Nt1330 Unit 4 Lab Report

The relatively steady DBP may be due to the Windkessel effect which the rise in BP is much absorbed by the elasticity of the major arteries.3 (p197) Both subjects exhibited a rise in MAP, when calculating the PP (Pulse pressure dividing by 2 then adding the DBP) as expected to supply blood and oxygen to the exercising muscle tissues as well as decrease in MAP once they entered the recovery stage due to decreased need for blood and oxygen. 5(p.1205) Both resulted in average HR, SBP, and RPP during maximal cycle ergometer exercise which can conclude to say subjects performed well. Resting RPP may have been “much higher than average” due to unfamiliarity with the protocol, anticipation to the exercise resulting in higher than their normal resting pressure3(p.201), muscle tension in arm causing erroneous BP reading, BP technician may not have been skilled and experienced at measuring near accuracy, and/or subjects’ health condition on the experiment day. In addition, Table 17.4 data in the Laboratory Manual was obtained during treadmill exercise and we used a cycle ergometer instead, which may have altered the result. BP technician also had a hard time recalling SBP and DBP when blood pressure was being

Results: At basal level Heart rate was recorded at 834 (mean  SEM) bpm (beats per minute), the end point reading was 773 bpm, which was a significant decrease by p=0.0394 (figure 1).

The Q is the first wave downward, or negative, wave form of the QRS complex. The R wave is the first positive or upward, deflection. The R wave can occur with or without a Q wave. The T wave represents ventricular repolarization. The QT indicated the time from ventricular depolarization to repolarization. The wave of electricity it continues traveling through the myocardium to atrioventricular node. The AV node it coordinates the incoming electrical impulses from the atria and relays the impulse to the ventricles through a bundle of specialized muscle fibers. The atria pump blood into the ventricles and then the ventricles pump blood out of the heart. Chambers of the heart fill with blood during a relaxation phase diastole and eject blood during a contraction phase systole. Atrial

he first part of the experiment, exercise 1, dealing with heart rate and temperature can be seen in Table 1. It was apparent that temperature decreased the heart rate and this was probably due to same principles surrounding nerves. If the temperature is too low it is harder for ions to pass through the membrane and cause an action potential thus decreasing the contraction of the heart. The visual representations of this exercise can be seen in Figure 1 (before cold ringers) and Figure 2 (after cold ringers).

It is hypothesized that if subject #3 is reclining for 3 minutes, their arterial rate and heart rate will decrease because their body is relaxing and their heart is not doing any work. This drop is caused by the PNS system sending a signal to the cardioinhibitory center to lower heart rate. When the body is at rest, HR does not need to be increased. While the subject was sitting quietly, the baseline BP and HR was taken. BP was 105 mmHg and HR was 66 bpm. After 3 minutes of reclining, the subjects BP increased to 121/71 mmHg and HR decreased to 62 bpm. The cause of this could have been student error or the subject may have been uncomfortable during the experiment. After reclining for 3 minutes, the subject immediately stood up It is hypothesized that their arterial pressure and heart rate will stay the same because the subject is not moving therefore blood is being pooled in the lower extremities and not getting back to the heart. This will cause a decrease in HR and BP. But the body will sense this and activate the SNS response to release norepinephrine to increase BP and HR or to get it back to what BP and HR was initially. After standing for 3 minutes, the subjects BP went from 129/70 mmHg to 121/75 mmHg and HR went from 86 bpm to 80 bpm. As stated previously, blood was starting to pool into the legs. The results do not necessarily support the hypothesis because there was a decrease in BP and HR. This could be because the SNS had not been activated just yet because the body did not sense a change in BP and/or HR. The body will sense a decrease in returned blood and will act upon it by increasing BP and HR to get more blood coming to the heart. After 3 minutes, BP decreased from 129/70 mmHg to 121/75 mmHg and HR decreased from 86 bpm to 80 bpm. The results showed a decrease in BP as well as HR. As stated in the hypothesis it was expected to

The two main parts to the cycle are systole and diastole. Systole is the contraction phase of the cycle, pumping the blood, and diastole is the relaxation phase of the cycle, blood filling the chambers (Reece 921). While the blood pumps out of the heart, the arteriole blood pressure is raised; however, during the relaxation phase, the aortic valve closes thus dropping the arteriole blood pressure (Harris-Haller 243). Because of this inconsistency in blood pressure during the cardiac cycle, the mean arterial pressure compensates for these fluctuations by calculating mean values (Harris-Haller 244). An electrocardiogram is a graph that represents “the electrical activity of the heart [and] plots sequential events of excitation and recovery of a heartbeat,” and it is summarized by four main parts to the heart wave (Harris-Haller 240). The P wave shows the depolarization of the wave over the atria, the QRS complex shows the ventricle depolarization process, and the T wave shows the repolarization of the ventricles (Harris-Haller 241). Exercise can also have an impact on the blood pressure and pulse by increasing both (Moeini 431). In addition, the respiratory rate when one is exercising can often increase as well in

The purpose of this experiment is to show how the cardiac and respiratory system react after exercise. Each system differs at rest and after exercise. We observed the respiration rate, the blood pressure (bp), and our pulse during resting and after exercise. Everyone exercised for five minutes. We chose to run a flight of stairs in the same building of our class. After exercise we would check off everything that we listed to see the bp, pulse, and breathing. To check our bp and pulse we used an electronic cuff called the sphygmomanometer to do our counting. Once we completed our exercise we would each have a two-minute break. For that break we would recheck on the new differentness and check how much has changed from before exercising and after

Figure 1 shows that the systolic and diastolic pressure while the subject was sitting down, 119/64, is lower than that of the other body positions and exercise. Standing showed the second lowest systolic and diastolic pressure, 121/83. Lying down showed a slightly higher blood pressure of 123/84. The highest blood pressure, 133/94, was measured when the subject had just completed some physical activity. Figure 2 and 3 display, respectively, the difference between heart contractions at rest and after exercise, as illustrated by the greater number of contractions following exercise in the same amount of time compared to resting conditions. In addition to displaying the interval lengths for three sequential beats from Figures 2 and 3, Table 1 also includes the heart rate for before and post exercise, 102 bpm and 132 bpm, respectively. Figure 4 shows similar

The heart is a muscle that is divided into four chambers. The top of the heart has two atria while two ventricles are located on the bottom. When the heart is healthy, the heartbeat will begin in the right atrium. The right atrium will send an electrical signal across the heart spreading throughout the atria to the AV node, then to the ventricles. This electrical impulse, occurring about 60 to 100 times per minute, causes the heart to contract. Each contraction equals a single heartbeat. According to the Human Diseases and Conditions article , under some conditions, almost all heart tissue is capable of starting a heartbeat, or becoming the pacemaker. A dysrhythmia occurs when:

The purpose of this experiment was to model the changes of the cardiac system under different forms of stress in a non-invasive fashion: primarily using a sphygmomanometer cuff, a stethoscope, and an electrocardiogram. As different stressors were placed upon the subjects, their cardiac systems responded accordingly to the diverse stimuli. We recorded and calculated quantitatively their responses so to further understand each component of the cardiac system.

For this experiment students sought to demonstrate how cardiac function was regulated. Students made hypothesizes for clamping, drug injections, and stimulation with effects of arterial pressure and heart rate in mind. Students performed various tests in order to fully obtain results for this experiment which included the injection of drugs and their effects, using and removing a clamp and that effect, and finally used an electrical simulation machine in order to stimulate nerves to test that effect. The main hypothesizes depended on each treatment and each prediction was made specifically to fit a certain set of conditions. These various tests were performed to obtain a better understanding of cardiac function and its physiological aspects. Understanding cardiac function is not only very important to science but very important to the

Based on the results, it can be seen that the addition of pilocarpine decreased the heart rate of the frog and the addition of atropine further decreased the heart rate. The data collected is shown in Table 6. Effect of Epinephrine Before the addition of epinephrine, the heart rate was found to be 20 bpm, and after the addition of epinephrine the heart rate was found to be 44 bpm. Based on these results, it can be seen that the addition of epinephrine increases heart rate. The data collected is shown in Table 7.

The pacemaker of the heart, the sinoatrial (SA) node, generates the impulses that trigger the contractions of the heart chambers. In a very sequential, coordinated rhythm at a rate of 75 times per minute, it depolarizes faster than the other pacemaker cells of the heart preceding them with their impulses. Located in the superior right atrium, these spontaneously depolarizing myocytes trigger a depolarization wave, via gap junctions, to the left atrium and the atrioventricular (AV) node, lying in the inferior right atrium. Gap junctions, in the intercalated discs, allow the rapid transmission of ions to adjoining myocytes. Furthermore, the electrical signal can conduct through the adjoining myocytes, allowing it to operate as one functional

Anova 1, with values of each section of time after injection of Ringer's solution, shows a p-value of 0.9513. Thus, we are sure at more than 95% that values aren't significantly differents between the three groups. So Ringer's solution have no effect on heart rate or amplitude. Ringer it's our normal conditions control, it doesn't affect heart rate or amplitude (=force of heart contraction).

A time that starts with contraction between the atria and ventricular relaxation is known as the cardiac cycle. The relaxation period also known as the diastole this occur when the chambers fills with blood. The blood will flow according to pressure. As the fluid from the vein into the left atrium the pressure gets higher and rises, initially move passively into the ventricles from the atria. As the left ventricle filled to its volume the mitral valves closes to prevent any backflow. The contraction from the left ventricle send the oxygenated blood by the aortic value to aorta as the semilunar valves closes to prevent backflow of blood into the left ventricles.