI
 Shoulder-hand syndrome; extremely rare but
consists of the development of pain and stiffness
in the left shoulder or hand and vasomotor
changes sometimes associated with muscle
atrophy.
TESTS IN MI
ECG:
 ST elevation, T inversion and Q-waves are in the
leads adjacent to the infarction.
 Leads opposite the infarct may show reciprocal
ST depression (eg. V1-4 in inferior MI, II, III and
AVF in anterolateral MI).
 The absence of Q-waves in a proven infarct is
associated with higher risk of subsequent MI.
ANATOMIC DISTRIBUTION BASED ON ECG LEADS

Leads Myocardium coronary artery

I , aVL High lateral wall Diagonal or proximal
LCX
V5 to V6 Lateral wall LCX
V1 to V2 Septal Proximal LAD
V2 to V4 Anterior wall LAD
II,III, aVF Inferior RCA or LCX
CREATINE KINASE
 Creatine kinase (CK/CPK) is an enzyme expressed
in a number of tissues.
 Function: it catalyses the conversion of creatine to
phosphocreatine degrading ATP to ADP (In cardiac
as well as other tissues, phosphocreatine serves as
an energy reservoir for the rapid regeneration of
ATP)
 The CK enzyme consists of two subunits, B (brain
type) or M (muscle type), Making three different
isoenzymes: CK-MM, CK-BB and CK-MB
 CK-BB occurs mainly in tissues, rarely of any
significance in the bloodstream
TESTS IN MI

Cardiac enzymes:
 CK:- Creatine Kinase; starts to rise at 4-6
hours, peaks about 12 hours and falls to normal in
48-72 hours. ( CK is also present in skeletal
muscles, and a rise in Ck may be due to IM
injection or vigorous physical exercise . 
 CK-MB:- Myocardiac isoenzyme-CK; is
more specific for myocardial injury.
TESTS IN MI
 Cardiac specific troponins-; troponin T and troponin
I are regulatory proteins with a very high specificity
for cardiac injury and more specific and sensitive
than CK-MB. Reaches peak in 2-4 hours after MI
and persists up to 7 days.

Serial estimations are necessary in doubtful cases, for it is the

change in enzyme levels which is of diagnostic value.
TESTS IN MI
 AST:- Aspartate Transaminase; starts to rise
about 12 hours, and reaches a peak on the first or
second day. 
 LDH:- Lactate Dehydrogenase; is liberated from
haemolysed RBCs and is therefore less specific.
It starts to rise after 12 hours, reaches a peak after
2 or 3 days and may be elevated for a week. LDH
estimation is useful when the diagnosis is
uncertain several days after a possible infarct.
TESTS IN MI

Other blood tests:

 Urea and Electrolytes
 Full blood count
 ESR can rise to 80mm/h and take some
weeks to return to normal. Similarly glucose
can be upset and lipids may be raised from
the first 24h post-Mi for up to 3 weeks.
TESTS IN MI
CXR:
 This is mainly to exclude aortic dissection, look for
signs of failure including pulmonary oedema, watch
for changes in cardiac size enlargement may
indicate previous myocardial damage or pericardial
effusion.
Radionuclide scanning:
 A pyrophosphate scan may show the site of
myocardial necrosis. A radionuclide ventriculogram
indicates the extent of impairment of ventricular
function and may give useful prognostic
information.
DIAGNOSIS

Diagnosis: Is made on the basis of 2 or 3 out of the;

history, ECG changes and enzyme changes being
suggestive of an MI.
 MANAGEMENT OF MI

Immediate management:
 Greatest risk of death is in the first hour; the
main immediate need is relief of pain and
prevention or treatment of arrhythmias and
complications.
 Correcting arrhythmias and giving
thrombolysis at home can lead to a 50%
reduction in mortality.
 IMMEDIATE MANAGEMENT CONTINUED
 In the first 3-4 hours when the risk of fatal
arrhythmias is highest, it is best for patients to be
cared for where there is immediate access to
resuscitation facilities usually in coronary care
unit (CCU).
 Patients seen and diagnosed after the first few
hours may be cared for at home if they are free of
cardiac failure and other complications.
 MANAGEMENT CONTINUED

Pain relief
 The patient is usually terrified and anxious;
assure him/her that recovery is the most likely
outcome and that the most dangerous phase of the
illness is already over and find time to talk to the
relatives.
 Oxygen therapy (35% oxygen) unless the patient
has COAD.
 Site an IV cannula for emergencies.
 PAIN RELIEF CONTINUED
 Morphine 5-10mg aliquots titrated against the
patient’s response.
 Diamorphine 2.5-10mg (at 1mg/minute) is
slightly more potent on a weight for weight basis,
and produces analgesia slightly more rapidly but
has no other advantages to compensate for its
expense.
 Either drug may be given subcutaneously or
intramuscularly. The amount of analgesia needed
tends to parallel the extent of myocardial damage
 PAIN RELIEF CONTINUED
 Glyceryl trinitrate (GTN) Start with 0.5mg
glyceryl trinitrate SL or spray (0.4mg intra
oral puff) for coronary artery vasodilatation.
 
 Prompt treatment with fibrinolytic and
antiplatelet drug reduces mortality by over
40% (heparin 5000units IV start, then
1000U/hour IVI for 24hours).
 PAIN RELIEF CONTINUED

Streptokinase (SK)
 If present in less than 12 hours after the onset of
pain, give streptokinase (SK) 1.5 million units in
100ml 0.9 saline IVI over 1 hour + asprin
150mg/day PO for >1month.

SK side effects:
 Hypotension.
 Anaphylaxis.
 PAIN RELIEF CONTINUED
CI of SK:
 Stroke or active bleeding in past 2 months.
 BP >200mmHg
 Surgery or trauma in past 10 days.
 Bleeding disorders.
 Pregnancy.
 Menstrual period.
 Proliferative DM retinopathy.
 Previous SK treatment in the past 5 days to 1 year).
PAIN RELIEF MANAGEMENT OF MI CONTINUED

Heparin 5000U/8h SC until mobilized, as

prophylaxsis against DVT.
If pain continue to give Isosorbide dinitrate
infusion 2-10/h IVI. If maximum tolerated
dose is inadequate, give diamorphine 5-
10mg IV as often needed. If pain still not
controlled, refer for angiography with a
view to surgery.
MANAGEMENT OF MI CONTINUED

Supplementation with an antiemetic like a

phenothiazine (prochlorperazine 12.5mg IM up to
6hourly or antihistamine (eg. cyclizine 50mg IV)
should be given. Metoclopramide activity closely
resembles that of phenothiazides.
MANAGEMENT OF MI CONTINUED

Arrhythmias;
Pain relief, rest reassurance and the correction of
hypokalaemia all play a major role in preventing
arrhythmias. Lignocaine is given after
resuscitation from AF or to treat ventricular
tachycardia with a rapid rate. It is also given if
multiple ectopics .
If lignocaine is ineffective, mexiletine may also be
used instead. Sometimes IV beta-blocker (eg.
atenolol 5-10mg ) may be helpful.
MANAGEMENT OF ARRHYTHMIAS CONTINUED

 Ventricular fibrillation should be treated

with an immediate d.c. shock sometimes use
a defibrillator.
 Atrial tachycardia, flutter or fibrillation are
best treated with digoxin.
 If the arrhythmia causes severe hypotension,
synchronised d.c. shock treatment should be
considered.
 MANAGEMENT OF MI CONTINUED

 Discontinue pre-infarction cardiac drugs.

 Prohibit smoking.
 Continue monitoring ECG, CXR, cardiac
enzymes and U&E for 2-3 days.
 Examine heart, lungs and legs for
complications at least daily.
SUBSEQUENT MANAGEMENT OF MI

 Ifuncomplicated, the patient may sit out of

bed on day two, walk freely on day 5 and
heparin may be discontinued, go home on
day 7-10 and return after 4-12 weeks,
depending on degree of heavy
manual/clinical labour.
SUBSEQUENT MANAGEMENT OF MI CONTINUED
The 5 favourable prognostic signs.
 No pre-existing hypertension.
 Normal heart size.
 No significant arrhythmias after day one.
 No post-Mi pulmonary oedema.
 No post-MI angina.
These patients are at very little risk and best plan is
to discharge them not taking any drugs as these
encourage doctor-dependency and will have side
effects.
THE 5 FAVOURABLE PROGNOSTIC SIGNS CONT.

 He/she should not drive for 1 month, advise slowly to

increase exercise, considering a planned fitness training
programme.
 Specifically mention to him and his partner that sexual
activity may be safely resumed. Ask for any fears of
returning to a normal life.
 Arrange for a lipid test if not done on a sample during the
first 24 hours and discourage risk factors strongly.
 All other patients are reviewed at 4-6 weeks for:
 Repeat ECG and CXR (to look for cardiac size and
aneurysm).
SUBSEQUENT MANAGEMENT OF MI CONTINUED

 If angina recurs, treat it conventionally, perform an

exercise test, and consider coronary angiography.
 Start an exercise program and a -blocker (eg. atenolol
50mg/24h PO) to improve prognosis. Give -blocker to
all patients if except low risk patients (above), CI eg
asthma, unstable DM .
 Consider asprin 75mg/24h PO. Warfarin anticoagulation
has a very limited effect on mortality, but may reduce re-
infarction risk.
 Consider ACE inhibitor if any LVF (known to reduce
mortality).
STEMI
PREVENTION OF IHD
May be primary or secondary prevention.
 Primary prevention is the term used for measures
which are applied in the absence of clinical
manifestations of disease, whereas secondary
prevention refers to measures put into practice
after the disease has become apparent, usually as
a result of development of angina or following
myocardial infarction.
 Secondary prevention already seen above in
management of the three syndromes.
PRIMARY PREVENTION IN IHD
 Cigarette Smoking. Stopping smoking reduces the
risk of subsequent infarction. The improvement is
greatest for the young patients and increases with the
length of abstention.

 Plasma cholesterol. High density lipoprotein (HDL)

containing cholesterol appears to have a protective effect
against atheroma, whereas cholesterol in the low density
and very low density (LDL and VLDL) appear to
promote atheroma and its complications if present in
excess.
PRIMARY PREVENTION IN IHD CONTINUED
 The reduction of high plasma cholesterol
concertrations (above 7 mmol/litre) reduces risk
of ischaemic heart disease.

 Dietary measures (of low cholesterol diet with

increased ratio of polyunsaturate fractions to
saturated fat) may have to be supplemented with
drugs such as cholestyramine, particularly in
those with familial hypercholesterolerolaemia.
PRIMARY PREVENTION IN IHD CONTINUED
Other dietary factors. these are both too numerous and
the evidence often too tenuous to discuss.
 The best current recommendation is for a mixed diet
with no more than a third of the total energy requirement
derived from fat. At least a third of the fat should be
polyunsaturated from fish or vegetable source rather than
animal fat.
 An adequate fruit, vegetable and fibre intake and a low
proportion of refined carbohydrate is required
PRIMARY PREVENTION IN IHD CONTINUED
 Blood pressure. Even mild degrees of hypertension are
strong correlated with an increased risk of ischaemic
heart disease. Unfortunately it has been difficult to show
that treatment of the hypertension reduces this risk,
possibly because the damage has already been done by
the time it is instituted.
 In general, primary prevention is likely to be more
effective if modest and practicable measures are aimed at
a wide section of community than if rigorous ones are
imposed on a small minority.
PRIMARY PREVENTION IN IHD CONTINUED
 Obesity. on its own is a relatively weak risk factor for
ischaemic heart disease; however its correction is often
an important step in the treatment of other risk factors.

 Exercise. Clinical ischaemic heart disease is more

prevalent in sedentary sections of the community than
those who take regular exercise. Although there is little
direct evidence that the sedentary will improve their
prognosis by physical activity, regular daily exercise to
the point of mild breathlessness is recommended, and is
unlikely to do harm.