Physiology Good Answers PDF

G. more than 10 mEq of sodium ions are lost in the faeces H. the mucosa of the large intestine absorbs chloride ions in an exchange transport process I. aldosterone enhances sodium transport capability J. the storage colon is represented by the distal half of the colon 250. Which statements followin...

G. more than 10 mEq of sodium ions are lost in the faeces H. the mucosa of the large intestine absorbs chloride ions in an exchange transport process I. aldosterone enhances sodium transport capability J. the storage colon is represented by the distal half of the colon 250. Which statements following the composition of the faeces are true? A. 10 to 20 per cent of the solid matter is represented by fat B. 2 to 3 per cent of the solid matter is represented by protein C. the odour of faeces is caused by derivatives of bilirubin D. 30 per cent of the solid matter is represented by dead bacteria E. The white colour of the faces is caused by the presence of urobilin in the faeces F. the faeces normally are composed only of solid matter G. skatole is an odoriferous product H. the brown colour of faeces is caused by hydrogen sulfide I. undigested roughage is represented by the food and dried constituents of digestive juices, such as bile pigment and sloughed epithelial cells J. the odour of faeces is independent of the person’s colonic bacterial flora and the type of food eaten 251. Events of the cardiac cycle for left ventricular function – indicate the correct correlation(s): A. Isovolumic contraction → B B. Isovolumic contraction → A C. Ejection → B D. Ejection → C E. Rapid inflow → D F. Slow inflow → F G. Isovolumic relaxation → C H. Diastasis → E I. Atrial systole → A J. Isovolumic relaxation → D 252. Events of the cardiac cycle for left ventricular function – indicate the correct correlation(s): A. J: Atrial relaxation, A-V valve closes B. G: Aortic valve opens, A-V valve opens C. C: Aortic valve closes D. D: A-V valve opens E. B: A-V valve closes F. E: All valve close G. I: Ejection, aortic valve opens H. F: All valve open I. A: Aortic valve opens J. H: Isovolumic relaxation, 253. Events of the cardiac cycle for left ventricular function – indicate the correct correlation(s): A. E: Mitral valve closes B. C: All valves closed C. D: Isovolumic relaxation, open A-V valves D. I: Ejection, open aortic valve E. F: Aortic valve closes F. A: Aortic valve opens G. B: Diastasis, all valves are open H. J: Isovolumic contraction, open A-V valves I. H: Mitral valve opens J. G: Isovolumic relaxation, all valves are closed 254. Events of the cardiac cycle for left ventricular function – indicate the correct correlation(s): A. H: Rapid inflow, mitral valve is open B. F: Isovolumic contraction, open A-V valves C. E: Ejection, all valves are open D. G: Ejection, aortic valve is open E. B: Aortic valve opens F. A: Isovolumic contraction, all valves are close G. I: Ejection, open aortic valve H. C: Mitral valve closes I. J: Diastasis, all valves are open J. D: Isovolumic relaxation, all valves are open 255. Events of the cardiac cycle for left ventricular function – indicate the correct correlation(s): A. E: Isovolumic contraction, open A-V valves B. C: Isovolumic relaxation, all valves are open C. G: Atrial contraction D. A: Diastasis, all valves are open E. D: Ejection, aortic valve is open F. I: Aortic valve closes at the end of ejection G. F: Diastasis H. B: Ejection, all valves are open I. H: Ejection, open aortic valve J. J: Mitral valve opens on the beginning of rapid inflow 256. The curves from figure represent: A. C: Ventricular volume B. B: Ventricular pressure C. A: Phonocardiogram D. F: Aortic pressure E. F: Atrial pressure F. G. H. I. J. 257. A. B. C. D. E. F. G. H. I. J. 258. A. B. C. D. E. F. G. H. I. J. 259. A. B. C. D. E. F. G. D: Phonocardiogram B: Electrocardiogram C: Electrocardiogram D: Ventricular pressure A: Ventricular volume Indicate the correct correlation(s): The “c” wave occurs when the atria begin to contract. The “v” wave occurs during the atrial contraction while the A-V valves are closed. The curve E represents the atrial pressure. The “v” wave occurs toward the end of ventricular contraction. The “a” wave is caused by atrial contraction. The “c” wave occurs when the ventricles begin to contract. The “a” wave is caused by atrial fibrillation. The “c” is caused by opening of the A-V valves because ventricular isovolumic relaxation. The “a” wave is caused by ventricular contraction. The “c” wave is caused mainly by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles. On the volume-pressure diagram: Point D: Mitral valve closes. Period E: Intraventricular volume decreases. Point C: Mitral valve opens. Period E: Intraventricular pressure decreased. Point A: Mitral valve opens. Point C: Aortic valve opens. Point B: Aortic valve closes. Point D: Aortic valve closes. Point A: Aortic valve opens. Point B: Mitral valve closes. On the volume-pressure diagram – cardiac cycle phases are: Period H: the ventricular volume increases but the ventricular pressure is constant Period E: Isovolumetric relaxation (the ventricular pressure decreases but the ventricular volume is constant) Period F is including atrial contraction. Period F is not including diastasis. Period G: the ventricular pressure decreases but the ventricular volume is constant Period H: Period of ejection Period E: the ventricular pressure increases but the ventricular volume is constant H. Period F: the ventricular volume decreases but the ventricular pressure is constant I. Period G: Isovolumetric contraction (the ventricular pressure increases but the ventricular volume is constant) J. Period F: Period of filling 260. On the volume-pressure diagram: A. V1: end diastolic volume (about 120 mL). B. Period E: ejection (the ventricular volume decreases to 50 milliliters). C. Period F: ventricular filling (the ventricular volume normally increases to about 120 milliliters) D. Period H: isovolumic relaxation (the pressure inside the ventricle decreases to 2-3 mmHg). E. V2: end diastolic volume (about 120 mL). F. V2: end systolic volume (about 50 mL). G. Period G: isovolumic contraction (the pressure inside the ventricle increases to about 80 mm Hg) H. V3: stroke volume (120-50=70 mL). I. V1: end systolic volume (about 50 mL). J. V3: stroke volume (120+50=170 mL). 261. Indicate the correct statement(s): A. The heart is composed of the atrial syncytium and the ventricular syncytium. B. Potentials are conducted from the atrial syncytium into the ventricular syncytium only by the A-V bundle. C. The cardiac muscle is striated in the same manner as in vascular muscle. D. Cardiac muscle is refractory to restimulation during the action potential. E. The atria provide the major source of power for moving blood through the body’s vascular system. F. Each atrium is a weak primer pump for the ventricle G. In cardiac muscle the action potential is caused by opening of the voltage activated fast sodium channels and the L-type calcium channels. H. The premature ventricular contractions cause wave summation, as occurs in skeletal muscle. I. The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized excitatory neurons. J. Decreasing heart rate decreases duration of cardiac cycle. 262. Phases of cardiac muscle action potential: A. Phase 0 (depolarization), fast sodium channels open B. Phase 1 (initial repolarization), fast calcium channels open. C. Phase 2 (plateau), calcium channels open and fast potassium channels close D. Phase 0 (depolarization), fast potassium channels open E. Phase 2 (plateau), calcium channels open and fast sodium channels open F. Phase 1 (initial repolarization), fast sodium channels close. G. Phase 4 (resting membrane potential) averages about +20 millivolts. H. Phase 3 (rapid repolarization), calcium channels open and slow potassium channels close. I. Phase 3 (rapid repolarization), calcium channels close and slow potassium channels open. J. Phase 4 (resting membrane potential) averages about −90 millivolts. 263. Indicate the correct statement(s): A. The strength of contraction of cardiac muscle depends to a great extent on the concentration of sodium ions in the extracellular fluids B. The calcium release channels in the sarcoplasmic reticulum membrane are also called ryanodine receptor channels. C. The strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the extracellular fluids D. Transport of calcium back into the sarcoplasmic reticulum is achieved with the help of a sodium-calcium exchanger. E. Sodium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction F. Transport of calcium back into the sarcoplasmic reticulum is achieved with the help of a calcium–adenosine triphosphatase (ATPase) pump. G. The duration of contraction of cardiac muscle is mainly a function of the duration of the action potential. H. Calcium entering the cardiomyocytes triggers the release of calcium into the sarcoplasm from the sarcoplasmic reticulum. I. Sodium entering the cardiomyocytes triggers the release of calcium into the sarcoplasm from the sarcoplasmic reticulum. J. The calcium release channels in the sarcolemma are also called ryanodine receptor channels. 264. Indicate the correct statement(s): A. The a wave in the atrial pressure curve occurs when the ventricles begin to contract. B. The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called the systole. C. The right atrial pressure increases 100 to 120 mm Hg during atrial contraction. D. If the atria fail to function the no difference can be noticed. E. The atrial contraction usually causes an additional 20 percent filling of the ventricles F. The heart beating at a very fast rate does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction. G. There is a delay of more than 0.1 second during passage of the cardiac impulse from the atria into the ventricles. H. The total duration of the cardiac cycle is directly proportional to the heart rate. I. The delay of action potentials conduction on A-V node allows the atria to contract ahead of ventricular contraction. J. Each cycle is initiated by spontaneous generation of an action potential in the sinus node 265. Indicate the correct statement(s): A. When the left ventricular pressure rises slightly above 8 mm Hg the ventricular pressures push the semilunar valves open. B. Approximately 60 percent of the blood in the ventricle at the end of diastole is ejected during systole C. During the period of isovolumic relaxation the cardiac muscle tension is increasing but little or no shortening of the muscle fibers is occurring. D. During period of isovolumic (isometric) systole all valves are open. E. During period of isovolumic (isometric) relaxation all valves are closed. F. The first third of ejection is called the period of isovolumetric contraction. G. The period of rapid filling of the ventricles lasts for about the last third of diastole. H. During the period of isovolumic contraction no ventricular emptying occurs. I. The ventricles fill with blood during diastole. J. During the middle third of diastole, only a small amount of blood normally flows into the ventricles 266. Indicate the correct statement(s): A. The aortic and pulmonary valves prevent backflow of blood from the ventricles to the atria during the last third of ventricular diastole. B. The A-V valves are constructed with an especially strong yet very pliable fibrous tissue. C. The aortic and pulmonary valves are supported by the chordae tendineae. D. The A-V valves (i.e., the tricuspid and mitral valves) prevent backflow of blood from the ventricles to the atria during systole. E. The papillary muscles prevent the bulging of A-V valves too far backward toward the atria during ventricular contraction. F. Because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary valves are subjected to much greater mechanical abrasion than are the A-V valves. G. If a chorda tendinea becomes ruptured or if one of the papillary muscles becomes paralyzed the A-V valves cannot open. H. The A-V valves are open during ventricular contraction. I. The semilunar valves (i.e., the aortic and pulmonary artery valves) prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. J. For anatomical reasons, the semilunar valves require rather rapid backflow for a few milliseconds to cause closure. 267. Indicate the correct statement(s): A. The atrial T wave represents the stage of repolarization of the ventricles B. The T wave initiates contraction of the ventricles and causes the ventricular pressure to begin rising. C. The QRS complex begins slightly before the onset of ventricular systole. D. There is a rise in the atrial pressure curve immediately after the electrocardiographic S wave. E. The R wave is followed by atrial contraction. F. The T wave occurs slightly before the end of ventricular contraction G. The electrocardiogram waves are electrical voltages generated by the heart and recorded by the electrocardiograph from the surface of the body. H. The P wave is caused by spread of depolarization through the atria. I. The P wave is followed by atrial relaxation which causes the closing of A-V valves and second heart sound. J. About 0.16 second after the onset of the P wave, the QRS waves appear as a result of electrical depolarization of the ventricles 268. Indicate the correct statement(s): A. The ejection fraction is usually equal to about 0.6 (or 60 percent). B. The stroke volume output represents the difference between ventricular end-diastolic volumes and the ejection fraction. C. The remaining volume in each ventricle at the end of systole is called the end-systolic volume. D. As the ventricles empty during systole, the volume decreases about 70 milliliters (the stroke volume output). E. The fraction ejection fraction is usually equal to the stroke volume output. F. During diastole, normal filling of the ventricles increases the volume of each ventricle to a volume called the end diastolic volume. G. When the heart contracts strongly, the end-systolic volume may decrease to as little as 0 milliliters. H. By increasing the end-diastolic volume and decreasing the end-systolic volume, the stroke volume output can be decreased. I. The fraction of the end-diastolic volume that is ejected is called the ejection fraction. 269. 270. 271. 272. J. When large amounts of blood flow into the ventricles during diastole, the ventricular end-diastolic volumes can become as great as 100 liters in the healthy heart. The pressure changes in the aorta: A. Increasing after opening aortic valve B. Decreasing during isovolumic ventricular contraction C. Increasing during atrial contraction D. Increasing before closing mitral valve E. Increasing during isovolumic ventricular relaxation F. Increasing during third heart sound G. Decreasing during isovolumic atrial relaxation H. Increasing during diastasis I. Increasing during fast ejection J. Decreasing during rapid inflow The pressure in the left ventricle is: A. Decreasing before second heart sound B. Decreasing during ventricular filling C. Increasing after closing the mitral valve D. Decreasing before opening of aortic valve E. Increasing slightly during atrial contraction F. Increasing after open aortic valve G. Increasing suddenly during distasis H. Decreasing during isovolumic relaxation I. Increasing after closing aortic valve J. Decreasing after closing mitral A-V valve: A. Closes at the beginning of isovolumic relaxation B. Closure generates the first heart sound C. Closes at the beginning of isovolumic contraction D. Opens at the end of isovolumic contraction E. Closes after atrial repolarization F. Closure generates the second heart sound G. Opens at the beginning of rapid ejection H. Opens at the end of isovolumic relaxation I. Opens at the beginning of rapid inflow J. Closes after atrial contraction Aortic pressure curve: A. The pressure in the aorta decreases slowly throughout ventricular filling. B. Before the ventricle contracts again, the aortic pressure usually has fallen to about 80 mm Hg (diastolic pressure). C. The entry of blood into the aorta during systole causes the pressure to increase to about 120 mm Hg. D. After the second hear sound the blood stored in the distended elastic arteries flows continually through the veins back to the left atria. E. At the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes, the aortic pressure suddenly drop to diastolic pressure. F. The entry of blood into aorta during systole causes the walls of these artery to relax. G. After the aortic valve has closed, the pressure in the aorta becomes equal to left ventricular pressure. H. When the left ventricle contracts, the ventricular pressure increases rapidly until the aortic valve opens. I. When the left ventricle begin to contract, the aortic pressure increases rapidly until the aortic valve close. J. An incisura occurs in the aortic pressure curve when the aortic valve closes. 273. Indicate the correct statement(s): A. When the aortic and pulmonary valves close at the end of systole, one hears the second heart sound. B. The first hears a sound has a low vibration pitch and it is long-lasting. C. When listening to the heart with a stethoscope one does not hear the opening of the valves. D. When the valves open, the vanes of the valves and the surrounding fluids vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest. E. When the ventricles contract, one first hears a sound caused by closure of the aortic valves F. When the aortic and pulmonary valves open at the end of systole, one hears the second heart sound. G. When listening to the heart with a stethoscope one does not hear the closing of the valves. H. When the ventricles contract, one first hears a sound caused by closure of the A-V valves I. When the valves close, the vanes of the valves and the surrounding fluids vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest. J. The second hears a sound has a low vibration pitch and it is longlasting. 274. On the volume-pressure diagram of the cardiac cycle for normal function of the left ventricle we can see: A. During period of isovolumic relaxation (Phase IV) the intraventricular pressure decreases without any change in volume. B. Period of filling (Phase I) extends from end-systolic volume (50 milliliters) to the end-diastolic volume (120 milliliters). C. During period of ejection (Phase III) the volume of the ventricle decreases from end-sytolic volume to end-diastolic volume. D. During period of isovolumic relaxation (Phase IV) the intraventricular volume is named end-diastolic volume. E. Period of filling (Phase I) extends from the end-diastolic volume (120 milliliters) to end-systolic volume (50 milliliters). F. During period of ejection (Phase III) the volume of the ventricle decreases to end-systolic volume. G. During period of isovolumic contraction (Phase II) the pressure inside the ventricle increases to equal the diastolic pressure in the aorta (80 mm Hg). H. At the end of the period of ejection, the aortic valve closes, and the ventricular pressure falls back to the diastolic pressure level. I. During period of isovolumic contraction (Phase II) the pressure inside the ventricle increases to equal the systolic atrial pressure (120 mm Hg). J. At the end of the period of ejection, the aortic valve opens and the ventricular pressure falls back to the 80 mm Hg. 275. Indicate the correct statement(s): A. The load against which the muscle exerts its contractile force, which is called the afterload. B. Oxygen consumption has also been shown to be nearly proportional to the tension that occurs in the heart muscle during contraction multiplied by the duration of time that the contraction persists. C. Approximately 70 to 90 percent of heart muscle energy is normally derived from oxidative metabolism of fatty acids. D. The afterload of the left ventricle is usually considered to be the pressure in the aorta leading from the right ventricle. E. For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled. F. More than 70 percent of the heart muscle energy is normally derived from oxidative metabolism lactate and glucose. G. The degree of tension on the muscle when it begins to contract, which is called the preload. H. Much less chemical energy is expended even at normal systolic pressures when the ventricle is abnormally dilated. I. The heart muscle tension during relaxation is proportional to pressure times the diameter of the aorta. J. During heart muscle relaxation, most of the expended chemical energy is converted into work output. 276. Indicate the TRUE statement(s): A. The vagal fibers are distributed mainly to the ventricles. B. Stretch of the right atrial wall directly increases the heart rate by 10 to 20 percent. C. Within physiological limits, the heart pumps all the blood that returns to it by way of the veins. D. Strong stimulation of the sympathetic nerve fibers from the vagus nerves can stop the heartbeat for a few seconds E. cardiac output) often canbe increased more than 100 percent by sympathetic stimulation F. Strong sympathetic stimulation can increase the heart rate in young adult humans from the normal rate of 70 beats/min up to 180 to 200 G. Sympathetic stimulation can the force of heart contraction thereby increasing the volume of blood pumped and increasing the ejection pressure. H. Inhibition of the parasympathetic nerves to the heart can decrease cardiac pumping to a moderate extent. I. Strong vagal stimulation can decrease the strength of heart muscle contraction by 100 percent. J. The effect of vagal stimulation is mainly to increase the heart rate rather than to increase greatly the strength of heart contraction. 277. Indicate the correct statement(s): A. Contractile strength of the heart often is enhanced temporarily by a moderate decrease in temperature B. Prolonged elevation of temperature exhausts the metabolic systems of the heart and eventually causes spastic contraction. C. Increased body temperature, such as that which occurs when one has fever, greatly increases the heart rate. D. Any increase of the arterial pressure in the aorta will be follow by a decrease the cardiac output. E. Excess calcium ions cause the heart to move toward spastic contraction. F. High extracellular fluid potassium concentration depolarizes the cell membrane generating action potentials. G. Elevation of potassium concentration to only 8 to 12 mEq/L can cause severe weakness of the heart, abnormal rhythm, and death. H. Large quantities of potassium also can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle. I. A high potassium concentration in the extracellular fluids decreases the resting membrane potential in the cardiac muscle fibers and increases the intensity of the action potential. J. Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid and also slows the heart rate. 278. Indicate the correct statement(s): A. The strength of heart muscle contraction is caused almost entirely by calcium ions released from the sarcoplasmic reticulum. B. The T tubule action potentials in turn act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions. C. Cardiac muscle begins to relax a few milliseconds before the action potential ends. D. At the end of the plateau of the cardiac action potential, the influx of calcium ions to the interior of the muscle fiber is suddenly cut off. E. The sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle. F. A heart placed in a calcium-free solution will showed spastic contraction. G. The sarcoplasmic reticulum of cardiac muscle stores enough calcium to provide full contraction. H. Cardiac muscle begins to contract a few milliseconds after the action potential begins I. The strength of contraction of cardiac muscle depends to a great extent on the concentration of mucopolysaccharides in the extracellular fluids. J. Without the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably. 279. Effect of sympathetic stimulation on the heart and vessels: A. Bronchodilation (β2 adrenergic receptors) B. Increased myocardial strength (β1 adrenergic receptors) C. Cardioacceleration (β1 adrenergic receptors) D. Slowed rate (muscarinic receptor) E. Thermogenesis (β3 adrenergic receptors) F. Iris dilation (alpha adrenergic receptor) G. Vasoconstriction (alpha adrenergic receptor) H. Increases the overall activity of the heart I. Decreased force of contraction, especially of atria (muscarinic receptor) J. Vasodilation by (β2 adrenergic receptors) 280. Events of the cardiac cycle for left ventricular function: A. After opening of the aortic valve, the intraventricular volume rapidly increases B. After opening of the aortic valve, the intraventricular volume rapidly decreases C. If both the mitral and aortic valves are closed, the intraventricular volume does not change. D. After closing of the aortic valve, the intraventricular pressure rapidly increases E. After opening of the mitral valve, the intraventricular volume rapidly decreases F. After opening of the mitral valve, the intraventricular volume rapidly increases G. After closing of the aortic valve, the intraventricular pressure rapidly decreases H. If both the mitral and aortic valves are closed, the intraventricular pressure does not change. I. After closing of the mitral valve, the intraventricular pressure rapidly decreases J. After closing of the mitral valve, the intraventricular pressure rapidly increases 281. Organization of the atrioventricular (A-V) node – indicate the True correlation(s): A. E: S-A node B. D: Left ventricle C. B: Transitional fibers D. H: Right bundle branch E. A: Structures that bring depolarization from S-A node F. I: Myocardial fibers G. F: Distal portion of A-V bundle H. A: Right atrium I. G: Purkinje fibers J. C: A-V node 282. Organization of the atrioventricular (A-V) node – indicate the True correlation(s): A. F: A-V valve B. B: Purkinje fibers C. C: Sinus node D. A: Internodal pathways E. D: Atrioventricular fibrous tissue F. A: Left atrium G. G: Left bundle branch H. H: Right ventricle I. I: Ventricular septum J. E: Penetrating portion of A-V bundle 283. The intervals of time needed to pass different structures of conductive system: A. Delay in the interventricular septum = 4 second B. From sinus node to ventricular contractile myocardium = 0.16 second C. Delay in the penetrating A-V bundle = 0.04 seconds D. Delay in sinus node = 0.03 second E. From S-A node to atrial contractile myocardium = 0.3 seconds F. From sinus node to A-V node = 0.03 second G. From S-A node to A-V valve = 0.16 second. H. From sinus node to penetrating portion of A-V bundle = 0.12 seconds I. Delay in the S-A node itself = 0.09 second J. Delay in the A-V node itself = 0.09 second 284. Pacemaker of the heart: A. The A-V nodal fibers could discharge at an intrinsic rate of 40 to 60 times per minute. B. In normal conditions, nervous system generates the intrinsic rhythmical excitation of the heart. C. The Purkinje fibers have an autonomic discharge rate of 10–20/ minute. D. Other parts of the heart than sinus node, that exhibit intrinsic rhythmical excitation. E. The sinus node is the pacemaker because it has the fastest rate of rhythmical discharge. F. The A-V node is almost always the pacemaker of the normal heart. G. The A-V valve has an intrinsic discharge rate of 70-80/ minute. H. The Purkinje fibers could discharge at an intrinsic rate somewhere 15 and 40 times per minute. I. The sinus node is the ectopic pacemaker of the normal heart. J. The sinus node is almost always the pacemaker of the normal heart. 285. The rhythmical and conductive system of the heart: A. S-A node is in the superior posterolateral wall of the left ventricle. B. If the conductive system of the heart stops the ventricles contract 0.16’’ before the atria. C. In normal conditions, all portions of the ventricles are contracting almost simultaneously. D. Purkinje fibers conduct the cardiac impulses to all parts of the atria. E. The human heart has a special system for rhythmic self-excitation and repetitive contraction. F. The normal rhythmical impulses of the heart are generated in the sinus node. G. The Purkinje fibers ordinarily control the rate of beat of the entire heart. H. The rhythmical and conductive system of the heart is susceptible to damage by heart disease, especially by ischemia of the heart tissues. I. The internodal pathways conduct impulses from the sinus node to the atrioventricular node. J. Impulses from the atria are delayed before passing into the ventricles through sinoatrial node. 286. In the sinus nodal fibers: A. After the action potential is over, progressively more and more L-type calcium channels close. B. The inherent leakiness of the sinus nodal fibers to Na+ and Ca2+ causes the self-excitation. C. The hyperpolarization means the membrane potential of sinus nodal cells becomes (−90) millivolts at the termination of the action potential. D. Self-excitation of sinus node cells generates their own action potential. E. After the action potential is over the inward-leaking Na+ and Ca2+ overbalance the K+ outflow. F. The leakiness to sodium and calcium ions causes the sinus nodal fibers to remain depolarized all the time. G. The “resting” potential of the sinus nodal cells gradually decreases to hyperpolarize the cells. H. The rhythmical discharge of a sinus nodal fiber could continue throughout a person’s life. I. Activation of the fast sodium channels causes the action potential in sinus node cells. J. Between heartbeats, influx Na+ causes a slow rise in the membrane potential of sinus nodal cells. 287. Indicate the correct statement(s): A. The slow conduction in the transitional, nodal, and penetrating A-V bundle fibers is caused mainly by diminished numbers of gap junctions. B. A special characteristic of the A-V bundle is the inability of action potentials to travel backward from the ventricles to the atria. C. The atrioventricular node delays impulse conduction from the atria to the ventricles. D. Once the cardiac impulse enters the ventricular Purkinje conductive system, it opens the valves. E. In normal situation, the A-V bundle allows the re-entry of cardiac impulses from the ventricles to the atria. F. The Purkinje fibers could forcefully contract during impulse transmission. G. Usually, muscle bridges penetrate the fibrous barrier between atrial and ventricular syncytium boosting the cardiac impulse to re-enter the atria from the ventricles. H. The total delay in the A-V nodal and A-V bundle system is more than 0.10 second. I. The ends of the sinus nodal fibers connect directly with surrounding atrial muscle fibers J. Once the impulse reaches the ends of the Purkinje fibers, heart stops. 288. Indicate the correct statement(s): A. The hyperpolarization caused by vagal stimulation decreases the atrioventricular node delay of impulse conduction. B. Sympathetic stimulation increases the cardiac rhythm and conduction. C. Parasympathetic (vagal) stimulation slows the cardiac rhythm and conduction D. If the vagal stimulation is strong enough, it is possible to stop the rhythmical self-excitation of the entire heart. E. The beta-1 adrenergic stimulation increases the permeability of the fiber membrane to sodium and calcium ions. F. The increase in permeability to sodium ions is at least partially responsible for the increase in contractile strength of the cardiac muscle under the influence of sympathetic stimulation. G. Norepinephrine stimulates beta-1 adrenergic receptors, which mediate the effects on heart rate. H. The acetylcholine makes the “resting” membrane potential of the sinus nodal fibers considerably more positive than usual. I. Sympathetic stimulation decreased the rate of rhythmicity of the nodal fibers. J. The acetylcholine released at the vagal nerve endings greatly increases the permeability of the fiber membranes to potassium ions. 289. When A-V block occurs: A. When A-V block occurs the cardiac impulse fails to pass from the ventricles into the atria through the Purkinje system. B. After sudden A-V bundle block, the Purkinje system does not begin to emit its intrinsic rhythmical impulses until 5 to 20 seconds later. C. When A-V block occurs there is a blockage of transmission of the cardiac impulse from the central nervous system to the heart. D. Delayed resumption of heartbeat is called Stokes-Adams syndrome. E. Before the blockage, the Purkinje fibers had been “overdriven” by the rapid sinus impulses and, consequently, are in a suppressed state. F. A new pacemaker usually develops in the Purkinje system of the ventricles and drives the ventricular muscle at a rate of 15 to 40 bpm. G. The A-V nodal and Purkinje fibers can exhibit intrinsic rhythmical excitation at the normal rate of rhythm of the sinus node. H. When A-V block occurs the atria will beat at lower rate between 15 and 40 beats per minute.s I. The Purkinje fibers, when not stimulated from some outside source, discharge at a rate of 60 and 80 times per minute. J. A pacemaker elsewhere than the sinus node is called an “ectopic” pacemaker. 290. Mechanism of the sympathetic effect of the heart include: A. In the sinus node: norepinephrine → stop the rhythmical self-excitation. B. In the A-V node: norepinephrine → blocks conduction. C. Stimulation of beta-1 adrenergic receptors → ↑ permeability for Na+ and Ca2+. D. In the A-V node: norepinephrine → ↑ conduction velocity E. Norepinephrine → ↑ permeability for K+. F. In the ventricular myocardium: norepinephrine → ↑ contractile strength. G. In the sinus node: norepinephrine → accelerate self-excitation. H. Norepinephrine → stimulates cholinergic receptors in the heart. I. Norepinephrine → stimulates beta-1 adrenergic receptors in the heart. J. In the ventricular myocardium: norepinephrine → hyperpolarization. 291. A. B. C. D. E. F. G. H. I. J. 292. A. B. C. D. E. F. G. H. I. J. 293. A. B. C. D. E. F. G. H. I. J. 294. A. B. C. Electrocardiogram – indicate the True correlation(s): Q-T interval → A Ventricles → D RR interval → D RR interval → B Q-T interval → E P-R interval → B S-T segment → E Ventricles → F P-R interval → C S-T segment → C Electrocardiogram – indicate the True correlation(s): T wave → D P wave → E P-R interval → E P-R interval → B P wave → A Q-T interval → C S-T segment → A T wave → C Q-T interval → D S-T segment → B On the ECG trace – indicate the True correlation(s): F: No potential is recorded in the ECG when the ventricular muscle is completely depolarized A: The repolarization wave. D: The T wave is caused by potentials generated as the ventricles recover from the state of depolarization. B: The depolarization wave spreading through the ventricles. E: P-Q interval is the time between the beginning of electrical excitation of the atria and the ending of excitation of the ventricles. D: The R-R interval. E: The P wave is caused by electrical potentials generated when the atria depolarize before atrial contraction begins. A: QRS complex is caused by potentials generated when the ventricles depolarize before contraction. C: P-Q interval is the time between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles. C: The T-P segment. On the ECG trace (25 mm/sec and 10 mm/mV) there are: E: S-T segment is flat on the zero potential level. D: The Q-T interval. C: The R-R interval. D. E. F. G. H. I. J. 295. A. B. C. D. E. F. G. H. I. J. 296. A. B. C. D. E. F. G. H. I. J. 297. A. B. C. D. E. F. G. C: The QRS complex. B: The Q-T interval. E: The P-R interval. B: The depolarization wave spreading through the ventricles. D: The R-R interval. A: The P-R interval of about 4 mm (meaning 4x0.04 = 0.16 sec). A: The P-R interval of about 40 mm meaning 40x0.04 = 0.016 sec. On the ECG trace (25 mm/sec and 10 mm/mV) we can see: Negative P waves in V3 to V6 (abnormal). In leads V1 and V2, the QRS recordings of the normal heart are mainly negative (normal). Inverted T waves in V4 to V6 (abnormal). The P waves in leads V2 to V6 are mainly positive (normal). The T waves in leads V2 to V6 are mainly positive (normal). Abnormal (negative) QRS recordings in leads V1 and V2. In leads V4, V5, and V6, the QRS complexes are mainly positive (normal). Abnormal (positive) the QRS complexes in leads V3 to V6. Normal electrocardiograms recorded from the six chest leads. There is not normal ECG. On the ECG trace (25 mm/sec and 10 mm/mV) we can see: The positive P wave in lead aVR which is normal. The negative QRS complex in lead aVF which is normal. The negative QRS complex in lead aVR which is normal. The inverted T wave in lead aVF which is normal. The positive P wave in lead aVF which is normal. The positive T wave in lead aVF which is normal. The positive QRS complex in lead aVF which is normal. The inverted T wave in lead aVR which is normal. The positive QRS complex in lead aVR which is normal. The positive T wave in lead aVR which is normal. The ECG leads: The V1 to V6 are recorded with the positive electrode on the chest and two of the limbs connected to the negative terminal of the electrocardiograph. The term “bipolar” means that ECG is recorded from two electrodes. All leads from figure are in the same plane. The augmented unipolar limb leads are: V1, V2, V3, V4, V5, V6. The I, II, and III are named standard bipolar limb leads. The precordial limb leads are I, II, III, V1, V2, and V3. The V1 to V6 are recorded with the positive electrode on the chest and the indifferent electrode connected through equal electrical resistances to the right arm, left arm, and left leg at the same time. 298. 299. 300. 301. H. The augmented unipolar limb lead are aVR, aVL and aVF. I. The three standard electrocardiographic limb leads are: I, II and III. J. The precordial limb leads are aVR, aVL, aVF, V4, V5, and V6. The ECG morphology on leads: A. The QRS complex is negative in few standard limb leads, which is normal. B. The T wave is positive all leads, which is normal C. The QRS complex is positive in standard limb leads I and III, which is normal. D. The T wave is positive in limb lead aVR, which is normal. E. The QRS complex is negative in aVR, which is normal. F. The P wave is positive in all leads, which is normal. G. The T wave is positive in precordial leads, which is normal H. The P wave is positive in limb leads except aVR, which is normal. I. The QRS complex is positive in standard limb lead aVR, which is normal. J. The T wave is positive in limb leads except aVR, which is normal. The ECG leads: A. Leads I and II have the negative electrode on right leg. B. Leads V4, V5 and V6 have the electrode nearer to the base of the heart. C. Leads V1 and V2 have the electrode nearer to the heart apex. D. Leads II and III have the positive electrode on left leg. E. The lead aVR is the only lead having the positive electrode on right arm. F. Leads V1 and V2 have the electrode nearer to the base of the heart than to the apex. G. Leads aVF and aVL have no electrode. H. Leads I and III have the positive electrode on left arm. I. Leads I and II have the negative electrode on right arm. J. Leads I and aVL have the positive electrode on left arm. The ECG leads: A. Lead aVF has positive electrode on left leg. B. Leads I and III have the negative electrode on left arm. C. Leads I and II have the positive electrode on right arm. D. Lead I is different the lead V1. E. Lead aVL has negative electrode on right arm. F. Leads II and III have the positive electrode on right leg. G. Leads I and III have one of the electrodes on left arm. H. Leads V1 to V6, are recorded with one electrode placed on the anterior surface of the chest directly over the heart. I. Leads I, II, III, aVR, aVL, and aVF have electrodes on limbs. J. Lead aVF has positive electrode on right leg. Facts about the augmented unipolar limb leads: A. They are all named precordial leads. B. Two of the limbs are connected through electrical resistances to the negative terminal of the electrocardiograph, and the third limb is connected to the positive terminal. C. They are all similar to the standard limb lead recordings, except that the recording from the aVR lead is inverted. D. When the positive terminal is on the left leg, it is known as the aVL lead. E. When the positive terminal is on the left arm, the lead is known as the aVR lead. F. When the positive terminal is on the right arm, the lead is known as the aVR lead. G. When the positive terminal is on the right arm, the lead is known as the aVF lead. H. Two of the limbs are connected through electrical resistances to the third limb. I. When the positive terminal is on the left arm, the lead is known as the aVL lead. J. When the positive terminal is on the left leg, it is known as the aVF lead. 302. Characteristics of the normal electrocardiogram: A. The QRS complex is caused by potentials generated as the depolarization wave spreads through the ventricles. B. The P wave is caused by potentials generated as the ventricles recover from the state of depolarization. C. Both the P wave and the components of the QRS complex are repolarization waves. D. No potential is recorded in the ECG when the ventricular muscle is either completely polarized or completely depolarized. E. The R wave is caused by electrical potentials generated when the atria depolarize before atrial contraction begins. F. The QRS complex is caused by potentials generated when the ventricles depolarize before contraction. G. The T wave is caused by potentials generated as the ventricles recover from the state of depolarization. H. The QRS complex is caused by potentials generated when the atria depolarize before contraction. I. The P wave is caused by electrical potentials generated when the atria depolarize before atrial contraction begins. J. The QRS complex is caused by potentials generated as the repolarization wave spreads through the ventricles. 303. P-Q or P-R interval from the normal electrocardiogram: A. The interval from the beginning of the QRS complex to the end of the T wave is called the Q-T interval. B. The time between the beginning of the P wave and the beginning of the QRS complex is called the P-Q segment. C. The normal Q-T interval duration is more than 0.50 second. D. The normal P-R interval is about 0.26 second. E. The Q-T interval ordinarily is about 0.35 second. F. The time between the beginning of the P wave and the beginning of the QRS complex is called the P-R interval. G. Contraction of the ventricle lasts almost from the beginning of the Q wave to the beginning of the T wave. H. The normal P-R interval is about 0.16 second. I. The time between the beginning of the QRS complex and the beginning of the T wave is the interval between the beginning of electrical excitation of the ventricles and the beginning of excitation of the atria. J. The time between the beginning of the P wave and the beginning of the QRS complex is the interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles. 304. The standard bipolar limb leads: A. The standard bipolar limb leads record positive Q waves. B. In recording limb lead I, the negative terminal of the electrocardiograph is connected to the left arm and the positive terminal is connected to the right arm. C. To record limb lead II, the negative terminal of the electrocardiograph is connected to the right arm and the positive terminal is connected to the left leg. D. To record limb lead III, the negative terminal of the electrocardiograph is connected to the left arm and the positive terminal is connected to the right leg. E. The standard bipolar limb leads record positive P waves. F. In recording limb lead I, the negative terminal of the electrocardiograph is connected to the right arm and the positive terminal is connected to the left arm. G. To record limb lead II, the negative terminal of the electrocardiograph is connected to the right arm and the positive terminal is connected to the right leg. H. To record limb lead III, the negative terminal of the electrocardiograph is connected to the left arm and the positive terminal is connected to the left leg. I. The standard bipolar limb leads record positive T waves. J. The standard bipolar limb leads record positive S waves. 305. Indicate the correct statement(s): A. Extending the ECG to allow assessment of cardiac electrical events while the patient is ambulating during normal daily activities is called ambulatory electrocardiography. B. Improvements in digital technology permit transmission of digital ECG data and rapid “online” computerized analysis of the data as they are acquired. C. Standard ECGs provide assessment of cardiac electrical events over a brief duration, usually while the patient is resting. D. Ambulatory ECG monitoring is typically used when a patient demonstrates symptoms as pain. E. Ambulatory ECGs provide assessment of cardiac electrical events over a brief duration, usually while the patient is resting. F. Ambulatory ECG monitoring is typically used when a patient demonstrates symptoms as chest pain, syncope (fainting) or near syncope, dizziness, and irregular heartbeats. G. Extending the ECG to allow assessment of cardiac electrical events while the patient is ambulating during normal daily activities is called standard electrocardiography. H. Ambulatory ECG monitoring is typically used when a patient demonstrates symptoms that are thought to be caused by transient arrhythmias or other transient cardiac abnormalities. I. Standard ECGs provide assessment of cardiac electrical events more than 24 hours. J. Extending the ECG to allow assessment of cardiac electrical events while the patient is ambulating during normal daily activities is not possible. 306. Indicate the correct correlation(s): A. Left ventricular hypertrophy → C B. Normal ECG → B C. Right ventricular hypertrophy → D D. Right bundle branch block → E E. Normal ECG → A F. Right bundle branch block → A G. Left bundle branch block → C H. Right ventricular hypertrophy → E I. Left ventricular hypertrophy → B J. Left bundle branch block → D 307. Indicate the correct correlation(s): A. Normal axis orientation→ A B. Normal axis orientation→ E C. Right axis orientation because right bundle branch block→ B D. Right axis orientation because right ventricular hypertrophy → C E. Right axis orientation because right bundle branch block → A F. G. H. I. J. Left axis orientation because left axis orientation → D Left axis orientation because left axis orientation → C Left axis orientation because left bundle branch block → B Right axis orientation because right ventricular hypertrophy → D Left axis orientation because left bundle branch block → E 308. Indicate the correct statement(s) about the mean vector through the partially depolarized ventricles: A. When the vector extends straight upward, it has a direction of 0 degrees. B. When the vector extends from the person’s left to right, it has a direction of +180 degrees C. When the vector extends straight upward, it has a direction of −90 degrees. D. When the vector extends from above and straight downward, it has a direction of +180 degrees. E. Most of the depolarization wave of the ventricles, the base of the heart remains positive with respect to the apex of the heart. F. In a normal heart, the mean QRS vector, is about +59 degrees. G. When a vector is exactly horizontal and directed toward the person’s left side, the vector is said to extend in the direction of 0 degrees. H. When a vector is exactly horizontal and directed toward the person’s left side, the vector is said to extend in the direction of +90 degrees. I. When the vector extends from above and straight downward, it has a direction of +90 degrees J. When the vector extends from the person’s left to right, it has a direction of +270 degrees. 309. In the hexagonal reference system, the directions of the leads are: A. Lead aVL has an axis of about +30 degrees B. Lead I has an axis of about +90 degrees C. Lead I has an axis of about 0 degrees D. Lead aVL has an axis of about -30 degrees E. Lead II has an axis of about +60 degrees F. Lead III has an axis of about +120 degrees G. Lead aVF has an axis of about +90 degrees H. Lead II has an axis of about +120 degrees I. Lead II has an axis of about +50 degrees J. Lead aVR has an axis of about +90 degrees 310. Electrocardiogram during repolarization—the T wave: A. The positive end of the overall ventricular vector during repolarization is toward the apex of the heart. B. The normal T wave in all three bipolar limb leads is positive. C. The greatest portion of ventricular muscle mass to repolarize first is the subendocardial myocardium. D. The outer apical surfaces of the ventricles repolarize before the inner surfaces E. The high blood pressure inside the ventricles during contraction greatly reduces coronary blood flow to the epicardium slowing depolarization near the apex of the heart. F. The greatest portion of ventricular muscle mass to repolarize first is the entire outer surface of the ventricles, especially near the apex of the heart. G. The positive end of the overall ventricular vector during repolarization is toward the base of the heart. H. The inner apical surfaces of the ventricles repolarize before the outer surfaces I. The high blood pressure inside the ventricles during contraction greatly reduces coronary blood flow to the endocardium slowing repolarization in the endocardial areas. J. The normal T wave in all three bipolar limb leads is negative. 311. Change in the position of the heart in the chest could change the orientation of the mean QRS vector: A. Shift to the right occurs at the end of deep expiration. B. Shift to the left occurs at the end of deep inspiration. C. Shift to the right occurs normally in tall people. D. Shift to the left occurs when a person lies down. E. Shift to the left occurs at the end of deep expiration. F. Shift to the left occurs quite frequently in obese people. G. Shift to the left occurs when a person stands up. H. Shift to the right occurs at the end of deep inspiration. I. Shift to the right occurs normally in obese people. J. Shift to the left occurs quite frequently in tall people. 312. The left axis deviation could occur when: A. The left ventricle hypertrophies as a result of aortic valvular stenosis B. The left ventricle hypertrophies as a result of congenital heart conditions in which the left ventricle enlarges while the right ventricle remains relatively normal in size C. The right ventricle hypertrophies as a result of tricuspid valvular regurgitation D. The left bundle branch is blocked E. The right ventricle hypertrophies as a result of interventricular septal defect F. The right ventricle hypertrophies as a result of congenital pulmonary valve stenosis G. The left ventricle hypertrophies as a result of hypertension H. The left ventricle hypertrophies as a result of aortic valvular regurgitation I. The right ventricle hypertrophies as a result of tetralogy of Fallot J. The right bundle branch is blocked 313. Decreased voltage of the electrocardiogram could be a result of: A. Pulmonary emphysema B. Bundle branch block C. Diminished myocardial mass D. At the end of deep expiration E. Pleural effusion F. When a person stands up G. A series of old myocardial infarctions H. Fluid in the pericardium I. Hypertrophy of the muscle J. Peritoneal effusion 314. Current of injury: A. Flows between the pathologically depolarized and the normally polarized areas, even between heartbeats B. Could be caused by infectious processes that damage the muscle membranes C. Has maximum intensity when the heart becomes totally depolarized D. Could appears in the ECG during an attack of severe angina pectoris E. The negative end of the injury potential vector points toward the normal cardiac muscle. F. Never appears after acute coronary thrombosis G. Could be caused by mechanical trauma H. Stops during the T-P interval I. Could be caused by ischemia of local areas of heart muscle J. Flows from the diseased ventricles to normal atria 315. Abnormalities in the T wave – indicate the correct statement(s): A. One means for detecting mild coronary insufficiency is to have the patient exercise and to record the ECG, noting whether changes occur in the T waves. B. The recording of positive T waves in limb leads when the patient exercise is abnormal. C. The T wave is normally negative in all the standard bipolar limb leads. D. Shortening of depolarization of cardiac muscle could be produced by decreasing current flow through the potassium channels. E. The T wave becomes abnormal when the normal sequence of repolarization does not occur F. Mild ischemia causes shortening of depolarization of cardiac muscle that can cause T-wave abnormalities. G. Changes in the T wave during digitalis administration are often the earliest signs of digitalis toxicity. H. If the base of the ventricles would repolarize ahead of the apex the T wave in all three standard leads would be positive. I. The ischemia might result from relative coronary insufficiency that occurs during resting state. J. When conduction of the depolarization impulse through the ventricles is greatly delayed, the T wave is almost always of opposite polarity to that of the QRS complex. 316. Analyze the ECG strips (limb leads) from figure and indicate the correct correlation(s): A. Atrial fibrillation → C B. Sinus bradycardia → A C. Cardiac arrest → A D. Atrial premature beat → D E. Atrial fibrillation → E F. Sinus rhythm → B G. Ventricular tachycardia → D H. Sinus tachycardia → C I. Sinoatrial nodal block → D J. Ventricular fibrillation → E 317. Analyze the ECG strips (limb leads) from figure and indicate the correct correlation(s): A. Sinoatrial block → D B. Ventricular fibrillation → B C. Atrial fibrillation → C D. Atrial fibrillation → B E. Sinus rhythm → C F. Complete atrioventricular block → D G. Sinus rhythm → E H. Electrical alternans → E I. Ventricular paroxysmal tachycardia → A J. Atrial paroxysmal tachycardia → A 318. Analyze the ECG strips (limb leads) from figure and indicate the correct correlation(s): A. Ventricular paroxysmal tachycardia → A B. Premature ventricular contractions → B C. Atrial paroxysmal tachycardia—onset in the middle of the record → A D. Second-degree atrioventricular block, showing a “dropped beat” → E E. Sinus rhythm → D F. Atrial fibrillation → B G. Cardiac arrest → E H. Ventricular fibrillation → D I. Atrioventricular nodal premature contraction → C J. Complete atrioventricular block → C 319. A. B. C. D. E. F. G. H. I. J. 320. A. B. C. D. E. F. G. H. I. J. 321. A. B. C. D. E. F. G. The causes of the cardiac arrhythmias are: Allowing to sinus node to be the pacemaker of the heart Having action potential conduction delayed in A-V node Abnormal pathways of impulse transmission through the heart Starting the atrial depolarization from S-A node Allowing the heart impulse to pass from atria to ventricle only by A-V bundle. Having the Purkinje fibers “overdriven” by the rapid sinus impulses Blocks at different points in the spread of the impulse through the heart Abnormal rhythmicity of the pacemaker Shift of the pacemaker from the sinus node to another place in the heart Spontaneous generation of spurious impulses in almost any part of the heart Some causes of tachycardia include: A-V block Weakening of the myocardium Toxic conditions of the heart Increased body temperature Vagal stimulation Severe blood loss The well-trained athlete’s heart Ventricular escape Stimulation of the heart by the sympathetic nerves Anesthesia Indicate the correct statement(s): The term “bradycardia” means a slow heart rate, usually defined as fewer than 100 beats/min. The heart rate increased and decreased no more than 5 percent during quiet respiration. In patients with carotid sinus syndrome, the baroreceptors in the carotid sinus region of the carotid artery walls are excessively sensitive. The term “tachycardia” means fast heart rate, which usually is defined as faster than 60 beats/min in an adult When the athlete is at rest, excessive quantities of blood pumped into the arterial tree with each beat initiate cause tachycardia. If body temperature increases more than 40.5°C, the heart rate may decrease because of progressive debility of the heart muscle because of the fever. Sinus arrhythmia can result from any one of many circulatory conditions that alter the strengths of the sympathetic and parasympathetic nerve signals to the heart sinus node. H. The well-trained athlete’s heart is often larger and considerably stronger than that of a normal person. I. The “respiratory” type of sinus arrhythmia, results mainly from “spillover” of signals from the medullary respiratory center into the heart. J. The heart rate increased and decreased by as much as 30 percent during quiet respiration. 322. Second-Degree Block: A. When there are “dropped beats” of the ventricles. B. When the action potential is sometimes strong enough to pass through the bundle into the ventricles and sometimes not strong enough to do so C. Is defined as a delay of conduction from the atria to the ventricles but without actual blockage of conduction. D. Means that the impulse from the sinus node is blocked before it enters the atrial muscle. E. When there will be an atrial P wave but no QRS-T wave. F. Appears when the conduction through the A-V bundle is depressed so much that conduction stops entirely. G. Could be caused by an abnormality of the bundle of His-Purkinje system. H. When conduction through the A-V bundle is slowed enough to increase the P-R interval to 0.25 to 0.45 second. I. Never require implantation of a pacemaker. J. When the P-R interval is prolonged 0.20 - 0.25 second. 323. Conditions that can either decrease the rate of impulse conduction in A-V bundle or block the impulse entirely are as follows: A. Fever B. Pain C. Ischemia of the A-V bundle D. The “respiratory” type of sinus arrhythmia E. Sympathetic reflex stimulation of the heart F. Extreme stimulation of the heart by the vagus nerves G. Ischemia of the A-V node H. Stimulation of the β1 adrenergic receptors of the heart I. Compression of the A-V bundle by scar tissue J. Inflammation of the A-V node or A-V bundle 324. Complete A-V Block (Third-Degree Block) features: A. The P waves become dissociated from the QRS-T complexes. B. The ventricles “escaped” from control by the atria and are beating at their own natural rate. C. The Purkinje system begins discharging rhythmically at a rate of 60 to 80 times per minute and acting as the pacemaker of the ventricles. D. There is no relation between the rhythm of the QRS complexes and that of the -T waves E. There is no relation between the rhythm of the left ventricle and that of right ventricle. F. There is no correlation with the Stokes-Adams syndrome. G. These patients do not need an artificial pacemaker H. After sudden cessation of A-V conduction the ventricles start their own beating following a delay as a result of overdrive suppression. I. C