ECG cardiac infarction and ischemia
43,414views
00:00 / 00:00
Videos
Notes
ECG cardiac infarction and ischemia
Year 1
Playlist
Skin histology
Introduction to pharmacology
Skin anatomy and physiology
Wound healing
Introduction to biostatistics
Types of data
Vaccinations
Inflammation
Nuclear structure
Pharmacodynamics: Agonist, partial agonist and antagonist
DNA structure
Anemia: Clinical (To be retired)
Anatomy of the heart
Hypertension
Hypertension: Clinical (To be retired)
Myocardial infarction
Clinical trials
Mitosis and meiosis
Calcium channel blockers
Class III antiarrhythmics: Potassium channel blockers
Pharmacokinetics: Drug elimination and clearance
Pharmacokinetics: Drug metabolism
Pharmacokinetics: Drug absorption and distribution
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Opioid agonists, mixed agonist-antagonists and partial agonists
Cardiac muscle histology
Blood histology
Artery and vein histology
Arteriole, venule and capillary histology
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
Osmotic diuretics
Carbonic anhydrase inhibitors
Bone histology
Cartilage histology
Skeletal muscle histology
Central nervous system histology
Peripheral nervous system histology
Diabetes mellitus
Phenylketonuria (NORD)
Homocystinuria
Familial hypercholesterolemia
Fats and lipids
Cholesterol metabolism
Carbohydrates and sugars
Proteins
Extracellular matrix
Cytoskeleton and intracellular motility
Cell signaling pathways
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Amino acid metabolism
Nitrogen and urea cycle
Nucleotide metabolism
Introduction to biostatistics
Types of data
Probability
Mean, median, and mode
Range, variance, and standard deviation
Standard error of the mean (Central limit theorem)
Normal distribution and z-scores
Type I and type II errors
Study designs
Ecologic study
Cross sectional study
Case-control study
Cohort study
Randomized control trial
Sensitivity and specificity
Positive and negative predictive value
Test precision and accuracy
Atrophy, aplasia, and hypoplasia
Hyperplasia and hypertrophy
Metaplasia and dysplasia
Bone tumors
Osteomyelitis
Osteoporosis
Osteomalacia and rickets
Septic arthritis
Cauda equina syndrome
The Oral Microbiota and Systemic Health
Bacterial structure and functions
Nasal cavity and larynx histology
Trachea and bronchi histology
Bronchioles and alveoli histology
Inheritance patterns
Mendelian genetics and punnett squares
Hardy-Weinberg equilibrium
DNA mutations
Neuromuscular junction and motor unit
Pharmacodynamics: Drug-receptor interactions
Cholinergic receptors
Adrenergic receptors
Blood products and transfusion: Clinical (To be retired)
Muscle contraction
Sliding filament model of muscle contraction
Nervous system anatomy and physiology
Parasympathetic nervous system
Slow twitch and fast twitch muscle fibers
Enteric nervous system
Sympathetic nervous system
Resting membrane potential
Neuron action potential
Cell membrane
Selective permeability of the cell membrane
Blood groups and transfusions
Blood components
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Body fluid compartments
Movement of water between body compartments
Platelet plug formation (primary hemostasis)
Coagulation (secondary hemostasis)
Clot retraction and fibrinolysis
Carbon dioxide transport in blood
Bones of the vertebral column
Bones of the vertebral column
Joints of the vertebral column
Joints of the vertebral column
Joints of the wrist and hand
Bones of the upper limb
Fascia, vessels and nerves of the upper limb
Anatomy of the brachial plexus
Anatomy of the arm
Muscles of the forearm
Vessels and nerves of the forearm
Muscles of the hand
Anatomy of the sternoclavicular and acromioclavicular joints
Anatomy of the glenohumeral joint
Anatomy of the elbow joint
Anatomy of the radioulnar joints
Paired t-test
Two-sample t-test
Hypothesis testing: One-tailed and two-tailed tests
Methods of regression analysis
Spearman's rank correlation coefficient
Mann-Whitney U test
Chi-squared test
Kaplan-Meier survival analysis
Incidence and prevalence
Relative and absolute risk
Odds ratio
Attributable risk (AR)
Direct standardization
Indirect standardization
Disease causality
Selection bias
Information bias
Confounding
Innate immune system
Complement system
T-cell activation
B-cell activation and differentiation
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Upper respiratory tract infection
Heart failure
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Dyslipidemias: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Familial hypercholesterolemia
Deep vein thrombosis and pulmonary embolism: Pathology review
Chronic venous insufficiency
Ischemia
ECG cardiac infarction and ischemia
Angina pectoris
Aneurysms
Asthma: Clinical (To be retired)
Chronic bronchitis
Emphysema
Pulmonary hypertension
Idiopathic pulmonary fibrosis
Bronchiectasis
Lung cancer
Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)
Respiratory distress syndrome: Pathology review
Myocardial infarction
Vasculitis
ACE inhibitors, ARBs and direct renin inhibitors
Adrenergic receptors
Adrenergic antagonists: Alpha blockers
Class II antiarrhythmics: Beta blockers
Adrenergic antagonists: Beta blockers
Antiplatelet medications
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Pulmonary corticosteroids and mast cell inhibitors
Arteriole, venule and capillary histology
Microcirculation and Starling forces
Blood pressure, blood flow, and resistance
Resistance to blood flow
Lymphatic system anatomy and physiology
Laminar flow and Reynolds number
Compliance of blood vessels
Pressures in the cardiovascular system
Physiological changes during exercise
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Frank-Starling relationship
Pressure-volume loops
Changes in pressure-volume loops
Cardiac work
Cardiac preload
Cardiac afterload
Law of Laplace
Baroreceptors
Renin-angiotensin-aldosterone system
Chemoreceptors
Electrical conduction in the heart
Action potentials in pacemaker cells
Action potentials in myocytes
Cardiac excitation-contraction coupling
Cardiac contractility
ECG basics
Cerebral circulation
Coronary circulation
Respiratory system anatomy and physiology
Reading a chest X-ray
Lung volumes and capacities
Anatomic and physiologic dead space
Alveolar surface tension and surfactant
Ventilation
Regulation of pulmonary blood flow
Zones of pulmonary blood flow
Pulmonary shunts
Ventilation-perfusion ratios and V/Q mismatch
Airflow, pressure, and resistance
Diffusion-limited and perfusion-limited gas exchange
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Carpal tunnel syndrome
Assessments
ECG cardiac infarction and ischemia
Flashcards
0 / 20 complete
USMLE® Step 1 questions
0 / 1 complete
High Yield Notes
8 pages
Flashcards
ECG cardiac infarction and ischemia
of complete
Questions
USMLE® Step 1 style questions USMLE
of complete
External Links
Transcript
Content Reviewers
Rishi Desai, MD, MPHAn electrocardiogram - an ECG - or the dutch and german version of the word - elektrokardiogram or EKG, is a tool used to visualize “gram” the electricity “electro” that flows through the heart “cardio”.
An ECG tracing specifically shows how the depolarization wave moves during each heartbeat - which is a wave of positive charge - looks from the perspective of different sets of electrodes.
This particular set of electrodes is called lead II, with one electrode on the right arm and the other on the left leg, so essentially when the wave’s moving toward the left leg electrode, you get a positive deflection, like this big positive deflection correspond to the wave moving down the septum.
To read an ECG there are a few key elements to keep in mind, one of them includes figuring out if part of the heart has is suffering from ischemia or has undergone an infarction.
The term ischemia means that blood flow to a tissue has decreased, which results in hypoxia, or insufficient oxygen in that tissue, whereas infarction goes one step further and means that blood flow has been completely cut off, resulting in necrosis, or cellular death. That typically happens if blood flow has been cut off for about 20 minutes.
In the heart, ischemia and infarction can be transmural, affecting the entire thickness of the myocardium, or subendocardial, affecting just the innermost part of the myocardium - the part just beneath the endocardium.
Out of all four chambers of the heart, the ECG is most sensitive to transmural or subendocardial ischemia or infarction in the left ventricle because that’s the chamber with the thickest walls and therefore has the most cardiac tissue.
Alright, let’s start with subendocardial ischemia, which might happen when there’s incomplete blockage - let’s say 70% - in a coronary artery.
In that situation, at rest there’s enough blood flowing through to meet the demand of the myocardium, but during exercise there’s not enough to meet the increased demand of the myocardium.
Summary
Cardiac ischemia means that blood flow to the cardiac muscle tissue has decreased, which can lead to poor oxygen supply or hypoxia. Myocardial infarction means that the blood flow is completely cut off, resulting in cellular death or necrosis of the affected part of the heart muscle.
ECG changes associated with myocardial infarction and ischemia can be difficult to differentiate. Generally, ischemia will present with inverted T waves and flat or downsloping ST-segment depression, whereas myocardial infarction will show ST-segment elevation, T wave inversion, and Q waves.
The best way to differentiate acute myocardial infarction (AMI) from ischemia is to look at the changes in multiple leads. AMI will typically cause ST elevation in two or more contiguous leads, while ischemia may only cause ST elevation in one lead. In addition, AMI will usually cause Q waves, while ischemia typically does not.
Sources
- "Medical Physiology" Elsevier (2016)
- "Physiology" Elsevier (2017)
- "Human Anatomy & Physiology" Pearson (2017)
- "Principles of Anatomy and Physiology" Wiley (2014)
- "The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction" The American Journal of Emergency Medicine (2009)
- "Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction" Journal of the American College of Cardiology (2000)
Copyright © 2023 Elsevier, except certain content provided by third parties
Cookies are used by this site.
USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME). COMLEX-USA® is a registered trademark of The National Board of Osteopathic Medical Examiners, Inc. NCLEX-RN® is a registered trademark of the National Council of State Boards of Nursing, Inc. Test names and other trademarks are the property of the respective trademark holders. None of the trademark holders are endorsed by nor affiliated with Osmosis or this website.
