The Pathological Progression of Myocardial Infarction: A Timeline of Changes

Myocardial infarction, commonly known as a heart attack, is a serious medical condition that occurs when blood flow to the heart is blocked, leading to tissue damage and potentially life-threatening complications. The pathological progression of myocardial infarction follows a predictable sequence of events, with macroscopic and microscopic changes occurring over time.

Immediately after the infarct occurs, there are usually no visible changes to the myocardium. However, within 3-6 hours, maximal inflammatory changes occur, with the most prominent changes occurring between 24-72 hours. During this time, coagulative necrosis and acute inflammatory responses are visible, with marked infiltration by neutrophils.

Between 3-10 days, the infarcted area begins to develop a hyperaemic border, and the process of organisation and repair begins. Granulation tissue replaces dead muscle, and dying neutrophils are replaced by macrophages. Disintegration and phagocytosis of dead myofibres occur during this time.

If a patient survives an acute infarction, the infarct heals through the formation of scar tissue. However, scar tissue does not possess the usual contractile properties of normal cardiac muscle, leading to contractile dysfunction or congestive cardiac failure. The entire process from coagulative necrosis to the formation of well-formed scar tissue takes 6-8 weeks.

In summary, understanding the timeline of changes that occur during myocardial infarction is crucial for early diagnosis and effective treatment. By recognising the macroscopic and microscopic changes that occur over time, healthcare professionals can provide appropriate interventions to improve patient outcomes.

Valvular Murmurs

Valvular murmurs are a common topic in medical exams, and it is crucial to have a good of them. The easiest way to approach them is by classifying them into systolic and diastolic murmurs. If the arterial valves, such as the aortic or pulmonary valves, are narrowed, ventricular contraction will cause turbulent flow, resulting in a systolic murmur. On the other hand, if these valves are incompetent, blood will leak back through the valve during diastole, causing a diastolic murmur.

Similarly, the atrioventricular valves, such as the mitral and tricuspid valves, can be thought of in the same way. If these valves are leaky, blood will be forced back into the atria during systole, causing a systolic murmur. If they are narrowed, blood will not flow freely from the atria to the ventricles during diastole, causing a diastolic murmur.

Therefore, a diastolic murmur indicates either aortic/pulmonary regurgitation or mitral/tricuspid stenosis. The loud first heart sound is due to increased force in closing the mitral or tricuspid valve, which suggests stenosis. the different types of valvular murmurs and their causes is essential for medical professionals to diagnose and treat patients accurately.

The T wave on an ECG indicates ventricular repolarisation and is typically positive in all leads except AvR and V1. Abnormal T wave findings may suggest strain, bundle branch block, ischaemia/infarction, hyperkalaemia, Prinzmetal angina, or early STEMI. The P wave represents atrial depolarisation, while atrial repolarisation is hidden by the QRS complex. The PR interval is determined by the duration of conduction delay through the atrioventricular node. Finally, the QRS complex indicates ventricular depolarisation.

This patient has high cholesterol and hypertension, both of which require immediate attention.

Medications:
The patient will start taking atorvastatin 20 mg once a night to address their high cholesterol. After three months, their cholesterol and full lipid profile will be rechecked, and the therapy will be titrated to maintain a total cholesterol of <5. If necessary, the dose may be increased to 40 mg once a night.

For hypertension, the patient will start taking a calcium channel blocker as they are over the age of 55. The blood pressure will be monitored regularly, and if it rises above 150/90, additional treatment may be necessary.

Monitoring:
The patient’s cholesterol and full lipid profile will be rechecked after three months of treatment with atorvastatin. The aim is to see a 40% reduction in non-HDL cholesterol. If this is not achieved, a discussion of adherence, lifestyle measures, and the possibility of increasing the dose will take place.

The patient’s blood pressure will also be monitored regularly. If it rises above 150/90, additional treatment may be necessary.

Treatment Options for ST-Elevation Myocardial Infarction (STEMI)

ST-Elevation Myocardial Infarction (STEMI) is a medical emergency that requires immediate intervention. The diagnosis of STEMI is confirmed through cardiac sounding chest pain and evidence of ST-elevation on the ECG. The primary treatment option for STEMI is immediate revascularization through primary percutaneous coronary intervention (PCI) and placement of a cardiac stent.

Therapeutic alteplase, a thrombolytic agent, used to be a common treatment option for STEMI, but it has been largely replaced by primary PCI due to its superior therapeutic outcomes. Aspirin is routinely given in myocardial infarction, and clopidogrel may also be given, although many centers are now using ticagrelor instead.

High-flow oxygen and intravenous morphine may be used for adequate analgesia and resuscitation, but the primary treatment remains primary PCI and revascularization. Routine use of high flow oxygen in non-hypoxic patients with an acute coronary syndrome is no longer advocated.

It is crucial to avoid delaying treatment for STEMI, as it can lead to further deterioration of the patient and increase the risk of cardiac arrhythmia or arrest. Therefore, waiting for troponin results before further management is not an appropriate option. The diagnosis of STEMI can be made through history and ECG findings, and immediate intervention is necessary for optimal outcomes.

Treatment Options for ST Elevation Myocardial Infarction (STEMI)

When a patient presents with a ST elevation myocardial infarction (STEMI), prompt and appropriate treatment is crucial. The gold standard treatment for a STEMI is a primary percutaneous coronary intervention (PCI), which should be performed as soon as possible. In the absence of contraindications, all patients should receive aspirin, ticagrelor, and low-molecular-weight heparin before undergoing PCI.

Delaying PCI by treating the pain with sublingual glyceryl trinitrate (GTN), aspirin, and oxygen, and reviewing the patient in 15 minutes is not recommended. Similarly, giving the patient aspirin, ticagrelor, and low molecular weight heparin without performing PCI is incomplete management.

Thrombolysis therapy can be performed on patients without access to primary PCI. However, if primary PCI is available, it is the preferred treatment option.

It is important to note that waiting for cardiac enzymes is not recommended as it would only result in a delay in definitive management. Early and appropriate treatment is crucial in improving outcomes for patients with STEMI.

Managing Acute Shortness of Breath: Prioritizing ABCDE Approach

When dealing with acutely unwell patients experiencing shortness of breath, it is crucial to follow the ABCDE approach. The first step is to address Airway and Breathing by sitting the patient up and administering high flow oxygen to maintain normal saturations. Only then should Circulation be considered, which may involve cannulation and administering IV furosemide.

According to the latest NICE guidelines, non-invasive ventilation should be considered as part of non-pharmacological management if simple measures do not improve symptoms.

It is important to prioritize the ABCDE approach and not jump straight to administering medication or inserting a urinary catheter. Establishing venous access and administering medication should only be done after ensuring the patient’s airway and breathing are stable.

If the patient has an adequate systolic blood pressure, iv nitrates such as glyceryl trinitrate (GTN) infusion could be considered to reduce preload on the heart. However, most patients can be treated with iv diuretics, such as furosemide.

In cases of acute pulmonary edema, close monitoring of urine output is recommended, and the easiest and most accurate method is through catheterization with hourly urine measurements. Oxygen should be given urgently if the patient is short of breath.

In summary, managing acute shortness of breath requires a systematic approach that prioritizes Airway and Breathing before moving on to Circulation and other interventions.

Diagnostic Tests for Secondary Hypertension: Assessing the Causes

Secondary hypertension is a condition where high blood pressure is caused by an underlying medical condition. To diagnose the cause of secondary hypertension, various diagnostic tests are available. Here are some of the tests that can be done:

Magnetic Resonance Imaging with Gadolinium Contrast of Renal Arteries
This test is used to diagnose renal artery stenosis, which is the most common cause of secondary hypertension in young people, especially young women. It is done when a renal bruit is detected. Fibromuscular dysplasia, a vascular disorder that affects the renal arteries, is one of the most common causes of renal artery stenosis in young adults, particularly women.

Echocardiogram
While an echocardiogram can assess for end-organ damage resulting from hypertension, it cannot provide the actual cause of hypertension. Coarctation of the aorta is unlikely if there is no blood pressure differential between arms.

24-Hour Urine Cortisol
This test is done to diagnose Cushing syndrome, which is unlikely in this case. The most common cause of Cushing syndrome is exogenous steroid use, which the patient does not have. In addition, the patient has a normal BMI and does not have a cushingoid appearance on examination.

Plasma Metanephrines
This test is done to diagnose phaeochromocytoma, which is unlikely in this case. The patient does not have symptoms suggestive of it, such as sweating, headache, palpitations, and syncope. Phaeochromocytoma is also a rare tumour, causing less than 1% of cases of secondary hypertension.

Renal Ultrasound
This test is a less accurate method for assessing the renal arteries. Renal parenchymal disease is unlikely in this case as urinalysis, urea, and creatinine are normal.

Diagnostic Tests for Secondary Hypertension: Assessing the Causes

Coronary Arteries and their Associated ECG Changes

The heart is supplied with blood by the coronary arteries, and blockages in these arteries can lead to myocardial infarction (heart attack). Different coronary arteries supply blood to different parts of the heart, and the location of the blockage can be identified by changes in the electrocardiogram (ECG) readings.

Left (obtuse) Marginal Artery: This artery supplies the lateral wall of the left ventricle. Blockages in this artery can cause changes in ECG leads I, aVL, V2, V5, and V6, with reciprocal changes in the inferior leads.

Anterior Interventricular (Left Anterior Descending) Artery: This artery supplies the anterior walls of both ventricles and the anterior part of the interventricular septum. Blockages in this artery can cause changes in ECG leads V2-V4, sometimes extending to V1 and V5.

Posterior Interventricular Artery: This artery is a branch of the right coronary artery and supplies the posterior walls of both ventricles. ECG changes associated with blockages in this artery are not specific.

Right (Acute) Marginal Artery: This artery supplies the right ventricle. Blockages in this artery can cause changes in ECG leads II, III, aVF, and sometimes V1.

Right Mainstem Coronary Artery: Inferior myocardial infarction is most commonly associated with blockages in this artery (80% of cases) or the left circumflex artery (20% of cases). ECG changes in this type of infarct are seen in leads II, III, and aVF.

Understanding Coronary Arteries and ECG Changes in Myocardial Infarction

Appropriate Management for a Patient with Unstable Angina

Unstable angina is a serious condition that requires urgent medical attention. In the case of a patient displaying textbook signs of unstable angina, such as crushing chest pain occurring at rest, admission to the hospital is necessary. Sending the patient home with only glyceryl trinitrate (GTN) spray is not appropriate, as the patient is at high risk of having a myocardial infarction (MI). Instead, the patient should be seen by Cardiology for consideration of an urgent elective angiogram.

Prescribing ramipril and simvastatin is not indicated unless there is evidence of hypertension. Lifestyle advice, including exercise recommendation, is also not appropriate for a patient with unstable angina. The immediate problem should be addressed first, which is the need for an angiogram.

It is important to differentiate between unstable and stable angina. Unstable angina presents with symptoms at rest, indicating a significant worsening of the patient’s cardiac disease. On the other hand, stable angina only presents with symptoms on exertion.

Sending the patient for percutaneous coronary intervention (PCI) is not necessary unless there is evidence of an MI. The pain experienced due to angina will alleviate itself most commonly at rest, unless the angina is unstable. Therefore, an urgent elective angiogram is the appropriate management for a patient with unstable angina.