Larger Waves Seen on the Oscilloscope Represent the Ventricular Contraction

Activity 1: 1. Explain why the larger waves seen on the oscilloscope represent the ventricular contraction. During ventricular contraction the force to pump the blood is greater compared to atrial contraction. Therefore, a lot of force is needed in order to provide the systemic circulation with blood that gets send throughout the entire body. The smaller waves represent the contraction of the atria. 2. Explain why the amplitude of the wave did not change when you increased the frequency of the stimulation. (Hint: relate your response to the refractory period of the cardiac action potential.) How well did the results compare with your prediction? Due to a longer refractory period (unlike the skeletal muscles) the cardiac muscle is incapable of wave summation. As a result the amplitude of the wave did not change during the experiment although the frequency of the stimulation was increased. The cardiac action potential is longer vs. the skeletal muscle potential. The amplitude of the ventricular systole did not changed with more frequent stimulation because a new contraction could not begin until the relaxation phase. The results matched my prediction. 3. Why is it only possible to induce an extrasystole during relaxation? Only until the resting membrane potential is again established in cardiac muscle cells, and is maintained until the next depolarization arrives, only then an induced extrasystole can occur, i.e. during relaxation. Only after repolarization the depolarization of cardiac cells can occur. Cardiac muscle is incapable of reacting to any stimulus before approximately the middle of phase 3, and will not respond to a normal cardiac stimulus before phase 4. 4. Explain why wave summation and tetanus are not possible in cardiac muscle tissue. How well did the results compare with your prediction? Because the ventricles must contract and relax fully with each beat to pump blood. Therefore the cardiac muscle cells have a longer refractory period and are incapable of wave summation and tetanus. The prediction was matched by the results of the experiment. Activity 2: 1. Explain the effect that extreme vagus nerve stimulation had on the heart. How well did the results compare with your prediction? If vagal stimulation is excessive the heart will stop beating. After a short time the heart resumed beating, and the heart rate increased to normal values. My prediction matched the results. 2. Explain two ways that the heart can overcome excessive vagal stimulation. After excessive vagal stimulation, the ventricles resume their contraction after a short period of time. This is known as vagal escape and is due to the initiation of a rhythm by the Purkinje fibers or sympathetic reflexes. 3. Describe how the sympathetic and parasympathetic nervous systems work together to regulate heart rate. The sympathetic and parasympathetic nervous systems are part of the ANS. The sympathetic nervous system is known as the “fight of flight” and the parasympathetic nervous system is known as “resting and digesting”. Both supply nerve impulses to the heart. Even when at rest both of the nervous systems work, but the parasympathetic nervous system is more active. The sympathetic nervous branch becomes more engaged when it is needed (ex: exercise, danger). By stimulating the parasympathetic nervous system the heart rate will decrease without directly changing the force of contraction. On the opposite side, by stimulating sympathetic nervous system the rate and force of contraction of the heart are increased. 4. What do you think would happen to the heart rate if the vagus nerve was cut? This will lead to an increase in the heart rate. The SA node will generate action potentials 100 times per minute. Without the vagus nerve there will be no more feedback from the parasympathetic nervous system. Both the parasympathetic and sympathetic nervous systems form a checks-and-balances system that provides the right parameters so the heart functions in an optimum way. If you eliminate one, then the balance is broken and the heart will suffer damage. Activity 3: 1. Explain the effect that decreasing the temperature had on the frog heart. How do you think the human heart would respond? How well did the results compare with your prediction? By decreasing the temperature of the Ringer’s solution resulted in a decreased heart rate for the frog. This is due to the fact that the frog is poikilothermic animal – it lacks an internal homeostatic regulatory mechanism, thus its internal body temperature changes depending on the temperature of its external environment. On the opposite side humans are homeothermic, even when the external temperature fluctuates the body’s internal mechanism will try to keep the internal temperature between 35.8-38.2 C. If the external temperature drops then the heat promoting center in the hypothalamus gets activated. To conserve energy the human heart will reduce its heart rate. In extreme cases of low external temperatures the human body becomes hypothermic. My predictions matched the results. 2. Describe why Ringer's solution is required to maintain heart contractions. The Ringer’s solution consists of essential electrolytes – chloride, sodium, potassium, calcium, and magnesium, and it provides the necessary environment for the frog’s heart so that spontaneous cardiac actions potentials can occur. The Ringer’s solutions provide the means for the isolated intact frog’s heart to be viable. 3. Explain the effect that increasing the temperature had on the frog heart. How do you think the human heart would respond? How well did the results compare with your prediction? By increasing the temperature of the Ringer’s solution resulted in an increased heart rate for the frog. This is due to the fact that the frog is poikilothermic animal – it lacks an internal homeostatic regulatory mechanism, thus its internal body temperature changes depending on the temperature of its external environment. The human body is homeothermic, and an increase of the external temperature triggers a response from the heat-loss center in the hypothalamus. This is done in order to keep the internal body temperature within the normal ranges. Also the heart rate will increase. In extreme high temperatures the body becomes hyperthermic due to failed thermoregulation. The results matched my prediction. Activity 4: 1. Describe the effect that pilocarpine had on the heart and why it had this effect. How well did the results compare with your prediction? Pilocarpine is a cholinergic drug (an acetylcholine agonist). When administered, the heart rate decreased from the base line of 61 to 46. Pilocarpine is a chemical modifier that mimics the action of acetylcholine on muscarinic receptors. It decreases the frequency of action potentials by binding to muscarinic cholinergic receptors embedded in the plasma membrane of the SA node cells. Indirectly the potassium channels are opened, and the calcium and sodium channels are closed. As a result the heart rate decreases. 2. Atropine is an acetylcholine antagonist. Does atropine inhibit or enhance the effects of acetylcholine? Describe your results and how they correlate with how the drug works. How well did the results compare with your prediction? Atropine, a chemical modifier, inhibits the effects of acetylcholine. Atropine antagonizes the muscarinelike actions of acetylcholine. During the experiment, pilocarpine decreased the heart rate to 46. When atropine was administered the heart rate increased to 71. The results matched my prediction. 3. Describe the benefits of administering digitalis. Digitalis increases the force of contraction and decreases the heart rate. This chemical modifier can help those with weakened hearts that need to allow maximum time for venous return and increased stroke volume. Those that suffer from congestive heart failure are prescribed digitalis. 4. Distinguish between cholinergic and adrenergic chemical modifiers. Include examples of each in your discussion. Chemical modifiers that inhibit, mimic, or enhance the action of acetylcholine in the body are labeled cholinergic (for ex. pilocarpine is an agonist and atropine is an antagonist). Chemical modifiers that inhibit, mimic, or enhance the action of epinephrine in the body are labeled adrenergic (for ex. epinephrine is an agonist). Activity 5: 1. Describe the effect that increasing the calcium ions had on the heart in this activity. How well did the results compare with your prediction? An increase in calcium ions resulted in an increased heart rate from the baseline of 59 to 69. The rate of depolarization and the force of contraction both increased. The results did not match my prediction. 2. Describe the effect that increasing the potassium ions initially had on the heart in this activity. Relate this to the resting membrane potential of the cardiac muscle cell. How well did the results compare with your prediction? The potassium concentration is greater inside the cardiac muscle cell vs. the outside of the cell. The resting membrane potential favors the movement of potassium ions more than sodium or calcium ions. The ratio of extracellular and intracellular concentrations of potassium determines mainly the resting membrane potential of cardiac muscle cells. By increasing the potassium ions initially the heart rate dropped to 28 and then it became erratic. Thus, the resting membrane potential decreased and also the force of contraction by increasing the potassium ions. The results matched my prediction. 3. Describe how calcium channel blockers are used to treat patients and why? Those that suffer from high blood pressure and abnormal heart rates can benefit from calcium channel blockers. They block the movement of calcium through the ion channels of the plasma membrane, throughout all the phases of the cardiac action potentials. If less calcium gets through, then both the rate of depolarization and the force of contraction are reduced.