CoverModule 1.0. Homeostasis, Membranes, Electrophysiology and ANS1.1. Homeostasis1.1.1. Homeostasis Defined1.1.2. Homeostatic Control Systems1.1.3. Feedback Response Loop1.2. Cell Transport; Water & Solutes1.2.1. Fluid Compartments1.2.2. Osmosis1.2.3. Diffusion of Solutes1.2.4. Active Transport1.2.5. Bulk Transport1.3. Electrophysiology1.3.1. Ions and Cell Membranes1.3.2. Membrane Potentials1.3.3. Graded Potential1.3.4. Action Potentials1.3.5. Refractory Periods1.3.6. Propagation of an Action Potential1.4. The Synapse1.5. The Autonomic Nervous System1.5.1. Organization of the Nervous System1.5.2. Structural Organization of the ANS1.5.3. The SNS and the PNS1.5.4. The Enteric Nervous System1.5.5. Physiology of the ANS1.5.6. Neurotransmitters of the ANS1.5.7. Receptors of the ANS1.5.8. Actions of the Autonomic Nervous System1.5.9. Table of Actions for the SNS and PNS and Some Common DrugsModule 2.0. Skeletal Muscle and Special Senses2.1. Structural Organization of Skeletal Muscle2.2.1. Neuromuscular Junction, Excitation-Contraction Coupling2.2.2. Muscle Contractures and Cramps2.3. Whole Muscle Contraction, Fiber Type, Fatigue and Muscle Pharmacology2.3.1. Motor Units2.3.2. Factors that Influence the Force of Contraction2.3.2. Factors that Influence the Force of Muscle Contraction2.3.3. Energy Source for Muscle Contraction2.3.4. Skeletal Muscle Fiber Types2.3.5. Fatigue2.3.6. Muscle Pharmacology2.4. Smooth Muscle2.4.1. Smooth Muscle Contraction2.5. Control of Body Movement2.5.1. Voluntary Control of Muscle2.5.2. Reflexes2.6. Taste and Smell2.6.1. Taste2.6.2. The Sense of Smell2.7. Vision2.7.1. Structure of the Eye2.7.2. Focusing Light on the Retina2.7.3. Converting Light to Action Potentials2.7.4. The Retina2.7.5. Phototransduction2.7.6. Receptive Fields2.8. Hearing and Equilibrium2.8.1. The Nature of Sound2.8.2. The Hearing Apparatus2.8.3. Sound Vibrations to Action Potentials2.8.4. The Sense of Balance and EquilibriumModule 3.0. Cardiovascular System3.1. Structure of the Heart3.1.1. Chambers and Circulation3.2. Cardiac Cell Action Potentials3.2.1. Action Potentials in Cardiac Muscle Cells3.2.2. Action Potentials in Cardiac Autorhythmic cells3.2.3. Cellular Mechanisms of Inotropy and Chronotropy3.3. Electrophysiology of Heart Muscle3.3.1. Heart Conduction System3.3.2. Electrocardiogram (ECG)3.3.3. Abnormal ECG - Current of Injury3.4. The Cardiac Cycle3.4.1. Cardiac cycle3.4.2. Cardiac Measurements and Pressure Volume Loops3.5. Blood vessels and Blood Pressure3.5.1. Arteries and Veins3.5.2. Capillaries3.5.3. Blood Pressure Regulation and Shock3.5.4. Capillary Exchange3.5.5. Myogenic and Paracrine Regulation of Vasoconstriction and Vasodilation3.6. Blood3.6.1. Composition of Blood3.6.2. Hematopoeisis3.6.3. Breaking Down Red Blood Cells3.6.4. HemostasisModule 4.0. Urinary and Respiratory Systems4.1. Function and Structure of the Kidney4.1.1. Urinary System Function4.1.2. Functional Anatomy of the Urinary System4.1.3. The Nephron: Functional Unit of the Kidney4.1.4. The Renal Corpuscle: Bowman's Capsule4.2. Physiology of Urine Production4.2.1. Filtration4.2.2. Renal Clearance4.2.3. Tubular Reabsorption4.2.4. Urine Concentration and Dilution4.2.5. Hormonal Regulation of Urine Production4.3. Acid/Base Balance4.3.1. Buffers4.3.2. Acid/Base Disturbances4.4. The Respiratory System4.4.1. Respiratory System Structure and Function4.4.2. Respiratory Membrane4.4.3. Respiratory pressures and Inspriation/Expiration4.4.4. Alveoli and Surfactant4.4.5. Pneumothorax4.4.6. Pressure-Volume Loops and the Work of Breathing4.5. Gas Exchange and Transport4.5.1. Gas Laws4.5.2. Partial Pressure Gradients in the Lung4.5.3. Alveolar Gas Equation4.5.4. Oxygen and Carbon Dioxide Transport in the Blood4.5.5. Alveolar Ventilation4.5.6. Ventilation/Perfusion Ratio4.6. Chronic Bronchitis and Emphysema4.6.1. Respiratory Control by the Medulla Oblongata4.6.2. Chemicals that Regulate VentilationModule 5.0. Digestive, Endocrine and Reproductive Systems5.1. Functional Anatomy of the Digestive System5.1.1. Layers of the Digestive Tract5.1.2. Enteric Nervous System5.1.3. Organs of the Digestive System5.2. Digestion5.2.1. Carbohydrates5.2.2. Proteins5.2.3. Lipids5.2.4. Lipoproteins5.3. Regulation of Digestive Secretions5.4. Endocrine System5.4.1. Overview of the Endocrine System5.4.2. Hormone Receptors5.4.3. Hormones of the Body5.4.4. Other Hormones: Melatonin and Pheromones5.5. The Hypothalamus and Pituitary Gland5.5.1. Structure and Function of the Hypothalamus and Pituitary Gland5.5.2. The Posterior Pituitary5.5.3. The Anterior Pituitary5.5.4. Growth Hormone5.5.5. Prolactin5.5.6. Thyroid Hormones5.5.7. Adrenal Hormones5.6. Pancreas5.6.1. Insulin and Glucagon5.6.2. Diabetes Mellitus5.7. Reproductive System Anatomy5.7.1. Female Reproductive Anatomy5.7.2. Male Reproductive Anatomy5.7.3. Sexual Development at Puberty5.7.4. Male Reproductive Endocrine Axis5.7.5. Spermatogenesis5.7.6. Female Reproductive System: Oogenesis5.7.7. Ovulation and Fertilization5.7.8. The Ovarian Cycle5.7.9. The Uterine Cycle5.7.10. PregnancyAppendix A. GenderAppendix B. The Placebo EffectB.2.1. The Placebo EffectB.2.2. Examples of the Placebo EffectB.2.3. How do Placebos Work?B.2.4. Are Placebos Ethical?B.2.5. How do we validate actual effectiveness of placebosB.2.6. Tips for evaluating scientific evidenceB.2.7. What about Faith Healings
3.3.3

Abnormal ECG - Current of Injury

3.3.3 - Abnormal ECG – Current of Injury

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Images by JS BYU-I F17

Abnormal ECGs could result in another 20 pages or more, we will discuss a couple of important abnormal patterns derived from what we call a “current of injury”.  When an area of the heart experiences a current of injury, due to damaged cells, this current of injury ends up causing the baseline “isoelectric” line to either raise or lower. This is because damaged cells have trouble maintaining resting membrane potentials and thus become depolarized. This abnormal depolarization creates an area in the heart that has negative charges on the outside of the cells in that region. The negative charge creates an abnormal dipole, meaning it creates a current when the heart should not be having a current. As a result, the ECG machine, which has been programmed to not see current at rest in the heart, automatically adjusts the baseline (isoelectric point) to filter out what it considers background noise, making a new baseline.

Typically this current of injury occurs in the ventricles and will not become evident until the end of the “S” wave. Why? This is because when the ventricles are fully depolarized (at the end of the “S” wave), all of the ventricular cells are depolarized and this “current of injury” is temporarily suspended (no more dipole because all the cells are now negative on the outside) and the ECG machine will return to the original or “normal” isoelectric baseline. However, as the ventricles repolarize and switch the nondamaged cells back to a positive polarity on the outside surface again, the current of injury will return because the damaged cells will again appear more negative on the external surface, making the dipole at rest appear again and causing the ECG machine to make another adjustment. The resulting ECG will show different abnormal waves depending on the severity of the current of injury. Some of these abnormal waves will be addressed below.

Inverted T waves

To understand an inverted T wave, lets first review normal T waves. Normal T waves are upright because the first cells to repolarize are epicardial cells and the last are the endocardial cells. This pattern of repolarization results in a vector opposite to that of depolarization because the electrical vector has a positive tail moving towards a negative sensor (if we set up the ECG sensor pads to simulate lead II). Thus, for the T wave to be inverted it must repolarized in the opposite direction, or stated another way the endocardium must repolarize before the epicardium.  

Hypoxia in the endocardium can induce a state where the endocardium repolarizes before the epicardium. How? As the endocardium gets less oxygen than normal, the production of ATP decreases which in turn reduces the activity of the Na/K ATPase pump and activates the IK (ATP) channels. The reduction in pump activity induces a relative depolarization in the hypoxic cells and the activation of the I K (ATP) channels leads to a quicker repolarization. Therefore, rather than depolarizing and repolarizing last, the endocardium will now depolarize and repolarize before the epicardium, switching the electrical vector. The switched electrical vector will now have a positive tail moving towards a positive sensor (inferior lateral part of the heart) and this causes the T wave to deflect down instead of up.  Upside down T waves are shown in the image above (top left).

ST depression

A classic ST depression is caused by a negative vector at rest (due to hypoxic cells) that is oriented towards a positive sensor. The image above shows this in the top right corner as a blackened area on the inferior lateral wall of the left ventricle. Notice that the electrical vectors are oriented in a way that the “average” vector would extend in an inferior/lateral direction. If sensors were set up to simulate lead II, we would have a negative tail vector (-à) oriented towards a positive sensor and this would cause an ECG deflection in an upward direction.

Thus, because the background vector is causing an upward interference, the ECG machine will set the isoelectric point above its normal point. In the picture below, you can see that compared to the normal ECG, the current of injury has caused the ECG baseline to deflect upward. The other waves including P, Q, and R all occur relative to this new baseline (deflected upward because of the current of injury).  At the “S” wave however, all the cells of the ventricles are depolarized and so all the cells are negative on the outside surface. We don’t have an area of negative setting up a dipole with an area that is still positive. So, at this point, the ECG will try to draw a line at the original base line (at the point of the S wave). However, as the heart repolarizes, the repolarization will move past the hypoxic cells and leave them still negative on the outside (after repolarization) but everywhere else repolarized to positive on the outside. The ECG will sense a background current of injury again and gradually deflect upward again to finish the T wave. This creates a shape recognized as an ST depression and suggests that there is an area of endocardium that is hypoxic.The abreviation for this is called NSTEMI or nonSTEMI, which stands for Non ST Elevated Myocardial Infarction. 

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Image by JS BYU-I W19

ST elevation

A classic ST elevation is caused by an area of hypoxic cells that involves the entire thickness of an area of the ventricular wall (usually toward the inferior pole of the ventricle). The image above shows this in the bottom center as a blackened area that crosses the entire wall thickness. This is often called a “transmural” infarct. Notice that the electrical vectors are oriented in a way that the “average” vector would extend in more of a superior direction. If sensors were set up to simulate lead II, we would have a negative tail vector oriented towards a negative sensor and this would cause an ECG deflection in an downward direction.

This downward deflection is again called a “current of injury” but is a downward deflection this time. In the picture below, you can see that compared to the normal ECG, the current of injury has caused the ECG baseline to deflect downward. The other waves including P, Q, and R all occur relative to this new baseline (deflected downward because of the current of injury). At the “S” wave however, all the cells of the ventricles are depolarized and so all the cells are negative on the outside surface. We don’t have an area of negative setting up a dipole with an area that is still positive. So, at this point, the ECG will try to draw a line at the original base line (at the point of the S wave). However, as the heart repolarizes, the repolarization will move past the transmural injury and leave them still negative on the outside (after repolarization) but everywhere else repolarized to positive on the outside. The ECG will sense a background current of injury again and gradually deflect downward again to finish the T wave. This creates a shape recognized as an ST elevation and suggests that there is an area where hypoxia exists across an entire area of ventricular thickness. Transmural infarcts reflect that there is even greater loss of blood flow than the inverted T waves or the ST depression. Sometimes a patient can reveal an ST depression that converts to an ST elevation which would suggest that heart damage is progressing and could suggest that emergency intervention is necessary. The abreviation for this is called STEMI, which stands for ST Elevated Myocardial Infarction. 

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Image by JS BYU-I W19

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