The Dive Response (04/11/13 prac)

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The physiological basis, methodology, results, and clinical relevance of the Dive Response, from the 04/11/13 Human Physiology lab.

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The Dive Response (04/11/13 prac) The dive response enables aquatic mammals to conserve oxygen by decreasing heart rate and blood flow to the extremities. In terrestrial animals, oxygen consumption actually rises as a result of submersion in cold water in order to prevent core temperature from dropping, so the bradycardia (resting HR conserve heat. In this lab, we triggered the dive response by suddenly submerging the subject’s face in cold water (~10°C), stimulating the trigeminal nerve receptors around the nose. As water temperature decreases, stimulation of the receptors is enhanced, and the severity of the bradycardia increases. Enhanced stimulation of these receptors results in an inhibition of the cardiovascular centre, as well as subsequent reduction in heart rate through both enhanced parasympathetic output and reduced sympathetic output to the heart. We compared the circulatory effects of the dive response with breath-holding, and found that while the dive response initiates bradycardia and there are minimal O2/CO2 effects, breath-holding initiates tachycardia, hypoxia and hypercapnia. For these first two experiments, we attached a finger pulse transducer to the middle finger of the volunteer and to the PowerLab panel. For both experiments, the volunteer held their face over the water to establish a resting heart beat for 15 seconds, then for the dive response they submerged their head under water for 30 seconds (another person tapped their back every 10 seconds to keep time) and for the next experiment the volunteer held their breath above the water for 30 seconds. For both experiments, a further 30 seconds of ‘recovery’ was recorded after breathing resumed. In peripheral occlusion of the dive response, venous return to the heart is disrupted, but the amount returned is also reduced along with cardiac output. We replicated that by blocking venous return and then measuring the decrease in the volume of the calf when the cuff was removed (as the gradual increase could not be detected by the transducer, but the sudden decrease could). For a third experiment, we attached a blood pressure cuff and sphygmomanometer to the volunteer’s right thigh, and a respiratory belt (attached to the PowerLab panel) around the right calf. After a 10 second resting control, we repeated the above tests: resting with face above the water, holding breath with the face above the water, and submerging the face into the water. For the 30 seconds that the variables were being performed, the cuff was inflated to 100mmHg. The cuff was ripped off to allow for the most sudden volume change to be recorded by the transducer. After this there was a 10 second resting recovery period. We recorded the change in volume at this point for all three sets of conditions. Class data: Not available. My data: During the dive response, my heart rate stated the same initially but the pulse amplitude increased (from 0.000585 to 0.00115, suggesting an increased stroke volume). At the end of the dive, my heart rate had risen (from 56.66 BPM to 72.53 BPM) and the pulse amplitude had lowered slightly (from 0.00115 to 0.000875, showing a higher rate and slightly lower stroke volume). 30 seconds after the dive, my heart rate began to return to resting (from 72.53 BPM to 65.36 BPM) but the pulse amplitude continued to increase (from 0.000875 to 0.001375) suggesting that stroke volume was still increased to compensate for the hypoxia. Tachycardia occurred instead of bradycardia – I expect that this was because the water was too warm at 10°C, but also because I panicked slightly as I felt water travelling up my nose. As expected, during breath holding my heart rate rose similarly and the pulse amplitude decreased in shorter, shallower beats (Rest: 67.44 BPM, 0.00062; 15s in: 83.68 BPM, 0.00052; End: 89.56 BPM, 0.00046; Recovery: 70.77 BPM, 0.0005). Lastly, with the leg blood volume, the change in volume was decreased in the dive response (at rest, the change was 0.18V, whereas it was 0.09V in the dive response), but increased during breath-holding (to 0.33V). The lower change in the dive response is expected, as stroke volume is decreased so there is less blood to return to the heart, meaning that less will accumulate when return is occluded. In the breath-hold, there is increased cardiac output to address the tissue hypoxia, so there will be more blood to return to the heart, resulting in a larger accumulation when return is occluded. The dive response is more of a survival mechanism than a pathological presentation. However, the circulatory effects of breath holding were clear, and could be similar in pathologies in which air flow and gaseous exchange is restricted, such as emphysema, pulmonary fibrosis, and asthma. Clinically, the dive response can be used to restore sinus rhythm to those with paroxysmal supraventricular tachycardia. This can occur with digitalis toxicity, or in Wolff-Parkinson-White syndrome in which a person has an extra pathway for impulses to travel in the heart.

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