1. (30 points) Electrical activity stimulates the muscular contractions needed f
ID: 3479168 • Letter: 1
Question
1. (30 points) Electrical activity stimulates the muscular contractions needed for the heart to function as a pump.
- Describe the roles of K+, Na+, and Ca2+ in the production of a pacemaker potential and an action potential in a contractile cardiocyte.
- How does electrical activity in the pacemaker cells stimulate electrical activity in the contractile cells?
- How does the plateau phase in the contractile cells enable normal heart function?
- Explain how hyperkalemia and hypokalemia would affect heart function and why those effects would be observed.
- Digoxin is a positive inotropic agent. What does that mean and by what mechanism does it influence heart function?
- Metoprolol is a negative chronotropic agent. What does that mean and by what mechanism does it influence heart function?
Explanation / Answer
- At the peak of each impulse, K+ ions go from ICF to ECF and bring about repolarization. K current declines, and a channel permeable to both Na+ and K+ is activated (h channel) and the membrane begins to depolarize, forming the first part of the prepotential. Ca2+ channels then open. The calcium current (ICa) due to opening of T channels completes the prepotential, and ICa due to opening of L channels produces the impulse.
- Depolarization initiated in the SA node spreads radially through the atria and converges on the AV node. A delay of about 0.1 s (AV nodal delay) occurs before excitation spreads to the ventricles. From the top of the septum, the wave of depolarization spreads in the rapidly conducting Purkinje fibers to all parts of the ventricles in 0.08–0.1 s.
- The sarcoplasmic reticulum of cardiomyocytes is not very extensive and does not provide a sufficient store of calcium ions. A large amount of calcium enters the cardiomyocytes through L-type calcium channels on the cardiomyocyte membrane during the plateau Phase of the cardiac action potential, that is essential for cardiac contraction
- Hypokalemia cause significant Q-T interval prolongation with subsequent risk of torsade des pointes, ventricular fibrillation and sudden cardiac death. Hyperkalemia cause peaked T waves, wider QRS complexes and result in bradycardia, asystole and sudden death.These effects are due to affection of cardiac resting membrane potential and repolarisation phase of action potential.
- Digoxin is a positive inotropic agent, that means it causes increased force of cardiac contraction.
By inhibiting the Na+/K+-ATPase, digoxin cause intracellular sodium concentration to increase. This then leads to an accumulation of intracellular calcium via the Na+-Ca++ exchange system. Increased intracellular calcium causes more calcium to be released by the sarcoplasmic reticulum, thereby making more calcium available to bind to troponin-C, which increases contractility (inotropy).
- Metoprolol is a negative chronotropic agent. This means metoprolol decreases heart rate.
Mechanism – it decreases speed of the depolarizing effect of Ih (hyperpolarisation current), and the rate of spontaneous discharge decreases, decreasing heart rate.
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