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Transcript
Myocardial infarction. Clinical forms, laboratory
and ECG diagnosis. Early signs and complications.
Principles of treatment of noncomplicated
myocardial infarction
•
Prof. S.M.Andreychyn
Clinical forms of IHD
• 1. Sudden coronary death or heart arrest
(HA)
• 1.1. HA with following resuscitation.
• 1.2. HA with following mortal outcome.
• 2. Angina pectoris (AP)
• 2.1 Stable angina at exertion.
• 2.1.1 Stable angina at exertion (
functional class should be determined).
• 2.1.2 Stable angina at exertion in
angiographically intact vessels
(coronary syndrome X).
• 2.2. Angiospastic angina (angina in rest,
spontaneous, variant, Prinzmetals’ angina)
• 2.3. Unstable angina.
• 2.3.1. Primary angina.
• 2.3.2. Progressive angina.
• 3. MYOCARDIAL INFARCTION (МI)
• 4. CARDIOSCLEROSIS (postinfarctional,
focal and diffuse)
• 5. MYOCARDIAL ASCHEMIA WITHOUT
PAIN
• 6. CARDIAC RRHYTHM DISORDERS
(form)
• 7. HEART FAILURE (stage, functional class)
Classification of IM
• Acute myocardial infarction with the presence of wave Q
(transmural).
• Acute myocardial infarction without Q wave.
• Acute subendocardial myocardial infarction.
• Acute myocardial infarction (undefined).
• Recurrent myocardial infarction.
• Repeated myocardial infarction.
• Acute coronary insufficiency.
Myocardial infarction (MI)
• It is necrosis of area cardiac to the
muscle, that is
predefined by an ischemia that arises
up sharply as a result
of disparity of coronal blood stream
to the requirements of
myocardium in oxygen.
Causes of IHD
•
•
•
•
•
85 % - stenotic atherosclerosis of coronary arteries
10 % - spasm of coronary arteries
5 % - transitory thrombocytes aggregates
100 % - combination of these factors
Morbidity in males is 4 times higher than in females
Provocation factors
•
•
•
•
•
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•
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•
Smoking
Dyslipidemia
Arterial hypertension
Diabetes mellitus
Obesity
Dietary factors
Thrombogenic factors
Lack of physical activity
Alcohol abuse
The accumulation of cholesterol in the
vascular wall - atherosclerotic plaque
• Schematic of MI:
1 - subendocardial
2 - transmural
3 - subepicardial
4 - intramural
2
Myocardial infarction can be:
•
•
•
•
Time of occurrence:
-primary;
-second (after 1 month. following the first);
- recurrent (in the range of 72 hours. Before 28 days
after the first).
Clinical variants of MI
•
•
•
•
•
•
Anginous variant
Abdominal variant
Asthmatic variant
Arrythmic cariant
Cerebral variant
Asymptomatic variant
Clinics – main symptom
• Pain pattern simillar to angina pectoris but pain intensity
is much more severe that is why nitrates can’t release
pain. Pain duration is longer.
If patient feels pain, you must ask him about:
• 1. The nature of pain.
• 2. Localization.
• 3. Duration.
• 4. Irradiation.
• 5. Contact with the physical, emotional stress,
movements, breathing, eating, and other factors.
• 6. Effect of different drugs on pain.
Pain syndrom
Pain syndrom
The second severity of symptoms is
dyspnea. It may be accompanied by
pain or be the only sign of MI.
Next complains can be tachycardia, different
arrhythmias, high temperature, swelling.
Diagnosis of MI:
• Typical history and clinical presentation.
• Characteristic of ECG changes.
• There are three zones on ECG:
• - Zone of ischemia - negative or high T wave;
• - Zone of damage - shift segment S-T;
• - Zone of necrosis – Q wave larger then ¼ R wave
Wave T
•
•
•
•
Shows the process of rapid ventricular repolarisation.
Always positive in I - II, aVF, V2 - V6.
In the third, aVL, V1 can be positive or negative.
Duration 0.12 - 0.16 s, amplitude 2.5 - 6mm.
Wave Q
•
•
•
•
It is excitation interventricular septum.
Duration to 0.03 sec., height does not exceed ¼ wave R.
Sometimes can not register.
Registration Q wave even small amplitude in leads V1 V3 pathology.
Stages of MI
І. Superacute (before the development of necrosis) –
clinical pattern of prolonged attack of anginous pain
(duration 30 min – 2 hours).
Acute stage
• ІІ. Acute stage (development of myocardial necrosis) – 2
– 7 days
• - pain disappears;
• - manifestation of heart failure
Subacute period
• ІII. Subacute period (initial organization of a scar,
displacement of nectoric tissues with connective one) – 3
weeks.
Postinfarctional stage
• IV. Postinfarctional stage (final
organization of a scar), lasts for 3-6
month).
ST segment elevation
QS wave
Display units infarction on ECG
•
•
•
•
•
•
I - the front wall of the left ventricle
II - intermediate (repeats I or III toward pathology)
III - postlateral diaphragmatic or right ventricle
aVR - basal parts of the left ventricle
aVL - upper lateral departments of left ventricle
aVF - diaphragmatic departments or right ventricle
•
•
•
•
•
V1 - front wall
V2 - front wall
V3 – partition (septum)
V4 - top
V5 – lower lateral departments of the left
ventricle
• V6 – lower lateral departments of the left
ventricle
ECG signs of acute myocardial infarction
with Q wave
• Anterior MI - presence of Q or QS waves in V1 - V4.
• Lower (posterior diaphragmatic) - the presence of Q or QS
waves in II, III and aVF leads.
• Side - the presence of Q or QS waves in and aVL, V5 - V6.
• Posterior - reciprocal ECG changes in V1 - V2 leads.
Blood tests
• Serum troponin I or T levels (or CK-MB if troponin is not
available).
• Full blood count.
• Serum creatinine and electrolyte levels, particularly
potassium concentration, as hypokalaemia is associated with
an increased risk of arrhythmias, especially ventricular
fibrillation (grade B recommendation).
• Serum creatinekinase (CK) level.
• ALT, AST, LDG levels
• Leucocitosis
• Serum lipid levels (fasting levels of total cholesterol, lowdensity-lipoprotein cholesterol, high-density-lipoprotein
cholesterol and triglycerides) within 24 hours.
• Blood glucose level.
Scheme of coronarography
Treatment of MI
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A - Aspirin and Antianginal therapy
B - Beta-blocker and Blood pressure
C - Cigarette smoking and Cholesterol
D - Diet and Diabetes
E - Education and Exercise