CVS Physiology-Virtual Experiments
Online Virtual Experiments:
1. For Virtual Experiment Visit this link. Click on "Exercise 5: Cardiovascular Dynamics".
Click on one of the following titles:
- Vessel Resistance,
- Pump Mechanics.
2. For Virtual Experiment Visit this link. Click on "Exercise 6: Cardiovascular Physiology".
Click on one of the following titles:
- Electrical Stimulation,
- Modifiers of Heart Rate.
Virtual Experiment on Thermal & Chemical effects on frog heart:
Virtual Experiment on Refractory period of the heart:
Virtual Experiment on Starling law of the heart:
Virtual Experiment on Heart block:
Virtual Experiment on ECG and Exercise:
Virtual Experiment on The meaning of heart sound:
Virtual Experiment on ECG and Finger Pulse:
Virtual Experiment on Electrical axis of the heart:
Virtual Experiment on ECG and Heart block:
Virtual Experiment on Abnormal ECGs:
Virtual Experiment on Cooling and peripheral blood flow:
Virtual Experiment on Blood Pressure and Gravity:
Virtual Experiment on Blood Pressure and Body Position:
Virtual Experiment on Deep breathing and Cardiac function:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES & INTRODUCTION" and read it. Read the file "Steps" in the main "Deep breathing and Cardiac function" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file. You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ & LAB REPORT".
Virtual Experiment-Physiology Simulator
- Heart
- Blood vessels
1. Starling’s Law of the Heart
The sarcomere is the fundamental contractile unit of skeletal and cardiac muscles. Sarcomeres are laid down next to one another and give these muscles their characteristic banded or 'striated' appearance. The sarcomeres in both types of muscles are made up of thick and thin filaments, which are laid down so that thin filaments are attached to the Z-line at the end of the sarcomere and overlap with thick filaments in the center of the sarcomere. According to the sliding filament theory, the thick and thin filaments slide over one another to shorten the sarcomere and the muscle fiber.
In human skeletal muscle, an action potential in a motor neuron produces an action potential in the fibers it supplies, and this action potential initiates a single muscle contraction or ‘twitch’. In the heart, the pacemaker cells in the sinoatrial (SA) node of the heart create an action potential, which stimulates a contraction of all cardiac fibers. The mechanism of contraction in cardiac and skeletal muscle is similar in many ways. A contraction is produced by an increase in the amount of intracellular calcium, and the calcium ions react with troponin on the thin filaments to expose myosin binding sites on the actin molecules. Myosin uses ATP to repeatedly make and break bonds with actin to create a sliding between adjacent thick and thin filaments. This making and breaking of bonds, called crossbridge cycling, creates tension and draws the thick and thin filaments across one another and decreases sarcomere length.
The amount of tension produced by a single twitch depends upon the amount of overlap between the thick and thin filaments. When a sarcomere is at an optimum length, the thick and thin filaments can create the maximum number of crossbridges, and therefore produce maximum tension. Changing the length decreases the number of crossbridges that can be formed and decreases the amount of tension. In skeletal muscle, dramatic changes in muscle length are prevented by restricting the range of motion around a joint. However, the heart has no such safeguard.
During
the cardiac cycle, the heart muscle goes through a period of contraction
(called systole) followed by a period of relaxation (called diastole). During
diastole, if there is an increase in the volume of blood entering the heart,
the heart will fill with more blood before it contracts (i.e., the end
diastolic volume will increase). This increase in volume will stretch the walls
of the heart, and the sarcomeres will be stretched. According to the sliding
filament theory, this increase in sarcomere length should change the amount of
overlap between the thick and thin filaments and change the amount of tension
produced by the heart contraction.
In this experiment, you will correlate the size of the contraction of an exposed frog heart with the length of the muscle fibers. A thread connects the ventricle of the heart to a transducer, which is held on a metal stand. You will raise the transducer on the stand to stretch the heart, and measure the amplitude of the heart contraction. This relationship between the end diastolic volume (length of the muscle fibers) of the heart and the amount of tension produced is known as Starling’s Law of the Heart.
The Dissection: A frog is anesthetized with MS-222, pithed, and then placed ventral surface uppermost in a dissection dish. A pair of scissors is used to remove the skin over the pectoral girdle and throat, and the pectoral girdle is cut in the midline and along the left lateral margin. The cut girdle and associated muscles are removed to expose the heart.
A metal hook is placed through the ventricle. A short length of thread connects the hook to a displacement transducer, which is interfaced to a computer through a Data Acquisition Unit. A contraction of the heart produces a deflection of the transducer arm and a deflection of the line tracing on the screen (see video).
The Experiments: You will raise the transducer to stretch the heart, and measure the amplitude of the contraction. In this way you will determine the relationship between stretch and the amount of tension produced by cardiac muscle (see Table).
2. Extrasystole of the frog heart:
The mechanical activity of the heart, also known as the cardiac revolution or the cardiac cycle, is composed by the rhythmical succession of the distinct phases (see video):
Systole or the contraction phase of the cardiac muscle and
Diastole or the relaxation phase of the cardiac muscle
The excitability of the cardiac muscle is proven to be variable, in systole the myocardium becomes unexcitable; in diastole the cardiac excitability reaches the highest levels.
Objective: demonstration of the phases of the cardiac cycle of the frog heart and the evolution of its excitability by using the graphical method.
Principles: The phases of cardiac cycle of the frog heart are recorded on a graphical surface and the effect of electrical stimuli on the heart is determined.
Graphical recording (see figure):
The graphical recording consists in two moments:
-the graphical recording of the normal mechanical activity of the heart (figure-A);
-the graphical recording of the effect of electrical stimuli on the mechanical activity of the heart, first in systole and then in diastole (figure-B).
The normal cardiogram is sinusoid and we can distinguish the two phases of the cardiac cycle: systole, the ascending side of the cardiogram (S); and diastole, the descending side of the cardiogram (D). By applying the experimental electrical stimuli we obtain different responses according to the phase of the cardiac cycle in which the frog's heart is found:
- in systole there is no change of the general aspect of the cardiogram;
- in diastole the cardiogram changes and shows an extra-systole (ES) which is followed inevitably by a prolonged resting period (PRP).
Conclusions
In each systole the myocardium is unexcitable (it is crossing a periodic non- excitable phase).
The biological significance of the periodical non-excitable phase, which is long and covers the duration of the whole systole, is to assure the controlled contraction of the myocardium, without any disturbs. ln diastole, the myocardium becomes excitable and if there is an artificial stimuli the response will be an extra-systole. Any extra-systole is constantly followed by a prolonged resting period. The invariable presence of the prolonged resting period after each extra-systole is due to losing a physiological systole (generated by the Sino-atrial node) which finds the myocardium in the non-excitable phase following the contractionphase of the extra-systole.
3. Humoral & electrolytes effect on the frog heart:
The cardiac automatism is the ability of the cardiac muscle to contract rhythmically and independently without the intervention of other extra cardiac regulating factors. This property provides the heart the ability to contract rhythmically even when all the nervous, vascular and physical connections of the organ with the rest of the body ceased. The completely isolated heart can continue its activity if the following conditions are assured (video):
Perfusion (the circulation of a liquid through the cardiac compartments) with a solution under a certain pressure; the solution used for perfusion must provide the energetic substrate necessary to the cardiac activity;
optimal temperature.
Under these circumstances the heart will continue its activity independently for a long time.
Principle: Recording the mechanical activity of the isolated frog heart on a graphical surface, while the heart is being perfused with isotonic fluid containing various concentrations of ions (Ca++, K+) and chemical mediators (epinephrine and acetylcholine).
Graphical recordings
The graphical recordings consist of:
1. Recording the cardiogram while perfusing the isolated heart with Ringer's solution;
2. Recording the cardiogram while perfusing the isolated heart with calcium ions-free solutions (we accomplish this by using an ammonium oxalate solution);
3. Recording the cardiogram while perfusing the isolated heart with a calcium chloride solution. While perfusing the heart with a calcium chloride solution the heart increases its contraction amplitude; by immediately repeating the administration of calcium in the solution calcium rigidity appears (the heart stops in the systole)
4. Recording the cardiogram while perfusing the isolated heart with a potassium chloride solution; while perfusing the heart with a potassium chloride solution the heart decreases the amplitude of its contraction; by immediately repeating the administration of potassium in the solution the potassium inhibition appears (the heart stops in diastole).
5. Recording the cardiogram while perfusing the isolated heart with an epinephrine solution; while perfusing the heart with a solution of epinephrine, the heart increases the amplitude and frequency of its contraction;
6. Recording the cardiogram while perfusing the isolated heart with an acetylcholine solution. While perfusing the heart with a solution of acetylcholine the heart decreases the amplitude and frequency of its contraction.
These changes in the cardiac activity lead to the conclusion that even if the heart presents a functional autonomy, its activity can be influenced by the specific action of some humeral factors.
NOTES: Effect of extracellular ion Concentration: The ions that affect cardiac muscle function are the same ions (K+, Ca2+, and Na+) that influence membrane potentials in other electrically excitable tissues. However, cardiac muscle responds to these ions differently than nerve or skeletal muscle tissue does. For example, the extracellular levels of Na+ rarely deviate enough from normal to significantly affect cardiac muscle function.
Excess K+ (hyperkalemia) in cardiac tissue causes the heart rate and stroke volume to decrease. A twofold increase in extracellular K+ results in heart block, which is the loss of action potential conduction through the heart. The excess K+ in the extracellular fluid causes partial depolarization of the resting membrane potential, resulting in reduced amplitude of action potentials and, because of the reduced amplitude, a decreased rate at which action potentials are conducted along cardiac muscle cells. As the conduction rates decrease, ectopic action potentials can occur. In many cases, partially depolarized cardiac muscle cells spontaneously produce action potentials because the membrane potential reaches threshold. Elevated blood levels of K+ can produce enough ectopic action potentials to cause fibrillation. The reduced action potential amplitude also results in less Ca2+ entering the sarcoplasm of the cell; thus, the strength of cardiac muscle contraction lessens. Although the extracellular concentration of K+ is normally small, a reduction in extracellular K+ (hypokalemia) causes the resting membrane potential to become hyperpolarized; as a consequence, it takes longer for the membrane to depolarize to threshold. Ultimately, the reduction in extracellular K+ results in a decrease in heart rate. The force of contraction is not affected, however.
A rise in the extracellular concentration of Ca2+ (hypercalcemia) produces a greater force of cardiac contraction because of a higher influx of Ca2+ into the sarcoplasm during action potential generation. Elevated plasma Ca2+ levels have an indirect effect on heart rate because they reduce the frequency of action potentials in nerve fibers, thus reducing sympathetic and parasympathetic stimulation of the heart. Generally, elevated blood Ca2+ levels lower the heart rate. A low blood Ca2+ level (hypocalcemia) increases the heart rate, although the effect is imperceptible until blood Ca2+ levels are reduced to approximately one-tenth of their normal value. The reduced extracellular Ca2+ levels cause Na+ channels to open, which allows Na+ to diffuse more readily into the cell, resulting in depolarization and action potential generation. However, reduced Ca2+ levels usually cause death due to tetany of skeletal muscles before they decrease enough to markedly influence the heart’s function.
4. Cardiac vagal stimulation :
The cardiograms obtained after the graphical recordings (see video) look like one of the following (figure)
Analyzing the cardiogram we can notice the following:
-after the electrical stimuli's on the vagus for 2-3 seconds we witness a decrease of the amplitude of the cardiac contractions and the cardiac pause in diastole (figure 1) (this effect is due to acetylcholine release from the vagal-myocardic synapse);
—after the electrical stimuli's on the vagus for a longer period of time we witness a decrease of the amplitude of the cardiac contractions and the cardiac pause in diastole for a few seconds and then the heart will continue its activity regardless the continuous application of electrical stimuli's on the vagus (figure 2). The phenomenon is called the "escape of the heart from the vagal influence" and it is considered to be due to:
distension of the myocardium after passive accumulation of blood in the ventricle (Starling effect)
acetylcholine depletion
reflex epinephrine production
5. Factors affecting a blood flow through a vessel:
The set up of this virtual experiment is shown in the figure. The video demonstrates the procedure. The results of such experiment is shown in table.
Questions:
1. Describe the relationship between pressure and blood flow.
2. What kind of change in the cardiovascular system would result in a pressure change?
3. Why would such a change cause problems?
4. Describe the relationship between radius and blood flow rate, linear or exponential?
5. Physiologically, what could cause the radius of a blood vessel to change in our
bodies?
6.
In a clogged artery, what has happened to the radius of the artery? How
has this affected blood flow? What could be done to fix this condition?
7. When a blood vessel bifurcates (splits) into two smaller
vessels, the radii of the two smaller vessels add up to a larger
cumulative radius than the radius of the original vessel. However, blood
flow is slower in the two vessels than in the original. Why?
8. What is the advantage of having slower blood flow in some areas of the body, such as in the capillaries of our fingers?
9.
Describe the relationship between viscosity and blood flow. Is fluid
flow versus viscosity an inverse or direct relationship?
10. Predict the effect of polycythemia vera on blood flow rate.
11. How would blood viscosity alter with dehydration of the body?
12. What would happen to blood flow if the body were dehydrated?
13. Is the effect of viscosity greater or less than the effect of radius on fluid flow?
14. Describe the relationship between vessel length and blood flow.
15. Why is vessel radius a more important factor in controlling blood flow resistance than vessel length?
6. The effect of CO, Resistance
& elasticity on BP:
The arterial pressure is the force exerted by the blood flow on arterial walls. The following video shows the setup of this experiment. The Table shows the results obtained from such an experiment.
The arterial pressure is generated by:
A) Ventricular contractions - in each systole the heart pushes in the arteries a new quantity of blood over the previous one, which leads to creating and maintaining a certain blood pressure in these vessels. An increase in CO is associated with an increase in systolic and diastolic BP (but without marked changes in pulse pressure).
B) Arterial wall elasticity does not allow the systolic pressure to exceed a certain level and the diastolic pressure to fall under a certain level (maintains the diastolic pressure). A decrease in vascular elasticity is associated with a slight increase in systolic BP and larger reduction in diastolic BP (i.e. increase pulse pressure).
C) Peripheral resistance - created in arterioles by the frictional force of the blood with a large surface represented by the summation of walls of the arterioles.
Objective: Demonstration of the way in which these three factors (that generate the arterial pressure) influence the values of this parameter.
7. BP measurement:
Measurement of the arterial tension by indirect methods (see the video): The indirect methods for determining the arterial pressure measure the tension which is exerted by blood on the Wall of the blood vessel by applying the manometer or an intermediary component on the anatomic projection of the examined artery. These methods are frequently used in clinical investigations. From the variety of indirect methods which determine the arterial pressure (Riva-Rocci, Korotkov etc) the most frequently used is the auscultatory method (Korotkov method).
The auscultatory method (Korotkov)
Principle: Exert a well determined decreasing pressure on the cutaneous projection area of the humeral artery, listening closely to the audible sounds with a stethoscope applied distally from the place where we exert the pressure. Record the following:
-the pressure when we start hearing the restored circulation on the compressed segment of the artery;
-the pressure when we can hear the restored normal circulation through the compressed artery.
8. Factors affect CO: Pump Mechanics experiment:
In this virtual experiment, it is important to recall the figure that represents a summary of various factors that affect CO. The following figure represents the labeled set up of this virtual experiment. This video represents the procedure followed in this experiment by changing one parameter in a time while keeping other parameters that affect CO fixed. The table shows the results of changing different parameters (one in a time) on the CO. The results in this virtual experiment are not necessarily applied to what is happing actually in the human body. This is because in human body, the factor that induces a change in one parameter may affect other parameters in different way. For example, sympathetic nervous system activation increases heart rate and venoconstriction (in favor of increase CO), increases contractility of cardiac muscle (causing a decrease in ESV and consequently SV which is in favor of increase CO), while at the same time decreasing the ventricular filling time (decrease the EDV which tends to reduce CO) because of the increase in the heart rate.
Questions:
How would a decrease in left flow tube radius affect flow and pump rate? Predict the outcome here.
As the
stroke volume was increased, what happened to the rate of the pump?
What would happen to the pump rate if you decreased the
stroke volume?
What would occur if blood were returned to the left
side of the heart at a faster rate than it left the right side of the heart?
What might occur if the valves became constricted?
In people with a high-fat diet, arteriosclerosis (a decrease in vessel diameter) is a common problem. What would the heart have to do to ensure that all organs are getting the adequate blood supply?
Compare the effect on flow rate of decreasing the right flow tube radius vs. the effect of decreasing the left flow tube radius (while keeping all other variables constant).
Recall that the flow tube between the left and middle beakers represents a vein, while the flow tube between the middle and right beakers represents an artery. In a living system, would you expect the vein or the artery to be more susceptible to a change in radius? Why?
What happens to flow rate when you decrease the pressure in the left beaker? Why?
What might be a cause of pressure decrease in the left beaker?
What happens to flow rate when you decrease the pressure in the right beaker? Why?
What might be a cause of pressure decrease in the right beaker?
What happens to flow rate when you increase the pressure in the right beaker? Why?
What might be a cause of pressure increase in the right beaker?
9. Physiological
and pharmacological experiments on Isolated Heart Muscle in a virtual
laboratory
(see video)
Receptor agonists and antagonists: competitive inhibition: For receptor-mediated effects, in addition to the physiological neurotransmitter or hormonal substances, there are other substances (drugs) available for pharmacological experiments that bind to the receptors and, thereby, compete competitively with the physiological substance for binding to the receptor. The relative proportion of receptors occupied by either type of molecule is determined by the affinity of the respective molecules for the receptor. If the drug substance has the same receptor-mediated effect as the physiological substance, then it is referred to as an agonist. If the drug molecule only occupies the receptor, without causing the receptor-mediated effect, it is simply blocking the receptor`s availability for the physiological substance (or agonist), and is so referred to as an antagonist. Agonist and antagonist drugs can often be found that are much more specific in their affinity for the different sub-types of receptors than the respective physiological agonist. For example, the nicotinic and muscarinic sub-types of Ach receptors are defined by their selective binding of the drugs, nicotine and muscarine, respectively.
Pilocarpine is a non-selective muscarinic acetylcholine receptor agonist in the parasympathetic nervous system.
The antagonist of Ach is atropine, which selectively binds muscarinic receptors, such as those on cardiac cells. The control of pupil size is a classic example of the physiological antagonism of the sympathetic and parasympathetic nervous systems; the papillary constricting effect of the parasympathetic nervous system is blocked by atropine.
Through activation of β-adrenergic receptors, epinephrine (released from adrenal gland) and norepinephrine (releases from sympathetic nervous system) increases the heart muscle contraction (positive inotropic effect) and heart rate (positive chronotropic effect).
Another important group of cardioactive drugs are the digitalis glycosides, which include g-strophantin (or ouabain). These are an important group of cardioactive drugs because they are among the few drugs which can increase the power of the heart (positive inotropic effect) in, for example, heart failure and bradycardia (negative chronotropic effect). The cardiac glycosides act in principle at every cell membrane, because they primarily inhibit the all over the place Na+-K+ pump. However, there is a therapeutic dose, at which the strength of cardiac contractions is increased without the biology of other cells, especially nerve cells, being affected. Their mechanism of action is quite clear. Their enhancement of cardiac contractile force is explained by an ouabain-induced inhibition of Na+-K+ pump, leading to an increase in the intracellular Na+, thus decreases the Na+ membrane gradient and so indirectly reducing the Na+-Ca++ membrane exchange (which exchange intracellular Ca++ for extracellular Na+) and increasing cellular retention of Ca++. This resultant increase in cytosolic Ca++ increases the degree of muscle contraction (see figure).
Calcium acts as a second messenger in the mediation of either adrenergic or cholinergic receptor activation but is also a key mediator of electromechanical coupling in muscle cells. In electromechanical coupling, it is the cytosolic Ca++ concentration that determines the strength of cardiac contractions, and the cytosolic Ca++ concentration is governed by the amount of Ca++ released from intracellular stores and the amount of extracellular Ca++ entering the cell from outside.
Recording the mechanical activity of the isolated frog heart on a graphical surface, while the isolated heart is being perfused:
With calcium ions free solutions (we accomplish this by using calcium chelating agent such as ammonium oxalate solution) we recorded a decrease of the cardiac contraction amplitude (negative inotropic effect).
With an excess of calcium chloride, the heart increases its contraction amplitude (positive inotropic effect); and bradycardia (negative chronotropic effect) by immediately repeating the administration of calcium in the solution calcium rigidity appears (the heart stops in the systole). This typically results from the direct effects of calcium ions upon the contractile process of cardiac muscle. A marked reduction in the calcium ion concentration has effects similar to those observed with high potassium levels.
Excessive levels of sodium ions result in depression of cardiac function, negative inotropic effect and negative chronotropic effect which is thought to stem from their competition with calcium ions at some critical site during the contractile process. At the other extreme, a deficiency of sodium ions in the extracellular environment leads to the development of a potentially lethal condition called cardiac fibrillation. In this situation, the cardiac muscle contracts at an extremely high rate and in an uncoordinated fashion such that little or no blood is actually pumped by the heart.
With an excess of potassium chloride, the heart decreases the amplitude of its contraction (negative inotropic effect); and bradycardia (negative chronotropic effect). By immediately repeating the administration of potassium in the solution the potassium inhibition appears (the heart stops in diastole).
With a decreasing temperature, heart rate decreases and vice versa.
10. Experiments
on Langendorff heart preparation
(see video1, video2, video3 & video4): In the so-called Langendorff
set-up, the isolated heart (no sympathetic or parasympathetic innervation)
with the aorta is perfused, whereby the coronary vessels are continuously
flushed in a retrograde manner (thus, with closed aortic valves) with
oxygenated and temperature-controlled Krebs solution (contains Na, K, Cl, Ca,
MgSO4, HCO3, PO4, glucose, albumin, and tromethamine [THAM], Bubble in 95% O2
and 5% CO2, pH of 7.4) that washes out from the severed vessels of
the venous system. The completely isolated heart can continue its activity if
the following conditions are assured: perfusion (the circulation of a liquid
through the cardiac compartments) with a solution under a certain pressure; the
solution used for perfusion must provide the energetic substrate necessary to
the cardiac activity; optimal temperature. Through a heat exchanger that is
controlled by a thermostat (the device on the left of the shelf), the
temperature of the perfusion solution is maintained at 37°C. With an average
flow of 10 mL/min, which is monitored by a flow meter, the hydrostatic
pressure of the reservoir (left of the screen display) that supplies the
perfusion system is set. The isovolumetric pressure changes in the left
ventricle are measured using a pulmonary artery balloon catheter (introduced
via the venus pulmonalis), a mechano-electric transducer and Statham amplifier
(with a fixed setting of 1 mV/2 mmHg), and they are recorded on the
chart recorder (on the bottom). The result outcome of this virtual experiment is shown in figure.
Clinical Relevance: The treatment of heart disease is one of the most common activities in daily medical practice. Cardiac diseases differ a lot in their clinical characteristics and have different causes. To understand the mode of action of cardiac medications, you need to know about the physiological processes that control cardiac activity and how these processes are affected by different drugs. You will work with the physiologically-important transmitters and test the effects of drug substances that are widely-used as heart medications. The virtual laboratory used here replicates the classic experimental heart model, the so-called “Langendorff heart”. This model and the type of experiments that you will be performing represent the standard procedure that continues to be used for screening for cardioactive drugs in the development of new heart medications.
Ach has negative chronotropic effect on heart through muscarinic receptors while its antagonist is atropine, which selectively binds muscarinic receptors, and blocking the receptor`s availability for the Ach and abolishes Ach effect.
As with cholinergic receptors, adrenergic receptors can be antagonized by specific drug substances. Propranolol is an adrenergic "β-blocker" that has potent effects on the heart and is an important heart medication. It directly affects the force of cardiac contractions by acting on β-adrenergic receptors and blocking the actions of NE and adrenaline, and can lower blood pressure and reduce tachycardia. As with cholinergic receptors, adrenergic receptors can be antagonized by specific drug substances. Phentolamine acts as an antagonist at α-adrenergic receptors, which play virtually no role in the heart muscles. It acts on α-adrenergic receptors of smooth muscle cells of blood vessels and of the intestinal wall.
Another important group of cardioactive drugs are the digitalis glycosides, which include g-strophantin (or ouabain). These are an important group of cardioactive drugs because they are among the few drugs which can increase the power of the heart (positive inotropic effect) in, for example, heart failure and bradycardia (negative chronotropic effect). The cardiac glycosides act in principle at every cell membrane, because they primarily inhibit the all over the place Na+-K+ pump. However, there is a therapeutic dose, at which the strength of cardiac contractions is increased without the biology of other cells, especially nerve cells, being affected. Their mechanism of action is quite clear. Their enhancement of cardiac contractile force is explained by an ouabain-induced inhibition of Na+-K+ pump, leading to an increase in the intracellular Na+, thus decreases the Na+ membrane gradient and so indirectly reducing the Na+-Ca++ membrane exchange (which exchange intracellular Ca++ for extracellular Na+) and increasing cellular retention of Ca++. This resultant increase in cytosolic Ca++ increases the degree of muscle contraction (see figure).
Calcium channel blockers or calcium antagonists, such as verapamil, have a broad therapeutic utility in heart disease. They reduce the power of cardiac contractions (negative inotropic effect) (and so reduce blood pressure) and can also normalize an increased heart rate. It should be noted, in particular, that Ca++-channels are involved in electromechanical coupling in all muscle cells, although they are not always regulated by the same mechanisms. This explains why Ca++ channel blocker drugs is not selective for heart muscle but also act on the smooth muscles of blood vessels, causing vasodilation of peripheral blood vessels, including the coronary arteries. Thus, Ca++ channel blocker drugs are often used to reduce high blood pressure. Drugs that block slow inward calcium channels are used to reduce pacemaker firing rate by slowing the rate of rise of depolarizing pacemaker potentials. These drugs also reduce conduction velocity at the AV node, because those cells, like SA nodal cells, depend on the inward movement of calcium ions to depolarize.
11. Frogs Heart block
The human heart will beat when removed from the body, and will continue to beat for several hours when kept in the appropriate conditions. This observation indicates that the rhythm for the cardiac cycle comes from within the heart itself. The cells responsible for controlling the heart beat cycle are located in the sinoatrial (SA) node, which is located in the right atrium. These cells have a membrane potential that changes over time. The membrane potential is depolarized by the pacemaker potential and when it reaches threshold, an action potential is produced. This action potential creates a single contraction of the entire heart. These events repeat every second or so, with the result that the resting heart contracts or ‘beats’ at a frequency of about 70 times each minute in a resting individual.
The pacemaker cells in the SA node are electrically connected to one another and to adjacent atrial fibers by gap junctions. The action potential ‘hops’ across these junctions between the atrial muscle fibers and initiates a contraction of both atria. The atria and the ventricles are not connected by gap junctions; rather they are electrically connected by a second group of specialized cells called the atrioventricular (AV) node, which is located close to the center of the heart. These small, specialized muscle cells do not contract; rather they receive the action potential from the atria and slowly relay it through the AV node via gap junctions. The action potential is then rapidly conducted via the AV bundle and Purkinje fibers to the fibers that make up the myocardium of both ventricles. This delayed conduction of the action potential through the AV node insures that the ventricles contract sometime after the atria contract.
The heart is composed almost entirely of large, strong muscle fibers, which are responsible for the pumping action of the heart. Other smaller, specialized cardiac cells are weakly contractile and produce the rhythm for, and conduct it to, the rest of the heart. While the pacemaker for the heart is in the SA node, the other specialized cells in the AV node, the AV bundle, and the Purkinje fibers can also produce their own rhythmic discharge of action potentials. However, the rate of electrical activity from these cells is much slower than that shown by the SA node and is usually masked by the action potentials that drive the cardiac cycle. In some people, one or more of these cells produce an occasional action potential and a heart contraction that is not synchronized with the normal cardiac cycle. These additional contractions are called ‘ectopic beats’ and are said to be generated by an action potential from a cell called an ‘ectopic pacemaker’.
In this lab (see video), you will use a photoreceptor to monitor the movements of an isolated frog heart by watching a line tracing on the screen of a virtual monitor (see video). This system allows you to watch the heart and correlate the line tracing on the screen with the contractions of the atria and the ventricle. You will loop thread around the heart and tie a knot in the thread. Pulling the ends allows you to pull the knot tight around the heart and interrupt action potential conduction between the regions on either side of the ligature. The goal is to place the thread between the atria and ventricles to have them beat asynchronously, so that the SA node drives the atrial contractions and an ectopic pacemaker drives the ventricle contractions at a slower rate. A frog is anesthetized with MS-222, pithed, and then placed ventral surface uppermost in a dissection dish. A pair of scissors is used to remove the skin over the pectoral girdle and throat, and the pectoral girdle is cut in the midline and along the left lateral margin. The cut girdle and associated muscles are removed to expose the heart.
The heart is carefully removed from the frog and placed in a Petri dish containing frog Ringer's solution. Fine metal pins are placed though the aortic arch and into the transparent resin lining the dish. The last metal pin is pushed through the tip of the ventricle and into the resin to hold the stretched heart to the dish. The dish is placed on a photoreceptor so that the heart movements create a deflection of the line tracing on the screen.
A length of thread is placed under the heart and a loose knot is tied. The location of the thread is adjusted and the knot is tightened in an effort to obstruct action potential conduction through the heart, and change the cardiac rhythm (see the results).
12. ECG and exercise
The human heart is composed almost entirely of large, strong muscle fibers, which are responsible for the pumping action of the heart. Other smaller, specialized cardiac cells are weakly contractile and produce the rhythm of the heart. The pacemaker for the human heart is located in the sinoatrial (SA) node, which is a group of small, specialized cardiac cells in the right atrium. Gap junctions provide an electrical connection between the cells in the SA node and the muscle fibers in the atria. As a result, an action potential in a pacemaker cell evokes an action potential in all of the cells in the SA nodes and an action potential in, and a contraction of, all of the fibers in both atria.
The atria and the ventricles are not connected by gap junctions; rather, they are electrically connected by a second group of specialized cells called the atrioventricular (AV) node, which is located close to the center of the heart. These small, specialized muscle cells in the AV node do not contract; instead they slowly relay the action potential through the AV node via gap junctions. When it has reached the other side of the AV node, the action potential is rapidly conducted via the AV bundle and Purkinje fibers to the fibers of both ventricles, which produces an action potential and contraction. This delayed conduction of the action potential through the AV node ensures that the ventricles contract sometime after the atria contract.
During the normal cardiac cycle, there is a sequential contraction of the atria and the ventricles, followed by a period of relaxation as the heart fills with blood. Since these sequential contractions are initiated by an action potential, the action potential must first take place in all atrial fibers, and then in all ventricular fibers. This synchronous electrical activity in so many cardiac muscle cells produces currents that can be monitored with electrodes placed on the skin; the resulting recording is called the electrocardiogram, or ECG. The human ECG consists of five waves, which are expressed as the P-wave, the QRS complex, and the T-wave. The following three components of the ECG can be correlated with the action potentials in the atria and ventricles.
• The P-wave is produced by atrial depolarization.
• The QRS wave is created by repolarization of the atria and depolarization of the ventricles.
• The T-wave is produced by repolarization of the ventricles.
Exercise can induce a dramatic increase in heart rate. In this lab you will compare the ECG from a student volunteer at rest and immediately after exercise. You will illustrate the increase in heart rate by measuring the time interval between the R-waves from successive cardiac cycles. You will also examine the effect of exercise on the time intervals between the various components of the ECG (see video). The goal is to determine whether the increase in heart rate changes the timing between atrial and ventricle action potentials, or simply decreases the time interval between cardiac cycles. See the table.
1. The skin on the underside of each wrist is abraded with an alcohol swab.
2. Three electrodes are attached to the volunteer's skin -- one on each wrist and a third on the left ankle. The three electrodes now form Einthoven's triangle where the electrodes are in what is known as Lead I orientation.
3. The cables are attached to the Data Acquisition Unit and the ECG is painlessly recorded.
4. After the ECG is recorded, the volunteer is asked to exercise and then sit quietly while the ECG is recorded during recovery.
13. ECG and finger pulse
The cardiac cycle consists of a contraction of the atria, a contraction of the ventricles, and then a period of rest. An action potential in the pacemaker cells in the sinoatrial (SA) node is conveyed directly to the atrial fibers across gap junctions, and to the ventricles via the atrioventricular (AV) node. The action potential passes slowly through the AV node and delays excitation of the ventricles, thus insuring that the ventricles contract after the atria. The synchronous action potential activity in the muscle fibers of the atria and then the ventricles produces currents that can be detected with electrodes placed on the skin and the recording, called the electrocardiogram (ECG), can be correlated with action potentials in the atria and ventricles.
• The P-wave is produced by atrial depolarization.
• The QRS wave is created by repolarization of the atria and depolarization of the ventricles.
• The T-wave is produced by repolarization of the ventricles.
The heart acts as a pump; it takes blood from the veins at a low pressure and contracts to push the blood into the arteries at a higher pressure. In the relaxed heart, venous blood flows into the atria and then into the ventricles. The atria contract and push their blood into the ventricles. Now the ventricles contract; the ventricular blood pressure increases and closes the AV valves, which make the ‘lub’ heart sound. The blood is now trapped inside the ventricles because the semilunar valves are kept shut by the high arterial blood pressure. The ventricles continue to contract, increasing the blood pressure in the ventricles until it is greater than the blood pressure in the arteries. At this point, the semilunar valves open and the volume of the ventricles decrease as they discharge blood into the arteries. The ventricles relax, the ventricular pressure declines, and the higher arterial pressure closes the semilunar valves, which make the ‘dup’ heart sounds. The role of the heart is to provide sufficient pressure for the blood to flow through the blood vessels and back to the heart. Blood leaves the arterial system continuously through the capillaries, but enters intermittently from the heart. This is analogous to pumping up a leaky tire; air is pumped into the tire, but the air constantly leaks out of the tire. Thus, the tire pressure increases as air is pumped in and then slowly declines as air passes out through the holes. In a similar way, the arterial blood pressure changes during the cardiac cycle; the blood pressure is at its highest level (called the systolic pressure) when the heart contracts, and slowly declines as blood passes out through the capillaries. The lowest arterial blood pressure is called the diastolic pressure and is recorded immediately before the ventricle contracts to push more blood into the arteries. The systolic and diastolic pressures are the values given to patients during medical evaluations.
The flow of a liquid through a tube depends upon many factors, including the radius of the tube and the pressure pushing the liquid down the tube. Imagine a syringe filled with water; no water will leave the syringe unless you apply pressure to the plunger. Further, the rate of flow will depend upon the amount of pressure you apply to the plunger; the greater the pressure the greater the flow. In the arteries, the change in the blood pressure during the cardiac cycle will affect the blood flow through the arterial system. When the blood pressure is high, more blood will be forced out of the arterial system than when the blood pressure is low. Therefore, the heart changes the blood pressure and creates a ‘pulsatile’ flow of blood through the arterial system. This changing blood flow can be detected by feeling a patient’s ‘pulse’ on the wrist or the neck, or using a movement detector attached to the finger.
Most blood vessels show some degree of compliance, and expand when the internal pressure increases. This tends to dampen out the pressure oscillations created by the heart, with the result that there is little or no pulsatile flow in the capillaries. One feature created by the compliance of the aorta is the ‘dicrotic notch’, which is a transient increase in blood pressure produced by the wall of the aorta quickly returning to its original size. When blood is pushed into the aorta by the left ventricle, the blood pressure increases and the aorta expands. This small increase in the radius of the aorta is maintained by the high blood pressure, but as the blood pressure declines between heart contractions, this force is overcome by the elasticity of the aorta wall. This recoil of the stretched vessel wall creates a transient increase in blood pressure as the elastic fibers in the wall of the aorta quickly return the vessel to its original size. This transient increase in blood pressure is called the ‘dicrotic notch’ and takes place a short time after the semilunar valves shut.
In this lab (see video), you will use a finger pulse unit to monitor the flow of blood through the finger of a student volunteer. You will also listen to the heart sounds and record the ECG, and examine the relationship between these three signals during the cardiac cycle (see figure). The 0.22 sec in the figure represents the blood conduction time. It measures the duration between the R wave of a cardiac cycle and the peak of the corresponding pressure wave in the pulse recording. This is roughly how long it takes blood to travel from your heart to the tip of your finger through arteries. If you assume that the distance from your heart to your finger is ~1 meter, calculate the velocity that blood is traveling by dividing 1m by the blood conduction time:
Blood conduction velocity (m/s) = 1 m / conduction time (sec). Bernoulli’s Principle states that when the velocity of a fluid is high, the pressure is low, and when the velocity is low, the pressure is high (see figure) as shown in a flow of water into a venturi meter. The kinetic energy increases at the expense of the fluid pressure, as shown by the difference in height of the two columns of water. An example of real life is atherosclerosis which occurs when a deposit formed on an arterial wall. This means a smaller cross-sectional area at clogging site, leads to faster flow velocity and a drop in pressure.
1. The skin on the underside of each wrist is abraded with an alcohol swab.
2. Three electrodes are attached to the volunteer's skin; one on each wrist and a third on an ankle. The cables are attached to the Data Acquisition Unit.
3. Blood flow is monitored with a finger pulse unit, which consists of a cable and a sensitive movement detector held in a small plastic chamber. The finger pulse unit is strapped to a volunteer's finger with the movement detector on the fingertip; the cable from the unit is attached to the Data Acquisition Unit.
4. A stethoscope is placed on the skin over the volunteer's heart, and an event marker, which is also connected to the Data Acquisition Unit, is used to indicate when the lub and dup heart sounds take place.
5. The ECG, finger pulse, and heart
sounds are displayed on the computer screen.
14. Electrical axis of the heart
A contraction of the heart is initiated by pacemaker cells in the sinoatrial (SA) node. During the cardiac cycle, the signal travels through the heart to produce synchronous action potential activity in, and a contraction of, the atria and then the ventricles. This electrical activity creates large currents, which spread from the heart throughout the body. Electrodes placed on the skin can pick up these electrical currents, and the recorded response is called the electrocardiogram, or ECG. The different waves of the ECG can be correlated with the action potentials in the atria and ventricles.
• The P-wave is produced by atrial depolarization.
• The QRS wave is created by repolarization of the atria and depolarization of the ventricles.
• The T-wave is produced by repolarization of the ventricles.
In the classroom setting, the ECG
is usually recorded with three electrodes placed on the skin on each wrist and
the left ankle. The electrodes are connected to the Data Acquisition Unit (DAQ)
in ‘Lead I’ orientation, so that signals are recorded from the two electrodes on
the wrists, and the ankle electrode is connected to ground. The DAQ measures
the difference between the signals from the wrists, and amplifies this ECG for
display on a recording device. If the heart were in the midline of the chest,
the distance between the heart and each recording electrode would be the same,
so the two electrodes would deliver the same signal to the DAQ. Under these
conditions, the difference between the two signals would be zero and the
display would be a flat line. In most people the heart is located to the left
of the midline, so any signal from the heart arrives at the electrode on the
left wrist before it reaches the electrode on the right wrist, because the
signal has a shorter distance to travel. The signals from the two electrodes
will not be the same, so the differential output from the DAQ will display the
characteristic ECG.
This lab assumes that the
amplitude of the ECG is an indication of how far the heart lies off the
midline. In this lab, you will measure the amplitude of the QRS complex with
the electrodes in Lead I orientation, where the recording electrodes are placed
on the wrists. Then you will switch the electrode orientation to Lead III,
where the recording electrodes are placed on the left wrist and the left ankle.
A second QRS measurement will indicate the relative distance between the two
electrodes and the heart, and the data will be used to calculate the angle at
which the heart lies in the chest. This means that if you draw a line along the
septum between the atria, the ventricles, and the tip of the heart, this line
would exit the left side of the body. The angle this line makes with horizontal
is often referred to as the axis of the heart (see video). The figure demonstrates the calculation results.
1. The skin on the underside of each wrist is abraded with an alcohol swab.
2. Three electrodes are attached to the volunteer's skin; one on each wrist and a third on the left ankle. The three electrodes now form Einthoven's triangle, where the electrodes are in what is known as Lead I orientation.
3. The cables are attached to the
Data Acquisition Unit and the ECG is painlessly recorded.
15. Cooling and peripheral blood flow
The human circulatory system is ‘closed’ and consists of a heart, blood vessels, and blood. Other organisms have an ‘open’ circulatory system where organs are simply immersed in a large ‘bath’ of blood or hemolymph. One advantage of a closed system is that the amount of blood flowing through a vessel can be controlled, so that blood can be directed to different organs based on need. One disadvantage of a closed system is the large amount of friction between the blood and the walls of the vessels, which results in a decline in blood pressure as blood travels through the circulatory system. A high arterial blood pressure is achieved by the heart, which acts as a pump to push blood into the arteries and provides sufficient pressure for blood flow through the blood vessels and back to the heart.
According to the Poiseuille Equation, the flow of fluid through a rigid tube is inversely proportion to the fourth power of the radius. So, if tube A has a radius of 2 and tube B has a radius of 1/2 (if all other variables are kept constant) the flow of fluid through tube A will be (2 to the fourth power) 16 units, and the flow of fluid through tube B will be (1/2 to the fourth power) 1/16th of a unit. Clearly, the radius of a tube has a huge effect on the flow of fluid. Now, if we turn to the circulatory system, the flow of blood down arterioles is controlled by sphincters, which are bands of smooth muscle that wrap around a blood vessel. Contraction of these smooth muscles decreases the radius of the arterioles and dramatically decreases blood flow to the tissues downstream. In this way, sphincters can decrease the radius of an arteriole (a phenomenon called ‘vasoconstriction’) to shunt blood away from certain organs and, therefore, allow blood to flow to others. The sympathetic nervous system can create vasoconstriction in the arterioles to certain organs, and cooling can also cause sphincter contraction and dramatically decrease blood flow to the fingers.
In this lab, you will examine the effect of changing temperature on blood flow to the fingers (see video). This will be achieved by monitoring blood flow through a volunteer's finger while a bag of ice is applied to (and subsequently removed from) his wrist. Blood flow is monitored with a finger pulse unit, which consists of a cable and a sensitive movement detector held in a small plastic chamber. The finger pulse unit is strapped to a volunteer's finger with the movement detector on the finger tip, and the cable from the unit is attached to the Data Acquisition Unit. In this way, the pulsing flow of blood through the finger can be displayed on the computer screen (see figure).
In this lab you will study the effect of
cooling on blood flow using an ice bag placed on the volunteer's wrist.
Questions:
Panel A represents the peripheral blood flow without ice. On application of ice, the blood flow was decreased (panel B1), Explain. On continuous application of ice (panel B2), the blood flow was returned back to it original flow rate observed during rest. Explain.
On removal of ice (panel C), immediately the peripheral blood flow was
overshooted above the resting level and gradually return back its
resting level. Explain.
16. Blood pressure and gravity
The human circulatory system consists of a heart, blood vessels, and blood. The heart acts as a pump to push blood into the arteries and provides sufficient pressure for blood flow through the blood vessels and back to the heart. Blood leaves the arterial system continuously through the capillaries, but enters intermittently from the heart. This is analogous to pumping up a leaky tire; air is pumped into the tire at a certain rate, but the air constantly leaks out of the tire. Thus, the tire pressure increases as air is pumped in and then slowly declines as air passes out through the holes. In a similar way, the arterial blood pressure increases to its highest level (called the ‘systolic pressure’) as blood is pumped in, and then slowly declines to its lowest level (called the ‘diastolic pressure’) value just before the ventricles contract again. The systolic and diastolic pressures are the values recorded during medical evaluations.
A high blood pressure must be produced in the arteries, because the pressure declines as blood travels through the circulatory system. If the heart creates an arterial blood pressure that is too high, blood will flow too quickly through the capillaries and blood vessels may burst, creating aneurisms. A low arterial blood pressure will slow blood flow and certain organs like the brain may malfunction because they do not carry a store of metabolites to maintain life when there is insufficient blood supply.
The arterial blood pressure must be kept within defined limits and is controlled by a negative feedback system. Baroreceptors in the carotid sinus measure the pressure of the blood as it enters the brain. Any change in carotid blood pressure is relayed to the cardiovascular control center in the brain and adjustments are made to return the blood pressure back to normal. Thus, the pressure of the blood going to the brain is kept constant and the brain is constantly perfused with blood. This system does not consider other parts of the body, and any complications that may be encountered due to gravity. This lab examines the arterial systolic blood pressure in a student volunteer with his hand in two locations: by his side and above his head. When a blood pressure cuff is placed on the upper arm, the two hand locations allow measurements to be taken with the cuff at the same level as the heart and in line with the ear. Blood pressure measurements are made using a blood pressure cuff, or sphygmomanometer. The cuff is wrapped around the upper arm and inflated, to compress the brachial artery and stop blood flow to the arm. The cuff pressure is slowly released and the pressure at which blood flow starts up again is taken as the systolic blood pressure. During a medical examination, a stethoscope is used to listen to the turbulent flow of blood through the partially open brachial artery. However, the noise in the teaching lab usually makes this an impossible task, so a finger pulse unit is used to detect blood flow. Blood pressure is measured using a sphygmomanometer (blood pressure cuff), which is firmly strapped around the volunteer's upper left arm. The operator uses the bulb to inflate the cuff and squeeze the arm. When the pressure in the cuff is greater than the blood pressure in the brachial artery, the vessel collapses and blood flow to the lower arm ceases. A valve is used to slowly release cuff pressure and, when the cuff pressure is slightly less than the systolic blood pressure in the brachial artery, the vessel transiently opens when its highest (systolic) pressure is achieved.
Traditionally, the operator uses a stethoscope to listen for the turbulent flow of blood through the narrow artery. However, the noise in the teaching lab makes this process difficult. Therefore, the procedure has been modified to monitor blood flow with a finger pulse unit, which consists of a cable and a sensitive movement detector held in a small plastic chamber. The finger pulse unit is strapped to a volunteer's finger with the movement detector on the fingertip, and the cable from the unit is attached to the Data Acquisition Unit. With this setup, the pulsing flow of blood through the finger can be displayed on the computer screen (see video).
In this lab, you will measure the systolic blood pressure from a volunteer. The result of systolic blood pressure while the left arm is at the side of the volunteer (i.e. the cuff is at the level of the heart) or the left arm is elevated above the head (the cuff is above the level of the heart of the volunteer) is measured and is shown in Table. Diastolic pressure is more difficult to determine using a finger pulse monitor, so this experiment will focus on systolic pressure.
Questions:
A. Why does the systolic BP is lower when the left arm is above the head of the volunteer than when his left arm is on his side?.
B. Why the elevation of right arm does not affect the BP level?
17. Blood pressure and body position
The human circulatory system consists of a heart, blood vessels, and blood. The heart acts as a pump to push blood into the arteries and provides sufficient pressure for blood flow through the blood vessels and back to the heart. Blood leaves the arterial system continuously through the capillaries, but enters intermittently from the heart. This is analogous to pumping up a leaky tire; air is pumped into the tire at a certain rate, but the air constantly leaks out of the tire. Thus, the tire pressure increases as air is pumped in and then slowly declines as air passes out through the holes. In a similar way, the arterial blood pressure increases to its highest level (called the systolic pressure) as blood is pumped in, and then slowly declines to its lowest level (called the diastolic pressure) value just before the ventricles contract again. The systolic and diastolic pressures are the values recorded during medical evaluations.
A high blood pressure must be produced in the arteries, because the pressure declines as blood travels through the circulatory system. If the heart creates an arterial blood pressure that is too high, blood will flow too quickly through the capillaries and blood vessels may burst, creating aneurisms. A low arterial blood pressure will slow blood flow and certain organs like the brain may malfunction because they do not carry a store of metabolites to maintain life when there is insufficient blood supply.
It is clear that the arterial blood pressure must be controlled within carefully defined limits, and this is achieved by a negative feedback system. Baroreceptors in the carotid sinus measure the pressure of the blood as it enters the brain. Any changes in carotid blood pressure are relayed to the cardiovascular control center in the medulla of the brain. An increase in blood pressure stimulates the parasympathetic nervous system to slow the heart rate and decrease the cardiac output; less blood will enter the arterial system and blood pressure will decrease. A decrease in blood pressure stimulates the sympathetic nervous system to increase cardiac output, by increasing heart rate and stroke volume, and to contract certain arteriole sphincters to decrease blood loss from the arterial system. Both strategies increase the amount of blood in the arteries and, therefore, increase blood pressure.
In a standing person, blood must flow against gravity as it travels from the heart to the brain; clearly, the pressure of the blood as it leaves the heart will be greater than in the carotid sinus. In a person who is lying down, blood will not flow against gravity from the heart to the brain, so the blood pressure at these two locations will be similar. If the pressure of the blood entering the brain is constant irrespective of body position, will the systolic arterial blood pressure be different if a person is standing or lying down? This lab addresses this question by measuring the systolic blood pressure from a student in these two positions.
Blood pressure measurements are made using a blood pressure cuff, or sphygmomanometer. The cuff is wrapped around the upper arm and inflated to compress the brachial artery and stop blood flow to the arm. The cuff pressure is slowly released and the pressure at which blood flow starts up again is taken as the systolic blood pressure. During a medical examination, a stethoscope is used to listen to the turbulent flow of blood through the partially open brachial artery. However, the noise in the teaching lab usually makes this an impossible task, so a finger pulse unit is used to detect blood flow. In this lab, you will measure the effects of body position on the systolic blood pressure by making measurements from a student volunteer who is standing and lying down.
Blood pressure is measured using a sphygmomanometer ('blood pressure cuff'), which is firmly strapped around the volunteer's upper left arm. The operator uses the bulb to inflate the cuff and squeeze the arm. When the pressure in the cuff is greater than the blood pressure in the brachial artery, the vessel collapses and blood flow to the lower arm ceases. A valve is used to slowly release cuff pressure and, when the cuff pressure is slightly less than the systolic blood pressure in the brachial artery, the vessel transiently opens when its highest (systolic) pressure is achieved.
Traditionally, the operator uses a stethoscope to listen for the turbulent flow of blood through the narrow artery. However, the noise in the teaching lab makes this process difficult. Therefore, the procedure has been modified to monitor blood flow with a finger pulse unit, which consists of a cable and a sensitive movement detector held in a small plastic chamber.
The finger pulse unit is strapped to a volunteer's finger with the movement detector on the fingertip, and the cable from the unit is attached to the Data Acquisition Unit. With this setup, the pulsing flow of blood through the finger can be displayed on the computer screen.
In this lab, you will measure the systolic blood pressure from a volunteer who is standing and then lying down (see video). Diastolic pressure is more difficult to determine using a finger pulse monitor, so this experiment will focus on systolic pressure. The results are shown in Table.
Question:
Why does the systolic BP in supine position is lower than in standing position?