Official BPK 407

Distinguish between "unipolar" leads and "bipolar leads".

"Lead" in general represents the direct 'imaginary' line or plane between two electrodes, which can be either a bipolar or unipolar. Bipolar indicates that there are 2 electrodes of opposite polarity (one negative and one positive/recording); unipolar indicates that there is no negative pole, rather there is a positive/recording electrode and a reference electrode. For example, in a 12-lead ECG there are 3 bipolar limb leads (Lead I, II, and III), there are 9 unipolar limb limbs (3 augmented voltage limb leads which are calculated from the 3 bipolar limb leads; 6 precordial or chest leads (V1-V6). There will also be a reference electrode placed. Each lead shows a scalar (1 dimensional) projection in the plane that it is in, which is a component of the 3 dimensional vector measured from all of the lead recordings to overall generate the mean electrical axis.

How does the average pulse wave amplitude from the rest and each time period in recovery compare? Do you see any variation or trend?

(From Dr. Carter) The pulse wave increases from rest to exercise because as the blood pressure increases, the pulse wave needs to as well, both to keep up with the demands of the exercising body (faster HR needed, larger stroke volume and thus cardiac output needed, overall to increase perfusion rate to the working muscles). As the body returns to its resting state the pulse wave amplitude should and will also return to normal. For our subject specifically, the left ventricle had to contract more forcefully during recovery for a number of reasons.

List 3 desirable characteristics of an ECG electrode.

- Easily manipulated by the operator (easily accessible, easy to put on and remove) - inexpensive to make - provides low and stable impedence when placed on the skin (impedence = the resistance of the electrical circuit to the alternating current)

How does using a pressure cuff which is too narrow affect the reading of SP? Explain briefly.

A blood pressure cuff has a distensible rubber bladder inside the nondistensible outer material; the purpose is so that when you inflate the bladder it exerts even pressure on the limb under the cuff to that the pressure in the cuff is directly transferred to the brachial artery. If the BP cuff is too narrow then the pressure thats in the cuff will be higher than the actual pressure that is exerted on the artery so you end up with an overestimation of actual BP.

Do muscle fibers have a refractory period like nerve fibers?

A refractory period is a short period of time following a stimulus where if another stimulus came along it would not generate another action potential. Yes muscle fibers do have a refractory period like nerve fibers. It is the depolarizing AP that travels down the T-tubules opening Cav 1.1 in the T-tubule sarcolemma and RyR1 channels in the SR membrane that allows the cytoplasmic calcium spike. This allows cross bridge cycling and muscle fiber contraction. As long as calcium and ATP is available, sustained contraction can occur. You can have high frequency of muscle fiber AP's to allow summation and then tetany (sustained muscle contraction). The muscle fibers still have a refractory period but the cytoplasmic calcium and ATP may still be present and not yet returned to the SR before the next muscle fiber AP is generated. Muscle fibers transmit action potentials the same as nerve fibers (neurons) do where sodium channels open allowing sodium influx (depolarization) which then inactivate and potassium channels then open to allow potassium efflux (repolarization). The sodium channels inactivate and it takes a brief time period for them to reset, hence a refractory period.

Are the systolic and diastolic blood pressures from Exercises 1 and 2 identical? What are the possible sources of variation? (repeat BP measures on L arm)

Although very similar, the BPs are not identical, with SPs being closer than DPs. Side note: Sources of error or variation with experimental measurements does NOT refer to whether the experimenter has done something incorrectly like position of taping or markers, rather it refers to true experimental errors like in the equipment, experimental design, etc. Specifically, random errors refer to errors that cause the results to spread in any direction of the true value, systematic errors refer to errors that cause the result to always be skewed in one direction, and parallax error refers to when the position on a needle on a scale is read at an angle and not straight on. Possible sources of error in this case could be: the LabScribe Program is very accurate in identifying the SP since it is simply the first upward tracing on the Pulse Channel) however DP is less easily identifiable (because the DP is the first upward pulse wave of the successive pulse waves that have consistent heights after the SP wave); this would explain how the SPs are closer in value than the DPs movement or shifting of the BP cuff - arm interface or pulse plethysmograph-finger interface during recordings Since the subject rested between exercises 1 and 2, their BP simply could have gone down due to increasing resting time; they became more relaxed Simple biological variation as well Between exercise 1 and 2 the BP cuff was resituated on the subject, this particular subject had arms small in diameter so fitting of the BP cuff was not exact

What is "ambulatory BP" measurement, and what are its advantages compared to clinic BP measurement?

Ambulatory BP measurement is when your BP is measurement as you move around during your normal daily life using a small digital BP machine that is attached to a belt around your body that's connected to a cuff around your arm. In this way you can get a clear idea of how your BP changes throughout the day. You can see if your BP medicine is working throughout the entire day, including when you sleep. It avoids 2 problems often associated with clinic BP measurement. With clinic BP measurement you may be subject to 2 types of problems: White coat hypertension = an overestimation of BP because the patient is anxious or nervous from being in a physician office Masked hypertension = the person's true hypertension is masked, where they have normal BP in the physician office but they have high BP during many other time periods of the day

Define the term electrode with respect to human physiological recordings.

An electrode is a type of transducer that converts the biological ionic current traveling through the body's cells to an electric current intended to flow through the electrode cable. More generally a transducer senses a physical phenomenon and produces an electrical signal, converting one form of energy to another.

Surface electrodes are prone to "cross-talk". What does this mean?

An electrode will be placed over a muscle and ideally will record electrical activity that occurs within motor units of the muscle it overlays. Cross-talk refers to electrical activity in other muscles that the electrode detects and records when you are trying to just record electrical activity from one muscle.

Did the LP values of the subject at rest go up or down as his or her HP values increased?

As the subjects LP values increased, their HP values decreased. Then as the subject's LP values decreased, their HP values increased. Therefore LP and HP show to have an inverse relationship. This makes sense since LP is associated with sympathetic activity and HP is associated with vagal activity; the 2 parts of the autonomic nervous system (sympathetic and parasympathetic) tend to oppose one another in activity/function.

Which muscles, Pronator or Biceps, had the most EMG activity during losing?

Both muscles had very similar EMG activity during losing; the EMG activity difference is not significant.

Define the term "common mode rejection".

Common mode rejection is a process provided by a differential amplifier that solves the problem of 60 Hz interference. It is an electronic subtraction of the common signal that is experienced by each of the recording electrodes. 60 Hz interference is a form of electrical activity provided from power lines, lights and electrical equipment that cannot be filtered out, so to remove it you can take the voltage recordings at each of the 2 recording electrodes and subtract them which ends up canceling this 60 Hz interference; this is common mode rejection.

Which muscles, anterior or posterior, had the most EMG activity during extension?

During extension, we got expected results when the hand was open and when closed making a fist: posterior forearm muscles had more EMG activity during extension.

Give 3 reasons for exercise stress testing (EST).

EST is an accessible and inexpensive method to evaluate suspected coronary disease and to evaluate its severity if present by engaging the individual in exercise for a total time of 8-12 minutes. Most commonly a multi-stage bicycle or treadmill test is performed where there are small increments in work rate and several work periods of about 3-5 minutes in length each. The small increments in work rate allow you to see the patient's threshold for say myocardial ischemia and the exercise is to be stopped when the patient is fatigued; where the final work rate is considered the PWC max (maximum physical work capacity) of that person. Three reasons for EST are to diagnose an abnormal response to exercise that indicates CVD (cardiovascular disease), to assess physical tolerance of CVD patients and to assess physical fitness of non-CVD patients.

What electrical and mechanical events take place in the heart during the R wave?

Electrically speaking, the R wave represents ventricular depolarization. Mechanically speaking, the R wave represents ventricular contraction. At this point in the cardiac cycle the electrical signal has reached the Purkinje fibers which spread the depolarization wave across the ventricular cardiomyocytes (ventricular depolarization). Mechanically speaking, following atrial contraction the AV valves close so that now both the AV valves and the semilunar valves are closed, the ventricles depolarize so that the cardiomyocytes begin to contract and build pressure within the ventricles (isovolumic ventricular contraction). When the ventricular pressure is more than the arterial pressure on the vessel side of the semilunar valves, the semilunar valves open expelling blood out to the body (ST segment).

Describe the current research evidence regarding the effectiveness of an exercise program for hypertensive subjects. Describe the optimal exercise program for hypertensive subjects.

Exercise has an anti-inflammatory effect through its action on the sympathetic nervous system as well as the hypothalamus/pituitary/adrenal glands; it increases your vagal tone. It has direct effects on BP. Current research suggests that the most effective exercise for hypertensive subjects is moderate intensity aerobic exercise. Examples include speed walking, jogging, light running, dancing, sub-maximal cycling, swimming, etc. It has been found to lower resting BP in patients with mild to severe hypertension. Physical activity leads to many vascular, immune and neuroendocrine changes, a few of which are: Vascular changes like increased lumen diameter and neoangiogenesis (new blood vessels forming). Anti-inflammatory effect: Reduced levels of C-reactive protein (elevated with high BP) and reduced inflammatory cytokines. Enhanced baroreceptor sensitivity, reduced NE levels and reduced peripheral vascular R. Aerobic exercise will induce physiological hypertrophy where the heart increases in mass but function is improved because there is more ventricular dilation (increasing the capacity of the pump). Aerobic exercise has been found to be almost completely free of secondary/side effects; it reduces resting BP. When it comes to patients with Stage 2 hypertension, research suggests they should be treated pharmacologically before beginning training to not put added stress on the cardiovascular system. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369613/ In contrast to aerobic exercise training, resistance training and isometric exercise is not recommended as the only form of exercise for patients with hypertension because it is not found to be associated with a significant reduction of SP or DP. Moreover there is significant elevation of pressure within the thoracic cavity during these forms of exercise putting more pressure on the vasculature close to the heart.

Describe 5 factors that can affect the relationship between amount of force exerted and muscle activity as measured by electromyography.

Factors that can affect the relationship between force generated and EMG activity recorded (so if the force that is generated does not match up with the EMG activity recorded): Cross talk - there could be cross talk between muscles so that the force that is generated may be the same but the electrode is picking up more EMG activity from nearby muscles. Other muscles doing the work - depending on the body positioning, a large amount of force could be produced not because the muscle is more active but because force is provided by other muscles; so the force would be large but the EMG activity recorded would be small. Fatigue - a muscle that is fatiguing with have an increase in EMG activity but its force generation would be depleting Lever class (skeletal muscle - bone organization) - if the lever is very efficient there will be more output (force generated) for less input (less EMG activity recorded) MU distance from electrode (with MU recruitment) - to increase muscle force there is recruitment of more MUs (also an increased firing of motor neurons) which according to the size principle, smaller MUs are recruited first then large if needed. Because of this, increasing MU size with increasing force should mean proportional increase in EMG activity. But this may not be true because EMG activity also depends on the distance of the MU from the electrode; if it is very far then the electrode will pick less of the electrical activity up.

Compare the parameters for the EMG bursts from the gastrocnemius (G) during each of the activities. When was G activity the greatest? The least?

G was most active when rocking forward with one leg (then second most active during plantar flexion while standing on the toes). This contrasts the activity of TA, suggesting they are antagonistic muscles (muscles that act on the same body part to produce opposing movements; they will be active during opposite times, when TA contracts, G will relax and vice versa). G was least active when standing erect with both legs (then second least active during dorsiflexion during squat). This suggests that both TA and G are not very involved in maintaining balance while standing or contribute in smaller amounts because that is all that is needed.

Distinguish between prehypertension, Stage 1 hypertension, and Stage 2 hypertension.

Google doc page 34 and 35

Be able to recognize the following arrhythmias, give a physiological explanation of the cause of the arrhythmia, and a physiological explanation of the shape of the resulting ECG waveform from the arrhythmia.

Google doc page 7 & 8

Give a detailed explanation of how HR and BP change with time in a normal subject who is rapidly moved from supine to a 70 degree head up tilt (HUT) position.

HUT position can be induced with a tilt table, in this way there is no skeletal muscle pump available to aid in VR, so the HUT can be a test of baroreceptor (BR) response strength and thus orthostatic tolerance (the strength of your BRs, how well you can handle standing without syncope). When you take a normal subject and lay them supine on a tilt table their perfusion pressure and mean arterial blood pressure (MAP) are consistent across their body (there is no head to toe gradient). Then once you tilt them on the tilt table you are inducing orthostatic stress on their body, which results in a perfusion pressure gradient from head to toe where pressure increases as you go further down the body due to the force of gravity. While in this upright position the most important thing is to maintain cerebral perfusion, as well as BP and blood volume. If the body is unable to do so (has a lack of orthostatic tolerance) then this results in gravity induced venous pooling in the lower body, which reduces BP and worse cerebral ischemia. The body's last defense when this occurs is syncope (loss of consciousness due to cerebral ischemia) so that the body goes into supine position remobilizing blood back to the brain. There are defense mechanisms in place to prevent this from happening as soon as the normal subject is moved from supine to HUT position: In standing, the first line of defense is the skeletal muscle pump, where contractions of the leg muscles propel the sequestered venous blood back to the heart to increase VR. However in a HUT this defense is not available so the first line of defense is the BRs. There are two sets of baroreceptors (arterial BRs in the carotid sinus and aortic arch and cardiopulmonary BRs in the right atrium, ventricles and pulmonary arteries); the reasoning for this is to ensure BP is regulated on both the high pressure side (arterial BRs) and the low pressure side (venous side and pulmonary circulation). The arterial BRs on the high pressure side in the carotid sinus and aortic arch act primarily to regulate HR and contractility of the heart through SNS and PSNS channels stemming from the CNS (cardiovascular control centre in the medulla). The cardiopulmonary BRs are located on the lower pressure side in the right atrium, ventricles and pulmonary arteries and they primarily act to ensure adequate VR. BOTH of the BRs contribute to the BR reflex: When the subject is tilted there is a venous pooling effect seen in the lower region of the body which reduces the amount of blood effectively circulating (hypovolemia); consequently there is a decrease in the central venous pressure so a decrease in venous return and thus CO so drop in BP. The arterial and (to a lesser extent) the cardiopulmonary BRs sense this drop in BP and trigger their cardiopulmonary baroreflex to overall increase VR (a drop in BP causes a reduction in BR firing rate): Increase in TPR (total peripheral resistance) Vasoconstriction to the extremities and splanchnic circulation mediated by the SNS - to redistribute blood flow and dip into the blood reservoir held by splanchnic circulation Reduction in venous compliance (less volume change for a given pressure change; less venous distension so redistribution of blood volume kept on the venous side of circulation) A proposed line of defense following is humoral agents (hormones) like epinephrine (increase HR) and ADH (increase blood volume) through the SNS and RAAS. But this response takes time so is more delayed; might not be important for the immediate response to orthostasis. Last line of defense is syncope - loss of consciousness due to inadequate cerebral perfusion will cause the person to collapse, become supine, remobilize blood back to the brain and restore consciousness.

Are the BP values obtained for the right arm the same as those obtained for the left arm? Explain any differences.

However, in our subject SP seems to be slightly higher and DP seems to be lower or about the same. Differences could be due to the sources of error described in question 1 or the fact that the subject may not have been relaxed enough (not relaxed for the full 5 minutes as they were in Exercise 1 and 2) in the movement from exercise 2 to exercise 3. Some outlandish and highly unlikely reasoning the subject could have situs inversus with dextrocardia so for all we know her right arm is closer to her heart.

If a person had poor hearing acuity (ie. was "hard of hearing") when they measure BP with a cuff and stethoscope, how would their readings compare with the actual measures of SP and DP?

If a person had poor hearing acuity, they would likely underestimate SP (recorded SP would be lower than the true value because they would hear the first Korotkoff sound later) and would likely overestimate DP (recorded DP would be high than the true value because they would hear the Korotkoff sounds disappear earlier).

Over what range of pressures should you calibrate the aneroid manometer? Why?

In general you calibrate an instrument over a range of values that you expect to measure. The aneroid manometer values that we expect to measure will be about 40-200 mmHg for this BP lab. The reason for this range specifically is we do not expect to need to inflate the cuff over 200 mmHg because this would be unnecessary and we do not expect the subjects DP to reach levels under 40 mmHg because that's medical emergency status.

What happens to the BP in the subject's left leg when they stand?

In going from sitting to standing there are significant increases in BP values also due to orthostatic stress. The increase in BP values going from sitting to standing is to a much larger degree than when the subject went from supine to sitting, or in measuring from the left arm and left leg when sitting.

Pushing the calibration button generates a 1 mV square wave. What is the purpose of recording a calibration signal on the electrocardiogram.

In recording the calibration signal, one can now measure the height (in millimeters) of the square wave and generate the conversion factor that 1 mV = ____ mm on the electrocardiogram. This is essential for calculating amplitudes of the QRS complex or ST segment depression for instance.

Compare the BPs before and after dynamic exercise. How long does it take your subject's BP to return to the resting level?

It is important to not that there is a difference between strength exercise and aerobic exercise; strength exercise is like during isometric force generation or heavy lifting where as aerobic exercise involves more cardio where the heart needs to pump blood to the working muscle. There is a marked increase in BP always seen with strength exercises but there is much more variation in BP seen with aerobic exercise. BP should drop after aerobic exercise but it doesn't always. The body is very good at regulating blood flow (HR, vasoconstriction/ vasodilation, etc); with aerobic exercise blood flow increases to certain structures like active/ working skeletal muscle, reduces to other structures like the stomach, intestines, kidney, while other structures like the brain need to have constant perfusion. In this exercise, we should see the DP stay approximately constant during exercise and afterwards in recovery and we should see the SP increase when the subject is exercising and decrease in recovery until it goes back to normal or even below normal. This is partly exhibited by our subject, the DP stays pretty much constant with some fluctuation and the SP increases from rest to recover time of zero (corresponds to exercising). Then as recovery time progresses the subjects SP decreases. Interestingly toward the end of recorded recovery time the subject's HR, SP and DP rose slightly when it was expected to continue dropping. Possibly attributable to subject movement or emotional stimulation.

How can one record a 12 lead ECG with only 10 electrodes?

Leads can share the same electrode so the standard 12 lead ECG only needs 10 electrodes. The electrodes within the 12 lead ECG consist of 1 reference electrode, 3 recording electrodes associated with the 3 bipolar limb leads, and 6 recording electrodes associated with the 6 precordial or chest leads. The 3 augmented voltage limb leads are calculated from the 3 bipolar limb leads and do not require electrode placement. The circle of axis is created by the 3 bipolar limb leads and 3 augmented voltage leads which 'fill in' the angles that Leads I, II and III do not thus allowing a good idea of the total electrical activity of the heart. More electrodes are not needed.

Compare advantages and disadvantages of mercury sphygmomanometers versus aneroid sphygmomanometers. Why are aneroid manometers replacing mercury manometers in many clinical settings?

Mercury sphygmomanometers are more accurate, are less likely to need to be recalibrated, and are easier to maintain. They contain mercury (a liquid) so require a level surface and are less mobile. However they are being abandoned in clinical settings because of the associated risk of mercury spills. Aneroid sphygmomanometers require routine maintenance and recalibration every 6 months and need to be handled gently to avoid decalibrating. They can be cheaper and are more mobile; however they do have a range of quality and pricing with different models.

In what way does motion artifact look different than wandering baseline?

Motion artifact looks like a sudden upward or downward deflection on the tracing caused my movement of the electrode at the electrode-skin interface. Whereas wandering baseline is where the whole tracing gradually moves upwards then gradually downwards caused by either excessively deep respiration, electrode paste/jelly drying up, the electrode pulling away from the skin, or by excessive tension on the patient cable (between patient and recording device).

Explain the difference between "wire" or "patient cable" and "lead" with respect to electrocardiography.

Named in electrocardiography, the patient cable (cable being a bundle of wires) transmits the electrical signal from the electrode to the electrocardiograph (the machine). Whereas a "lead" represents the direct 'imaginary' line or plane between two electrodes, which can be either a bipolar or unipolar lead. Bipolar indicates that there are 2 electrodes of opposite polarity (one negative and one positive/recording); unipolar indicates that there is no negative pole, rather there is a positive/recording electrode and a reference electrode. For example, in a 12-lead ECG there are 3 bipolar limb leads (Lead I, II, and III), there are 9 unipolar limb limbs (3 augmented voltage limb leads which are calculated from the 3 bipolar limb leads; 6 precordial or chest leads (V1-V6). There will also be a reference electrode placed. Each lead shows a scalar (1 dimensional) projection in the plane that it is in, which is a component of the 3 dimensional vector measured from all of the lead recordings to overall generate the mean electrical axis.

What is the normal BP response to dynamic exercise? How does this differ from the response to isometric exercise? Explain the main physiological factors (at a systems level, not a molecular level) in each case.

Normally during dynamic exercise SP will increase as work rate increases and DP will remain constant. During dynamic exercise the body's working muscle requires more oxygen, this increased oxygen supply (and consumption) is provided by the body increasing HR and stroke volume (SV) which overall increases cardiac output (CO) (CO=HR*SV). This process just described increases arterial BP, especially during systole because the heart has an increased contractility during dynamic exercise. Since SP is the pressure exerted by the blood on the walls of the arteries during contraction of the heart it increases whereas DP pressure is during relaxation so there will be less of a change. Another factor is that DP is largely affected by total peripheral resistance (TPR) - during dynamic exercise there is a blood flow shift away from the gut and kidney (via vasoconstriction of arterioles to these organs) and toward the active working skeletal and cardiac muscle (via vasodilation) - the overall net effect reduces TPR. It is the decrease of TPR but the increase of CO that tends to cancel eachother out and keep DP approximately constant. To sum up, the combo of increased contractility of the heart muscle and thus increased CO will increase SP and the balance of a decrease in TPR but increase in CO causes DP to remain constant. Normally in isometric exercise both SP and DP increase as the work rate increases. The magnitude of this increase depends on a few factors: the amount of muscle mass involved in the contraction and the strength of the contraction, as well as whether the upper or lower limbs is involved. Since energy is still consumed through cross-bridge formation to produce tension in the isometric muscle we refer to work being done, even though technically there's no work done (W=F*d; the force was not performed over a distance). With isometric exercise there is a smaller work rate than dynamic exercise, this means there is less energy and oxygen consumption, so less needs to be supplied. Thus CO will be lower (any increase is almost all due to HR not SV). There's also less of a vasodilatory response to the skeletal and cardiac muscle because not as muscle blood supply is needed. The isometric contraction of the muscle exerts a pressure on the blood vessels which can partially or completely occlude them which increases TPR. To sum up, the combo of more CO, less vasodilatory response (so more TPR) and increased pressure exerted on the blood vessels (so more TPR) causes an overall increase in TPR. This causes an increase in both SP and DP.

How does the heart rate from the subject at rest and at 0, 30, 60, 90, and 120 seconds after exercise (recovery) compare? Is there any variation between the rates for each time period? Is there a trend and what is it?

Normally during exercise HR increases a ton, then in the 1-2 min post-exercise it drops immediately to about 10-20 mmHg above normal resting value. The heart rates at rest and at 0, 30, 60, and 90 seconds after exercise are 63, 112, 97, 92, and 90 bpm respectively. HR at rest is lowest, understandably so. At recovery time of 0 seconds which is essentially like during exercise HR has increased dramatically; following this as recovery time goes on the HR decreases. Yes there is variation between the rates for each time period; there seems to be a trend where the rate of decrease is largest at the start of recovery and the rate of decrease reduces over time.

Explain how each of the two types of electronic BP devices works. Which one is more sensitive to movement?

One type of electronic BP meter is the oscillometric BP meter: it is the most common and is based on surges of pressure from ventricular contraction transmitting from the artery to within the cuff. Blood flowing through the artery between SP and DP causes vibrations in the arterial wall which then get detected by the cuff; when the cuff is fully inflated it's cuff pressure is more than the artery pressure so the vessel is occluded. As the cuff is deflated below SP, the reduction in cuff pressure means less pressure is transmitted to the artery so blood is allowed to recede and advance against the occluded artery in pulses corresponding to ventricular contraction. Vibrations are transferred from arterial wall, through the air inside the cuff and into a transducer in the monitor that then converts the measurements into electrical signals. Another type of electronic BP meter is the auscultatory BP meter which has a small microphone in the pressure cuff that gets centered over the brachial artery. It 'hears' the Korotkoff sounds and therefore sends signals to a micropressor when it 'hears' the tapping sounds first appear (SP) and then again when they disappear (DP).

During exercise testing, signs and symptoms of possible CVD may occur. List at least 4 of these other than HR or BP responses.

Other signs and symptoms indicating possible CVD: -Claudication = discomfort/ pain in the legs due to peripheral atherosclerosis -Dyspnea = shortness of breath -Hyperpnea = disproportionate hyperventilation; labored or rapid breathing -Cyanosis (blueness) of the lips or nail beds -Change in face color to ashen or pale -Clammy skin -Weak pulse -Weak voice; posture slumping -Mental confusion; disorientation; lethargy; stuper -Post-exercise syncope; lightheadedness; dizziness; nausea; vomiting; headache -Persistent fatigue -Indigestion; influenza-like symptoms

Which muscles, anterior or posterior, had the most EMG activity during flexion?

Our results are not to be expected: during flexion with the hand open, the posterior forearm muscles were more active than the anterior forearm muscles. Possible reasons for this unexpected result are cross talk between muscles, static tension generated in the posterior forearm muscles during flexion, or the fact that the fingers were extended (an action performed by posterior forearm muscles). During flexion when the hand was closed making a fist we did get expected results where the anterior forearm muscles had more EMG activity.

How does the subject's BP change when the subject resumes breathing after apnea?

Our subject's BP fluctuates once they resume breathing; we suspect inaccuracy in our recorded measurements since they are unlike what we would expect. We would expect the baroreceptors to sense the drop in SP and DP during continued apnea and see it as a systemic decrease in BPs; so they will act to compensate by increasing HR and increasing peripheral vasoconstriction. When the subject releases their held breath the intrathoracic pressure will suddenly drop so there is much less pressure exerted on the left ventricle and aorta. Consequently there will be a further drop in BP (not exhibited by our subject). From that drop in intrathoracic pressure there is also a large increase in venous return (reversal of the collapse of thoracic veins) which consequently increases stroke volume and CO. What happens here with the large increase in VR, SV and thus CO but existing peripheral vasoconstriction is an arterial pressure overshoot that last about 4-8 seconds. After this the baroreceptor reflex kicks in to reduce BP by slowing HR and reducing peripheral vasoconstriction.

In what units should P-wave amplitude be reported?

P-wave amplitude would be recorded in millivolts.

What is PAR-Q and what is it used for?

PAR-Q stands for Physical Activity Readiness Questionnaire. It is more of a first level screening tool to do before starting exercise to identify adults where physical activity may be inappropriate or where medical advice regarding physical activity may be required for them.

How can parallax error be avoided when reading the aneroid manometer?

Parallax error is error in measurement because the experimenter was looking at some angle to the instrument instead of straight on. With the aneroid manometer, avoid this by placing it at any height for the observer to look at the needle on the pressure gauge straight on.

Describe in detail the proper procedures for measuring SP and DP using an aneroid sphygmomanometer.

Patient must be seated in a chair in a quiet room for about 5 minutes, with their legs uncrossed, feet on the floow and back supported. Their arms should be supported, slightly flexed at heart level (because BP changes if the cuff is above or below the heart (0.8 mmHg/cm)). The patient should have no caffeine or have smoked within 30 minutes before the measurement. If it is a new patient be sure to measure BP on both arms, but if subsequent visits on the arm with the higher BP reading. Ensure the pressure cuff is the correct size to exert an even pressure on the limb; if it is too narrow then the pressure within the cuff will be higher than the pressure actually pressing on the artery so this will result in an overestimation of BP. Position the cuff on the upper arm so that the bladder is centered over the brachial artery (medial humerus) and so the distal end of the cuff is about 2 cm superior to the antecubital fossa (bend of the elbow). You want mid-cuff to be about mid-sternum level. This way you can place the stethoscope to the brachial artery medial and superior to the antecubital fossa not touching anything but the patient's skin; firmly but with as little pressure as possible so as not to distort the artery. The aneroid manometer pressure gauge should be at an appropriate height so the measurer can read it without parallax error. Have as little exterior noise around the patient while measuring; so no talking by anyone. Now begin measurement: Close the thumb wheel on the bulb. Inflate the cuff quickly to about 30 mmHg above where the pulse disappears (about 150 mmHg for young healthy patient at rest OR about 200 mmHg for hypertensive or young healthy patient during exercise) Deflate the cuff about 2-3 mmHg/second (slowly) by opening the thumb wheel slightly; while doing so listen to the Korotkoff sounds: the first faint clear tapping that increases in intensity is associated with SP (record this); while the DP is associated with when the sounds disappear (record this). When the sounds disappear rapidly release all the cuff pressure. Wait about 1 minute at least before taking another measurement to allow blood that has accumulated in the forearm to leave via the venous circulation.

Does flexion or extension affect the strength of EMG activity in either muscles?

Pronator teres appears to have similar EMG activity strength in both flexion and extension movements. This makes sense because in both winning and losing the subject is trying to generate force through pronating the hand/ medially rotate the forearm at the elbow. Biceps brachii has noticeably less EMG activity during winning and much more activity during losing. We would expect the biceps brachii to be more active during flexion. WINNING IS FLEXION AND LOSING IS EXTENSION? yes IF SO WHY ARE OUR BICEPS MORE ACTIVE DURING LOSING? Answer = Just know in what actions the muscles are meant to be active; research can get messy

Which muscles, Pronator or Biceps, had the most EMG activity during winning?

Pronator teres had the most EMG activity during winning; the EMG activity difference between pronator teres and biceps in winning is obvious. This makes sense because as the subject is winning they are acting to forcefully pronate their right hand, medially rotating their right forearm at the elbow.

In what way does 60 Hz interference look different than skeletal muscle tremor?

Skeletal muscle tremor produces interference on the ECG tracing that is irregular in height and frequency, due to the subject talking, laughing, shivering, moving, or any other skeletal muscle contractions. To overcome this interference the subject is simply instructed to relax, hold still and stop talking. Whereas 60 Hz interference is a regular interference pattern affected the entire tracing seen at 60 Hz frequency and is produced from poor skin preparation (electrode-body interface issues), electrical equipment noise, muscle noise, etc. This can be solved with good skin preparation, having a differential amplifier and reference electrode, as well as having a proper setup placed in the order of power source - recording device - patient.

What is the standard barometric pressure at sea level? At SFU?

Standard barometric pressure at sea level is 760 mmHg and at SFU is about 730 mmHg but can fluctuate. The Earth has a gravitational field producing a force that pulls gas molecules towards its centre so that as you go closer to its center/ lower in the atmosphere there is an increase in density of gas molecules. Thus there is an increase in barometric pressure as you reduce altitude from SFU to sea level.

If you are administering an exercise ECG, you should stop the exercise if you see certain abnormalities. Name 3 of these.

Stop the exercise if you see: -ST segment depression (horizontal or down sloping) more than 2 mm -Patient is experiencing severe angina pectoris (pain/ discomfort in upper chest) -More than 30% of the beats are premature ventricular contractions (PVC = ventricles show disorganizes electrical activity where they become spontaneously depolarized; could be a leak in the annulus fibrosis) -The PVC are at different parts of the cardiac cycle -The R portion of the PVC is superimposed on the T wave -Ventricular tachycardia (get medical help) -Ventricular fibrillation = uncoordinated ventricular contraction (very severe, get medical help) -Abnormal blood pressure (BP) responses: more than 250 mmHG SP or more than 115 mmHg DP

How do the HRV ratios from the first through the fifth minute of the rest period compare? Is your subject more or less "stressed" as the rest period passes?

Stress tends to be associated with a high LP and low HP, thus an HRV ratio that is elevated (LP/HP) indicating there is more sympathetic influence on heart rate at rest. The HRV ratios increase from minute 1 to minute 4, but after minute 4 they tend to decrease. This suggests as the rest period progresses the subject is getting more "stressed", but then they get to a point about 4/5 minutes in where they begin to relax. Suggested reasoning could be that the initial event of being recorded and watched could "stress" the subject, then once the initial distress is over and the subject is used to the exercise, they begin to relax.

Compare the parameters for the EMG bursts from the tibialis anterior (TA) during each of the activities. When was TA activity the greatest? The least?

TA was most active during rocking backward with one leg (then second most active when rocking backward with both legs) suggesting it functions in dorsiflexion of the foot at the ankle. TA was least active during standing erect with both legs (then second lease active during rocking forward with both legs).

When measuring BP, after reaching the 5th Korotkoff sound, what should the measurer do?

The 5th Korotkoff sound (Phase 5) is the DP where the sounds disappear. The measurer should rapidly release all the pressure within the cuff.

Are the BP values from the leg the same as those obtained from the arms? Explain any differences.

The BP values from the leg are notably higher than those for the arms due to the effects of orthostatic stress on the vasculature. Orthostatic stress is how the force of gravity acts on the body while in an upright position; while upright there is a pressure gradient that results in the body's vasculature due to the force of gravity. Imagine the heart as a starting point, as you go from the heart to the brain there is a 30 mmHg decrease and as you go from the heart to the feet there is about a 100 mmHg increase; thus there is more pressure within the vasculature as you go from head to feet. An analogy is a large column of water; larger pressures will be exhibited at the bottom of this water column so if you have a taller column of water (taller person) then you will have a larger pressure gradient going from surface to base (or rather head to toe). This is evident in this exercise. Firstly, in going from supine to sitting, there is a large rise in SP and small increase in DP. When the left hand is raised high, the force of gravity acts on the blood redistributing the blood within the left arm resulting in smaller BP recordings. 'On the other hand', if the right arm is raised this will similarly redistribute the right arm's blood so BP recordings from the left arm should be higher.

Why is the ECG bandwidth an important consideration?

The ECG bandwidth is the range of frequencies that the ECG machine is responsive to and that can be reproduced on the tracing. It is an important consideration because you want to filter certain frequencies that you know are associated with interference. With ECG it is common to do a band pass where the ECG machine filters certain frequencies between say 0.5-40 Hz (it lets through all frequencies within this range); this range is common to good ECG machines. After filtering these frequencies the ECG machine will then amplify the ones let through.

The laboratory manual describes three techniques which increase the loudness and clarity of the Korotkoff sounds. Name these and describe briefly the way each one works.

The Korotkoff sounds are the sounds of blood flowing through the brachial artery heard through a stethoscope but pressure is applied to the BP cuff during sphygmomanometry; they change during varying cuff pressure and we use them to determine SP and DP. 3 ways to increase loudness and clarity of these sounds: Raise the arm overhead before the cuff is inflated; this will drain the blood from the forearm Inflate the cuff rapidly; this avoids trapping blood from the forearm in the forearm After the cuff is inflated, squeeze the fist 8-10 times; this will vasodilate the forearm All 3 of these ways act to increase the pressure gradient between the artery directly below the cuff and the artery distal to the cuff.

How does the MEA of the heart calculated for deep inspiration differ from the MEA at rest? Explain.

The MEA is the average of all the instantaneous vectors generated as the ventricles depolarize; it is the resultant electrical conduction pathway through the heart. The normal MEA is anywhere between -30 degrees to +105 degrees (specific to BPK 407 since there's no real consensus on the true MEA). Since the heart is suspended from connective tissue in the thorax it hangs within the thoracic cavity; located to the left of the body's midline, hanging with its apex directed left and downward. When someone performs a deep inspiration, the diaphragm contracts and moves downward making more space in the thoracic cavity so the heart can hang more vertically and less left. This increases the MEA of the heart from about 59 to 70 degrees. The reverse happens during a deep expiration. The calculations of the MEA for a deep inspiration and at rest would be the same, however the result would differ as stated above: at rest the MEA would sit around 59 degrees and during a deep inspiration it would increase to about 70 degrees.

In what units should P-R Interval be reported?

The P-R interval is from the beginning of the P wave to the beginning of the QRS complex (onset of ventricular depolarization) and it should be reported in milliseconds.

How does the average P-R interval from rest and each time period in the recover compare? Do you see any variation or trend?

The P-R interval represents A-V conduction time: the time taken for the conduction of the electrical signal to spread over the atria, through the AV node and Bundle of His, and down the bundle branches. The P-R interval is largest at rest (0.143 s) and smallest at recovery time of 0 seconds (0.103 s)(aka during exercise the P-R interval reduces). It gradually increases getting closer to resting level as recovery time progresses.

Which phases of the cardiac cycle are represented by the Q-T interval and the T-Q segment? When comparing a pre-exercise ECG trace with an exercise ECG trace (obtained doing moderate exercise on a bicycle ergometer, HR = 155 bpm), how would you expect the QT interval and the T-Q segment to change? Give a physiological explanation.

The Q-T interval is the time between the beginning of the QRS complex and the end of the T wave following; it encompasses ventricular depolarization and atrial repolarization in the QRS complex as well as ventricular repolarization in the T wave. The T-Q segment is the time interval between the end of the T wave and the beginning of the following QRS complex; it encompasses atrial depolarization in the P wave. During exercise heart rate increases, so I would expect to see both intervals shorten slightly due to faster depolarization of both the atria and ventricles to allow faster contraction as well as faster repolarization of both to allow less relaxation time.

How does the average Q-T interval from rest and each time period in recovery compare? Do you see any variation or trend?

The Q-T interval represents ventricular contraction time: the time taken for the electrical signal to spread through the Purkinje fibers over the ventricular cardiomyocytes, depolarizing the ventricles, followed by ventricular contraction. The Q-T interval is largest at rest (0.390 s) and smallest at recovery time of 0 seconds (0.283 s). It gradually increases getting closer to resting level as recovery time progresses; this is similar to the P-R interval.

On which of the following - Lead I, Lead II, or Lead III - would you expect the QRS complex to have the highest positive amplitude? Explain.

The QRS complex represents ventricular depolarization and atrial repolarization. You would expect Lead II to have the QRS complex with the highest positive amplitude because Lead II is the one that is most commonly used to measure the heart's activity since it runs along/aligns with the conduction pathway of a normal heart. This conduction pathway is otherwise known as the mean electrical axis (MEA).

List at least 4 things (not including pathological conditions) which would produce a lower amplitude R-wave on an electrocardiogram.

The R wave amplitude is the voltage between the Q wave preceding the R-wave and the peak of the R-wave; it represents early ventricular depolarization. Reasons why the R-wave would have a lower amplitude could be (googled; most pathological): 1. Left ventricular hypertrophy 2. Right ventricular hypertrophy 3. Anterior Myocardial Infarction 4. Variation of normal but diminished anterior cardiac forces 5. Incorrect lead placement - if there is precordial lead reversal https://www.ncbi.nlm.nih.gov/pubmed/6212033

What events take place in the cardiovascular system during the R and pulse waves?

The R wave represents ventricular contraction pushing blood out to the rest of the body, the arteries being a pressure reservoir (lots of smooth muscle and elastic tissue) withstand the high pressure and volume changes during ejection by expanding, storing pressure and energy within their walls. The arteries reflexively vasoconstrict releasing that stored energy, which further propels blood through the circulatory vessels. The pulse wave represents that pulse of blood that is propelling through the rest of the body. Despite the attenuation of pulsatile flow of blood through the larger arteries by the arterial walls, there is still some pulsatile flow evident as you get to smaller arteries - gone by the time you get to capillaries. Note that there is a slight time delay (R-pulse Interval) between the electrical/mechanical events of ventricular contraction and the measure of the blood volume change as the pulse wave passes the plethysmograph.

How does the average R-Pulse interval from rest and each time period in recovery compare? Do you see any variation or trend?

The R-Pulse interval represents the time delay between the electrical event of ventricular depolarization (R-wave) in the heart and the mechanical event in the circulatory system of blood volume increase past the plethysmograph. The R-Pulse interval is largest at rest (0.266 s) and smallest at recovery time of 0 seconds (0.190 s). It gradually increases getting closer to resting level as recovery time progresses; this is similar to the P-R, Q-T and T-P intervals. NOTE: P-R, Q-T, T-P AND R-PULSE INTERVAL ARE ALL LARGEST AT REST AND THEN SMALLEST AT THE RECOVERY TIME OF 0 SECONDS (DURING EXERCISE), THEN GRADUALLY INCREASE AS RECOVERY TIME PROGRESSES - SO INTERVAL TIMES SHORTEN DURING EXERCISE DUE TO THE INCREASE IN HEART RATE.

How does the average R-wave ECG amplitude from the rest and each time period in recovery compare? Do you see any variation or trend?

The R-wave ECG amplitude is largest at rest (0.555 mV) and smallest at the first recovery time of 0 seconds (0.379 mV). It gradually increases getting closer to resting level as the recovery time progresses. Why is this? (from Jim) During recovery from exercise there is no simple answer due to the individual variability in HR, BP and CO. That being said, the R wave amplitude change depends on the fitness of the individual, their age, gender and overall health of the heart. So you may or may not see an increase in height (amplitude) as recovery time progresses. If you did see an increase in R wave amplitude this means the heart is working harder to pump blood to the once/still active muscles (more ventricular depolarization/ contraction during each cycle aka stronger pumping).

How does the average T-P interval from rest and each time period in recovery compare? Do you see any variation or trend?

The T-P interval represents a time of electrical inactivity at the end of ventricular repolarization and before the beginning of atrial depolarization. The T-P interval is largest at rest (0.420 s) and smallest at recovery time of 0 seconds (0.137 s). It gradually increases getting closer to resting level as recovery time progresses; this is similar to the P-R and Q-T interval.

Give a detailed explanation of how HR and BP change with time in a normal subject who performs a Valsalva maneuver. Explain these expected results in physiological terms.

The Valsalva maneuver is the act of forced expiration but with the glottis or nose/mouth closed so that intrathoracic pressure (Pintra) increases. This can be performed voluntarily or done naturally like when straining during a bowel movement or when bracing to lift heavy objects. It stabilizes the abdominal and thoracic cavities and is thought to enhance muscle action. The Valsalva maneuver can be divided into 5 'phases': Phase I: the onset of strain During the onset of strain there is an abrupt elevation of SP and DP because of the rise in Pintra which transfers to the left heart and aorta. Sometimes the baroreceptors will sense this increase in BPs and with compensate by decreasing HR, but not always. Phase IIa: the continued strain As the person continues strain, the Pintra causes collapse of the thoracic veins which reduces venous return (VR) and thus cardiac output, so you see a rapid reversal of SP and DP (both decrease rapidly). Phase IIb: the baroreceptor response The baroreceptors sense the rapid drop in SP and DP and will activate their compensatory mechanisms: increase HR and increase peripheral vasoconstriction in order to increase cardiac output and venous return respectively. Phase III: the release of strain When the subject stops their forced expiration there is a drop in Pintra, so there is no longer a pressure transferred to the left heart and aorta, thus you will see an even further decrease in BP. Sometimes the baroreceptors sense the further BP drop and try to increase HR even more, but again not always. Phase IV: the arterial pressure overshoot From the drop in Pintra there is also no longer a collapse of the thoracic veins so you have a large increase in VR which means a large increase in SV and thus CO, however you still have existing peripheral vasoconstriction; the combination causes an arterial pressure overshoot that lasts about 4-8 seconds. Then the baroreceptors activate to reduce the BP overshoot by reducing heart rate and allowing peripheral vasodilation.

What are the problems in using manual auscultatory sphygmomanometry to measure exercise BP?

The accuracy of this method during exercise is questionable due to movement artifact; the subject should be sitting quietly with their arm slightly flexed at heart level, the pressure gauge at an appropriate height to read to avoid parallax error, while no one talks, etc, but measurement while exercising does not allow this measurement protocol to take place. To avoid this movement artifact experimenters often get the maximal exercise BPs immediately after exercise but this tends to underestimate since the BPs decrease dramatically within 1 minute of recovery.

When you make a calibration curve of the aneroid manometer with the mercury manometer, which variable is entered on the x-axis? Why?

The aneroid manometer is entered on the x-axis because the mercury manometer depends on what you set or pump the aneroid manometer to. The mercury manometer acts as the standard or 'criterion' measure of pressure that the aneroid manometer must be compared to. Mercury manometers are more accurate and less likely to become decalibrated, where as aneroid manometers require recalibration frequently because if not handled gently they can lose their calibration.

The arm is supposed to be supported at the level of the heart when taking BP readings. If the arm was raised above the heart, how would the BP reading be affected? Explain.

The arm is supposed to be at heart level because we want the pressure recordings from the brachial artery to resemble those closest to the heart (aorta/heart pressure); BP will change 0.8 mmHg/ 1 cm that the cuff is raised above of below the heart. If you raised the arm so that the cuff was above the heart, this allows the force of gravity to act on the blood within the vasculature, draining the arm of blood, so you would result in recordings of BP lower than the true.

Is there any effect on the blood flow through the subject's finger as the subject is performing leg exercises?

The blood flow through the subject's finger has increased both in rate of flow through the finger and in the amount of blood flowing through. Increased rate of blood flow is due to the increase in heart rate and thus cardiac output (CO = HR*SV). The increase in the amount of blood flowing through the subject's finger is due to the increase in stroke volume and (again) thus cardiac output during exercise.

How do BP and HR respond to the cold pressor test? Give a physiological explanation of the expected results.

The cold pressor test is a cardiovascular test where the subject immerses their hand into an ice bath for 1 minute where the heart rate and blood pressure changes are measured in response. This test proves to have clinical use, it has been found that elevated blood pressure response correlates to higher risk of hypertension and CVD. During the cold pressor test the subject had a rise in both systolic and diastolic blood pressure, with a more prominent systolic increase. Heart rate appears to rise during the cold pressor test as well. After removing the hand from the ice bath, the subject's systolic blood pressure and heart rate gradually lowered returning to close to resting values. The subject's diastolic blood pressure continued to fall 18.5 mmHg past resting level. Theoretically the subject is expected to have an increase in blood pressure due to vascular sympathetic activation, while the heart rate response is less well defined having high inter-individual variability. Physiologically speaking, the cold pressor test involves sensory afferent nerves of the hand sensing the change in temperature and sending this information to higher centers, which triggers systemic sympathetic activation resulting in vasoconstriction. The vasoconstriction increases TPR which results in a sustained increase in blood pressure. With regards to heart rate, as stated, there is more variability observed between individuals, but the general responses will either be an unchanged heart rate or an increased heart rate. If there is an increase in heart rate seen throughout the test this is due to an increase in sympathetic activity and a decrease in the vagal outflow.

What event recorded on the Pulse channel corresponds to the dichrotic notch? What causes a dichrotic notch?

The dichrotic notch is caused by aortic valve closure. It matches up with a downward deflection following the pulse wave on the Pulse channel. The aortic valve closes at the end of ventricular repolarization (end of the T wave), it closes because the ventricles have now relaxed enough where the ventricular pressure is less than the aortic pressure. Valve closure ensures no back flow of blood from aorta to left ventricle.

What is the expected effect on arterial BP of wrapping a pressure cuff or tourniquet around a subjects upper thigh (assume that the pressure exerted on the tissue is 200 mmHg)? Explain in physiological terms.

The effect of the cuff or tourniquet on the upper thigh would be to stop blood flow through the vein or artery below the material so that blood flow is blocked distal to the cuff/ tourniquet. Micro scale you get ischemia distal to the cuff/ tourniquet which means less oxygen supply so causes glycolytic mechanisms to take over; build up of carbon dioxide so an acidotic state occurs. Macro scale you get effects during inflation and deflation of the cuff/ tourniquet; when you inflate it this causes an increase in TPR and an increase in the effectively circulating blood volume (because less is distributed to the leg and more can circulate in the upper body/ other leg). So it leads to an increase in central venous pressure as well as increase in arterial BP.

Give two examples of subconscious bias in BP measurement. How can such errors be minimized? Note: the answer is NOT "to be more aware of and try to avoid bias"; give more concrete suggestions.

The knowledge that both SP and DP tend to rise during isometric and that only SP tends to rise during dynamic exercise can lead the experimenter to note BP's closer to what is expected than maybe what is observed. To avoid this, the experimenter could be out of the room during the special condition performed, then re-enter when the condition is concluded. Or keep them in the room and completely unaware of the exercise; eyes closed, ear plugs, etc, then have them measure the BP. A tendency for the experimenter to record BP measurements to the nearest value that ends in zero instead of what it truly may be. For instance a BP of 121 mmHg for SP, experimenters unconsciously report 120 mmHg instead of the true. To avoid this, say aloud the exact value seen during the SP moment during Phase 1 of Korotkoff sounds to have a second experimenter write it down. Then do this again for DP as soon as Phase 5 comes around.

Why would you expect the BP to change after the subject has been standing for 5 minutes? Why would there be a change?

The person will have blood pooling in the lower extremities due to orthostatic stress which in turn causes central hypovolemia (less effectively circulating blood in the central thoracic region). The person's regulatory mechanisms will activate to continue cerebral perfusion. Skeletal muscle pump, baroreceptors, maybe hormones (RAAS, etc) and then syncope at last resort. When the subject has been standing for 5 minutes the subject may exhibit signs of orthostatic hypotension; this is when there is a drop in SP of at least 20 mmHg (or drop of DP of at least 10 mmHg) in the first 3 minutes of standing. There are two possible mechanisms responsible for this drop in blood flow and thus drop in blood pressure values: Failure of the autoregulatory mechanisms (arterial and cardiopulmonary baroreflexes) - where these mechanisms fail to cause the necessarily changes in vasculature and HR to counteract the drop in BP Drop in effectively circulating blood volume due to venous pooling in the lower region of the body from orthostatic stress; which in turn leads to central hypovolemia and consequently low venous return If the subject has good orthostatic tolerance (strong baroreceptor response) and the skeletal muscle pump works to increase venous return; there is less of an effect of orthostatic hypotension.

When current flows toward the positive electrode, does the EKG stylus deflect up, down or remain unchanged?

The positive electrode is the recording electrode and when positive current (positive charge movement represents a propagating depolarizing) moves toward this positive electrode there is an upward deflection of the stylus on the tracing.

What is the effect of raising each hand on the BP in the left arm? Explain your results.

The purpose of raising either arm was to see the effects of orthostatic stress on the peripheral circulation and resulting change in BP. Orthostatic stress is how the force of gravity acts on the body while in an upright position; while upright there is a pressure gradient that results in the body's vasculature due to the force of gravity. Imagine the heart as a starting point, as you go from the heart to the brain there is a 30 mmHg decrease and as you go from the heart to the feet there is about a 100 mmHg increase; thus there is more pressure within the vasculature as you go from head to feet. An analogy is a large column of water; larger pressures will be exhibited at the bottom of this water column so if you have a taller column of water (taller person) then you will have a larger pressure gradient going from surface to base (or rather head to toe). This is evident in this exercise. Firstly, in going from supine to sitting, there is a large rise in SP and small increase in DP. When the left hand is raised high, the force of gravity acts on the blood redistributing the blood within the left arm resulting in smaller BP recordings. 'On the other hand', if the right arm is raised this will similarly redistribute the right arm's blood so BP recordings from the left arm should be higher.

What is the purpose of shaving hair, abrading (rub vigorously), and applying ethanol at the skin where an electrode is to be placed?

The purpose of these three things is to prepare the skin for electrode placement to improve the electrical conductivity of the skin; shaving the hair improves contact between the electrode and skin, abrading removes any dead skin cells that would just impede the signal, and applying ethanol (a lipid solvent) removes the skin's natural oils.

What is the purpose of the reference electrode in electrocardiography (and other electrical recordings from the body)?

The reference electrode removes the electrical noise found within the body and in doing so improves the quality of the tracing. It records the electrical noise naturally occurring within the body, providing a reference voltage (offset) for the other electrodes placed on the body to refer to.

Is there a linear relationship between the muscle activity (EMG) and the grip strength (force)?

The relationship between muscle activity (EMG) and grip strength (force) is approximately linear; it is not an absolute one-to-one relationship but it is very close.

Are the BP values from the right forearm the same as those obtained with the cuff on the right upper arm? Explain any variations that you see.

The values of the right upper arm and right forearm are not the same. As expected the values for SP and DP of the right forearm are less than the corresponding values for the right upper arm. This is expected because as you increase the measurement distance from the heart there with be less of a prominent SP and DP recordings. Furthermore, in the upper arm you have a large brachial artery supplying the arm with blood, but by the time you get to the forearm this single brachial artery has branched which distributes blood flow and will result in diminished blood pressure recordings.

Which Korotkoff sound should be taken as SP? As DP?

The very first K-sound should be taken as SP, it is a clear, faint tapping that increases in intensity. The last K-sound should be taken as DP or rather immediately after the last sound.

Would an elite endurance athlete have a normal MEA or would it be shifted? If it is shifted, in what direction would the shift be?

Ventricular hypertrophy can cause shifting of the MEA; where an increase in cell size increases the ventricular muscle mass (more cardiomyocytes present) thus increasing the electrical activity within the area of hypertrophy. You can have right axis deviation where the MEA is shifted above 150 degrees from right ventricular hypertrophy or you can have left axis deviation where the MEA is shifted less than -30 degrees from left ventricular hypertrophy. Hypertrophy can be considered pathological or physiological, in the case of an elite endurance athlete it would be physiological hypertrophy due to their exercise and training. This is where the heart increases its mass and improves its function due to an increase in volume it experiences (exercise tends to increase blood volume). Physiological hypertrophy is eccentric hypertrophy where the cell's increase in cell length (vs concentric: increase in cell width) which increases the ventricle contractility and also the ventricular capacity thus increasing end diastolic volume, stroke volume and thus cardiac output. I would assume the MEA would be normal despite the improved functioning of the heart because it is symmetrical change versus pathological hypertrophy can be focused to one ventricle versus the other.

When the positive electrode and the negative electrode are at the same electrical potential (ie same voltage) does the ECG stylus deflect up, down or remain unchanged? Explain.

Voltage is the force that causes a current to flow. According to Ohm's Law (V=I*R or rather I=V/R) if there is zero voltage difference between two points then zero current will flow. The positive electrode is the recording electrode and when positive current (positive charge movement represents a propagating depolarizing) moves toward this positive electrode there is an upward deflection of the stylus. Conversely, if positive current moves away from this positive electrode there is a downward deflection of the stylus on the tracing. So if there is the same electrical potential (same voltage) between the two poles of a bipolar limb lead then zero current will flow, thus the stylus will remain unchanged.

Which of the following would you expect to produce a negative R-wave in a subject with a normal MEA of the heart - aVR, aVL, or aVF? Explain.

We know the normal MEA of the heart is between -30 and +150 degrees. aVR points directly -150 degrees so it would have a negative R-wave depicted, aVL points directly -30 degrees so it could have a positive or negative deflection depending on the individual, and aVF is points directly +90 degrees so it most likely would have a positive deflection of its R-wave.

When someone holds a heavier barbell the electromyogram recorded from electrodes over the active muscle increases. Explain why.

When a heavier barbell is involved, more tension is required from the muscle to support it. To increase this tension production there needs to be more neural activation of the muscle. This is done by recruiting more motor units (a motor neuron and all the muscle fibers it innervates) as well as increasing the frequency of firing of motor neurons to produce summation (then tetany). A motor neuron conducts the motor neuron AP where impulses are transmitted to the muscle fiber at the NMJ. A muscle AP (map) is produced and propagates along the muscle fiber, then actin and myosin filaments couple together to undergo cross bridge cycling, thus producing tension in the muscle. The EMG records the ionic potential occuring along this MU just described. There is very good correlation between the tension produced by the muscle and EMG magnitude.

Should you calibrate the aneroid manometer by starting at the high end of the range and going down, or at the low end of the range and going up? Why?

When calibrating, space the calibration points about 10 mmHg apart; start at the upper end of the range (200 mmHg) then go down 10 mmHg increments until you reach the lower end of the range (40 mmHg). The reasoning for this is to avoid hysteresis and more simply because it is technically easier to inflate the cuff fully and gradually let pressure out of the cuff with ample control than it would be to inflate to 40 mmHg and inflate the cuff by exactly 10 mmHg increments each calibration point. Hysteresis is when some instruments show a slightly difference response/ measurement/ recording when they are raised through their range compared to if they were lowered through their range; so as practice it is best to lower the BP through the range.

What are the expected changes in arterial BP and HR in a subject who has been lying quietly, then stands up rapidly?

When someone stands up rapidly after being lying down quietly they are immediately subjected to orthostatic stress which is how the force of gravity acts on the body, specifically the vasculature. When you take a normal subject and lay them supine on their perfusion pressure and mean arterial blood pressure (MAP) are consistent across their body (there is no head to toe gradient). Then once they stand orthostatic stress on their body results in a perfusion pressure gradient from head to toe where pressure increases as you go further down the body due to the force of gravity. Initially when they stand the blood will immediately drain from the head and neck causing slight dizziness or lightheadedness, but the body will activate mechanisms to ensure cerebral perfusion following this. If the body is unable to do so (has a lack of orthostatic tolerance) then this results in gravity induced venous pooling in the lower body, which reduces BP and worse cerebral ischemia. The body's last defense when this occurs is syncope (loss of consciousness due to cerebral ischemia) so that the body goes into supine position remobilizing blood back to the brain. There are defense mechanisms in place to prevent this from happening as soon as the normal subject is moved from supine to standing: In standing, the first line of defense is the skeletal muscle pump, where contractions of the leg muscles propel the sequestered venous blood back to the heart to increase VR. There are two sets of baroreceptors (arterial BRs in the carotid sinus and aortic arch and cardiopulmonary BRs in the right atrium, ventricles and pulmonary arteries); the reasoning for this is to ensure BP is regulated on both the high pressure side (arterial BRs) and the low pressure side (venous side and pulmonary circulation). The arterial BRs on the high pressure side in the carotid sinus and aortic arch act primarily to regulate HR and contractility of the heart through SNS and PSNS channels stemming from the CNS (cardiovascular control centre in the medulla). The cardiopulmonary BRs are located on the lower pressure side in the right atrium, ventricles and pulmonary arteries and they primarily act to ensure adequate VR. BOTH of the BRs contribute to the BR reflex: When the subject is tilted there is a venous pooling effect seen in the lower region of the body which reduces the amount of blood effectively circulating (hypovolemia); consequently there is a decrease in the central venous pressure so a decrease in venous return and thus CO so drop in BP. The arterial and (to a lesser extent) the cardiopulmonary BRs sense this drop in BP and trigger their cardiopulmonary baroreflex to overall increase VR (a drop in BP causes a reduction in BR firing rate) - this increases sympathetic activity and decreases parasympathetic activity: Increased HR Increase in TPR (total peripheral resistance) (MAP = CO*TPR) Vasoconstriction to the extremities and splanchnic circulation mediated by the SNS - to redistribute blood flow and dip into the blood reservoir held by splanchnic circulation Reduction in venous compliance (less venous distension so redistribution of blood volume kept on the venous side of circulation) A proposed line of defense following is humoral agents (hormones) like epinephrine (increase HR) and ADH (increase blood volume) through the SNS and RAAS. But this response takes time so is more delayed; might not be important for the immediate response to orthostasis. Last line of defense is syncope - loss of consciousness due to inadequate cerebral perfusion will cause the person to collapse, become supine, remobilize blood back to the brain and restore consciousness.

What effect does apnea have on the subject's BP?

When the subject holds their breath there is an increase to their intrathoracic pressure which in turn puts more pressure on the thoracic vessels. At first this will act to elevate SP and DP because that intrathoracic pressure is transferred to the left heart and aorta. With continued apnea, the intrathoracic pressure will cause collapse of the thoracic veins which reduces the venous return back to heart, consequently reducing cardiac output and thus a rapid reversal of SP and DP is exhibited. This rapid reversal (decrease) can be seen in the above table during our subject's apnea.

You need values for three things to calculate workrate on the Monark cycle ergometer. What are these?

Work rate is given in Watts. To calculate work rate on the Monark it needs to be in kiloponds. We know 1 Watt = 6.12 kp*m/min; so to calculate work rate in kp we need: Distance per revolution (6 m/rev) The revolutions per minute the person is to be cycling at (60 rpm) The conversion factor mentioned above (1 Watt = 6.12 kp*m/min)

Since the pressures are determined using changes in the pulse amplitude, would slowing the rate at which pressure is released from the cuff make your readings more accurate?

Yes and no. You want to release pressure from the cuff at about a rate of 10 mmHg/sec, if you release the pressure too quickly then you may not catch the SP in time, in this way yes if you slowed the rate at which pressure is released it would be more accurate. However, if you release pressure too slowly then what you get is a backup of pressure in the vasculature resulting in a SP reading that is most likely higher than what it should be.

Should aneroid sphygmomanometers be serviced on a regular basis? Explain.

Yes, aneroid sphygmomanometers require maintenance and calibration every 6 months because they are more complex than mercury sphygmomanometers. Aneroid means "operating without liquid [or fluid]" in Greek, so in the mercury one there is a fluid within the tube that simply needs to be read but in the aneroid one there is no fluid just air. There is risk of air leaks (although rare), there may be an incorrect zero (the zero mark indicated on the pressure gauge is not truly a pressure of zero due to air present in the bladder still), etc.

Should hypertensive patients be encouraged to use home electronic BP monitors? Explain.

Yes, hypertensive patients have high BP which can be dangerous if levels rise too high or fluctuate too excessively so they should monitor it using electronic BP monitors. Electronic BP monitors may not be as accurate as a manual aneroid manometer used in a clinic situation, however they are very consistent so the person can see any changes that have occured in their BP and get help accordingly. Also at home use of these electronic BP meters avoids two types of problems that sometimes occur during clinical measurements of BP: White coat hypertension = an overestimation of BP because the patient is anxious or nervous from being in a physician office Masked hypertension = the person's true hypertension is masked, where they have normal BP in the physician office but they have high BP during many other time periods of the day

Does the strength of the EMG in the muscles of the posterior forearm differ between extension with a weight and without a weight?

Yes, the EMG activity of the posterior forearm muscles increased about twice the amount during extension when holding a weight. So not as prominent of an increase as in (10).

The signal recorded on the Pulse channel is the rate of change of BP entering the subject's finger tip. When the signal is integrated, the waveform displayed on the Pulse Integral channel is similar to an arterial P curve. Is there a short plateau or dip during each cycle displayed on the Pulse Integral Channel?

Yes, there is a little dip followed by a slight plateau on the Pulse Integral Channel; this is referred to as the dichrotic notch and corresponds to aortic valve closure. It matches up with a downward deflection following the pulse wave on the pulse channel.

Does the strength of the EMG in the muscles of the anterior forearm differ between flexion with a weight and without a weight?

Yes, there is close to a 3 fold increase in the EMG activity of the anterior forearm muscles when holding the weight during flexion. This is to be expected, more tension is required of the muscle to move the load thus more EMG activity should be recorded.

Does flexion or extension of the fingers affect the strength of EMG activity in either group of muscles?

Yes, when the fingers were flexed (hand closed making a fist) much more EMG activity was found in the anterior forearm muscles. When the hand was open thus fingers were extended, there was a large increase in muscle activity seen in the posterior extensor muscles.

If you are a kinesiologist who is administering the exercise test, what should you do and say to the client if you see these signs/symptoms?

You should say "That's enough for today" so as to alarm the subject and do not attempt to interpret the results. After the test is concluded, suggest for the subject to see a clinician if the results are notable.

What would you do if you were trying to measure the QRS-wave amplitude and it was so large that it went off the EKG paper?

You would reduce the gain on the electrocardiograph (machine), because gain regulates the output or rather height of the ECG waveforms. Gain is output voltage/ input voltage; aka it is how much the original signal is amplified by.

What would you do if you were trying to measure the P-R interval and it was so small that it was hard to measure accurately?

You would take the average of several successive P-R intervals.

If your hematocrit was increased by 10, what would happen to your BP and why?

Your hematocrit is the ratio of your total blood volume that is taken up by red blood cells (RBC), so if this increased that means you have a higher oxygen carrying capacity of your blood which should correspond to a lower BP. Less blood supply will meet the same demands as before so CO can decrease thus BP will decrease.

If you were an exercise physiologist, how would you answer the following questions if you were asked them by a sedentary 35 year old male with a BP of 150/100? a) Do I have hypertension? b) Why should I be concerned about my BP? How dangerous is hypertension to my health? c) Which BP measurement is more important? SP or DP? d) What lifestyle modifications can I make in order to lower my BP and how effective are each of these modifications likely to be? e) Will I need to start taking drugs to lower my BP?

a) Yes, you do have hypertension, your blood pressure falls within the guidelines to classify you as having Stage 2 Hypertension. (His SP falls within the range of Stage 1 Hypertension (140-159) but his DP falls within the range of Stage 2 Hypertension (100 or higher) and treatment is determined by the highest BP category so he is Stage 2) b) Yes you should be concerned, hypertension is incredibly dangerous to your health. Hypertension can promote atherosclerosis which can lead to an increased risk of stroke, cardiovascular disease, myocardial ischemia or infarct and more. With high BP, there is turbulent flow of blood occuring in your blood vessels, this can cause damage to the cells that line the blood vessels providing a foundation for atherosclerotic plaque formation (a fatty deposit with a hard fibrous shell to it). You can have these fatty deposits in your coronary (heart) vessels reducing the blood flow to your heart which can cause heart pain (angina) whenever you do exercise. Or if this fatty deposit breaks off then it can get lodged in a vessel downstream and cause a stroke (if in a cerebral/ brain vessel) or a heart attack (in a coronary vessel), etc. Hypertension can also cause pathological cardiac hypertrophy, where your heart increases in muscle mass from larger cell sizes due to the pressure overload that it is dealing with. It does so in a way where it reduces functionality, so heart wall thickness increases and there's less ventricular capacity so you can't pump as much blood over time. Hypertension can be a silent killer; so you can be unaware you even have it or that it is truly that bad, then your first warning sign is a heart attack or stroke. c) With regards to risk of having CVD (a heart attack or stroke), the SP reading is given more attention [recently]. So if you have one person with an elevated SP/normal DP and another with normal SP/elevated DP; the one with elevated SP is at more risk. SP tends to increase with age as you get stiffening on the large arteries and long term build up of atherosclerotic plaque, indicating increasing risk of CVD. Reading the literature it mentions that traditionally diastolic has been considered more important in determining cardiovascular risk but that recently clinicians are putting more emphasis on systolic. d)To lower your BP you can do a number of dietary and lifestyle changes: Reduce your salt intake; this reduces the amount of water you retain and thus less plasma volume in your blood vessels. Reduce your caffeine intake because this acts as a positive inotrope (it increases the contractility of your heart; the force it contracts with at a given length); so lessen the caffeine and you lessen the force the blood shoots out of the heart at reducing your SP. Reduce your fat intake to lessen your risk of an atherosclerotic plaque forming or worsening. If you smoke, stop it - the chemicals cause blood vessel and bodily damage. If you drink, reduce your alcohol intake. Reduce your stress if possible - increases your LP and decreases your HP (so high HRV ratio). Increase your activity levels; exercise is a huge help in reducing BP. e) You have Stage 2 hypertension so it is recommended that you get started on a two-drug combination. There are thiazide-type diuretics that act to reduce your water retention. We can pair this with either an ACEI (angiotensin converting enzyme inhibitor) that acts to reduce functional ACE so lessens the amount of angiotensin II created and thus lessens its vasoconstrictor effect and lessens its sodium retention; or pair it with an ARB (angiotensin receptor blocker) to do the same things but instead of lessening ANGII formation it blocks its action; or pair it with a BB (beta blocker) to block beta-1 adrenergic receptors of the heart thus reducing CO and MAP; or pair it with CCB (calcium channel blockers) to block Cav1.2 (DHPR) to cause less vasoconstrictor tone and reduce cardiac muscle contractility to reduce MAP.