Frog Lab Report

6 June 2017

When the heart “skips a beat”, it is actually Just your heart’s normal cardiac rhythm being somehow interrupted and causing an extra beat or a skipped beat (compensatory pause). The atria are supposed to contract first, but in this case the ventricles contract first which is wrong and the heart has to then correct itself by pausing and waiting for the atria to contract again (1). This is what feels like a skipped beat, and it appears like one too on an ECG because there is a big pause between atrial contractions.

To cause the ventricles to contract early, an electrical tumulus (or one of many other problems that could potentially affect the heart, in this case it is electrical shock) must be applied during atrial relaxation to cause the ventricles to contract before the atria. Different chemicals, or reagents, cause different things to happen to the heart. Some reagents, like nor epinephrine, are released during stressful times and cause the heart rate to increase and contract with more force.

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This is an example of an excitatory neurotransmitter, which can be depleted in many ways, for example by a reagent that does the opposite of what it does, which would be to decrease heart rate (2). Some reagents, like, cause the heart rate to dramatically decrease and could potentially be harmful if not corrected. But, these effects can be inhibited by reagents like atropine and allow heart rate to return to normal. Others, like potassium chloride, could cause the heart to stop completely and are used for such methods like lethal injection in prisons.

Given all of this information, our hypothesis was that the frog hearts used in this experiment would follow the expectations that this background information tells us. When stimulated at the right time the heart would have an extra systole event, when iv en an excitatory neurotransmitter the heart rate and contraction force would increase, etc. The frog hearts, if they are healthy and functioning properly, will react normally to all of the stimuli/reagents applied to it. Materials and Methods: Before the dissection, the equipment and strength of the frogs heart beat needed to be tested.

So, ECG pins were inserted in both shoulders and right thigh of the frog via small incisions made with scissors. We first tested lead l, which involved placing the ground pin in the right thigh, the positive pin in the left shoulder, and the negative pin in the right shoulder. Once the pins were in place, the equipment was set up so that the settings were at single event mode, looms event interval, Oms event delay, 10ms pulse width, and single pulse. The SIU was set at 1 mA range, positive polarity, and 20. 0% of range. The settings were 2K gain, AC, 30HZ low frequency, and 0. kHz high frequency. Finally, the transducer amplifier was set at bridge mode, 100 filter, and 20 sensitivity. Once all of the equipment and the frog were set up, lead I ECG recordings were made until good records were recorded. The R wave, duration of atrial depolarization, duration of electrical A-V delay, duration of ventricular depolarization, and duration of electrical ventricular depolarizations were then measured. Then, the set up was changed to represent lead II, which only changed the location of the positive pin to the left thigh instead of shoulder.

Once this change took place, the same Now that baseline recordings were measured, the frog could be dissected. First, all four limbs were pinned to the dissecting pan with heavy pins. Next, the skin of the abdomen and chest (and some of the neck) was removed using forceps and scissors. It was removed in a rectangular shape, going across the abdomen and up the sides and then across the neck. Then the muscle was removed in the same fashion, and the heart was visible. The pericardium was removed unintentionally during muscle removal, so it was not possible to observe it.

Now that the heart was visible and accessible, a piece of thread approximately 20cm long was looped on both ends. One end was attached to a Z pin, which was attached to the very end where the apex is because that is Just tissue. The other end attached to an S-hook on a transducer connecting to the machinery and computer. The equipment and frog were positioned so that the string was taut when the ventricles relaxed. The heart was kept moist with ringers throughout the entire experiment. Observing the heart beat via the ECG on the computer, the atrial and ventricle contractions were observed and noted as to where in the recording they were.

Once these were established, the single event button was pressed at the peak of each ventricular contraction, maximum ventricular relaxation, peak of each atrial contraction, and maximum atrial relaxation. Now an extra-ventricular contraction needed to be made. To do this, two pin electrodes were used as “paddles” with the negative pin near the base of the heart and the positive pin near the apex. The accupulser/SllJ settings were changed to deliver single pulses of 20ms duration and 0. 5mA, and stimuli were applied at different times in the cardiac cycle using the single event button.

When a response to the stimulus was seen, two beats were allowed to go by before stimulating the heart again. Next, stimulus was applied to create the illusion of a heart blockage. The electrodes were rearranged to once again represent lead l, and thread was tied around the narrow groove of the heart between the atria and ventricles. As the recordings continued, the string was tightened more and more until evidence of an A-V conduction block became apparent (a ventricular beat did not follow every atrial beat).

Then the recording was continued until there was no ventricular contraction in the mechanical record. After these four tests were done, a new frog was used and dissected the same as the first one. The lead II setting proved to show better results than lead I during this experiment so that set up was used. For this part of the experiment, different reagents were injected into the liver of the frog and the results were observed on the ECG recordings. mL syringes were used to administer the reagents, and cleaned between each one by filling and emptying with ringers about six times each.

The first reagent was 0. 1% nor epinephrine, 0. 25mL were injected into the liver of the frog and the results were observed and recorded. Then 0. 1% epinephrine was injected, then 0. 1%, all using the same procedure. The next reagent used was 0. 5mL of, a beta-adrenergic antagonist (slows down heart), which needed to be almost immediately counteracted with so the heart would not begin to stop. The results of Just the metoprolol observed and recorded. Acetylcholine was then used, 0. 25mL immediately followed by 0. 25mL of 0. 5% atropine in order to restart the heart. Once the heart rate was back to normal (or as close as it would get at this point), the final reagents were injected. First was 1% calcium chloride in frog ringers, and finally the frog was given 2% potassium chloride which was the final reagent before the heart did not recover. All of the results were observed and recorded for all of the reagents. Results: The control baseline ECG recording before the dissection showed the lead I set up had a peak R wave amplitude of 70. 5mV and a visible P wave and QRS wave difficult to find the T wave).

The lead II set up had a peak R wave amplitude of -55mV as well as a visible P wave (again, hard to see the T wave). Using the R wave amplitudes for lead I and lead II, we were able to predict that our frog heart apex was most likely pointed down and towards the left lung. When the stimulus was applied during maximum atrial relaxation, the atrial contraction recordings began to visibly merge with the ventricular contraction recordings. It also caused the P waves to become very difficult to see, if they were even present at all.

The maximum R wave amplitude during this time was ”275mV. The same results happened when the stimulus was introduced during maximum atrial contraction (”275mV), maximum ventricular relaxation (”300mV) and maximum ventricular contraction (”300mV). The extra systole occurred about 750ms after the extra stimulus was introduced to the heart, and right after that the compensatory pause was both seen on the ECG as well as the frog heart itself. During this pause, the ventricles swelled much more than normal and then finally contracted.

It took a few tries to cause the extra systole to occur, but it finally did when the stimulus was introduced during maximum atrial relaxation. The maximum R wave amplitude after the compensatory pause was –300mv. When the A-V block was simulated, the ECG showed a complete separation of the ventricular contraction waves and the atrial contraction waves, as well as a huge decrease in amplitude in the QRS wave. The new maximum R wave amplitude was ”25mV. When the blockage was complete, there were no ventricular contractions of any kind and instead big pauses between atrial contractions.

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