Cardio Electrophysiology Flashcards
What is repurfusion injury and why does it occur?
After an ischemic event, as cellular respiration continues progress into the anaerobic stage, free radicals and other toxic waste products begin to concentrate at the injury site. Once perfusion is restablished, a “sudden increase in blood and oxygen flow…triggers the activation of the inflammatory process, release of cytokines, and results in further damage to cells and their membranes.”
Ikhlas M, Atherton NS. Vascular Reperfusion Injury. [Updated 2022 Aug 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK562210/
What are intercalated discs?
“A junction between two adjoining cells is marked by a critical structure called an intercalated disc, which helps support the synchronized contraction of the muscle (Figure 19.2.1b). The sarcolemmas from adjacent cells bind together at the intercalated discs. They consist of desmosomes, specialized linking proteoglycans, tight junctions, and large numbers of gap junctions that allow the passage of ions between the cells and help to synchronize the contraction (Figure 19.2.1c).”
Biga, L. M., Dawson, S., Harwell, A., Hawkins, R., Kaufmann, J., Lemaster, M., Matern, P., Morrison-Graham, K., Quick, D., & Runyeon, J. (2019). Chapter 19. The Cardiovascular System: The Heart. In Anatomy & Physiology (pp. 1153–1255). essay, Openstax/Oregon State University.
What type of junction is responsible for transmitting the action potential from pacemaker cells to the rest of the cardiomyocytes (cardiac fibers)?
Gap junctions allow pacemaker cells to transfer this depolarization wave to the other cardiac msucles fibers, allowing for the heart to contract in a coordinated manner.
List the important structures of the heart’s conduction system.
- The sinoatrial node (SA node)
- The atroventricular node (AV Node)
- The atrioventricular bundle (aka the bundle of His)
- Right and left bundle branches
- Purkinje fibers
Biga, L. M., Dawson, S., Harwell, A., Hawkins, R., Kaufmann, J., Lemaster, M., Matern, P., Morrison-Graham, K., Quick, D., & Runyeon, J. (2019). Chapter 19. The Cardiovascular System: The Heart. In Anatomy & Physiology (pp. 1153–1255). essay, Openstax/Oregon State University.
Describe the action potential pacemaker cells
Pacemaker cells have a series of sodium channels that persistently allow for a small influx of Na+. As Na+ continues to enter the nodal cells, the intracellular charge becomes more and more positive, until reaching a membrane potential of -40 mv. After reaching this -40 mv threshold, voltage-gated Ca2+ channels open and rapildy depolarizes the cell, until its membrane potential reaches +5 mv and the influx ceases due to the voltage-gated Ca2+ channels closing. Also, once the membrane potential reaches +5 mV, voltage gated K+ channels open and potassium begins to flow out of the cell to repolarize the membrane back to -60 mv.
Biga, L. M., Dawson, S., Harwell, A., Hawkins, R., Kaufmann, J., Lemaster, M., Matern, P., Morrison-Graham, K., Quick, D., & Runyeon, J. (2019). Chapter 19. The Cardiovascular System: The Heart. In Anatomy & Physiology (pp. 1153–1255). essay, Openstax/Oregon State University.
How does the electrical pattern of cardiac contractile cells and pacemaker cells differ?
Cardiac muscle cells experience a plateau phase in their membrane potential prior to repolarizataion. This refractory period ensures that cardiac cells doe not experience another action potential before they cycle through their contraction. Furthermore, contractile cells have a much more stable resting phase, at -80 mV for atrial and -90 mV for ventricular contractile cells.
Biga, L. M., Dawson, S., Harwell, A., Hawkins, R., Kaufmann, J., Lemaster, M., Matern, P., Morrison-Graham, K., Quick, D., & Runyeon, J. (2019). Chapter 19. The Cardiovascular System: The Heart. In Anatomy & Physiology (pp. 1153–1255). essay, Openstax/Oregon State University.
Compared to skelatal muscle, how does contraction differ in cardiac cells? What is the cause of this difference?
(Think about the plateau phase of a cardiac fiber impulse)
The contraction of cardiac fibers is much longer (250 ms vs 30 ms) to prevent tetany (when muscle cells remain involuntarily contracted - which would prevent adequate perfusion)
Compared to skelatal muscle, how does contraction differ in cardiac cells? What is the cause of this difference?
The contraction of cardiac fibers is much longer (250 ms vs 30 ms) to prevent tetany (when muscle cells remain involuntarily contracted - which would prevent adequate perfusion). This long refractory period is due to the opening of slow Ca2+ channels while a few K+ channels are simultaneously open (allowing for a slow influx of Ca2+ and slow efflux of K+), which allows for a slow repolarization of the membrane potential. Once the membrane potential reaches approximately zero, the Ca2+ channels close and the rest of the K+ channels open, repolarizing the resting potential to -80 mV for atrial and -90 mV for ventricular cardiac cells.
What determines which pacemaker cells regulate the rate of contracdtion?
The packemaker cells that reach the action potential threshold (-40 mV) the fastest, therefore, the SA node is the pacemaker of the heart in healthy individuals. Moving from the most superior pacemaker cells (the SA nodal cells) to the most inferior (Purkinje fibers), the autorhythmic impuse rate becomes slower and slower.
What is the rate the SA node sets as the pacemaker without any nervous system or endocrine input?
80-100 bpm
What is the rate the AV node sets as the pacemaker without any nervous system or endocrine input?
40-60 bpm
What is the rate the atrioventricular bundle (bundle of His) sets as the pacemaker without any nervous system or endocrine input?
20-30 bpm
What is the rate the Purkinje fibers set as the pacemaker without any nervous system or endocrine input?
15-20 bpm
In the cardiac cycle, what is systole?
The contractile phase
In the cardiac cycle, what is diastole?
The filling phases
What is preload?
Preload is the degree of stretch on the heart before it
contracts (End-diastolic volume)
* Greater preload increases the force of contraction
**Frank-Starling Law of the Heart
**– the more the heart fills with
blood during diastole, the
greater the force of
contraction during systole
What is contractility? What is directly responsible for the degree of contractility of the heart?
Contractility is the strength of contraction at any given
preload (due to cytosolic calcium concentrations)
What is afterload? What are two disease processes that increase afterload?
-
Afterload: Pressure that must be overcome before
a semilunar valve can open - Increases in afterload cause stroke volume to
decrease
– Blood remains in ventricle at the end of systole -
Hypertension and atherosclerosis increase
afterload
