The Effects Of Deep Breathing On Heart Rate And Blood Pressure Essay

The purpose of arterial pressure and the pulse lab is to determine the effect of posture and exercise on systolic and diastolic pressure and the heart rate. And also in order to find the differences in the reading taken under these condition compares to the baseline reading. The Sphygmomanometer and stethoscope are used to measure the systolic and diastolic blood pressure, counting the beat on the radial artery will give the reading for pulse rate and by using the lab scribe software and IWX214, the blood pressure will be measured. In the heart, the aorta and the carotid arteries have baroreceptors and the chemoreceptors that identify the changes in arterial pressure and the changes in

Comparing my Rebreathing Carbon Dioxide graph to my peers, I noticed that we all share an increase in both the breathing rate and depth. Talking to my peers, I noticed that we all mutually had the pressure of the pressure cuff go down once we finished this experiment. This release of pressure most likely occurred because during the different intervals – breathing normally, holding our breaths, slowly breathing, and breathing through the Ziploc bag – the kPa, or unit of pressure, gradually decreased. The relationship between breathing rate and breathing depth is that they strongly influence HRV, or heart rate variability. This is most efficient because the tidal volume decreases as heart rate does too, although the changes are insignificant.

Determining the Effect of Arousal on the Heart Rate and Blood Pressure of Adolescent Males

In healthy individuals, heart rate can be lowered 2 to 5 beats per minute during short-term relaxation interventions (Paul 1969; Melville, Chang, Colagiuri, Marshall, and Cheema 2011; Wallace, Benson, and Wilson 1971; Schandler and Grings 1976). Relaxation interventions can lower blood pressure 6 mmHG to 14 mmHG in systolic blood pressure (Melville et al 2011; Schandler and Grings 1976) and respiration rate can be lowered by 2 to 4 breaths per minute in healthy patients (Benson 1993; Paul 1969; Melville et al 2011; Wallace et al 1971).

The main purpose of this experiment, was to demonstrate and understand the effect of breath-holding on the heart rate (apnoea).

Figure 1. Compared effects of breathing in air (control treatment) and a simulated dive (apnea in 10C water) on human heart rate (n=6). Bars represent the combined mean heart rate of the subjects for both treatments over each measurement period. Error bars represent 95% CI.

As the intensity of exercise increased, so did the rates of the heart and breathing. After a small period of rest, the heart rate and breathing rate both decreased to a point close to their resting rate. This proved the stated hypothesis. First, the hearts average resting rate was recorded to be 76 bpm. The heart is therefore transporting oxygen and removing carbon dioxide at a reasonably steady rate via the blood. During the low intensity exercise (Slow 20) the heart rate increases to 107 bpm, which further increases to 130bpm at a higher intensity level (Fast 20). The heart therefore needs to beat faster to increase the speed at which oxygen is carried to the cells and the rate at which carbon dioxide is taken away by the blood.

We decided to measure the subject’s pulse and respiratory rates whilst sitting down because there would be no additional stress on their heart, which would increase their heart rate. Their heart rate should also return to its resting heart rate due to the decrease of muscle use.

Before performing this experiment we hypothesised that breathing exercises would cause the heart to relax, causing a decrease in heart rate and blood pressure. In addition, we predicted that the systolic pressure would decrease and the diastolic pressure would stay similar to the control test. Due to all of the three t-tests exceeding .05 (0.64659, 0.380067, 0.184003) the null hypothesis was accepted. The data didn’t show a significant change from the basal readings to the treatment readings so we failed to reject the null hypothesis.

After I measured heart beats in different positions such as immediately upon standing, after jumping twenty times, standing, deep breathing, and strong stimulus. I acknowledged that most of my hypothesis were right. By standing immediately from lying down position, I saw that my my heart rate was decreased because when we lying down, our hearts were in a resting period where they don’t need blood to pump to them as much as when we are walking, jumping, or doing other things. Similar to this position, by deep breathing would also cause our heart rate to decrease because as I looked up online, it said that our heart decreased when we took a deep breath because it referred to as the "valsalva maneuver", were taking a big breath in and then

The literature on the effects of exercise of cardiac output maintains the idea that exercise should affect cardiac output- pulse rate, systolic blood pressure, diastolic blood pressure, QRS-pulse lag, P-T and T-P intervals, because of increased heart rate. For our experiment, we tested this theory by measuring our cardiac output before and after some rigorous exercise. We measured the individual cardiac output and then combined the data to compose a class-wide data average. We compared the results of the experiment to what we expected, which was that exercise does affect our heart. Our data from this experiment supported the notion that exercise does, in fact, change cardiac output.

The effects of exercise on blood pressure, heart rate, respiration rate and electrical activity of the heart were assessed. The measurements of respiration rate, pulse rate and blood pressures were noted as described in Harris-Haller (2016). Data was first taken from subjects in a relaxed position and then followed by sets of reading after exercising based on one minute intervals. The data also noted sitting ECG traces from Harris-Haller (2016). The respiratory rate, pulse, blood pressure, P wave, QRS complex and T wave were defined for each subject. The class average was calculated for males and females and graphed to illustrate the results by gender for each cardiopulmonary factor.

This experiment was conducted to see how exercise affects breathing and heart rates. My hypothesis was that if exercise puts strain on the body, then the heart and breathing rates will increase and I was correct. This is because as the exercise increased the heart and breathing rates also increased. For example in trial #1 the resting heart rate was 96 beats per minute then after 1 minute of exercise it increased to 144 beats per minute and then increased again to 160 beats per minute after 4 minutes of exercise. After the exercise was completed the heart rate went back down to 132 beats showing that the heart rate is based off of the amount of exercise rather than it just going increasing or decreasing randomly. The breathing rate also increased

A blood pressure meter, commonly known as the sphygmomanometer is a device that is used to measure the blood pressure in people. Typically, it is comprised of a cuff that is inflatable that collapses and releases the artery and a mercury manometer that measures the pressure. It was invented by Samuel Siegfried Karl Ritter Von Basch in 1881, but Scipione Riva-Rocci created a more easily used device, that was later popularized by Harvey Cushing in surgery in the United States.

The heart rates of participants was tested before the step test, one minute, two minutes, and three minutes after the step test was performed in this experiment. Since heart rate increases while someone is performing physical activity, it was expected that heart rates of the students would be higher than before the step