ISCHEMIC HEART

DISEASE

department therapy №1
with course of endocrinology
proffesor Dudar L.V.
 Ishemic heart disease
/IHD/
is disease of the heart ,which occurs
when-ever there is an imbalance
between myocardial oxygen demand
and its supply.
 ETHIOLOGY:
 Atherosclerotic coronary artery disease (
98%);
 Coronary artery spasm;
 Coronary arteritis;
 Embolism;
 Systolical superexertion for the large
hypertrophy of the left ventricular for the
aortic stenosis and regurgitation, mitral
regurgitation,mitral valvule prolaps,
hypertrophic cardiomyopathy and other;
 Anemia.
 CORONARY RISK FACTORS :

Tabacco smoking, hypertension,

hyperlipidemia, diabetes, obesity,
physical inactivity, family history of
IHD, stress.
PATHOGENESIS:
CLINICAL PRESENTATION (The
main clinical form IHD )

 Sudden coronary death;

 Angina pectoris;
 Acute myocardial infarction;
 ARRHYTHMIAS’S;
 HEART INSUFFICIENCY (FAILURE).
 ACUTE MYOCARDIAL
INFACTION
 Acute myocardial infarction is myocardial
necrosis, developing due to thrombotic
occlusion ( or sometime prolonged spasm)
of coronary artery.
 ETIOLOGY and
PATHOGENESIS:
The maine cause of the acute myocardial
infarction is atherosclerosis coronary artery
(more than 90%) and pathogenesical
situatione, when “ thrombus sitdown on the
atherosclerotic plaque “ and occludes
coronary artery, stop,s coronary blood flow.
This is cause of the severe myocardial
ischemia and necrosis.
 Rarely myocardial infarction is caused by
coronary spasm, embolizatione, systolical
superexertione. Cocaine causes intens
coronary arterial spasm and users may
present with cocaineinduced angina pectoris
or myocardial infarction. Biochemical
disordes in area ischemia and necrousis is
the cause of the arrhytmias, heart failure,
card!ogenital shock and other
complicationes.
 SYMPTOMS and SIGNS:
About 75% of the patients experience
prodromal symptoms days to weeks before
the event,including unstable or crescendo
angina pectoris,shortness of
breath,fatigue.The first symptom of acute
myocardial infarctione is
deep,substernal,visceral paine described as
aching or pressure,ofne with radiatione to
the left substernal area, left arm or jaw and
stopn’t after intake nitroglycerin more then
30 minets .This is anginouss (painful)
varient of acute MI.
 In other case acute MI may starts with
cardiac asthma attak (asthmaticua
variant of acute MI),with acute paine
in the epigastrical region, vomiting and
nausea (abdominal variant),with
arrhythmias ( arrhythmical variant),
with cerebrovascular disorders
(cerebrovascular variant),with
cardiogenic collapse (collapsical
variant),also painless variant or painful
with atipical paine localization.
 ON EXAMINATION:
 The patient is usually restless, pale and sweating
and perhaps cyanosed.
 The heart may show no abnormality at the onset,
but the sounds may be distant or an abnormal
rhythm may be present. The pulse is often weak
(filamentical) and the rate more than 90. The blood
pressure characteristically falls, a systolic pressure
of 100 mm. Hg, or even 80, being recorded. On the
second or third days mild fever of 38-39 may occur.
Rarely may be auscultated systolic murmur in the
apex heart and basal rales in the lungs if there is
left ventricular failure.
 CLASSIFICATION:
Myocardial infarction (MI) may be:
 small-focal MI;
 large-focal MI;
 transmural (through-and-through) MI.
On localization:
 Subendocardial MI;
 Subepicardial MI.
 Anterior miocardial infarctione ( I,II,AVL)
(anteroseptal, anterolateral,
anteroinferior);
 Posterior miocardial infarction ( III,II,AVF)
(posterolateralis, posterobasal,
posteroseptal);
 Apical myocardial infarction ( V4);
 Lateral myocardial infarction (high lateral,
basal lateral) V5,V6;
 Diaphragmatic (inferior) myocardial
infarction ( III,AVF,V1)
 INVESTIGATIONS:
 Laboratory diagnostics:
genaral blood test is normal due 2 -3 days.
Polimorphonuclear leukocytosis may be due
3 – 5 -7 days mith maxim on 5 days and
often reaches levels of 12000 – 15000 l per
cub. ml and erythrocyte sedimentation is
accelerates on 5 days.
 Serum Enzymes:
 Myoglobin level incrise over 2 -4 hour after
infarct starts;
 Creatinine phosphokinas increase over 6-8
hours;
 LDH1 increase over 4-6 hours;
 AST increase over 8-24 hours.
 ECG changes:
The direct sings of the myocardial infarctione
are:
 Q wave is deep (profundus) and widthly;

 QS wave is the sing of the transmural

infarction;
 ST segment elevation to the apper.
ECG changes by the stage:
 Stage 1 (acute stage);
 Stage 2 (intermediate);
 Stage 3 (myocardial scarring).
 TREATMENT:
 Treatment is designed to relieve distress,
reverse ishemia, limit infarct size, reduce
cardiac work, prevent and treatment
complications. Myocardial infarctione is an
acute medical emergency and outcome is
significantly influenced by rapid diagnosis
and treatment.
 Emergency therapy:
1. Analgesia:
 Nitroglycerine 0.1%-10.0 intravinously
, drop by drop, slowly for schem: 4-6-
8-10 and more drops in minet with
arterial pression control or
sublingval over the 5-10 min.
 Narcotic`s drags : Morphine 1%- 1 ml
intravinously or subcutaneus with
Atropini sulfatis 0.1%-0.5 ml
subcutaneus . May be using other
narcotic drugs.
 Phentanilum 0.05% -2 ml intravinous
and other.
 Nitrous oxide may be administered in
addition to narcotic analgesics with
little or no depression of left ventricular
function.
2. Sedative and tranquilizers drugs
(diazepam, nozepam ,other);
3. Oxygen;
4. When the patient has high arterial
pressure or/and palpatetione we should
be administed B-adrenoblokers:
Propronolol or Atenolol .
ISCHEMIC HEART
DISEASE:
MYOCARDIAL
INFARCTION

department therapy №1
with course of endocrinology
proffesor Dudar L.V.
 Treatment aims
Treatment is designed to relieve distress,
reverse ishemia, limit infarct size, reduce cardiac
work, prevent and treat complications.
Myocardial infarction is an acute medical
emergency with outcome significantly
influenced by rapid diagnosis and treatment.
 Emergency therapy

1. Analgesia
 Nitroglycerine 0.1%-10.0 intravinously , drop by drop, slowly
for schem: 4-6-8-10 and more drops in min. with arterial
pressure control or sublingval over than 5-10 min.
 Narcotic`s drugs : Morphine 1%- 1 ml intravinously or
subcutaneusly with
 Atropin sulfatis 0.1%-0.5 ml subcutaneusly. May be using
other narcotic drugs.
 Phentanilum 0.05% -2 ml intravinous and other.
 Nitrous oxide may be administered in addition to narcotic
analgetics with little or no depression of left ventricular
function.
 Emergency therapy

 2.Sedative and tranquilizers drugs (diazepam,

nozepam ,other)
 3.Oxygen
 4.When the patient has hirth arterial pressure
or/and palpatetione we should be administed
B-adrenoblokers: Propronolol or Atenolol .
 TREATMENT
UNCOMPLICATED M I
 1.Regimen - bed rest with personnal
electrocardiographic monitoring.A catheter should be
introduced into peripheral vein and kept open by the
slow infusion of isotonic glucouse solutione. No
smoking.
 2.Diet – during the first 5 days,alow-calorial diet
divided into multiple small feedings , than diet 10.
 3.Analgesia
Narcotic drugs (morphini 1%-1.0, promedol2%-1/0)
Nitroglycerine 10mg i/v, drop by drop, other
 TREATMENT
UNCOMPLICATED M I
4. Trombolitic therapy
 Trombolitic therapy is most effective in the first hours after onset of
myocarrdial infarction.During the acute phase ofbQ-wave MI thrombolitic
drugs reduce hospital mortality between 30 and 50 per cent.Trombolitic drugs
are :
 Streptokinase - 1.5 millione U intravinous during 30 – 60 min.

 Alteplase – 100 mg i/v during 90 min

 Actilase (plasminogen activator) – 100 mg i/v during 3 hours

5.Concomitant antithrombotic therapy – Heparin therapy

 Heparine 5000 U subcutaneous 4 per days
 Aspirine 160-325 mg daily
 TREATMENT
UNCOMPLICATED M I
 6. Oxygen
 7. B-adrenergic blockers (anaprilinum,
metaprololum, other)
 8. Long-acting nitrates ( nitrosorbitum, sustac-
forte, cardiket, monoket )
 9. Cardiometabolic drugs
 TREATMENT COMPLICATED
MYOCARDIAL INFARCTION

 1. Analgesia
 2. Thrombolytic therapy
 3. Concomitent anti thrombotic therapy
 4. Nitroglycerini 10 mg i/v drop., than long-
acting nitrates
TREATMENT COMPLICATED
IM
In CARDIOGENIC SHOK this triatment
is combaned with a- or b- agonists
(biological amines) :
 Dopamine 0.5 to 1mg/kg/min i/v drop.
 Dobutamine 2.5 to 10 mg/kg min i/v drop
 Prednisolone 60mg i/v
 TREATMENT
 In LEFT VENTRICULAR FAILURE (CARDIAC
ASTHMA, PULMONERY EDEMA) basis treatment
combaned with
 Diuretics : Furasemidi ( Lasix) 80 – 120mg i/v bolus
 Nitroglicerini (Isoket, Monoket)10 mg i/v drop.
 Morphine 1% -1.0 ml i/v or s/c + Atropine
0.1%-1ml
 Oxygen with spiritus (ethanol) ingalation
 TREATMENT
 Sinus tachycardia – b-adrenergic blokers
(anapriline 20-40mg,methaprolol 25-50mg) ,
digitalis drugs oraly
 Sinus bradycardia – Atropine sulfate 0.1%- 1ml
s/c
 Paroxysmal ventricular tachycardia - Lidocaine 2
– 4 mg i/v bolus
 Atrial fibrillatione – Novocainamid 10%-10 ml
+ Mesatone 0.5ml i/v
 TREATMENT
 Ventricular fibrillatione – Lidocaine 2-4mg i/v
bolus,
 Electrical defibrillatione
 Extrasystolia (beats) – Kalium drugs, Lidocaine
2 mg i/v, b-Blockers
 Blockades - Atropine sulfate 0.1%- 1ml s/c
Prednisolone 30-60 mg i/v or oraly
Riboxine 5 ml i/v
TREATMENT AFTER HOSPITAL
PERIOD
Treatment after hospital period includs are:
- hypolipidemical drugs,
- prolongate nitrates,

- adrenoblocades drugs,

- aspirin,

- physical and

- psichological rehabilitation.
Thank you for attention!