The heart is composed of a specialized tissue called cardiac muscle, which are voluntary muscles that work off electrical stimulants. Cardiac muscles contain myocardial cells, which consist of autorythmic cells. The autorythmic cells make up the sinoatrial node and the atrioventricular node, which are specialized “pacemaker” cells that spontaneously depolarize and repolarize, when pacemaker channels open, the cells will depolarize to threshold, followed by calcium channels opening to depolarize the peak levels. Once the action potential has peaked, potassium channels open for a short amount of time, causing the falling phase known as the refractory period. The refractory period is prolonged as a safety feature of the heart to protect itself from contracting too quickly or “racing” at a much higher rate. The membrane potential falling below threshold signals for the pacemaker channels to open again and repeat the cycle. Firing of the sinoatrial node initiates this wave of depolarization, which spreads to the atria via electrical connections between cardiac muscle cells called gap junctions, causing the atria to contract. Eventually, the slow depolarization ensures the ventricles properly fill with blood and contract after the atria. The homeostatic process maintains a regular heartbeat.
We will be using this entire cycle throughout our experiment, including the addition of certain chemicals and environmental factors. We are using variables such as electrical stimulation to see how it effects the contractions and cycles of a heart. We also use chemicals such as epinephrine, sodium ions and calcium ions to also see their effects on the contractions of a heart. The purpose of these experiments are to show the correlation of how certain chemicals and environmental variables can effect the rate of a contracting heart without any voluntary control.
We began the experiment by testing the base heart rate without any stimulates added to it that may cause it to vary. We then used the PhysioEx software to simulate a heart stimulation electrode that is directly connected to the ventricular muscle tissue. Starting with a single stimulus rapidly hitting the heart we tested what the results of this electrical stimulation did to the heart, this added stimulant caused the heart to temporarily flat line after an extrasystole occurred. The next part of the experiment changed the electrode from a direct heart stimulator to a vagus nerve stimulation electrode that is now connected directly to the ventricular muscle tissue, with this electrode we were able to conduct multiple stimulus to the heart that caused the heart rate to slow down until it eventually flat lined but soon after picked back up once the stimulants ended.
Once the electrical stimulation experiments were completed, the next experiment was to test how temperature may effect the heart rate. We expected the heart rate to lower as the temperature decreased; the starting temperature was 5 degrees Celsius. This temperature, as expected, caused the heart rate to lower be 11 beats per minute. Next we tested the effect of increasing the temperature drastically up to 32 degrees Celsius, which we expected would raise the heart rate as the temperature grew. That is exactly what happened once we saw the heart rate raised from 50 beats per minute to 70 beats per minute. All the changes that the varying temperatures made to the heart were the exact results we expected prior to the experiments.
Although the body itself produces certain chemicals that certain organs such as the heart needs to function, we tested what would happen if we added these chemicals to the body at a higher rate than is normally produced, and also some external chemicals that may effect the heart directly. We began with Pilocarpine, which is a chemical used more commonly in certain medications. Once the Pilocarpine solution was dispensed onto the heart it almost automatically caused the heart rate to drastically lower in beats per minute, you can also conclude that Pilocarpine acts as an antagonist to the activity of the heart. After Pilocarpine, we flushed the heart and next tested the effects of Atropine on the heart. We did the same procedure by adding an Atropine solution directly onto the heart, which caused the heart to have an opposite effect than the Pilocarpine, causing the heart rate to increase in beats per minute. Just like Pilocarpine, Atropine is also classified as an antagonist to the effects on heart activity. The next chemical that we tested is one that is produced in the body itself, this chemical is Epinephrine which is more commonly known as “adrenaline” in the body. The Epinephrine solution was added directly to the heart and, as expected, caused the heart rate to rise higher than any other chemical that was tested. The next chemicals were also found naturally in the body, these chemicals being calcium, sodium and potassium ions. Calcium and sodium ions had the same effects causing the heart rate to fluctuate and not stabilize, meanwhile the potassium ions acted differently, slowing the heart and even going through periods of compensatory pause.
After completing all of these experiments and logging them thoroughly, we are able to show the effects various stimulants may have on the heart. Many people do not realize how even the smallest things such as temperature change can effect the rate at which your heart is beating, they also don’t realize how the consumption of something may effect it as well. To show an example of this, if a patient in a hospital was given an overdose of calcium ions their heart would be affected and show signs of fluctuation with an eventual decrease of heart rate in between each fluctuation. This can be treated and eventually corrected using drugs such as calcium channel blockers, which help to block the entry of calcium ions to the heart, thus aiding the heart in its attempts of stabilizing it’s natural heart beat.
The other example we can use is a 67 year old man that has come to an emergency room of a hospital suffering from palpitations, dizziness, and shortness of breath. As the main waits in the emergency room he collapses and goes into cardiac arrest, a good response to this situation is to use Epinephrine. To explain why you must first understand that going into cardiac arrest means there has been a sudden stop in the functioning of your heart causing the patient to stop breathing and lose consciousness. Epinephrine is a drug that helps raise the beats per minute of a minute, so using Epinephrine on a patient who is in cardiac arrest can help kick start their heart over again and raise it to it’s regular heart rate. Another drug that can be looked at is Atropine which is something else that can be used for a patient who is in cardiac arrest, although it does not raise the heart rate as quickly as Epinephrine it still acts the same and helps bring the heart rate of the patient up. Atropine can also be paired with a vagal nerve stimulation to help increase and regulate a patient’s heartbeat. This can be used on someone suffering from cardiac arrest or something from conditions such as bradycardia which causes a person to naturally have a slower heart rate than they are suppose to.