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Home , Korotkoff sounds, Pulse, Pulse pressure

LABORATORY HANDBOOK

Advanced (HL 2017 and HL 2018)

Karolinska Institutet • Department of Physiology and Pharmacology Postal address: 171 77 Stockholm Visiting address: Biomedicum, Solnavägen 9 Tel exp: 08-524 872 29

HEART SOUNDS & PRESSURE

Karolinska Institutet • Department of Physiology and Pharmacology Postal address: 171 77 Stockholm Visiting address: Biomedicum, Solnavägen 9 Tel exp: 08-524 872 29

Advanced Physiology KTH v.1 Sounds and 1

Heart Sounds and Blood Pressure

Introduction

The following laboratory exercise will be an introduction to of the heart, palpatory and auscultatory blood pressure measurement, and blood pressure regulation during orthostatic challenge.

Goals

Heart sounds

• Identify the first and second heart sounds during auscultation. • Locate where on the chest the different parts of the heart is best heard. • Auscultatory define and . • Know the mechanisms behind the heart sounds.

Blood pressure

• Perform palpatory and auscultatory blood pressure measurements. • Understand the relationship between the and systolic and diastolic pressure during auscultatory measurements. • Identify factors that affect the systolic and diastolic blood pressure. • Identify factors and sources of error that can affect a blood pressure measurement.

Orthostatic test

• Perform a simple orthostatic test. • Interpret a complete orthostatic test. • Understand how circulation is affected by standing up quickly, and how the body compensates for this. • Account for the symptoms that occur during orthostatic hypotension. • Understand the mechanism behind vasavagal (fainting).

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 2

BACKGROUND

Auscultation of the heart When the heart beats, vibrations are set up in the heart and the major blood vessels. These vibrations are caused by the acceleration or deceleration of the blood, when the kinetic energy is converted into sound energy. Furthermore, the extent of vibrations depend upon turbulent flow which in turn is a function of the velocity and viscosity of the blood.

The heart sounds can be divided into:

Heart sounds (normal and extra)

Accessory sounds (murmurs and friction rubs)

Heart sounds The heart sounds are normally dependent on ventricular function. The primary origin of the sounds is the turbulence that occurs due to closing of the valves.

The first heart sound (“lub”) occurs upon closure of the mitral and tricuspid valves.

The second heart sound (“dub”) arises from the shutting of the aortic and pulmonary valves.

The third heart sound is heard when the blood flows rapidly from the atria into the ventricles. It is predominantly heard in children and young, well-trained individuals.

The occurs during atrial contraction. It is considered to be pathological in all except infants and young children.

The first sound marks the beginning of systole and diastole starts with the second sound.

Accessory Heart Sounds An accessory heart sound that is strong enough to be palpated is called fremitus (fremissement in Swedish).

If the mouth of a valve is too narrow, this is called a stenosis. A stenosis can cause a murmur because of the resulting turbulent flow. Note also that an increased amount of blood trying to get through a normal sized valve (e.g. during exercise) can also cause a murmur. The most common sites for stenosis is the mitral or .

An insufficiency arises when a valve cannot shut tightly. An insufficiency can give rise to a murmur because of altered flow.

An insufficiency in the atrioventricular valves (tricuspid and mitral valves), and a stenosis in the semilunar valves (aortic and pulmonary valves) demonstrates itself during systole. The opposite is true during diastole (insufficiency is heard in the semilunar valves and a stenosis in the atrioventricular valves). These conditions can be congenital or acquired.

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 3

In the case of young, well-trained individuals, a soft murmur can be heard clearly during inspiration (increased venous return) and is most easily heard in the third left intercostal space (I3) at the sternal border.

There is a characteristic area (the point of maximal impulse, PM) where heart sounds or murmurs can be best heard. Unfortunately, this area can vary from person to person. In different illnesses, there will usually be a characteristic shift in the PM.

Figure 1 The sound from different valves can best be heard in different locations on the chest. Note that the sound can project to different sites without being pathological. This is especially true in the case of the aortic and pulmonary components. (Lännergren et al. Fysiologi, 1996).

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 4

Valve is Closed Open Closed

Fig. 2

ECG-registration

Valves Tricuspid Pulmonary Mitral Aortic

Heart sounds “LUB” “DUB” Heartcycle Diastole Systole Diastole

The The stethoscope has two possible modes of use. Low-pitched sounds are best heard with the bell side and high-pitched sounds with the flat diaphragm. Use the diaphragm side for blood pressure measurements. Make sure that the earpieces are set properly in your ears, they should point forwards and downwards in the same direction as the external ear canals to get the best sound quality.

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 5

Blood Pressure The blood pressure is regulated continuously for each tissue to get enough blood flow and to keep the arterial pressure relatively constant. There are two main factors that regulate the arterial pressure; and peripheral resistance. These are responsible for short term regulation of blood pressure. The total amount of fluid in the body will also affect the blood pressure over a longer period of time.

The true value of blood pressure in the arterial system must be measured by inserting a into a blood vessel. However, the method is not sufficiently easy and risk-free to be used except in exceptional cases such as research and intensive care.

The most satisfactory method is the auscultatory method where one listens to the altered sound caused by changes blood flow in the blood vessels. The blood pressure is measured by using a blood pressure cuff to compress a large , usually in the upper arm. The palpatory method is able to provide a good estimate of the systolic pressure.

Systolic-, diastolic-, - and . The systolic pressure is produced by the pumping of blood from the heart into the arterial system. The and the volume of blood that is already present in the arterial system are the determining factors for the amplitude of the pressure. A stiff blood vessel causes a considerably larger increase in systolic blood pressure than does an elastic blood vessel. The normal range is 90-119 mm Hg, 120-139 mmHg and ≥140 mm Hg.

The diastolic pressure is the lowest pressure that exists in the arterial system during the diastolic, or filling, phase. The blood pressure falls continuously because of the peripheral outflow of blood. Consequently a low increases the tendency for a low diastolic pressure because more blood leaves the during the longer time between heartbeats. The diastolic pressure is also affected by the peripheral resistance; causes an increase in the diastolic pressure. The normal range is 60-79 mm Hg, prehypertension 80-89 mm Hg and hypertension ≥ 90 mm Hg. The typical normal or textbook value of systolic/diastolic blood pressure is 120/80, expressed verbally as 120 over 80.

The is the difference between the systolic and diastolic pressure. The higher the pulse pressure, the larger pulsations in the vessels.

During the ejection phase, the blood pressure increases in the aorta (to the systolic pressure) and the elastic walls are stretched. A pressure equalisation then occurs with the resultant pulse wave continuing in a peripheral direction. This pulse wave moves more rapidly than the blood flows (3 –10 m/s compared to less than 0.5 m/s). The pulse wave represents the movement of the pressure increase through the circulation system.

The mean arterial pressure is of great importance for flow and transcapillary exchange. It is calculated as the sum of the diastolic pressure plus 1/3 of the pulse pressure.

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Auscultatory method of measuring blood pressure The figure below shows how the Korotkoff sounds are believed to develop.

Fig 3 The principle of auscultatory measurement of blood pressure in the arm (Jonson et al. Klinisk fysiologi. 1998). When the pressure in the cuff is greater than the systolic pressure (A), there is no flow in the blood vessel and no sound is heard. If one reduces the pressure just below the systolic pressure (B), a turbulent flow starts (phase I). The flow of blood increases progressively as the pressure in the cuff falls (phase II, characterised by a roaring sound and phase III, this becomes more and more clear). When the cuff pressure is equal to the diastolic pressure (C), the Korotkoff sound disappears (phase IV) because the blood vessel is no longer compressed. Phase V is when the sound disappears completely.

There are variations on this usual course of events. The most common is that the sound only subsides slowly. The standard procedure is then to accept the pressure at which the reduction in sound occurs as the diastolic pressure. If the difference between phases IV and V is less than 10 mm Hg, one should note both values (120/80-90). In certain cases, an auscultatory gap can exist. This is when all sound disappears from an interval between the systolic and diastolic pressures. The reason for this is unknown, but you should keep listening and slowly release pressure a short while after the diastolic sound has disappeared not to get a false high diastolic value due to the auscultatory gap.

Note! If the diaphragm of the stethoscope is placed over the without the cuff being inflated, there should be no sound. If a sound is heard this is due to a compression of the artery by the stethoscope resulting in turbulent flow.

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Sources of error Resting pressure: Somebody who is not relaxed can have a very variable blood pressure. Therefore, one should always try to measure the resting blood pressure as a lowest value. A person who is moving or not relaxed will get an inaccurately high measurement due to the cuff having to work against the muscle tone as well as static contractions giving a significant increase in blood pressure. Everything that activates the sympathetic nervous system can result in false highs; nervousness, pain, need to go to the bathroom, fear of the situation at the hospital or lab.

Characteristics of the artery: If the blood vessels are stiff, much greater cuff pressure is needed to compress them. Because of this, the cuff pressure might be increased insufficiently and the systolic pressure will not be obtained.

Limb position: The limb in which one measures the blood pressure must be at the same level as the heart. This avoids addition of a hydrostatic component to the blood pressure (Note, that the force of gravity acting on the limb and the heart is then the same!). This means that when the subject is laying down, the arm should be at the same level as half of the thoracic height.

Cuff error: The pressure in the cuff is not transmitted perpendicular through the tissue to compress the blood vessel but is dissipated through the cuff and the highest pressure is in the middle of the cuff. A cuff that is too small or poorly placed on the arm will not dissipate properly. The result is that one can get a too high, false, measure of the blood pressure. The width of the cuff should be at least 30% of that of the limb.

The stethoscope. The placement of the stethoscope can be a source of error during the blood pressure measurement. The sound will not be clear if the stethoscope is not placed directly above the artery. If too much pressure is applied, the artery can be compressed leading to turbulent flow.

Inaccurate inflation. The pressure in the cuff should be decreased with the correct speed. If it is lowered too quickly, the heart beats will not be heard often enough and the inaccuracy will be great. The result tends to be too low (the heart should have time to beat at least once/3mmHg). A value that is too high is possible with a slow inflation or deflation if this leads to stasis on the venous side.

Sphygmomanometer. The should work and be calibrated.

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 8

a) The dashed lines represent the distribution of pressure under the cuff. b) The correlation between the pressure in the cuff and the character of the auscultated sound.

Fig. 4 Lännergren et al. Fysiologi, 1996

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 9 Första tonen

Orthostatic test

The principle behind the orthostatic (ortho = straight or upright, static = position) test is to register blood pressure and heart rate while the subject is in a horizontal and vertical position. Due to the effect of gravity on the , a person in a supine or lying position has a central reservoir of blood in the lungs and heart. Between 400 to 700 ml is redistributed when one rises from a supine position. In addition to the redistribution of blood from the lungs to the legs, there is also a change in the of the lung so that the upper parts get a lower perfusion.

The reduced central blood volume leads to a reduced venous return which in turn leads to a reduced stroke volume. A reduction in stroke volume results in lowered arterial blood pressure. This is detected by the baroreceptors in the aortic arch and carotid sinus. The baroreceptors in the carotid sinus register a lower blood pressure than that generated by the heart since they are located approximately 30 cm above the heart in an upright position. In addition, it is thought that “low-pressure receptors” in the atrium and the large respond to the reduced central blood volume with an increased afferent discharge.

The afferent signals from the different receptors leads to increased sympathetic activity from the vasomotor centre. The peripheral resistance increases and the heart rate increases to maintain the mean arterial pressure. The increased sympathetic tone affects the capacitance blood vessels and leads to an increased venous return.

In the long run, there are also humoral compensation mechanisms. Secretion of antidiuretic hormone (ADH or vasopressin) from the neurohypophysis increases. In addition, the renin activity increases which acts via (increases peripheral resistance) to increase aldosterone secretion from the adrenal glands and thereby increase the re-absorption of Na+ and water in the kidneys. Fig 5. Response of some haemodynamic parameters in a normal person in response to a change in position (After Bevegård, 19973). The blood pressure is measure at the level of the heart.

STROKE VOLUME

HEART RATE

CARDIAC OUTPUT

PERIPHERAL RESISTANCE

BLOOD PRESSURE

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 10

Certain people have difficulties making the adjustment from a supine to a standing position, and develop orthostatic hypotension. When these individuals get up quickly, they feel light- headed. In more severe situations, people faint returning them to a horizontal position and blood circulation to the brain is restored.

Asympathetic orthostatic hypotension describes a situation when the mechanisms for compensating for the decreased blood pressure that occurs when changing position from supine to standing not are enough and in some cases there is no increase in heart rate. This can be seen in elderly individuals as a result of treatment with pharmaceutical agents that block the sympathetic system, or it can be caused by damage to the autonomic nervous system (such as in diabetes and Parkinson’s disease) or the blood pressure regulating area in the medulla oblongata (for example following a myocardial infarction).

Sympathetic orthostatic hypotension refers to an increased sympathetic tone or discharge which fails to maintain blood pressure at an appropriate level. There are two possible reasons for this; an inadequate effect of the sympathetic nerves on the blood vessels and/ or a reduced blood volume. Sympathetic orthostatic hypotension usually appears when the blood volume is reduced, such as after a large haemorrhage or bleeding over a longer time when a reduced renin activity leads to a decreased plasma volume. Tall individuals are affected to a greater extent by the effects of gravity and are thus more likely to be affected than short individuals.

Training increases blood volume and also improves sympathetic function. In more severe cases, where physical training is not sufficient, one can use pharmaceutical agents that increase the tone of the capacitive blood vessels.

Fig 6. Diagram of some of the compensation mechanisms that help to maintain blood pressure in a standing person (after Thulesius, 1970.

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Clinical use of the tilt bed

Orthostatic test Investigation of the causes of syncope (fainting), dizziness and sensation of sickness that occur upon changes in posture.

Rehabilitation Patients who have been bedridden for a long time can be trained to regain their orthostatic reflexes by means of the tilt bed. In this way, the renin activity can be increased stepwise and sympathetic function will be improved.

Simple Orthostatic test A simple test of orthostatic function can be done during a routine measurement of blood pressure. Once the blood pressure has been measured at rest, the subject will stand up and heart rate and blood pressure will be measured immediately and after 2 minutes.

Comprehensive Orthostatic test This is undertaken with a tilt bed to avoid the involvement of the muscle pump (activation of the muscle pump in the legs during movement will facilitate the venous return to the heart). It easier to control the speed of standing up, but this is a less “physiological” test. Heart rate and blood pressure are measured at rest and then every minute for 7 minutes after tilting the subject. In certain cases, a continuous record of ECG is also taken to study the sympathetic activity.

Change in heart rate I III

Normal range Fig 7 II Change in blood pressure

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Interpretation

A change in blood pressure from the resting value is marked along the x-axis. The change in heart rate from the resting value is marked along the y-axis. The co-ordinate values (x,y) for the seven time points obtained after tilting the subject are plotted.

In a normal subject, these values have returned to the normal range of resting values within 7 minutes. In the Figure above, this is marked as the “normal range”.

A final value that ends up in the area marked “I” shows that the blood pressure fell despite a rise in heart rate and is indicative of sympathetic orthostatic hypotension.

If the values end up in the area marked “II”, this indicates that there was no rise in heart rate when the blood pressure fell i.e. asympathetic orthostatic hypotension.

Over-compensation by the sympathetic system leads to increased heart and elevated blood pressure (III). Such a response may be an early symptom of hypertension.

Vasovagal reaction Either a reduced sympathetic tone or an increased parasympathetic tone (for example in very stressful situations, a decrease in central blood volume or venous return) can result in a decrease in heart rate and a fall in blood pressure and a risk of fainting. Fainting or syncope is often preceded by a vasovagal reflex in combination with dizziness, nausea, pallor and .

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 13

PROCEDURE – Auscultation of the Heart

Be organised and focussed when you listen. Use an onomatopoetic chorus to describe the rhythm (for example lub-dub lub-dub lub-dub etc).

Organisation Ideally, this laboratory procedure should be done in a QUIET room. Adjust your stethoscope so that you can hear well. Listen to one valve at a time. Begin by trying to identify the first heart sound.

In every examination, begin by listening to the rhythm. Auscultate the first heart sound. Then auscultate the second heart sound. Finally listen for possible systolic or diastolic murmurs.

Work in pairs. Be methodical. Follow the instructions below.

1. The subject should strip to the waist and lie comfortably on the examination table. The examiner should stand on the subject’s right side.

2. Palpate or feel where the heartbeat is strongest, this is the point of maximal impulse (PM). Mark that point on the chest. Is its rhythm regular? _____ Frequency: _____ beats/min

3. Palpate the radial pulse. Frequency: _____beats/min. A deficit is said to exist when the pulse is lower than the frequency of the heart.

Is there a deficit? Yes ( ) No ( ).

4. Place the stethoscope over the third left intercostal space near the sternal border. Make yourself familiar with the rhythm. Try to determine the systolic and diastolic phases.

5. Listen to:

a. The first heart sound

b. The second heart sound

c. The interval between the first and second heart sounds. Can you hear a systolic murmur?

d. The interval between the second and first heart sounds. Can you hear a diastolic murmur?

6. Make you subject take a long and deep inspiration. Focus on the second heart sound, can you hear a split in the sound?

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 14

7. Make your subject do a little intensive exercise, such as push-ups or sit-ups. Listen again to the heart. Now do you hear any murmurs? Yes ( ) No ( )

If yes, when? Systole ( ) Diastole ( )

Best area to hear this murmur

The following is an example of how one can describe the heart sounds.

“Regular rhythm with a heart rate of 80 beats/min. Normal heart sounds. Mid-systolic high-pitched murmur grade 3-4 can be heard in the second right intercostal space.

Additional questions – auscultation of the heart These questions are only for your assistance and can be used as a tool to see if you have understood the background and practical work during this exercise. If you chose to answer them, you can ask your instructor for help. 1. Were you able to identify a split in the second sound induced by breathing? What is the mechanism behind this split? 2. Do you know where you usually can best hear sounds from different parts of the heart? 3. Can you explain: a. the auscultatory definition of systole and diastole? b. the mechanisms behind the heart sounds? c. sinus ?

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 15

PROCEDURE – Blood Pressure Work in pairs. Do the measurements in duplicate. Fill in the results that you obtain in the spaces below.

1. Ask the subject to lie on the examination table and relax (ten minutes is the standard, but it is not necessary for this laboratory). Place the upper arm so that the is accessible.

2. While the subject is relaxing, measure the circumference of the upper arm. Select and place a cuff of the right size on the upper arm. Get the stethoscope ready. Palpate the brachial artery at the elbow. Make sure that you know where it is.

3. Palpate the radial pulse and note the frequency (_____/min). Inflate the cuff until the pulse disappears (_____ mm Hg). Increase the pressure a further 20 to 30 mm Hg. What is this pressure called?

Continue another 20-30 mmHg.

4. Place the stethoscope over the brachial artery and slowly extend the subject’s elbow. The subject has to be relaxed. Start to slowly deflate the cuff.

5. Remember the pressure at which you hear the first Korotkoff sound (_____ mm Hg) and when the Korotkoff sounds disappear (_____ mm Hg). Deflate the cuff completely. Was there any auscultatory gap? Yes ( ) No ( )

Blood pressure = _____/_____ mm Hg (systolic/diastolic).

6. Check with the laboratory assistant that you have done everything correctly. Swap with your partner and repeat the measurements.

Additional questions – blood pressure 1. What is the relationship between the Korotkoff sounds and the systolic and diastolic blood pressure during auscultatory measurements? 2. Which factors affect the systolic blood pressure? 3. Which factors affect the diastolic blood pressure? 4. Which factors can affect the blood pressure measurement? 5. What is the normal range for systolic and diastolic blood pressure?

Advanced Physiology KTH v.1 Heart Sounds and Blood Pressure 16

PROCEDURE – Orthostatic Test

IMPORTANT NOTE: If a vasovagal response occurs, end the test immediately. Return the tilt board back to a horizontal position and leave the subject with the legs slightly raised. 1. Choose a volunteer, preferably somebody who is tall and thin. Strap the subject securely in a horizontal position on the tilt board.

2. Assign the following duties: 1 data collector 1 timekeeper 2 heart rate measurers (foot pulse!) 2 blood pressure measurers (one for each arm)

3. Mark where the can be palpated on the front of the foot and at the . Mark also the point where the brachial artery can be best heard. Remember to calculate the heart rate based on a 15 second measurement; since you will not have time to measure it every minute.

4. After the subject has rested for 5-10 minutes, measure the resting blood pressure and heart rate. Next the laboratory assistant tilts the bed and the clock starts. Start measuring heart rate and blood pressure immediately.

5. Measure the heart rate and blood pressure every minute for the next 7 minutes. The data collector checks how the subject feels.

6. After the experiment is finished, tilt he bed back to the original position and release the subject. Mark the data in the table. Use the simple plot (Figure 7) to discuss and interpret your results

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Table 1

Heart Heart Average Blood Blood Average rate 1 rate 2 heart rate pressure 1 pressure 2 blood pressure

Rest

0 min

1 min

2 min

3 min

4 min

5 min

6 min

7 min

The subjects reactions: ______

______

______

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Additional questions – orthostatic test 1. How is circulation affected by a quick change in posture from supine to standing? 2. Which mechanisms compensate to maintain blood pressure when standing up quickly? 3. What are the two types of orthostatic hypotension? 4. List a couple of symptoms of orthostatic hypotension. 5. List some reasons for orthostatic hypotension. 6. What is the mechanism behind vasovagal syncope (fainting)? 7. What is the clinical use for the orthostatic test?

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DEMONSTRATION

Electrocardiogram (ECG)

Advanced Physiology KTH v.1 ECG 20

ECG

I Definition Electrocardiogram (ECG): the graphic recording of the small extracellular electrical activity produced by the movement of action potentials through cardiac myocytes.

II Basic Facts At rest, there is a potential difference across the cardiac muscle cell membrane of about –80 mV, with the inside negative with respect to the outside. Stimulation of the heart muscle cell gives rise to an action potential (AP, Fig 1) with a relatively long duration of 200 to 800 ms.

-80

Fig 1 AP causes the inside of the cell to become positive with respect to the outside i.e. depolarisation. This is then succeeded by a restoration of the ionic gradient i.e. repolarisation.

Advanced Physiology KTH v.1 ECG 21

If a strip of myocardium is depolarised, a wave of depolarisation spreads along the strip. This depolarisation gives rise to a so called di-pole in the heart, areas of different charges (positive and negative). If an electrode is placed at each end, the electrode towards which the depolarisation is spreading (positive pole) will record a positive deflection. The electrode from which the impulse is coming will record a negative deflection (Fig 2a).

Depolarization:

Di-pole (neg ➔ pos)

Upon repolarisation, the opposite happens. The electrode from which the depolarisation starts records a positive deflection and vice versa (Fig 2b).

Figure 2a Repolarization:

Di-pole (pos ➔ neg)

Figure 2b

The situation in the intact heart is more complicated because the simultaneous depolarisation comes from different directions. These changes in potential, when added together, produce a single resultant waveform – the ECG, which is recorded.

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Genesis of the ECG waveform 1. The impulse starts from the sinoatrial (SA) node and depolarisation spreads radially over the atria. A positive wave, known as the P wave, is recorded.

2. Excitation moves from the atria to the ventricles via the atrioventricular (AV) node and the bundle of His. Conduction through the AV node is slow which results in a delay before the depolarises which shows up as the isoelectric section between the P wave and the coming Q wave.

3. The septum of the ventricle depolarises from left to right. This gives the transitory, negative Q wave.

4. Depolarisation of the ventricular walls spreads from the endocardial surface to the epicardial surface. The thicker walls of the left ventricle have a greater muscle mass than the right ventricle. Thus the electrical resultant is dominated by the left ventricle and is recorded as a large, positive wave, the R wave.

5. The last parts of the ventricular walls to be activated are those which lie around the aorta and the pulmonary . The resultant electrical activity is due chiefly to the right side and one sees a small negative wave, the S wave.

6. After depolarisation of the ventricular walls, there is a short period before repolarisation during which there are no major changes in potential, which shows up as the isoelectric ST segment.

7. Since the action potential is longer in the muscle cells located on the inner side of the ventricle than those located on the outer surface, repolarisation occurs first on the outer surface and then on the inner surface of the ventricles. This inverses the di-pole as to presented previously (see Fig 2b). As a result, the repolarisation wave shows up as a positive wave instead of a negative. Thus, despite the , which represents repolarisation of the ventricles, being positive it marks a repolarisation not a depolarisation.

8. Sometimes an additional wave, the , can be seen whose origin is disputed. Many attributes it to repolarisation of the papillary muscles.

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Different types of recording In order to study the complex electrical activity of the heart it is not enough to only use 2 electrodes as seen in fig. 2. We have to be able to see the heart from different sides/angles and therefore, in a typical clinical setting we use 9 measuring electrodes. These 9 electrodes make up for 12 leads (a 12 lead ECG). Each lead consists of a positive and a negative electrode/reference point and together they create a measuring axis for that lead. Using 12 leads means we can, for example, distinguish the location of a pathological process in the heart, such as a heart attack, thus treat it correspondingly.

Exploring electrode

ECG recorder and printer

Figure 3

Wilson’s electrode (V) acting as a reference electrode When discussing the electrodes in the ECG one differentiates between unipolar and bipolar recordings.

Unipolar recording is done between one exploring electrode and a neutral or reference electrode. The most common reference electrode is called Wilson’s electrode made by coupling the three limb leads together (Fig 3) designated by the abbreviation V.

Bipolar recordings are made by recording the potential difference between any two electrodes. If these electrodes sit at the same distance from the heart, the potential difference recorded by the electrodes will depend on their placement with respect to the spread of depolarisation (position of the di-pole).

The limb leads I, II and III were the first recordings made at the end of the 19th century (Fig 4). At that time there were no amplifiers in routine medical use and to reduce the cutaneous resistance, subjects had to place their arm and legs in tubs of salt solution.

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Lead I records between the left and right arms with the left arm as the positive electrode. Lead II records between the right arm and the left leg with the leg as the positive electrode. Lead III records between the left arm and left leg with the leg as the positive electrode. Here, positive electrode means that a wave of depolarisation directed towards the electrode gives a positive wave on the recording.

Figure 4

Augmented unipolar leads: aVR, aVL, aVF The three augmented unipolar limb leads compare one limb electrode to the average of the other two. The exploring electrode sits on the right arm in aVR recording, on the left arm in aVL recording and on the left ankle aVF recording (Fig 5). The reference electrode is achieved by connecting the remaining corners in the triangle (R arm, L arm, L leg) via a resistance. For further discussion of this, consult your lab mentor or course textbook.

Figure 5

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Chest leads The most common types of chest electrodes are unipolar and have a Wilson electrode as the reference. They are labelled V1 to V6 and represent the positive electrodes, placed on the chest. In the clinical ECG exam the Wilson electrode is made up by the electrodes placed on the limbs (frontal leads) and the reference point (negative electrode) is calculated automatically by the ECG machine. When recording the ECG during exercise, the limb electrodes are often placed on the shoulders and the thighs, which helps to reduce artefacts due to movement and muscle activity.

Placement of the electrodes on the chest (Fig 6)

V1: Fourth intercostal space, right of sternum

V2: Fourth intercostal space, left of sternum

V4: Mid clavicular line, fifth intercostal space

V3: Halfway between V2 and V4

V5: Anterior axillary line, same level as V4

V6: Mid axillary line, same level as V4

Sometimes V7 is used at the edge of the axillary line, same level as V4 and V4R (corresponding to V4 but on the right side).

Figure 6

ECG recording theory The leads that are most often used clinically are:

• The bipolar limb leads: I, II, and III.

• The unipolar augment limb leads: aVR, aVL, and aVF.

• The unipolar chest leads V1, V2, V3, V4, V5, and V6.

The appearance of the ECG depends upon where the exploring electrode is placed. This means that the electrical activity stays the same but the recorded wave varies depending on what lead you look at. This could be compared to a “spotlight lamp”, whereas the light intensity one could see would differ depending on where you stand, e.g. in front of the lamp, on the side or perpendicular to it, where no light would be seen.

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For example, the same electrical activity recorded from different points:

Figure 7

In order to facilitate the recording of a routine ECG, an internationally recognised colour coding of the cables is used.

Red = right arm Yellow = left arm Green = left leg Black = right leg (earth on older machines, active lead on newer machines)

For the chest leads, one uses the colours red, yellow, green, brown, black and blue together with the letters a to f or numbers 1 to 6.

Electrical axis of the heart The heart’s electrical axis is routinely determined in the frontal plane. The electrical axis is a function of the heart’s position in the chest cavity, the absolute thickness of the muscle in the two ventricles and the condition of the ventricles. The calculations are based on approximations and it is only obvious changes in the electrical axis that are interesting. These include when the axis is outside normal ranges or sudden changes over time (e.g when. comparing two ECG recordings).

When calculating the heart axis one assumes that:

• the heart, which is the centre of electrical activity, is located in the centre of the chest cavity

• the chest is round

• the leads which are used in the calculations (leads I, II and II) are located equidistant from the heart

• the body’s tissues conduct electricity equally well

The body is considered to be an equilateral triangle = Einthoven’s triangle (Fig. 8). Each side of the triangle represents a frontal lead (I, II and III). Additionally, each side is “used” to calculate the augmented unipolar limb leads (aVR, aVL and aVR) with the positive electrode towards the perpendicular side (left/right shoulder and left foot).

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Figure 8

In Sweden the limb leads in the Einthoven’s triangle are printed out in a particular sequence on a six-channel ECG recorder (the most commonly found in hospitals here) known as the Cabrera system. In the Cabrera system one imagines that all frontal leads (their measurement axes) are brought together to cross the same central point (the heart).

In Figure 9, the heart is shown with exploring/positive electrodes arranged according to the Cabrera system. Limb lead I corresponds to 0º, aVL to -30º, II to +60º, aVF to +90º and III to +120º. In order to have the different electrodes with 30º between them, the Cabrera system inverts aVR to –aVR which then corresponds to +30º.

Figure 9

Note that in the figure, the large black arrow is the vector representing depolarisation of ventricles (QRS-complex). This shows the largest sum of electrical activity during the heart cycle which also corresponds to the heart axis. By noting in which lead the sum of the positive and negative parts of the QRS wave is greatest (Tip! look for the highest R-wave), one immediately sees roughly where the electrical axis lies. Read more about the heart axis in the next section.

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Calculate the heart axis

In order to calculate the mean vector, one measures the sum of the heights of the Q, R and S waves in each of the leads I, II and III. The negative deflections are subtracted from the positive deflections and the resultant sum is drawn as a vector on the respective side of a triangle (the base of the vector is placed at the centre of the side). One draws a perpendicular from the head of the arrows and where they meet, this indicates the head of the mean vector.

The electrical axis can be:

Normal axis: -30º >angle < +110º Right axis deviation: angle > +110º Left axis deviation: -30º -90º

Figure 10

Example from the figure above

I:

III:

Advanced Physiology KTH v.1 ECG 29 EXAMPLE OF AN ECG OBTAINED WITH A SIX CHANNEL ECG RECORDER

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LABORATORY HANDBOOK

RESPIRATION

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RESPIRATION LABORATORY

Introduction

The main function of the lungs is gas exchange. The way in which this function can be seen by analysing the blood gases, i.e. O2 and CO2, of arterial blood. If one suspects that a cause of illness is in the lungs or the chest, one can use further investigations of lung function in order to reach a diagnosis and establish the degree of impaired function. Spirometry – measuring lung volumes and ventilatory power – is one of these methods. During this laboratory exercise, you will perform static and dynamic spirometry measurements. In addition, you will investigate the acute respiratory and cardiovascular effects of . The purpose of this laboratory exercise is to provide experience in two common clinical methods of investigation and illustrate the physiological concepts within respiration.

AIMS 1. Be able to describe the components contributing to the work of breathing 2. Be aware of the major types of restrictive ventilation and which type of spirometry to use to identify them. 3. Be able to define and measure the different lung volumes and tests of ventilation. 4. Be aware of the concept of air trapping and dynamic compression as well as understand the flow-volume loops.

5. Know the effects of PCO2 and PO2 on ventilation. 6. Know the symptoms of carbon dioxide and oxygen poisoning. 7. Know the effect of breathing patterns on the size of the alveolar ventilation and by this means PCO2 and PO2. 8. Know the effects of pronounced hyperventilation and how it is treated. 9. Know the gas exchange mechanisms of the body.

This laboratory exercise consists of three parts:

1. Static spirometry Assessment of lung volumes

2. Dynamic spirometry Assessment of active ventilatory power

3. Holding breath The effects of carbon dioxide on regulation of breathing

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BACKGROUND

Static spirometry Static spirometry is used to assess lung volumes by recording inhalation- and exhalation volumes. With the spirogram that is obtained during static spirometry, the following lung volumes can be obtained.

IRV

TV VC

ERV

Figure 1. Spirogram showing the variations in lung volume during normal breathing and during maximal in- and exhalation.

Tidal volume (TV): volume of air during in- and exhalation under normal respiration

Inspiratory reserve volume (IRV): maximum volume that can be inspired following a normal inspiration.

Expiratory reserve volume (ERV): the maximal volume that can be exhaled after a normal expiration.

Residual Volume (RV): The volume remaining in the lung after a maximal exhalation. Approximately 20% of the total lung capacity always remains.

Vital Capacity (VC): The maximal volume exhaled after a maximal inhalation. (TV+IRV+ERV)

Total Lung Capacity is the volume in the lungs after a maximal inspiration (VC + RV)

Residual Quotient is RV/TLC usually about 20%. Functional Residual Capacity (FRC) is the volume that remains in the lungs after a normal expiration (FRC = ERV + RV).

NOTE: The sum of two or more volumes is always referred to as capacity.

The lung volumes that can be assessed during static spirometry are tidal volume, inspiratory- and expiratory reserve volume, and the vital capacity. To measure residual volume, a gas mixture with helium is used. Since helium diffuses slowly, it will not take place in the gas exchange. A known volume of gas (V0), with a known helium

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concentration (C0), is allowed to equilibrate with the air that remains in the lungs after a normal exhalation. The amount of helium is a constant. By measuring the concentration of helium, when equilibrium is reached (C1), FRC can be measured (see fig. 4.2).

Normal range of values:

Female: VC = 4.36 x height (m) - 0.024 x age in years – 2.54. Lower limit VC – 0.9.

Male: VC = 5.19 x height (m) - 0.022 x age in years –3.03. Lower limit VC – 1.1.

V =V +FRC tot 0 V0 x C0 = Vtot x C1 Figure 2.

Vtot = (V0 x C0)/C1 V C 0 0 C FRC 1 V0 +FRC = (V0 x C0)/C1 C1 0 Before equilibrium After equilibrium FRC = (V0 x C0)/C1 –V0

Heliumdilution method. The person breathes in a closed system, to determine FRC and RV. A gas mixture, with the inert gas helium, is used. C1 FRC Certain diseases of the lung can give characteristic changes in the spirogram. Static spirometry can be used in the diagnosis of restrictive lung diseases, which decreases the normal expansion of the lung. A restrictive condition results in a decreased tidal volume, increased breathing frequency and an increased work of breathing. The following conditions are examples of restrictive conditions: • Reduced mobility of the thorax (kyphoscoliosis, post-operative pain, extreme obesity) • Reduced movement of the diaphragm (during , ascites) • Decreased compliance (lung fibrosis, pneumothorax, large volume of blood in the lungs as a result of left cardiac failure) • Reduced functional volume (tuberculosis, lung cancer).

Gas content of air In a volume of gas of known composition at a given pressure, each gas exerts a partial pressure, which is proportional to its share of the volume. For example, at standard atmospheric pressure (760 mmHg) oxygen makes up 21% of the air. Therefore, at sea level, the partial pressure for oxygen is 0.21 x 760 which corresponds to a partial pressure of about 160 mm Hg. At a high altitude there is still 21% oxygen in the air, but since the total pressure decreases, the partial pressure of oxygen will be reduced. This will decrease the gas exchange resulting in an increase in ventilation.

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In the table below, the partial pressures for the components of air are shown in kPa or in parentheses as mm Hg. Although the SI notation for pressure is kPa, many physiologists continue to use mmHg as the unit of measure for partial pressure. To convert mmHg to kPa, divide by 7.5.

Partial Pressure, kPa (mmHg)

Gas Inspired air Expired air Alveolar air

Oxygen 21.17 (158.8) 15.33 (115) 13.33 (100)

Carbon dioxide 0.03 4.4 (33) 5.3 (40)

Water vapour - 6.27 (47) 6.27 (47)

Nitrogen 80.13 (601) 75.33 (565) 76.4 (573)

Total pressure 101.3 (760) 101.3 (760) 101.3 (760) Tabel 1. Partial pressure in kPa (mmHg). As the air passes the nose and airways (dead space) it is heated to 37 oC causing water vapour to evaporate to the inhaled air from the epithelium in the airways. As can be seen in Table 1, the expired air is fully saturated with water vapour from the walls of the airways (the important function of the dead space). The water vapour content of the air depends upon the temperature and pressure (see the table on the next page). The expired air with a temperature of 37 ºC has a Pwater of 6.27 kPa (47 mm Hg) which means that the water content is 6.27/101.3= 6%. At 20 ºC, the air has a water content of only 2%, and the partial pressure is thus 2.3 kPa (17.5 mm Hg).

Properties of gases and the calculation of spirometry results As is well known, the volume of gases varies with pressure and temperature. In order to measure the lung volumes, we breathe into a spirometer or pneumotachograph. The volume measured must then be corrected for the temperature difference between the lungs and the measuring apparatus as well as for the difference in water vapour content. In this way, one obtains a standardised measurement that is not dependent on the actual temperature. The ideal gas law states that PV = nRT where P is pressure V is the gas volume n is the number of moles R is the gas constant (= 8.33 J x mol-2 x K-1) T is absolute temperature in kelvins (= ºC + 273)

Lung Spirometer

P0=760-47 (dry gas) P1V1/ P1=760-PH2O at room temp (rt) P0V0 T1 /T0 V0=lung volume

V1=measured volyme BTPS ATPS

Advanced Physiology KTH v.1 Respiration T0=273+37=310 35

T1=273+rumstemp

For a quantity of gas, PV/T = constant.

V0 (BTPS) = V1 (ATPS) x ((760- Pwater)/760-47) x (310/273 + room temperature)

i.e. V0 (BTPS) = V1 (ATPS) x factor

BTPS = body temperature and pressure, saturated; ATPS = ambient temperature and pressure

The volume in BTPS can be calculated according to the formula above or more simply by extracting the appropriate factor from the table below.

Factors to Convert Gas Volumes from Room Temperature Saturated to 37oC.

Factor to Convert When Gas With Water Volume to 37oC Temperature is oC Vapor Pressure (mm Hg)* of

1.102 20 17.5 1.096 21 18.7 1.091 22 19.8 1.085 23 21.1 1.080 24 22.4 1.075 25 23.8 1.068 26 25.2 1.063 27 26.7 1.057 28 28.3 1.051 29 30.0 1.045 30 31.8 1.039 31 33.7 1.032 32 35.7 1.026 33 37.7 1.020 34 39.9 1.014 35 42.2 1.007 36 44.6 1.000 37 47.0

th *H2O vapour pressures from Handbook of Chemistry and Physics (34 ed. Cleveland: Chemical Rubber Publishing Co 1952), p. 1981.

Note: These factors have been calculated for barometric pressure of 760 mmHg. Since factors at 22oC for example are 1.0904, 1.0910 and 1.0915, respectively, at barometric pressures 770, 760 and 750 mmHg. It is unnecessary to correct for small deviations from standard barometric pressure.

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The air in the lungs has a volume about 10% greater than that measured at 20 ºC. Different gases have dissolve differently depending on the fluid present. The solubility is proportional to the concentration in the surrounding gas phase, which is why the amount of oxygen and carbon dioxide is dependent on their partial pressure in the alveoli. The amount of oxygen physically dissolved in the arterial blood is quantitatively very little but even the saturation of haemoglobin is governed by the partial pressure of oxygen which becomes very important in situations where the partial pressure of oxygen is low such as high altitude.

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Dynamic spirometry Dynamic spirometry is used to measure flow, especially during expiration.

To create a flow of air in to the lungs, the surrounding tissues need to create and change the pressure surrounding the lungs. These pressures are relatively small and are usually described in cmH2O. The air pressure is set at zero and the other pressures are described as deviations from this. After a normal exhalation, a negative pressure will be created by the elastic properties of the lung and thorax. The lung tissue wants to collapse (because of elastic fibers and surface tension) and the elasticity of the chest causes it to expand. The difference in pressure between the alveoli and that in the pleural cavity is the transpulmonary pressure. During an inhalation both the elastic resistance and the resistance caused by the friction of air against the airway must be overcome. This is increased in obstructive lungdisease. There is also friction between the thorax and lung.

Inflation of the lung is an active process that is initiated by a contraction of the diaphragm. The chest will expand and the pleural pressure will become more negative. The transpulmonary pressure will increase, the alveolar pressure drops below the atmospheric pressure and air can enter the lungs. A normal exhalation occurs due to relaxation of the muscles causing inhalation. The volume of the thorax decreases, the pleural pressure becomes more positive, the transpulmonary pressure decreases and the lung tissue collapses slightly due to its elasticity and surface tension in the alveoli. During a forced exhalation, the conditions are somewhat altered. The abdominal musculature is activated to empty the lungs from air, and the pleural pressure will during this type of exhalation become positive. This is due to the chest being able to reduce the volume of the thorax faster than the lung itself can collapse. A strongly forced exhalation will therefore not empty the lung of more air, a phenomenon called dynamic airway compression. If the pressure in the thorax rises above that in the airway, it will be compressed. Due to the resistance from friction, the driving force in the airway will decrease towards the mouth. The point where the pressures inside and outside the airway are equal is called the Equal Pressure Point (EPP). Normally, EPP will be located in the parts of the bronchial tree where cartilage prevents compression. However, during conditions with decreased elasticity of the lung, such as emphysema, the driving force of the air in the airway is missing and EPP is moved towards the alveoli. When there is no cartilaginous structures, the bronchiole will be compressed and air, peripheral to the compression, will be trapped – air trapping.

During an obstructive disease, such as asthma, the airway friction is increased. The airways increase in diameter during inhalations and decrease during exhalations, especially when they are forced, due to the pressure variations in the lung that occur during breathing. Therefore, an increase in airway friction is especially clear during a forced exhalation. Patients with obstructive conditions will have a longer exhalation, which may be accompanied by a wheezing. Characteristic findings with an obstructive condition are a normal VC, but decreased FEV1.0 and FEV1.0%.

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Flows and volumes FVC: forced vital capacity

FEV1.0: the volume of air forcibly expired in one second.

FEV1.0%: FEV1.0/FVC, considered normal if above 80%

PEF: Peak expiratory flow measured in l/min. This differs greatly between individuals but is useful for monitoring an individual.

FEF: Forced expiratory flow, describes the flow at a time when a given proportion of the FVC has been expired and this expressed as FEF75 for example. This measurement is considered to detect obstructive limitations at an early stage, since minor limitations will be seen late in expiration.

MVV: Maximal voluntary ventilation is the maximal volume that be breathed in and out during a given time. Typically, it is measured over a 15 second period and converted to l/min. MVV is reduced in both restrictive and obstructive disease. The measurement of dynamic lung function cannot be considered reliable in patients who are not maximally motivated during the investigation.

Figure 3

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Holding breath experiment: Control of respiration

Gas exchange in the body A normal breath consists of 78% nitrogen, 21% oxygen, 1% noble gases, eventual water vapour and a very small amount of carbon dioxide, 0.3%. (Figure 4).

Oxygen Oxygen Noble gas Noble gas Carbon dioxide Carbon dioxide Nitrogen Nitrogen

Figure 4a. Inspired (dry) air Figure 4b. Expired (dry) air

The interesting physiological question is what happens to the inspired air. A resting breath has a volume of about 500 ml which makes up only a small part of the volume (roughly 3 l) of the ventilated parts of the lung. Therefore, the gas mixture in the alveoli does not change much between inspiration and expiration. Oxygen diffuses into the blood and the carbon dioxide produced by metabolism goes in the opposite direction. So when we exhale, the composition of the expired air gives a measure of the alveolar air mixed with dead space.

The carbon dioxide content of the expired air at the end of each breath (the end-tidal volume) usually provides a good measure of the arterial PCO2 (about 5.3 kPa) as carbon dioxide diffuses easily. The expired air does not provide a reliable estimate of the oxygen content of arterial blood as oxygen does not diffuse as readily as carbon dioxide. A few percent of carbon dioxide has been added to the expired air and about the same amount of oxygen has been consumed. This is used to express the Respiratory Quotient (RQ);

RQ = Carbon dioxide produced/Oxygen consumed (about 0.82 at rest)

One can easily measure carbon dioxide production and thus oxygen consumption. For example if the expired air contains 4.3% CO2, and the breathing rate is 12/min, then

Carbon dioxide production = 500 x 12/0.043 = 258 ml/min

Oxygen consumption is 258/0.82 » 315 ml/min.

Normal oxygen consumption is about 250 ml/min and the difference between inspired and expired air is only a few percent. The body can easily extract the amount of oxygen that is needed at rest, during exercise and even in the situation of heart-lung resuscitation. The size of the alveolar ventilation depends upon amongst other things, the carbon dioxide production and the acid-base balance.

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Procedure

Static spirometry 1. The spirometry settings of lab chart will be open when you start. Please do not close down the window during the lab! You will see two channels. Channel 1 records flow and channel 2 records changes in volume during the breathing cycles.

Figure 5

2. Before you start the experiment, leave the mouthpiece on the table. Under the Flöde- menu, in the column to the right, press Spirometer (fig. 6). The apparatus tends to record some activity even at rest (when there is no flow). This is called drift. Correct for this drift by pressing the Zero-button (fig 7). This assures that no signal is recorded when the flow is zero. Wait until the computer has completed the process. Press OK.

Figure 7

Figure 6

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3. The subject, who should wear a nose-clip so that all air goes through the mouth, should sit/ stand so that he/ she cannot see the screen. Hold the mouthpiece so that the plastic tubes are upwards. Try breathing in the mouthpiece a couple of times before the experiment.

4. Start the experiment by pressing the Start-button in the lower right corner. The test will change to Stop. Breathe normally for a couple of breaths, then perform a maximal inhalation followed directly by a maximal exhalation. Note: it does not have to be fast. Take a couple of more breaths and finish by pressing the Stop-button.

5. To make the analysis, mark the volume-curve in channel 2 so that at least one normal and the maximal breath are included. Among the functions in the upper toolbar, there is a Zoom-button. Press this. Measure the lung volumes by using the marker (M) in the lower left corner. Put the marker at a point on the curve. The volume between the marker and the movable cross will be measured. See ”Using the computer software” if a problem occurs. The value will be displayed as Dt (measured between the marker and cross) in the textline at the top of the picture.

6. Press the button ”Chart Window” to return to the starting page (this is the case for the whole experiment). Zoom

Chart Window

Volumes Value when seated (l)

Tidal volume (l)

Inspiratory reserve volume (l)

Expiratory reserve volume (l)

Vital capacity (l)

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Vital capacity when laying down (l):______

Check with the instructor that you have performed the measurements correctly before you continue with the experiment.

7. When the first subject has performed the measurement, he/ she will lay down while the other people in the group measure their lung volumes. The measurement will then, for one of the persons in the group, be performed while lying down.

8. The other people in the group perform the measurement. For every new trial, it is enough to press the Start-button and for analysis, mark the part of the recording that is of importance (repeat number 3-5).

Was there a difference in vital capacity between standing and laying down?______

What is the reason?

______

______

______

______

Note that the variation in lung volumes, even between individuals of similar size and gender, is large, whereas a value is considered pathological only when it deviates with more than 20% from the norm. In one and the same individual however, the values only differ with ± 200 ml.

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Dynamic Spirometry The same starting page as with the static spirometry is used. The zeroing process should not have to be repeated. 1. Start the measurement by pressing the Start-button. The subject should breathe normally in the mouthpiece, perform a maximal inhalation and then exhale as quickly, as much and for as long as possible. Continue by breathing through the mouthpiece for a while and then stop the recording by pressing the Stop-button.

2. Select this trial in both recordings for the analysis (First select one recording, then press the [Shift]-button and hold it down as the other recoding is selected) and press the Zoom-button. In this trial, you also use the marker and cross to find the following parameters. Volume and Flow Value

Forced vital capacity (l)

Forced expiratory volume in 1 sec (l)

FEV1.0% = FEV1.0/FVC x 100 (%)

Peak expiratory flow (l/min)

3. Compare the values that you get with the values from those that the computer yields by, when the curves are still selected, go under the Spirometry-menu and choose Report.

Figure 8 Figure 9

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WHO CAN HOLD THE LONGEST? In this part of the lab, we will do a small experiment to understand how respiration is regulated. Divide the students in 2 groups with more or less 4-6 people each group. Group 1 the experimental person will hold the breath as long as he/she can. Group 2 the experimental person will take 3-4 deep breaths (close to vital capacity) and then hold his/her breath as long as he/she can.

1. Discuss first which group do they think will hold the longest their breath. Why? This will be our hypothesis. 2. According to each group, the experimental person will be seated on a chair and be relaxed as much as possible. One colleague will measure the heart frequency by in the for 15 s. 3. Experimental person in group 1 holds the breath as long as possible and a colleague takes the time. Experimental person in group 2 takes 3-4 deep breaths and holds breath as long as possible and a colleague tales the time. Remember that isn’t a competition. 4. Right after holding breath is stopped measure heart frequency again. 5. Change the roles so the experimental person is different. 6. Fill the table with the time holding breath and the heart frequency before and after holding breath.

Group 1

Experiment Time holding HF before HF after person breath (s) holding breath holding breath

Average

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Group 2

Experiment Time holding HF before HF after person breath (s) holding breath holding breath

Average

Discuss the following questions. 1. Which group could hold the breath the longest? 2. Is it in accordance with your hypothesis in the beginning? Why or why not?

Additional questions 1. Which gas in the arterial blood, CO2 or O2, regulate normal breathing in healthy people? 2. Explain respiratory acidosis and alkalosis. What happens in the experiment? Relate with the bicarbonate buffering system. 3. Which receptors are activated in the regulation of the respiration that were activated with the experiment? Where are they? What do they detect? Where do they act? 4. What happen with the heart frequency during the experiment? Why? 5. In which anatomic structure is regulated the respiration? How does it happen that respiration occurs without we need to think about it? 6. What happens when someone hyperventilates for long time? Which symptoms can occur and what mechanism is the cause of those symptoms.

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