dvfs

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ISCHEMIC
CARDIOPATHY
STUDENTS
William Cruz
Kevin Herrera
Jorge Pacheco
Angie Chamba
Sonia Quijilema
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. ISCHEMIC CARDIOPATHY
It is the situation produced by the deprivation of oxygen to the tissues and the inadequate
elimination of the metabolites, resulting from the imbalance between the coronary supply
and the myocardial oxygen demand.
ETIOLOGY
Any cause that abnormally leads to reduced blood flow due to obstruction of coronary
vessels and / or increased myocardial oxygen needs. As: atherosclerosis, thrombosis,
coronary spasm or dynamic stenosis, muscle dysfunction, among others.

3. CARDIOVASCULAR RISK
FACTORS
CONSEQUENCES
Among those that are more common, we have:
 Ischemic Cascade: They induce ventricular dysfunction and arrhythmias without
causing angina; they include as a consequence the cessation of blood flow,
decreases the elastic properties of the myocardium, its contractile activity altering
the potential of transmembrane action appearing electrocardiographic changes,
finally releasing adenosine, which stimulates nerve endings, causing pain.
 Transient Ischemia: This is an episode in which the myocardium is becoming
more resistant to a new ischemic episode.
 Stunned myocardium: Prolonged reduction in contractility secondary to
transient ischemia, that is, it is a phase through which the myocardium passes,
subsequently to this ischemia.
 Hibernating Myocardium: Contractile function of the intensely reduced
ischemic area secondary to chronic coronary flow reduction.
 Myocardial Necrosis: Cell death, either necrosis or ischemia secondary to deep
coronary flow decrease.
SIGNS AND SYMPTOMS
It is characterized by a pain, type of oppression or the perception of a weight, which is
usually located in the retrosternal region or in the entire anterior aspect of the thorax and
irradiated to the arms, neck or jaw; which we call "chest angina", reaching its maximum
intensity soon and that usually disappears gradually in 1 - 10 min.

4. STABLE CHRONIC CORONARY DISEASE
Clinically stable angina is considered, is one whose pattern has not changed in at least the
last two months. According to severity and functional limitation, effort angina is divided:
 Grade I: Regular physical activity does not cause pain; This appears with
strenuous, fast or prolonged efforts.
 Grade II: Mild limitation of physical activity; pain that appears when walking
with normal pace more than two trips or climbing more than one floor.
 Grade III: Acute limitation, pain present when climbing a floor or walking with
normal pace one or two crossings.
 Grade IV: Inability to carry out any activity, pain at rest.
DIAGNOSTIC
Among those recommended, are:
1. Electrocardiogram.
2. Test of effort.

5. 3. Stress tests with image: Stress test combined with imaging techniques such as:
scintigraphy which allows visualization and quantification of hypoperfused
areas, while echocardiography allows the detection and quantification of
hypocontractile zones; that determine both at rest and effort, as a consequence of
ischemia.
4. Echocardiography: Determines segmental defects of myocardial motility, and
evaluates ventricular function by measuring the ejection fraction
5. Coronary angiography: Cardiac catheterization allows the analysis of ventricular
function and knowledge of the degree and extent of coronary lesions.
TREATMENT
At first, limit the progression of coronary atherosclerosis through changes in lifestyle.
For anginal attacks treatment during one of them will be nitrates; for the prevention of
crises we will have beta - blockers, calcium antagonists, isosorbide mononitrate and
ivabradine. There are also surgical treatments such as myocardial revascularization and
percutaneous coronary intervention.
SÍNDROME CORONARIO AGUDO
Clinical manifestations that occur as a consequence of the rupture of an atheromatous
plaque followed by the formation of intravascular thrombosis, distal embolization and
obstruction of myocardial perfusion.
CLINICAL TABLE AND DIAGNOSIS.-
Thoracic pain; first differentiate coronary pain from that which is not, second to determine
the existence or not of an ACS (acute coronary syndrome); then specify if it is an unstable
angina or an MI (myocardial infarction).
SCA without ST segment elevation: Unstable angina and myocardial infarction
without ST elevation. - Because both unstable angina and non-ST-elevation infarction
share the same physiopathology, clinical picture and treatment, they are considered to be
parts of the same. entity and are grouped under the name of SCA without ST elevation.

6. TREATMENT.
 Pharmacological:
 Antiplatelet Agents: clopidogrel 300 - 600 mg (8 tablets), plus aspirin 300
mg.
 Anticoagulants: enoxiparin (1 mg / kg of weight every 12h)
 Antianginal: beta-blockers in combination with nitrates, or calcium
antagonists with bradycardic effect (diltiazem or verapamil).
 Interventionist or Invasive:
Early coronary angiography is recommended, followed by percutaneous or surgical
coronary revascularization according to the coronary anatomy, the degree of ventricular
dysfunction and the presence of comorbidities, especially diabetes, peripheral vascular
disease and renal failure.
Myocardial Infarction with Elevation of the ST Segment.- In this case there is an acute
necrosis of the myocardium of ischemic origin, secondary to the total thrombotic
obstruction of a coronary artery, which is translated into the ECG by persistent ST
elevation.
TREATMENT:
 Analgesia and initial measures: Mórfico Chloride 2 - 4 mg i.v. every 5 - 15 min.
 Reperfusion treatment.
 Fibrinolytics: Streptokinase 1.5 million units in 1 h.
 Primary angioplasty.
 Post-thrombolysis rescue angioplasty.
 Antiplatelet agents: ASA 160 325 mg.
 Anticoagulants: beta blockers, ACEIs, nitrates, calcium antagonists.
BIBLIOGRAPHY
Genover X. Bosch. "Ischemic Heart Disease" Farreras Valentí, Rozman Cricill; Internal
Medicine. 17th ed. Barcelona, Spain. Elsevier, 2016. Pages: 471 - 492.