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Acute Myocardial Infarction

Updated : August 29, 2022





Background

A myocardial infarction (MI), also referred to as a heart attack, occurs when blood flow to the heart’s coronary artery is reduced or interrupted, damaging the heart muscle. The most typical symptom is discomfort or pain in the chest, which radiates to the shoulder, arm, back, neck, or jaw.

It frequently lasts more than a few minutes and usually occurs in the center or left side of the chest. Other common symptoms are shortness of breath, cold sweat, nausea, fatigue, and dizziness.

Some individuals occasionally experience discomfort and may feel like heartburn. Women are more likely than men to present with neck pain, arm pain, or fatigue rather than chest pain.

Epidemiology

Almost 70% of the cases of acute myocardial infarction are caused by blockage from the atherosclerotic plaques. Atherosclerosis is a common cause, and risk factors for such diseases are frequently addressed in disease prevention.

Approximately 5% of persons over 75 have experienced a MI with little or no history of symptoms. About 5-10 % of individuals have premature mortality during the first year following myocardial infarction.

Anatomy

Pathophysiology

An atherosclerotic rupture triggers platelet aggregation, thrombus development, and an inflammatory chain of macrophages and monocytes. As a result, the aeration of the myocardium is reduced due to diminished oxygen supply through the coronary artery.

The endocardium undergoes apoptosis or experiences myocardial infarction due to the mitochondria’s inability to make ATP. The spatial distributions of coronary arteries are distinct and diagnostic, with a few exceptions caused by genetic differences.

For instance, the interventricular septum, anterior wall, and ventricular apex are supplied with blood by the left anterior descending coronary artery. The right coronary artery provides blood to the right ventricle. The inferolateral wall is supplied with blood by the left circumflex artery.

Etiology

Acute myocardial infarction is caused by reduced coronary blood flow. Ischemia of the heart occurs when the amount of oxygen available is insufficient to meet the demand. The causes of decreased coronary blood flow are various. Atherosclerotic plaque rupture and thrombosis occur in acutely restricted coronary blood flow.

Coronary artery embolism, which affects 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm are a few other causes of poor oxygenation and myocardial ischemia.

Other causes of acute myocardial infarction are trauma, drug abuse, vasculitis, Aortic dissection, coronary artery emboli, coronary artery anomalies, excessive demand from the heart in conditions such as anemia, and hyperthyroidism.

Modifiable Risk Factors 

  • Obesity
  • Dyslipidemia
  • Sedentary lifestyle
  • Hypertension
  • Diabetes Mellitus
  • Elevated levels of homocysteine
  • Peripheral vascular disease
  • Smoking

Non-Modifiable Risk Factors

  • Age
  • Sex
  • Family History
  • Male pattern baldness

Genetics

Prognostic Factors

Acute MI has a significant mortality rate, with most deaths occurring before hospitalization. About 50% of patients experience readmission during the first 12 months following the initial MI.

At least 5%-10% of survivors expire within the first year after a MI, and nearly half require hospitalization within the same year. The overall prognosis is determined by the degree of muscle damage. Furthermore, the prognosis is also determined by the ejection fraction, age, and comorbidities.

Factors that affect the positive outcome are: 

  • Advanced age
  • Diabetes Mellitus
  • Congestive heart failure
  • Elevated BNP level
  • Depression
  • Delayed reperfusion
  • Vascular diseases
  • Stroke

Clinical History

Physical Examination

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Medication

 

timolol

10

mg

Orally

every 12 hrs



reteplase 

10 units intravenous bolus (above 2 minutes), after that Next dose given 30 minutes after initial (for total combined dose of 20 units) Treatment should start as soon as possible after onset of acute myocardial infarction Use a separate intravenous line for each bolus injection so that no other drugs are infused or administered at the same time.



tenecteplase 

Inject, as early as possible (inside 30 minutes) after onset of acute myocardial Infarction. 30 to 50 mg intravenous bolus above 5 seconds once (based on body mass)

<60 kg: 30 mg

60 to 70 kg: 35 mg

70 to 80 kg: 40 mg

80 to 90 kg: 45 mg

>90 kg: 50 mg
Indicated to restore function for hemodialysis Catheters (Orphan)



 
 

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK459269/

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Acute Myocardial Infarction

Updated : August 29, 2022




A myocardial infarction (MI), also referred to as a heart attack, occurs when blood flow to the heart’s coronary artery is reduced or interrupted, damaging the heart muscle. The most typical symptom is discomfort or pain in the chest, which radiates to the shoulder, arm, back, neck, or jaw.

It frequently lasts more than a few minutes and usually occurs in the center or left side of the chest. Other common symptoms are shortness of breath, cold sweat, nausea, fatigue, and dizziness.

Some individuals occasionally experience discomfort and may feel like heartburn. Women are more likely than men to present with neck pain, arm pain, or fatigue rather than chest pain.

Almost 70% of the cases of acute myocardial infarction are caused by blockage from the atherosclerotic plaques. Atherosclerosis is a common cause, and risk factors for such diseases are frequently addressed in disease prevention.

Approximately 5% of persons over 75 have experienced a MI with little or no history of symptoms. About 5-10 % of individuals have premature mortality during the first year following myocardial infarction.

An atherosclerotic rupture triggers platelet aggregation, thrombus development, and an inflammatory chain of macrophages and monocytes. As a result, the aeration of the myocardium is reduced due to diminished oxygen supply through the coronary artery.

The endocardium undergoes apoptosis or experiences myocardial infarction due to the mitochondria’s inability to make ATP. The spatial distributions of coronary arteries are distinct and diagnostic, with a few exceptions caused by genetic differences.

For instance, the interventricular septum, anterior wall, and ventricular apex are supplied with blood by the left anterior descending coronary artery. The right coronary artery provides blood to the right ventricle. The inferolateral wall is supplied with blood by the left circumflex artery.

Acute myocardial infarction is caused by reduced coronary blood flow. Ischemia of the heart occurs when the amount of oxygen available is insufficient to meet the demand. The causes of decreased coronary blood flow are various. Atherosclerotic plaque rupture and thrombosis occur in acutely restricted coronary blood flow.

Coronary artery embolism, which affects 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm are a few other causes of poor oxygenation and myocardial ischemia.

Other causes of acute myocardial infarction are trauma, drug abuse, vasculitis, Aortic dissection, coronary artery emboli, coronary artery anomalies, excessive demand from the heart in conditions such as anemia, and hyperthyroidism.

Modifiable Risk Factors 

  • Obesity
  • Dyslipidemia
  • Sedentary lifestyle
  • Hypertension
  • Diabetes Mellitus
  • Elevated levels of homocysteine
  • Peripheral vascular disease
  • Smoking

Non-Modifiable Risk Factors

  • Age
  • Sex
  • Family History
  • Male pattern baldness

Acute MI has a significant mortality rate, with most deaths occurring before hospitalization. About 50% of patients experience readmission during the first 12 months following the initial MI.

At least 5%-10% of survivors expire within the first year after a MI, and nearly half require hospitalization within the same year. The overall prognosis is determined by the degree of muscle damage. Furthermore, the prognosis is also determined by the ejection fraction, age, and comorbidities.

Factors that affect the positive outcome are: 

  • Advanced age
  • Diabetes Mellitus
  • Congestive heart failure
  • Elevated BNP level
  • Depression
  • Delayed reperfusion
  • Vascular diseases
  • Stroke

timolol

10

mg

Orally

every 12 hrs



reteplase 

10 units intravenous bolus (above 2 minutes), after that Next dose given 30 minutes after initial (for total combined dose of 20 units) Treatment should start as soon as possible after onset of acute myocardial infarction Use a separate intravenous line for each bolus injection so that no other drugs are infused or administered at the same time.



tenecteplase 

Inject, as early as possible (inside 30 minutes) after onset of acute myocardial Infarction. 30 to 50 mg intravenous bolus above 5 seconds once (based on body mass)

<60 kg: 30 mg

60 to 70 kg: 35 mg

70 to 80 kg: 40 mg

80 to 90 kg: 45 mg

>90 kg: 50 mg
Indicated to restore function for hemodialysis Catheters (Orphan)



https://www.ncbi.nlm.nih.gov/books/NBK459269/

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