Episode 35 - Cardiovascular system - Heart rate

Welcome to episode 35 of Pulse of Physiology. I'm your host, Dr. Jim Davis, and today we're discussing the regulation of heart rate, which is a crucial factor in maintaining cardiovascular function. Heart rate is influenced by both intrinsic pacemaker activity and extrinsic factors, such as the autonomic nervous system and circulating hormones. In the next episode, we'll build on this by exploring the conduction system of the heart, but for now, let's break down how heart rate is controlled and how it impacts overall cardiac function. So to start off, we need to understand what is meant by "chronotropic agents." The term "chronotropic" comes from the Greek word "chrono," which means "time." So when we talk about "chronotropic agents," we're referring to things that influence the timing of the heart contractions. Chronotropic agents are categorized into positive and negative types. Positive chronotropic agents increase heart rate. Negative chronotropic agents decrease heart rate. Examples of these agents include norepinephrine, which is a positive chronotropic agent which increases heart rate by enhancing sodium permeability in pacemaker cells. Acetylcholine is a negative chronotropic agent which slows heart rate by increasing potassium permeability. Now, the autonomic nervous system plays a major role in heart rate modulation with input from both sympathetic and parasympathetic branches. The sympathetic nervous system increases heart rate by releasing norepinephrine, which binds to beta-1 adrenergic receptors on pacemaker cells. This leads to an increase in sodium permeability, allowing more sodium to enter the cell. A steeper drift phase in the pacemaker potential means the membrane potential reaches threshold sooner. Ultimately, more frequent action potentials causes heart rate to increase. Now, the parasympathetic nervous system, on the other hand, decreases heart rate through acetylcholine bind to muscarinic cholinergic receptors on pacemaker cells. This results in increased potassium permeability, causing potassium to leave the cell. Ultimately, this hyperpolarizes the membrane, making it more negative and harder to reach threshold. However, it's important to note that there is still more sodium leaving the cell than there is potassium leaving the cell. Otherwise, we'd never hit threshold, which would mean your heart rate would stop. Now, a flatter drift phase means it takes longer to reach threshold, which reduces that heart rate. Now, heart rate directly influences how much blood fills the ventricles before contraction. This affects endiastolic volume, which in turn influences stroke volume and cardiac output. Now, endiastolic volume is the amount of blood in the heart at the end of diastole, which means the end of relaxation, which means the end of filling. Now, when someone has a low heart rate, they have more filling time, which means endiastolic volume will be higher. And ultimately, this leads to a stronger contraction according to the Frank Starling law, which we'll discuss in more detail during the stroke volume episode. The heart has more time to stretch and fill with blood, which leads to that greater stroke volume. Now, if someone has a high heart rate, this means that there is less filling time, which will lead to a lower endiastolic volume, which leads to a weaker contraction. At very high heart rates, ventricles don't have enough time to fill properly, which may actually reduce cardiac output. Now, this relationship explains why extreme tachycardia or extremely high heart rate can actually reduce cardiac efficiency despite the heart beating faster. So, let's summarize with our three key takeaways. Chronotropic agents influence heart rate with norepinephrine increasing heart rate and acetylcholine decreasing heart rate. The sympathetic nervous system speeds up heart rate by increasing sodium permeability while the parasympathetic nervous system slows it down by increasing potassium permeability. Finally, heart rate impacts filling time and endiastolic volume with slower heart rates allowing for more filling and greater stroke volume. And so that's all for episode 35 of the Pulse of Physiology. I hope this episode has clarified the mechanisms for controlling heart rate and their effects on cardiac output. Join me next time for episode 36 where I'll explore the conduction system of the heart and how electrical impulses coordinate ventricular contractions. Until then, keep questioning, keep exploring, and stay curious.