L10: Cardiac muscle 2 Flashcards
Diastolic Ca2+ leak> steady increase in membrane potential> triggers a Ca2+ release event before electrical stimulation.
> Arrhythmia
Ca2+ leak during diastole> cross-bridge cycling occurring during diastole> incomplete relaxation> reduces the amount of filling that can occur during diastole in preparation for the next heart beat
Each of these localised Ca2+ sparks will trigger the Na+/Ca2+ exchange in that region. Ca2+ is extruded by Na+/Ca2+ exchange in these localised areas. Because 3Na+ per 1 Ca2+ has an electrogenic effect> +ve charge in> depolarise the localised regions. If sufficient depolarisation occurs> these diastolic leaks will trigger a Ca2+ transient.
how does NCX contribute to myocyte membrane potential?
In the context of myocyte membrane potential, NCX is involved in both depolarization and repolarization phases. During the action potential, when the myocyte is depolarized, the influx of sodium ions through voltage-gated sodium channels leads to an increase in intracellular sodium concentration. NCX then utilizes this increased intracellular sodium concentration to extrude sodium out of the cell, simultaneously exchanging it for calcium ions.
The extrusion of calcium through NCX helps in the repolarization phase of the action potential. Calcium plays a significant role in the contraction of myocytes, and its removal from the cytoplasm during repolarization is crucial for relaxation and preventing sustained contractions. By transporting calcium out of the cell, NCX contributes to reducing the intracellular calcium concentration, allowing the myocyte to relax and prepare for the next contraction.
increase HR.
What happens to time in systole and diastole?
Increase HR> decreasing the time for diastole more than systole> reducing time for filling. Counterintuitive if want to increase SV.
Increase in HR means there is less time for filling and less time for ejection.
force of contraction (in the heart) is modulated by:
2 main ways to change the strength of contraction?
Frank-Starling concept
The Frank-Starling concept, also known as the Frank-Starling law or the Frank-Starling mechanism, describes the relationship between the length of cardiac muscle fibers and the force of contraction in the heart. It states that the greater the stretch (preload) placed on cardiac muscle fibers, the greater the force of contraction and subsequent stroke volume (the amount of blood pumped out of the heart with each beat).
The Frank-Starling concept is based on the intrinsic properties of cardiac muscle fibers. When the muscle fibers are stretched, such as by an increased volume of blood returning to the heart during diastole (the relaxation phase of the cardiac cycle), it leads to an increased sarcomere length. This increased sarcomere length enhances the overlap between actin and myosin filaments, optimizing the cross-bridge formation and allowing for a more forceful contraction.
The underlying mechanism behind the Frank-Starling concept involves the increased sensitivity of the contractile proteins (actin and myosin) to calcium ions. When the muscle fibers are stretched, it promotes an optimal alignment of the contractile proteins and the calcium release channels within the sarcoplasmic reticulum of the muscle cells. This alignment allows for a more efficient interaction between calcium ions and the contractile proteins, leading to an enhanced force of contraction.
The Frank-Starling concept is essential for maintaining cardiac output, which is the amount of blood pumped by the heart per minute. By increasing the force of contraction in response to increased preload, the heart can adapt to changes in venous return and maintain an adequate cardiac output to meet the body’s demands. It ensures a balance between the blood entering the heart and the blood ejected from the heart, optimizing the pumping efficiency.
The Frank-Starling mechanism has clinical implications as well. In conditions such as heart failure, where the heart’s ability to pump effectively is compromised, the Frank-Starling mechanism may be impaired. This can result in decreased contractility and reduced stroke volume. Medical interventions such as the use of inotropic drugs or mechanical devices aim to augment cardiac contractility and restore the Frank-Starling mechanism to improve cardiac function.
Overall, the Frank-Starling concept describes how the heart adjusts its force of contraction based on the degree of stretch of the cardiac muscle fibers, ensuring an efficient pumping of blood and maintaining cardiac output.
