The Dive Response (04/11/13 prac)

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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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