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 Contraction2.3.3. 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

Heart Conduction System

Cardiac muscle cells have the ability to conduct action potentials from cell to cell through the gap junctions of the intercalated disks. This conduction, however, cannot account for the ordered, synchronous contractions observed in the heart. To ensure the proper sequence of contraction and to speed the conduction of the action potentials through the heart muscle, the heart is equipped with a specialized conduction system composed of non-contractile cardiac muscle cells that are modified for the task of generating and conducting action potentials. The autorhythmic cells discussed in the previous section are part of this system.

Electrical Conduction System of the Heart.
 Image was drawn by BYU-Idaho student Nate Shoemaker Spring 2016

Located on the posterior wall of the right atrium near the site of connection of the superior vena cava is the sinoatrial node (SA node). The SA node is composed of autorhythmic cells and is the “pacemaker” for the heart, generating the action potentials that initiate contraction. These action potentials then spread through the right and left atria, causing them to contract. Although cardiac muscle cells are perfectly capable of conducting action potentials from cell to cell, to achieve a synchronous contraction, the spread of depolarization must be tightly controlled. To aid the two atria in contracting simultaneously there is thought to be a special band of rapidly conducting tissue called Bachman’s bundle that quickly spreads the action potential to the left atrium.

Although physically connected by a ring of connective tissue called the cardiac skeleton, the atria and the ventricles are electrically isolated, such that the action potential cannot spread directly from the atria to the ventricles. Instead, the action potential is detected by the atrioventricular node (AV node) which is located in the floor of the right atrium near the interatrial septum. Again, there are specialized conduction pathways called the internodal pathways that quickly conduct the action potentials from the SA node directly to the AV node. The AV node then “delays” the action potential for approximately 0.15 seconds, allowing the atria to contract before the ventricles. This delay is due to the very slow speed of conduction in the AV node, ~0.05 m/sec. From the AV node, the action potential is conducted via the atrioventricular bundle (AV bundle or bundle of His) into the interventricular septum. In the septum the AV bundle splits into the right and left bundle branches that descend through the interventricular septum to the apex of the heart.

At the apex, the bundle branches split into numerous Purkinje fibers that then ascend the walls of the ventricles. The AV bundle, bundle branches, and Purkinje fibers conduct the action potentials much faster than the cardiac muscle fibers, 1-4 m/sec vs 0.3-0.4 m/sec, respectfully. This rapid conduction creates a more coordinated contraction of the ventricular muscle. Also, since the action potentials, and hence contractions, spread from the apex toward the base of the heart the blood is pushed up toward the large arteries exiting the ventricles.

It should be noted that even though the SA node is the pacemaker, the other components of the conducting system are also capable of spontaneously generating action potentials. Each has its own intrinsic rate of generating action potentials, the SA node has a rate of 60-80/minute, the AV node a rate of ~40/minute and the AV bundle and Purkinje fibers a rate of ~20/minute. The reason the SA node is the “pacemaker” is simply because it has the fastest rate and reaches threshold before the other areas. If the SA node becomes damaged or stops functioning the AV node can take over and the heart will continue to beat, albeit at a slower rate.

Sometimes excitable cells (pacemaker cells) can grow in the heart in other places besides the nodes. When this happens, we call the location an ectopic focus. This is usually not life-threatening, but over time can disrupt the normal conductance of the heart and alter the heartbeat, making it beat faster than normal or slower than normal. In most cases, the faster rate of the SA node will mask the other cells, but if the SA node becomes compromised, ectopic foci can begin to control the heart rate, a scary situation because the ectopic foci is not modulated by the nervous system. Ectopic foci can also alter electrocardiogram readings (ECG), appearing as extra deflections and causing misdiagnosis.

Cardiac Excitation Coupling
BYU-Idaho image by Becky T: Created Fall 2018

Now that you know how action potentials are generated and conducted in the heart, we need to study how these action potentials lead to contraction of the cardiac muscle cells. We have already explained that cardiac muscle is very much like skeletal muscle and that the mechanism of contraction is the same in both muscle types. Therefore, the key to cardiac muscle contraction is also calcium. As with skeletal muscle, calcium is stored intracellularly in the sarcoplasmic reticulum. However, unlike skeletal muscle, cardiac muscle also relies on extracellular calcium for proper functioning. This means that the extracellular level of calcium is very important for heart muscle function.

Intracellular stores of calcium in the well-developed sarcoplasmic reticulum of skeletal muscle can help buffer against blood calcium level changes, but heart muscle does not have this advantage. The heart muscle sarcoplasmic reticulum is much less developed and heart muscle fibers are more sensitive to extracellular calcium level oscillations. In fact, small changes in blood calcium levels can cause heart arrhythmias.

As might be expected, there are some important ion channels that mediate the entry of calcium. The first is a voltage-gated calcium channel found in the membranes of the T-tubules (L-Type Calcium Channels). These are the same channels discussed earlier that are responsible for the plateau phase of the action potential. When the action potential descends into the T-tubules these channels open, allowing calcium to diffuse into the cell. This calcium then binds to calcium release channels found in the membranes of the SR (these channels are also known as Ryanodine receptor, RyR, channels). The binding of calcium to these channels causes them to open allowing calcium to diffuse out of the SR and bind to troponin initiating contraction. Thus, extracellular calcium triggers the release of sarcoplasmic reticular calcium. This process is referred to as calcium-induced, calcium release. Once the signal ends, a calcium ATPase (SERCA) in the membranes of the SR pumps the calcium back into the SR and contraction ends. Since some of the calcium that is now in the cell came from the extracellular fluid, a Na+-Ca2+ exchanger (secondary active transport 3 Na+ to 1 Ca2+) moves calcium from the cytoplasm back to the extracellular fluid. The strength of the muscular contraction in the heart is dependent on the amount of calcium that enters; hence, there are mechanisms to regulate how much calcium enters the cells.

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