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1. Describe the pathophysiological differences between UA, NSTEMI and STEMI 2. Compare and contrast signs and...

1. Describe the pathophysiological differences between UA, NSTEMI and STEMI

2. Compare and contrast signs and symptoms of UA, NSTEMI and STEMI.

5. What are the cardiac specific biomarkers used in diagnosing a patient with ACS? Make distinctions between which are elevated and the timing for when they become elevated.

6. Electrocardiography (ECG) is an important diagnostic test for people suspected of having a significant cardiac event. Identify what each of the following ECG findings indicate.

  1. The inverted T-wave
  2. ST segment elevation
  3. Abnormal Q-waves

7. Reperfusion therapy is necessary for patients diagnosed with STEMI. Explain the difference between percutaneous intervention (PCI) with stent insertion and coronary artery bypass graft (CABG).

Solutions

Expert Solution

1. Acute coronary syndrome (ACS) can be divided into subgroups of ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina.

UNSTABLE ANGINA

Unstable angina is also known as preinfarction angina.it occurs with an unpredictable degree of exertion or emotion and increase in occurence, duration and severity over time.pain may not be relieved with nitroglycerin.

PATHOPHYSIOLOGY

Unstable angina results when the blood flow to the myocardium is impeded.. Most commonly, this block can be from plaque formation in the blood vessels, intraluminal thrombosis, vasospasm, and elevated blood pressure. Often a combination of these is the provoking factor.

NSTEM I{non-ST segment elevation myocardial infarction}

Main predisposing fsctors are stable plaque, vasospasm as in Prinzmetal angina, coronary embolism, or coronary arteritis. Non-coronary injury to the heart such as cardiac contusion, myocarditis, or presence of cardiotoxic substances can also produce NSTEMI. Conditions relatively unrelated to the coronary arteries or myocardium itself such as hypotension, hypertension, tachycardia, aortic stenosis, and pulmonary embolism lead to NSTEMI because the increased oxygen demand cannot be met.

STEMI

ST-Elevation Myocardial Infarction (STEMI) is a very serious type of heart attack during which one of the heart’s major arteries (one of the arteries that supplies oxygen and nutrient-rich blood to the heart muscle) is blocked.

STEMI is most often caused by complete and persistent occlusion of a coronary artery by blood clot (thrombus). As soon as the coronary blood supply is interrupted, myocardial damage begins and the damage gets worsened with time.Timely management is necessary.

2...SIGNS AND SYMPTOMS

UNSTABLE ANGINA :

  • chest pain that feels crushing, pressure-like, squeezing, or sharp.
  • pain that radiates to your upper extremities (usually on the left side) or back.
  • nausea.
  • anxiety.
  • sweating.
  • shortness of breath.
  • dizziness.
  • unexplained fatigue.

STEMI

  

  • Chest pain or discomfort.
  • Shortness of breath.
  • Dizziness or light-headedness.
  • Nausea or vomiting.
  • Diaphoresis (sweatiness) unexplained by ambient temperature.
  • Palpitations (uncomfortable awareness of the heart beat)
  • Anxiety or a feeling of impending doom.

NSTEMI

  • shortness of breath.
  • pressure, tightness, or discomfort in your chest.
  • pain or discomfort in your jaw, neck, back, or stomach.
  • dizziness.
  • lightheadedness.
  • nausea.
  • sweating.

CAEDIAC BIOMARKERS

1. TROPONIN : Level rises within 3 to 4 hours after myocardial injury.Level remains elevated upto 10 to 14 days.There are two variants, Troponin I and T ropnin T, among which Troponin I is cardiac specific.

2: creatinine kinase (CK) : level rises within 6 hours after the onset of chest pain.level peaks within 18 hours after damage and death of cardiac tissue.

3. CK-MB : Peak elevation occurs 18 hours after the onset of chest pain. Level returns to normal 48 to 72 hours later.

4 : MYOGLOBIN : Level rises within 2 hours after cell death, with a rapid decline in the level after 7 hours

5. LDH : Level rises 24 hours after MI. Level peaks between 48 and 72 hours and falls to normal in 7 to 14 days.

INVERTED T WAVE

The T wave is the ECG manifestation of ventricular repolarization of the cardiac electrical cycle.

The T wave is normally upright in leads I, II, and V2 to V6; inverted in lead aVR; and variable in leads III, aVL, aVF, and V1. In general, an inverted T wave in a single lead in one anatomic segment (ie, inferior, lateral, or anterior) is unlikely to represent acute pathology.T-wave inversions associated with coronary artery disease may result from myocardial ischemia (ie, unstable angina), non–ST-segment elevation acute myocardial infarction (NSTEMI-MI), or previous MI.

S-T Segment

The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.

  • The ST Segment represents the interval between ventricular depolarization and repolarization.
  • The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction

Causes of ST Segment Elevation

  • Acute myocardial infarction
  • Coronary vasospasm (Printzmetal’s angina)
  • Pericarditis
  • Benign early repolarization
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Ventricular aneurysm
  • Brugada syndrome
  • Ventricular paced rhythm
  • Raised intracranial pressure
  • Takotsubo Cardiomyopathy

Q WAVES

Q waves can be normal or abnormal. When abnormal, they indicate the presence of an ongoing or an old myocardial infarction. The ECG findings of a pathologic Q wave include a Q wave duration of > 40 milliseconds or size > 25% of the QRS complex amplitude. These need to be present in at least 2 contiguous leads to be considered abnormal.

Percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) are considered revascularization procedures, but only CABG can prolong life in stable coronary artery disease. Thus, PCI and CABG mechanisms may differ. However, the majority of infarcts are generated by non–flow-limiting stenoses, but PCI is solely focused on treating flow-limiting lesions. Thus, PCI cannot be expected to significantly limit newinfarcts, but CABG may do so through providing flow distal to vessel occlusions

A coronary artery bypass graft (CABG) is a surgical procedure used to treat coronary heart disease. It diverts blood around narrowed or clogged parts of the major arteries to improve blood flow and oxygen supply to the heart.

Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis


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