CHAPTER III

CASE ANALYSIS

The patient was a man, 55 years old who is a referral from Dr. Oen hospital with a
diagnosis of STEMI Inferior. He have Got therapy Ranitidine inj 1 amp, Ascardia 160
mg, 300 mg Plavix. He is referred to RSDM because ICU IN Dr oen was full.
Patients present with chest pain since 10 hours before coming to the hospital. Chest
pain is felt as crushed heavy objects, radiating to the left arm and neck. Chest pain is felt
when the patient is lying down resting. Pain is felt with a duration of> 20 minutes.
Patients sleep with 1 pillow. Complaints chest pounding denied. Shortness of breath (+),
PND (-), DOE (-), orthopneu (-), fever (-), palpitations (-).
Based on from physical examination with vital signs, it got blood pressure in
60/palpasi TD, pulse 51 x / minute, HR 51 x / min, RR 20x/menit, and the temperature of
36.5 C. General state of the patient to look weak, compos mentis, shortness of breath,
and nutritional status is enough. The skin is not visible cyanosis, in both eyes do not look
conjunctival anemic, JVP not increased, chest wall retraction is not obtained, the
impression is not dilated heart border, heart sounds S1 and S2 normal intensity and did
not reveal any abnormal heart murmur. Vesicular basis sound in both lung fields normal
In additional examination, laboratory tests of blood found to increase in leukocytes
(16.5 thousand / ul), blood sugar (304 mg / dl) SG0T (382 U / l), SGPT (382 U / l),
Troponin I (8.63 ug / L) , CKMB (171.0 ng / ml)
EKG obtained at a total AV block HR 49 x/ ', normoaxis, STEMI Posterior +
Inferior + RV, Occasional PAC.
Patients feel chest pain caused by damage (necrosis) of heart muscle due to blood
flow to the heart muscle is interrupted. As a result, there was myocardial ischemia. A
decrease in cardiac perfusion resulting in a decrease in the intake of oxygen and the
accumulation of products of metabolism of chemical compounds. The accumulation of
these metabolites arise because of inadequate oxygen supply, the myocardial cells
compensate by respiring anaerobically. As by-products of lactic acid. Lactic acid makes
the cell pH decreases. Changes in myocardial metabolism of these cells are stimulated
via the sympathetic afferent pain receptors in the primary sensory cortex area (area 3,2,1
Broadman) which causes pain in the chest.

This stimulation via sympathetic afferents to sympathetic ganglia, posterior root of
the spinal cord toward Th15. Here impulse sympathetic afferent somatic met with
impulses thoracic structures. Impulse runs through the spinothalamic tract to the
thalamus and cerebral cortex that are headed sensation of pain.
Patients feel shortness of breath caused by the damming is occurring in the lungs.
This is caused by the failure of the left ventricle pumps blood throughout the body, thus
resulting in the volume of blood remaining in the ventricle. The volume of blood left in
the ventricle causes an increase in pressure in the left atrium. Resulting in increased
retrograde pressure. With the increased pressure in the pulmonary veins of more than
20mmHg there will be a transudation of fluid into the lungs out. This is what causes
patients to feel short of breath.
When the pressure in the pulmonary artery and bronchial rises also occurred in the
interstitial tissue transudation bronchi, the tissue becomes edema and this will reduce the
size of the bronchial lumen, so the airflow becomes disturbed. In these situation it
breathing sounds is reads during expiration, expiratory murmur and expiratory phase
becomes longer, this situation is known as cardiac asthma.
Increased pressure in the alveolar capillaries resulting in transudation of fluid in the
interstitial tissue and alveoli that found the presence of the sound wet smooth crackles
and coarse wet crackles.