Clinical Discussion: Acute Myocardial Infarction And Chest Pain

Cardiovascular disease or CVD accounts for the maximum number of deaths all around the globe. The phrase refers to a collection of ailments that involves conditions like coronary artery disease, heart attack, stroke, and congestive heart failure. A person’s predisposition to CVD can be increased by both changeable and non-modifiable threat variables. Ethnicity, if there is a medical background of CVD in the family, gender, and age are non-modifiable risk factors (1). This is a clinical discussion about a patient who has an acute myocardial infarction. There is a discussion of the clinical signs and symptoms. The options at every phase ECG, the angiogram, and the observations done for the purpose of treatment are all thoroughly discussed. The differential diagnosis of the symptoms presented by the patient is also mentioned. ECG localization of myocardial infarction, acute coronary occlusion management, and all clinical aspects of myocardial infarction monitoring are enclosed. The outcome and next steps are also discussed.

Myocardial infarction is caused due to restricted inflow of blood to the heart muscle. The heart muscles that are affected start to die as a result of it. Pain in the chest is one of the most prevalent purposes for trying to seek emergency treatment, and it becomes complicated between cases of non-emergency and those with increased deaths and morbidity rates, like acute coronary syndrome (ACS), aortic dissection, and pulmonary thromboembolism (11). There are 3 main specifications for managing acute pain in the chest: physiological examination and medical document, electrocardiogram (ECG), and markers of atrophy of the myocardium. They must be analyzed together to get a secure strategy for the patient, particularly when starting out ACS is required. Radiography of the chest, computed tomography angiography (CTA), echocardiography, as well as other exams may be helpful in making a diagnosis. Acute coronary syndrome is identified in roughly 15-25 percent of patients who come to the ER with pain in the chest, and it, therefore, is its most common clinical symptom (12). As a result, the existence of angina is the most important determining factor of an ischemic etiology in the first phase of the assessment, which also is the clinical investigation (2).

Angina is frequently characterized as a feeling which can be termed as burning or pressurizing and breathing problems in the precordial area or any other area of the chest region, emanating to the neck, shoulder, and left arm. It generally worsens in less than minutes and is preceded by health problems such as nausea and perspiring. It is provoked by physical or psychological exertion and is alleviated by rest or the use of nitrates. It must also be noted that ACS can take place without evident precipitating variables, be symptom-free, or reveal as an ischemic equivalent, particularly in the older and patients with diabetes with neurological impairment (6). The patient in this case scenario presented with extended pain in the chest, which does not govern out acute coronary syndrome (ACS), but does elevate the risk of a situation linked with this coronary portrait, also including pericarditis or mechanical abnormalities (7). Dyslipidaemia, diabetes, high blood pressure, male gender, advanced age, obesity/metabolic disorder, cigarettes, reduced physical activity, chronic kidney disease, anxiety, and strain are some of the most crucial risk factors for atherosclerotic disease. Age, male sex, high blood pressure, and smoking were all vulnerability variables in this patient’s advancement of coronary artery disease. Patients with pain in the chest and ACS frequently have a vaguely defined medical assessment, with very little than 20% demonstrating substantial changes in the clinical assessment. This is useful in detecting differential diagnoses (for example, pericardial friction rubs in pericarditis) or implying the existence of risk variables for coronary artery disease. This is an essential subject since the majority of the mortality due to myocardial infarction occurs within the first 60 minutes of the onset of the disease, with 40-65 percent happening inside of the first hour and roughly 80 percent happeningwithin the first 24 hours (7).

A 66-year-old man went to the emergency room for treatment after experiencing intense pain in the chest for 24 hours. The patient was conscious that he was hypertensive and that he smoked. The patient appeared to be fine until 3 hours ago when he abruptly felt an ambiguous pain in the chest in the centre of his chest. The pain started in the substernal area and spread to the shoulder on the right side. The suffering was dull and aching, and it was becoming more severe over the course of a few hours. Exertion agitated the pain in the chest. Even when he rested, the pain did not go away.  There was excessive sweating linked with the pain in the chest, as well as a feeling of upcoming demise or fatality. There was some slight dyspnoea and palpitation with pain in the chest. The pain in chest was widespread rather than localised. There is no link between the pain in the chest and the amount of food consumed. There was no accompanying vomiting or hematemesis. There had been no history of abuse or mental conditions in the past. There had been no record of dizziness, syncope, or seizures. There had been no previous fever, sniffle, or production of sputum.  There was no background of significantly reduced urine output, either now or previously. It was common to conduct an evaluation of other systems. The patient has no history of diabetes or hypertension. There was no prior knowledge of exertional angina or dyspnoea. There had been no previous surgical history. There are no medications being taken by the patient. For the past 15 years, the patient has followed a high-fat diet and smoked one packet of cigarettes per day. There was no background of alleged drinking or potentially illegal substance abuse.  He lives alone in a sanitary environment. Provided his father’s untimely death at the age of 52 because of the “heart problems,” he admits to being concerned about his own health and quality of life. Every night, he consumes 2-3 cocktails to “calm his anxiety”(7). 

The pulse rate was 120 beats per minute (tachycardia) with a normal rhythm. There has been no bruit in the carotid arteries.

Blood pressure:

138/94 mmHg – Upper left – Sitting left

144/90 mmHg – Lower left – Sitting left

The jugular venous pressure (JVP) was not increased.

34/min respiratory rate, shallow accelerated breathing, abdominothoracic in nature

There are no signs of kyphoscoliosis and the wall of the chest is bilaterally symmetrical. Due to slight obesity, the apex is not observable. There have been no scars or veins that are dilated. There is tachycardia if the first heart sound is loud in frequency and the second heart sound is regular in frequency (normal split). There have been no extraneous sounds or murmurs. The patient was alert and well-aware of time and place. An ECG, X-ray of the chest, CBC, thorough metabolic panel, cardiovascular enzymes, lipase, and clotting studies were performed during the patient’s initial physical exam in the ED. His initial triage EKG (Figure 1) revealed V2-V6 T wave shifts are hyperacute in a usual sinus rhythm.; his potassium level was 4.3. With the exception of a troponin-I of 0.41, his other laboratory tests were uninteresting.

A 1.5-hour follow-up ECG (Figure 2) revealed normal sinus rhythm with substantial elevation in the segment of ST-segment in leads I, II, and V1 through V6, indicating an anterolateral MI. He was noticed to get a 100-percent blockage all along the middle part of the left anterior descending (LAD) artery during catheterization; no obstructions were observed in the right coronary artery or the circumflex artery. Stents were implanted throughout the LAD’s first and second diagonal divisions. Numerous occurrences of ventricular tachycardia, which settled with profound coughing, occurred during the process, as did an incident of ventricular fibrillation, which required cardioversion to sinus rhythm. According to the catheterization laboratory report, the patient had anterolateral apical hypokinesia and a left ventricular function of 40%.(figure 1)

One differential diagnosis for this patient who is having intense pain in the chest along with the pericardial effusion is aortic dissection. In the case of this condition the onset of pain is very sudden and of very strong intensity from the beginning. This pain is not like the pain of angina which comes and goes and escalates increasingly. This pain is described as excruciating and the location of the pain reflects the site and the progression of the dissection. The other signs such as pallor and excessive sweating are very much linked. In this condition when the physical examination discloses hypertensive crisis, there is a difference between the pulse of the limbs, indications of pleural and pericardial effusion,

diastolic murmur of aortic regurgitation which is different from the systolic murmur that is observed in the case of this patient. The spread of the dissection to those certain vessels can cause signs resembling ischemia of the organ systems that are irrigated by them, such as haemorrhagic stroke, acute myocardial infarction, mesenteric ischemia, and so on (9).

Pulmonary embolism is some other possible diagnosis for the clinical problem. This assumption is much less probable because there are no pulmonary symptoms, primarily dyspnoea. It is another very frequent problem of this illness, affecting more than 78 percent of patients. Up to 44% of patients experience unexpected chest pain, which is frequently pleuritic. Coughing and hemoptysis are also possible. Furthermore, no reference of right ventricular dysfunction expressions, such as jugular stasis and hypotension, was formed on admission at the other service (8).

The following medications have been administered to the patient:

T. Aspirin 75 mg OD

 T. Ticagrelor 90 mg BD (after an initial loading dose of 180 mg)

T. Atorvastatin 80 mg OD HS

 T. Metoprolol.

As the patients left ventricular 50 mg OD ejection fraction was 40%-45%

T. Ramipril with hypokinesia in the LAD

2.5 mg BD territory T.

Lasix + spironolactone (20/50) mg od (7).

Trying to restore the flow of blood and circulation to the muscles of the heart that are affected as soon as possible is the goal of treating myocardial infarction. This can occur through a variety of means, varying from medication to surgery. It is very highly probable that treatment will include a combination of the methods listed below (10).

Supplemental oxygen is frequently given to people who are having breathing difficulties or have a low level of oxygen in blood oxygen, in addition to other heart attack treatment options. The oxygen can be inhaled through a tube that is placed below the nose of the patient or the oxygen mask which can be placed on top of the nose so that the mouth and the nose can be covered. This enhances the quantity of oxygen in the blood and relieves the pressure on the heart (13).

Anti-clotting medicines such as aspirin and other medicines that help in thinning the blood 

Nitro-glycerine is a medication used to treat pain in the chest.  It is also a potent vasodilator, which means it induces blood vessels to dilate, allowing blood to flow more quickly (13).

Thrombolytic (clot-busting) medications: These intravenous (IV) medications disintegrate and dissolve blood clots. These medications are typically only used within the first 12 hours following a heart attack (8)

Anti-arrhythmia medications: Heart attacks frequently result in arrhythmias, which are irregularities in your heart’s normal beating rhythm. Some arrhythmias are potentially fatal. These malfunctions can be stopped or prevented with anti-arrhythmia medications.

Morphine is the most commonly used pain reliever during heart attack treatment. This can aid in the relief of chest pain (8).

Percutaneous coronary intervention (PCI) a technique used to restore blood flow to the concerned cardiac muscle. This operation, also known as PCI for short, involves inserting a piece of catheter-based equipment into a significant blood vessel. The catheter is threaded up to the obstructed artery on the heart after being implanted into the blood vessel through a small cut. When the device attains the obstruction, the supplier will pump up a small balloon on the extreme of the machine to broaden the blood vessel and clear the obstruction (8).

Acute myocardial infarction (AMI) follow-up care is an important component of the recovery procedure after an AMI. Family doctors, in collaboration with a cardiovascular subspecialist, play a critical position in the subacute administration of MI. This duration can last one to three months and starts after a revascularization process or after the choice not to revascularize is formed (4). Diet, exercise, and cessation of smoking are all important aspects of modifying the unhealthy habits influencing the lifestyle that should be discussed at discharge. Dietary advice should include details about the Mediterranean diet, which has been shown to lower cardiovascular and all-cause mortality rates. Whenever the interventions related to behavior are initiated in the hospital environment and are integrated with one month of supportive care, smoking cessation rates improve in patients with cardiovascular disease (5).

This is a case study of a 66-year-old man, who presented to the ED with intense pain in his chest. There was excessive sweating linked with the pain in the chest, as well as a feeling of upcoming demise or fatality (7). Similarly, Campo (2016), presented a case study of 52 year old suffering from myocardial infarction (MI) over many months but it went unrecognized by her clinicians or the nurses. The author also mentions the initial signs and symptoms of the condition. The author also mentions how crucial it is to rule out the differential diagnosis so that current treatment can be provided to the patient which otherwise can be fatal (3). In the case study presented above also differential diagnosis to heart attack has been mentioned and the rationale has been presented as to why it has been ruled out. The patient here has also been given proper treatment to prevent the condition. ECG was done as one of the investigations. The T wave is some other aspect to deem in an ECG of a patient complaining of pain in chest. The T wave in an ECG is a representation of the heart’s ventricles repolarizing. The large percentage of T waves must be favourable and irregular, with a delayed upstroke and a quick downstroke. T waves in limb prospects should be less than 5 mm, and T waves in chest prospects should be less than 10 mm.  During this patient’s initial ECG, it was critical to rule out any abnormalities in T wave presentation that could indicate underlying heart pathology (7).  ( Silva, et al. (2017), presented a case study of a 41 year old female who is suffering from haemophilia and suffered pain in the chest which was radiating from left hand. It was followed by chest tightness and breathing difficulties. In the above and this case study it was found that cigarette smoking and obesity was one of the prime cause of myocardial infarction. Blood pressure was high in both the cases. In the case study by Silva, the ECG represented elevation in the ST segment in lead II, III and aVF which led to diagnosis of MI (14).

·         Myocardial infarction is caused due to restricted inflow of blood to the heart muscle.

·         The heart muscles that are affected start to die as a result of it

·         The symptoms generally include pain in the chest that radiates from left arm, nausea, breathlessness, fatigue, excessive sweating.

·         If not addressed on time can be very fatal.