case presenation

heart attack

Chief complaints (CC)
Acute chest pain
History of present illness (HPI)
54 years old male presented in Emergency room with history of retrosternal chest pain, sudden onset, severe burning, at around 3 am awoke him from sleep, continuous for 4 hours, radiating to lef shoulder, not relieved by rest, associated with nausea. Pain not increase by inspiration or changing position.
Past medical history (PMHx)
No history of hypertension or diabetes.
None known
Current medications
Social history (SocHx)
Non smoker, bowel and dietary habits normal.
Family history (FHx)
Father died at 71, Myocardial infarct
Mother 76, known with hypertension
Physical examination (PE)
Examination male with average height and built lying on bed conscious and oriented. Pulse: 106 b/ min regular BP: 130/ 80 mmHg Temperature: 37.0
No pallor or jaundice No clubbing or splinter hemorrhages JVP not raised No carotid bruit No neck swelling No palpable lymph nodes
Pulses equally palpable on both sides, normal volume No radio femoral delay No lower limb or sacral edema No rashes
Cardiovascular examination Apex beat in 5th intercostal space at mid clavicular line, non sustained. No thrill or heave S1 and S2 with normal intensity. No gallop or murmur
Respiratory system Chest bilaterally symmetrical moving with respiration. Vesicular breathing No crepits or ronchi
Gastrointestinal system No hepatosplenomegaly Central Nervous System Normal sensory and motor exam.
Laboratory results (Lab)
Other investigations
ECG:  ST elevation & hyperacute T waves in V2-V4 An echocardiogram may be performed to compare areas of the left ventricle that are contracting normally with those that are not. One of the earliest protective actions of myocardial cells used during limited blood flow is to turn off the energy-requiring mechanism for contraction; this mechanism begins almost immediately after normal blood flow is interrupted. The echocardiogram may be helpful in identifying which portion of the heart is affected by an MI and which of the coronary arteries is most likely to be occluded. Unfortunately, the presence of wall motion abnormalities on the echocardiogram may be the result of an acute MI or previous (old) MI or other myopathic processes, limiting its overall diagnostic utility.
Differential diagnosis
Angina Pectoris
Acute abdomen (posterior infarct )
Case summary and impression
Summary 41 years old male presented with history of retrosternal chest pain, severe continuous for 4 hours then decrease in intensity associated with nausea.
Percutaneous Coronary Intervention= PTCA + stent The goals of therapy in acute MI are the expedient restoration of normal coronary blood flow and the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient's failure to recognize MI symptoms quickly and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals. “Time is muscle” guides the management decisions in acute STEMI, and an early invasive approach is the standard of care for acute NSTEMI.

Medical Options

Antiplatelet Agents, Supplemental Oxygen, Nitrates, Pain Control, Beta Blockers, Anticoagulant Agents,
Follow up
An individual patient's long-term outcome following an MI depends on numerous variables, some of which are not modifiable from a clinical standpoint. However, patients can modify other variables by complying with prescribed therapy and adopting lifestyle changes.
Long-Term Medications
Most oral medications instituted in the hospital at the time of MI will be continued long term. Therapy with aspirin and beta blockade is continued indefinitely in all patients. ACE inhibitors are continued indefinitely in patients with congestive heart failure, left ventricular dysfunction, hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to diet modification, is continued indefinitely as well. Post-MI patients with diabetes should have tight glycemic control according to earlier studies. The latest ACC/AHA guidelines recommend a goal HbA1c of less than 7%.
Restoration of coronary blood flow in MI patients can be accomplished pharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy is indicated for patients who present with a STEMI within 12 hours of symptom onset without a contraindication. Absolute contraindications to fibrinolytic therapy include history of intracranial hemorrhage, ischemic stroke or closed head injury within the past 3 months, presence of an intracranial malignancy, signs of an aortic dissection, or active bleeding. Fibrinolytic therapy is primarily used at facilities without access to an experienced interventionalist within 90 minutes of presentation. As a class, the plasminogen activators have been shown to restore normal coronary blood flow in 50% to 60% of STEMI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective within the first hour of symptom onset and when the door-to-needle time is 30 minutes or less.
Heart attack timeline
3:00 am pain debut
3:45 am calling emergency
3:55 am emergency arrives
4:20 am arriving to the loval hospital
4:30 am alerting the catheterization center
5:40 am arriving to catheterization center
5:55 am starting PTCA + stent implantation

in brief

Patient 54 years, Male 
Chest pain

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