chương 2, 3 màng TB, TK, cơ, tim

UNIT II Màng sinh lý học, thần kinh Đặc điểm sau mô tả rõ thay đổi thể tích tế bào xảy tế bào hồng cầu( cân 280 milliosmolar (mM) dung dịch NaCl) đặt 140 mM dung dịch NaCl chứa 20 mM urê, phân tử tương đối lớn xuyên qua ? A) Ban đầu, tế bào co lại, sau sưng tan rã B) Các tế bào co lại thời gian ngắn dần trở lại thể tích ban đầu C) Các tế bào sưng lên tan rã D) Các tế bào sưng lên thời gian ngắn dần trở lại thể tích ban đầu E) Khơng xảy thay đổi thể tích tế bào Nồng độ osmol đo dung dịch chứa 12 mM NaCl, mM KCl, mM CaCl2 ( đv mOsm/L) ? A) 16 B) 26 C) 29 D) 32 E) 38 F) 42 Câu 3-6: Nội bào (mM) 140 K+ Ngoại bào (mM) 14 K+ 10 Na+ 11 Cl− 10–4 Ca++ 100 Na+ 110 Cl− Ca++ Bảng mô tả nồng độ ion qua màng plasma ( huyết tương) tế bào mẫu Từ bảng này, trả lời câu hỏi sau : Điện cân cho Cl− qua màng tế bào ? A) mV B) 122 mV C) −122 mV D) 61 mV E) −61 mV Điện cân cho K+ qua màng tế bào ? A) mV B) 122 mV C) −122 mV D) 61 mV E) −61 mV Nếu điện màng tế bào – 80 mV lực đẩy lớn ion nào? A) Ca++ B) Cl− C) K+ D) Na+ Nếu có K+ xuyên qua tế bào hiệu việc giảm nồng độ ngoại bào K+ từ 14 xuống 1.4 mM là? A) 10 mV khử cực B) 10 mV ưu cực C) 122 mV depolarization (khử cực) D) 122 mV hyperpolarization (tăng phân cực) E) 61 mV depolarization F) 61 mV hyperpolarization Biểu đồ cho thấy mối quan hệ độ dài- độ căng đơn thể sarcomere (sợi cơ) ( Số liệu từ Gordon AM, Huxley AF, Julian FJ : Biểu đồ độ dài – độ căng nhóm sợi vân động vật có xương sống J Physiol 171:28P, 1964.) Tại độ căng đạt cao B C? A) Các sợi Actin nằm chống chéo lên B) Các sợi Myosin nằm chồng chéo lên C) Sợi Myosin chiều dài nhỏ D) Đĩa Z sợi nằm sát cuối sợi Myosin E) There is optimal overlap between the actin and myosin filaments F) There is minimal overlap between the actin and myosin filaments Khuếch tán đơn giản khuếch tán tăng cường có điểm chung là? A) Có thể bị chặn chất ức chế cụ thể B) Không cần ATP C) Cần protein vận chuyển D) Áp lực thẩm thấu E) Vận chuyển chất ngược chiều với gradient nồng độ Sự kích thích-co xương bao gồm trình trừ? A) Thủy phân ATP B) Gắn Ca++ với calmodulin C) Thay đổi cấu trúc thụ thể Dihydropyridine D) Khử cực màng ngang tubule (T tubule) E) Tăng độ dẫn Na+ màng sợi vân 10 A single contraction of skeletal muscle is most likely to be terminated by which of the following Độ co xương bị chấm dứt hoạt động sau đây? A) Closure of the postsynaptic nicotinic acetylcholine receptor ( Đóng thụ thể acetylcholine nicotinic sau sysnap.) B) Removal of acetylcholine from the neuromuscular junction ( Loại bỏ acetylcholine khỏi khớp thần kinh) C) Removal of Ca++ from the terminal of the motor neuron( Loại bỏ Ca++ khỏi điểm cuối nơ ron vận động) D) Removal of sarcoplasmic Ca++ ( Loại bỏ tương Ca++) E) Return of the dihydropyridine receptor to its resting conformation ( Thụ thể dihydropyridine trở lại hình dạng nghỉ) 11 Which of the following statements about smooth muscle contraction is most accurate? Điều sau co trơn xác nhất?) A) Ca++ independent ( Độc lập với Ca++) B) Does not require an action potential ( không yêu cầu Điện hoạt động) C) Requires more energy compared to skeletal muscle( yêu cầu nhiều lượng so với xương) D) Shorter in duration compared to skeletal muscle( Ít bền sơ với xương) 12 Which of the following best describes an attribute of visceral smooth muscle not shared by skeletal muscle? Điều sau mơ tả tốt thuộc tích trơn nội tạng mà khơng có xương A) Contraction is ATP dependent ( Co phụ thuộc ATP) B) Contracts in response to stretch ( Co lại tương tác với dãn)* C) Does not contain actin filaments ( Không chứa sợi Actin) D) High rate of cross-bridge cycling ( Tỉ lệ cao chu trình nối cầu) E) Low maximal force of contraction ( Lực co tối đa thấp) 13 The resting potential of a myelinated nerve fiber is primarily dependent on the concentration gradient of which of the following ions? Điện nghỉ sợi thần kinh có bao Miê-lin phụ thuộc vào nồng độ gradient ions sau đây? A) Ca++ B) Cl− C) HCO3− D) K+ E) Na+ 14 Calmodulin is most closely related, both structurally and functionally, to which of the following proteins? Calmodulin liên quan chặt chẽ nhất, cấu trúc lẫn chức năng, với proteins sau đây? A) G-actin B) Myosin light chain ( Myosin chuỗi nhẹ) C) Tropomyosin D) Troponin C 15 Which of the following is a consequence of myelination in large nerve fibers? Kết Miê-lin hóa sợi thần kinh lớn là? A) Decreased velocity of nerve impulses ( vận tốc xung thần kinh giảm) B) Generation of action potentials only at the nodes of Ranvier (hình thành điện đốt Ranvier) C) Increased energy requirement to maintain ion gradients ( Tăng lượng cần thiết để trì ion gradient) D) Increased membrane capacitance ( Tăng thể tích màng) E) Increased nonselective diffusion of ions across the axon membrane ( Tăng khuếch tán ko chọn lọc ions qua màng axon) 16 During a demonstration for medical students, a neurologist uses magnetic cortical stimulation to trigger firing of the ulnar nerve in a volunteer At relatively low-amplitude stimulation, action potentials are recorded only from muscle fibers in the index finger As the amplitude of the stimulation is increased,action potentials are recorded from muscle fibers in both the index finger and the biceps muscle What is the fundamental principle underlying this amplitude-dependent response? Trong chứng minh cho sinh viên Y Khoa, nhà thần kinh học dùng kích thích từ tính vỏ não để kích hoạt việc bắn dây thần kinh trụ tình nguyện viên Ở kích thích biên độ tương đối thấp, điện động ghi nhận từ sợi ngón trỏ Khi biên độ kích thích tăng, điện động ghi nhận sợi ngón trỏ bắp tay Nguyên tắc phản ứng phụ thuộc biên độ gì?) A) Large motor neurons that innervate large motor units require a larger depolarizing stimulus ( Các nơ ron vận động lớn mà phân bố thần kinh đơn vị vận động lớn địi hỏi kích thích khử cực lớn hơn.) B) Recruitment of multiple motor units requires a larger depolarizing stimulus ( Sự bổ sung lượng lớn đơn vị vận động địi hỏi kích thích khử cực lớn hơn) C) The biceps muscle is innervated by more motor neurons ( Cơ bắp tay phân bố thần kinh nhiều nơ ron vận động hơn) D) The motor units in the biceps are smaller than those in the muscles of the fingers (Các đơn vị vận động bắp tay nhỏ so với ngón tay) E) The muscles in the fingers are innervated only by the ulnar nerve ( Các bắp ngón tay phân bố thần kinh dây thần kinh trụ) 17 Similarities between smooth and cardiac muscle include which of the following? Sư tương đồng trơn tim là? A) Ability to contract in the absence of an action potential ( Khả co lại thiếu điện B) Dependence of contraction on Ca++ ions ( Sự co phụ thuộc vào ion Ca++) C) Presence of a T tubule network ( Sự diện mạng lưới T Tubule) D) Role of myosin kinase in muscle contraction ( Vai trò myosin kinase co cơ) E) Striated arrangement of the actin and myosin filaments ( Sự xếp vân sợi Actin Myosin) 18 In a normal, healthy muscle, what occurs as a result of propagation of an action potential to the terminal membrane of a motor neuron? Ở bình thường khỏe mạnh,điều xảy kết phát tán Điện hoạt động tới màng cuối nơ ron vận động?) A) Opening of voltage-gated Ca++ channels in the presynaptic membrane ( Mở kênh điện Ca++ màng trước synaptic.) B) Depolarization of the T tubule membrane follows ( Khử cực màng T tubule theo sau) C) Always results in muscle contraction ( Ln ln có kết tượng co ) D) Increase in intracellular Ca++ concentration in the motor neuron terminal ( Tăng nồng độ nội bào Ca++ cuối nơ ron vận động) E) All of the above are correct ( Tất điều đúng) 19 Which of the following decreases in length during the contraction of a skeletal muscle fiber? ( Cái sau giảm độ dài suốt trình co sợi xương?) A) A band of the sarcomere ( bó vân) Sarcomere: đơn vị co vân * B) I band of the sarcomere ( I bó vân) C) Thick filaments ( Sợi dày) D) Thin filaments ( Sợi mỏng) E) Z discs of the sarcomere ( Các đĩa Z sarcomere) 20 A cross-sectional view of a skeletal muscle fiber through the H zone would reveal the presence of what? hình ảnh mặt cắt sợi xương qua khu H có ? A) Actin and titin B) Actin, but no myosin ( Actin, ko có myosin) C) Actin, myosin, and titin D) Myosin and actin E) Myosin, but no actin ( Myosin, ko có actin) 21 Tetanic contraction of a skeletal muscle fiber results from a cumulative increase in the intracellular concentration of which of the following? Chứng co cứng sợi xương kết từ gia tăng tích lũy nồng độ nội bào sau đây? A) ATP B) Ca++ C) K+ D) Na+ E) Troponin 22 Malignant hyperthermia is a potentially fatal genetic disorder characterized by a hyperresponsiveness to inhaled anesthetics and results in elevated body temperature, skeletal muscle rigidity, and lactic acidosis Which of the following molecular changes could account for these clinical manifestations? Cao huyết áp ác tính rối loạn di truyền gây chết người, đặc trưng tăng phản ứng với thuốc tê dạng hít gây tăng nhiệt độ thể, độ cứng xương a xít lactic Thay đổi phân tử sau giải thích biểu lâm sang trên? A) Decreased voltage sensitivity of the dihydropyridine receptor ( Giảm độ nhạy điện áp thụ thể dihydropyridine) B) Enhanced activity of the sarcoplasmic reticulum Ca++-ATPase ( Tăng cường hoạt động lưới tương Ca++ - ATP) C) Prolonged opening of the ryanodine receptor channel ( Kéo dài việc mở kênh thụ thể ryanodine) D) Reduction in the density of voltage-sensitive Na+ channels in the T tubule membrane ( Giảm độ kênh nhạy điện áp Na+ màng T tubule) 23 Weightlifting can result in a dramatic increase in skeletal muscle mass This increase in muscle mass is primarily attributable to which of the following? Nâng tạ gây tăng lên đáng kể xương Việc tăng chủ yếu do? A) Fusion of sarcomeres between adjacent myofibrils( Sự dính liền sarcomere sợi nguyên cơ-sợi tơ cơ) B) Hypertrophy of individual muscle fibers ( Sự phì đại sợi đơn lẻ) C) Increase in skeletal muscle blood supply ( Tăng nguồn cung máu cho xương) D) Increase in the number of motor neurons ( Tăng số lượng nơ ron vận động) E) Increase in the number of neuromuscular junctions ( tăng số lượng khớp thần kinh 24 Which of the following transport mechanisms is not rate limited by an intrinsic Vmax? Cái chế vận chuyển ko bị giới hạn Vmax nội tại? A) Facilitated diffusion via carrier proteins ( Khuếch tán tăng cường thông qua protein vận chuyển) B) Primary active transport via carrier proteins ( Vận chuyển tích cực( vận chuyển vật chất qua màng tế bào ngược với gradient nồng độ) qua protein vận chuyển) C) Secondary co-transport ( Đồng vận chuyển thứ phát D) Secondary counter-transport ( Phản vận chuyển thứ phát) E) Simple diffusion through protein channels ( Khuếch tán đơn giản qua kênh protein) 25 Assuming complete dissociation of all solutes, which of the following solutions would be hyperosmotic relative to millimolar NaCl? Giả sử phân ly hoàn toàn tất dung dịch , dung dịch sau tăng độ thẩm thấu tương ứng với mM NaCl?) A) millimolar CaCl2 B) millimolar glucose C) millimolar KCl D) millimolar sucrose E) 1.5 millimolar glucose Questions 26 and 27 The diagram shows the change in membrane potential during an action potential in a giant squid axon Refer to it when answering the next two questions Biểu đồ cho thấy thay đổi điện màng điện hoạt động loài mực ống khổng lồ Dựa vào bảng để trả lời câu hỏi sau 26 Which of the following is primarily responsible for the change in membrane potential between points B and D? Điều sau chịu trách nhiệm cho thay đổi điện màng điểm B D A) Inhibition of the Na+, K+-ATPase ( Sự ức chế Na+, K+ - ATP) B) Movement of K+ into the cell ( Chuyển K+ vào bên tế bào) C) Movement of K+ out of the cell ( Chuyển K+ khỏi tế bào) D) Movement of Na+ into the cell ( Chuyển Na+ vào tế bào) E) Movement of Na+ out of the cell ( Chuyển Na+ khỏi tế bào) 27 Which of the following is primarily responsible for the change in membrane potential between points D and E? 14.E) The normal plateau level of the cardiac output function curve is 13 L/min This level decreases in any kind of cardiac failure and increases markedly during sympathetic stimulation TMP12 111 15.E) As seen in Chapter 9, the first heart sound by definition occurs just after the ventricular pressure exceeds the atrial pressure This causes the A-V valves to mechanically close The second heart sound occurs when the aortic and pulmonary valves close TMP12 105 16.D) The increase in potassium permeability causes a hyperpolarization of the A-V node, and this will decrease the heart rate Increases in sodium permeability will actually partially depolarize the A-V node, and an increase in norepinephrine levels increases the heart rate TMP12 102 17.D) Increased sympathetic stimulation of the heart increases heart rate, atrial contractility, and ventricular contractility and also increases norepinephrine release at the ventricular sympathetic nerve endings It does not release acetylcholine It does cause an increased sodium permeability of the A-V node, which increases the rate of upward drift of the membrane potential to the threshold level for selfexcitation, thus increasing heart rate TMP12 111 and 120 18.D) The impulse from the S-A node travels rapidly through the internodal pathways and arrives at the A-V node at 0.03 sec, at the A-V bundle at 0.12 sec and at the ventricular septum at 0.16 sec The total delay is thus 0.13 sec TMP12 118 19.D) During sympathetic stimulation, the permeabilities of the S-A node and the A-V node increase Also, the permeability of cardiac muscle to calcium increases resulting in an increased contractile strength In addition, there is an upward drift of the resting membrane potential of the S-A node Increased permeability of the S-A node to potassium does not occur during sympathetic stimulation TMP12 120 20.C) The atrial and ventricular muscles have a relatively rapid rate of conduction of the cardiac action potential, and the anterior internodal pathway also has fairly rapid conduction of the impulse However, the A-V bundle myofibrils have a slow rate of conduction because their sizes are considerably smaller than the sizes of the normal atrial and ventricular muscle Also, their slow conduction is partly caused by diminished numbers of gap junctions between successive muscle cells in the conducting pathway, causing a great resistance to conduction of the excitatory ions from one cell to the next TMP12 117 21.A) After the S-A node discharges, the action potential travels through the atria, through the A-V bundle system and finally to the ventricular septum and throughout the ventricle The last place that the impulse arrives is at the epicardial surface at the base of the left ventricle, which requires a transit time of 0.22 sec TMP12 118 22.D) The action potential arrives at the A-V bundle at 0.12 sec It arrives at the A-V node at 0.03 sec and is delayed 0.09 sec in the A-V node, which results in an arrival time at the bundle of His of 0.12 sec TMP12 118 23.D) Increases in sodium and calcium permeability at the S-A node result in an increased heart rate An increased potassium permeability causes a hyperpolarization of the S-A node, which causes the heart rate to decrease TMP12 120 24.A) Acetylcholine does not depolarize the A-V node or increase permeability of the cardiac muscle to calcium ions but causes hyperpolarization of the S-A node and the A-V node by increasing permeability to potassium ions This results in a decreased heart rate TMP12 120 25.A) The normal resting membrane potential of the S-A node is −55 mV As the sodium leaks into the membrane an upward drift of the membrane potential occurs until it reaches −40 mV This is the threshold level that initiates the action potential at the S-A node TMP12 116 26.D) An increase in potassium permeability causes a decrease in the membrane potential of the A-V node Thus, it will be extremely hyperpolarized, making it much more difficult for the membrane potential to reach its threshold level for conduction This results in a decrease in heart rate Increases in sodium and calcium permeability and norepinephrine levels increase the membrane potential, causing a tendency to increase the heart rate TMP12 120 27.A) If there is a failure in conduction of the S-A nodal impulse to the A-V node or if the S-A node stops firing, the A-V node will take over as the pacemaker of the heart The intrinsic rhythmical rate of the A-V node is 40 to 60 times per minute If the Purkinje fibers take over as pacemakers, the heart rate will be between 15 and 40 beats/min TMP12 119 28.D) The impulse coming from the S-A node to the A-V node arrives at 0.03 sec Then there is a total delay of 0.13 sec in the A-V node and bundle system allowing the impulse to arrive at the ventricular septum at 0.16 sec TMP12 118 29.D) The resting membrane potential of the sinus nodal fibers is −55 mV, and this is in contrast with the −85 to −90 mV membrane potential of cardiac muscle Other major differences between the sinus nodal fibers and ventricular muscle fibers are that the sinus fibers exhibit self-excitation from inward leaking of sodium ions TMP12 116 30.A) If the Purkinje fibers are the pacemaker of the heart, the heart rate ranges between 15 and 40 beats/min In contrast, the rate of firing of the A-V nodal fibers are 40 to 60 times a minute, and the sinus node fires at 70 to 80 times per minute If the sinus node is blocked for some reason, the A-V node will take over as the pacemaker; and if the A-V node is blocked, the Purkinje fibers will take over as the pacemaker of the heart TMP12 119 31.E) Sympathetic stimulation of the heart normally causes an increased heart rate, increased rate of conduction of the cardiac impulse and increased force of contraction in the atria and ventricles However, it does not cause acetylcholine release at the sympathetic endings because they contain norepinephrine Parasympathetic stimulation causes acetylcholine release The sympathetic nervous system firing increases the permeability of the cardiac muscle fibers, the S-A node, and the A-V node to sodium and calcium TMP12 120 32.A) By convention, the left arm is the positive electrode for lead I of an EKG TMP12 125 33.A) By convention, the left arm is the positive electrode for lead aVL of an EKG TMP12 126 34.E) The contraction of the ventricles lasts almost from the beginning of the Q wave and continues to the end of the T wave This interval is called the Q-T interval and ordinarily lasts about 0.35 sec In this particular example the Q-T interval is a little bit longer than average and equals 0.40 sec TMP12 123 35.B) The heart rate can be calculated by 60 divided by the R-R interval, which is 0.86 sec This results in a heart rate of 70 beats/min TMP12 121, 123 36.E) The contraction of the ventricles lasts almost from the beginning of the Q wave and continues to the end of the T wave This interval is called the Q-T interval and ordinarily lasts about 0.35 sec TMP12 123 37.B) By convention, the left leg is the positive electrode for lead II of an EKG TMP12 125 38.A) By convention, the left arm is the negative electrode for lead III of an EKG TMP12 125 39.D) Einthoven’s law states that the voltage in lead I plus the voltage in lead III is equal to the voltage in lead II, which in this case is 2.0 mV TMP12 125 40.E) As can be seen in Figure 12-3 (TMP12), the positive portion of lead aVF has an axis of 90° and the negative part of this lead has an axis of −90° Note the difference between the positive and the negative ends of this vector is 180° TMP12 130 41.B) The mean electrical axis can be determined plotting the resultant voltage of the QRS for leads I, II, and III The result is as is shown above and has a value of −50° TMP12 134 42.A) The heart rate can be calculated by 60 divided by the R-R interval, which is 0.68 sec This results in a heart rate of 88 beats/min TMP12 123 43.B) Note in Figure 12-14 (TMP12), which is shown above, that there is a QRS width greater than 0.12 sec This indicates a bundle branch block There is also a left axis deviation, which is consistent with a left bundle branch block TMP12 136 44.E) Systemic hypertension results in a left axis deviation because of the enlargement of the left ventricle Aortic valve stenosis and aortic valve regurgitation also result in a large left ventricle and left axis deviation Excessive abdominal fat, because of the mechanical pressure of the fat, causes a rotation of the heart to the left resulting in a leftward shift of the mean electrical axis Pulmonary hypertension causes enlargement of the right heart and thus causes right axis deviation TMP12 136 45.D) Lead II has a positive vector at the 60° angle The positive end of lead II is at −120° TMP12 130 46.D) Note that lead III has the strongest vector, therefore the mean electrical axis will be closer to this lead than to leads I or II The angle of lead III is 120°, and the resultant vector (mean electrical axis) is close to that lead and has a value of +105° TMP12 134 47.D) The diagnosis is right bundle branch block This can be determined by a rightward shift in mean electrical axis as well as the greatly prolonged QRS complex In right ventricular hypertrophy, the QRS complex is only moderately prolonged TMP12 137 48.D) The patient has a left axis deviation because of the large negative deflection of the R wave in lead III Also, her T wave was inverted in lead I, which means that it is in the opposite direction of the QRS complex This is characteristic of bundle branch block Also, the QRS complex had a width of 0.20 sec, a very prolonged QRS complex A QRS complex that has a width greater than 0.12 sec is normally caused by a conduction block All these factors indicate that this patient has a left bundle branch block TMP12 136 49.A) This patient has an acute anterior infarction in the left ventricle of the heart This can be determined by plotting the currents of injury from the different leads The limb leads are used to determine whether the infarction is coming from the left or right side of the heart and from the base or apex of the heart The chest leads are used to determine whether it is an anterior or posterior infarct When we analyze the currents of injury, a negative potential, caused by the current of injury, occurs in lead I and a positive potential, caused by the current of injury, occurs in lead III This is determined by subtracting the J point from the TP segment The negative end of the resultant vector originates in the ischemic area, which is therefore the left side of the heart In lead V2, the chest lead, the electrode is in a field of very negative potential, which occurs in patients with an anterior lesion TMP12 140 50.A) Since the deflection in this EKG is in lead I, the axis has to be 90° away from this lead Therefore, the mean electrical axis has to be +90° or −90° Since the aVF lead has a positive deflection, the mean electrical axis must be at +90° TMP12 134 51.A) At the J point the entire heart is depolarized in a patient with a damaged cardiac muscle or a patient with a normal cardiac muscle The area of the heart that is damaged will not repolarize, but remains depolarized at all times TMP12 139 52.A) Note that the QRS complex has a positive deflection in lead I and a negative in lead III, which indicates that there is a leftward axis deviation This occurs during chronic systemic hypertension Pulmonary hypertension increases the ventricular mass on the right side of the heart, which gives a right axis deviation TMP12 13 53.D) The QRS wave plotted on lead I was −1.2 mV and lead II was +1.2 mV so the absolute value of the deflections were the same Therefore, the mean electrical axis has to be exactly halfway in between these two leads, which is halfway between the lead II axis of 60° and the lead I negative axis of 180°, resulting in a value of 120° TMP12 134 54.D) A QRS axis of 120° indicates a rightward shift Since the QRS complex is 0.18 sec, this indicates a conduction block Therefore, this EKG, which fits with these characteristics, is a right bundle branch block TMP12 137 55.B) The EKG from this patient has a positive deflection in aVF and a negative deflection in standard limb lead I Therefore, the mean electrical axis is between 90° and 180°, which is a rightward shift in the EKG mean electrical axis Systemic hypertension, aortic valve stenosis, and aortic valve regurgitation cause hypertrophy of the left ventricle and thus a leftward shift in the mean electrical axis Pulmonary hypertension causes a rightward shift in the axis, and is therefore characterized by this EKG TMP12 136 56.D) Note in the following figure that the current of injury is plotted on the graph at the bottom This is not a plot of the QRS voltages but the current of injury voltages They are plotted for leads II and III, which are both negative, and the resultant vector is nearly vertical The negative end of the vector points to where the current of injury originated, which is in the apex of the heart The elevation of the TP segment above the J point indicates a posterior lesion Therefore, the EKG is consistent with acute posterior infarction in the apex of the heart TMP12 140 57.D) When a patient has no P waves and a low heart rate, it is likely that the impulse leaving the sinus node is totally blocked before entering the atrial muscle This is called sinoatrial block The ventricles pick up the new rhythm usually initiated in the A-V node at this point, which results in a heart rate of 40 to 60 beats/min In contrast, during sinus bradycardia you still have P waves associated with each QRS complex In first-, second-, and third-degree heart block, you have P waves in each of these instances, although some are not associated with QRS complex TMP12 144 58.C) Atrial fibrillation has a rapid irregular heart rate The P waves are missing or are very weak The atria exhibit circus movements, and atrial volume is often increased, causing the atrial fibrillation TMP12 151–152 59.A) Circus movements occur in ventricular muscle particularly if you have a dilated heart or decreases in conduction velocity High extracellular potassium and sympathetic stimulation, not parasympathetic stimulation, increase the tendency for circus movements A longer refractory period tends to prevent circus movements of the heart, because when the impulses travel around the heart and contact the area of ventricular muscle that has a longer refractory period, the action potential stops at this point TMP12 150 60.B) A sudden onset of A-V block that comes and goes is called the Stokes-Adams syndrome The patient depicted here has about 75 P-waves/min, which means that the atria are contracting normally But the A-V block that occurs allows only 35 QRS waves to occur each minute TMP12 145 61.D) By definition, first-degree A-V heart block occurs when the P-R interval exceeds a value of 0.20 sec, but without any dropped QRS waves In the following figure, the P-R interval is about 0.30 sec, which is considerably prolonged However, there are no dropped QRS waves During second-degree AV block or thirddegree A-V block, QRS waves are dropped TMP12 144 62.E) Note that the premature ventricular contractions (PVCs) have wide and tall QRS waves in the EKG The mean electrical axis of the premature contraction can be determined by plotting these large QRS complexes on the standard limb leads The PVC originates at the negative end of the resultant mean electrical axis, which is at the base of the ventricle Note that the QRS of the PVC is wider and much taller than the normal QRS waves in this EKG TMP12 147 63.B) This patient has atrial flutter characterized by several P waves for each QRS complex In this EKG, you see some areas that have two P waves for every QRS and other areas that have three P waves for each QRS Note the rapid heart rate, which is characteristic of atrial flutter, and the irregular R-R intervals TMP12 152 64.E) The average ventricular rate is 120 beats/min in this EKG, which is typical of atrial flutter Once again, note that the heart rate is irregular due to the inability of the impulses to quickly pass through the AV node because of its refractory period TMP12 123 65.A) Atrial fibrillation has a rapid irregular heart rate The P waves are missing or are very weak The atria exhibit circus movements, and often are very enlarged, causing the atrial fibrillation TMP12 151–152 66.C) Atrial fibrillation occurs often with patients with an atrial enlargement This causes an increased tendency for circus movements to occur The ventricular beat is irregular because impulses are rapidly arriving at the A-V node; however, many times the A-V node is in a refractory period Therefore the A-V node will not pass a second impulse until about 0.35 sec elapses after the previous one There is also a variable interval between when the atrial impulses reach the AV node This results in a very irregular heartbeat but one that is very rapid with a rate of 125 to 150 beats/min TMP12 151–152 67.E) The term paroxysmal means that the heart rate becomes rapid in paroxysms, with the paroxysm beginning suddenly and lasting for a few seconds, a few minutes, a few hours, or much longer Then the paroxysm usually ends as suddenly as it began and the pacemaker shifts back to the S-A node The mechanism by which this is believed to occur is by a re-entrant circus movement feedback pathway that sets up an area of local repeated self-re-excitation The EKG shown is ventricular paroxysmal tachycardia That the origin is in the ventricles can be determined because of the changes in the QRS complex that have high voltages and look much different than the preceding normal QRS complexes This is very characteristic of a ventricular irritable locus TMP12 149 68.C) Note in this EKG that a P wave precedes each of the first four QRS complexes After that we see a P wave but a dropped QRS wave This is characteristic of second-degree A-V block TMP12 145 69.B) A dilated heart increases the risk of occurrence of ventricular fibrillation because of an increase in likelihood of circus movements Also, if the conduction velocity decreases, it will take longer for the impulse to travel around the heart, which decreases the risk of ventricular fibrillation Exposure of the heart to 60-cycle alternating current or epinephrine administration increases the irritability of the heart If the refractory period is long, the likelihood of the re-entrant type of pathways decreases, because when the impulse travels around the heart, the ventricles remain in a refractory period TMP12 149 70.A) The risk of occurrence of ventricular fibrillation increases in a heart exposed to a 60-cycle alternating current A shortened ventricular refractory period and a decreased conduction through the heart muscle occur, which increases the probability of re-entrant pathways Therefore, when the electrical stimulus travels around the heart and reaches the ventricular muscle that was again initially stimulated, the risk of ventricular fibrillation increases if this muscle has a short refractory period TMP12 150 71.A) The heartbeat immediately following a premature atrial contraction weakens because the diastolic period is very short in this condition Therefore, the ventricular filling time is very short, and thus the stroke volume decreases The P wave is usually visible in this arrhythmia unless it coincides with the QRS complex The probability of these premature contractions increases in people with toxic irritation of the heart and local ischemic areas TMP12 146 72.E) The heart rate can be determined by 60 divided by the RR interval, which gives you a value of 150 beats/min This is tachycardia, defined as a heart rate greater than 100 beats/min TMP12 123 73.A) The relationship between the P waves and the QRS complexes appears to be normal and there are no missing beats Therefore, this patient has a sinus rhythm, and there is no heart block There is also no ST segment depression in this patient Since we have normal P and QRS and T waves, this condition is sinus tachycardia TMP12 143 74.B) During a Stokes-Adams syndrome attack total A-V block suddenly begins, and the duration of the block may be a few seconds or even several weeks The new pacemaker of the heart is distal to the point of blockade but is usually the A-V node or the A-V bundle TMP12 143 75.C) During atrial paroxysmal tachycardia the impulse is initiated by an ectopic focus somewhere in the atria If the point of initiation is near the A-V node the P wave travels backward toward the S-A node and then forward into the ventricles at the same time Therefore, the P wave will be inverted TMP12 146 76.A) This EKG has characteristics of atrial paroxysmal tachycardia This means the tachycardia may come and go at random times The basic shape of the QRS complex and its magnitude are virtually unchanged from the normal QRS complexes, which eliminates the possibility of ventricular paroxysmal tachycardia This EKG is not characteristic of atrial flutter since there is only one P wave for each QRS complex TMP12 148 77.E) First-, second-, and third-degree heart blocks as well as atrial paroxysmal tachycardia all have P waves in the EKG However, there are usually no evident P waves during atrial fibrillation, and the heart rate is irregular Therefore, this EKG is characteristic of atrial fibrillation TMP12 151-152 78.E) This patient’s heart rate is 40 beats/min, which can be determined by dividing 60 by the R-R interval This is characteristic of some type of A-V block TMP12 123 79.E) This EKG is characteristic of complete A-V block, which is also called third-degree A-V block The P waves seem to be totally dissociated from the QRS complexes, since sometimes there are three P waves and sometimes two P waves between QRS complexes First-degree A-V block causes a lengthened P-R interval, and second-degree A-V block has long P-R intervals with dropped beats However, this does not seem to be occurring in this EKG, since there is no relationship between the ORS waves and the P waves TMP12 145 ... ion qua màng plasma ( huyết tương) tế bào mẫu Từ bảng này, trả lời câu hỏi sau : Điện cân cho Cl− qua màng tế bào ? A) mV B) 122 mV C) −122 mV D) 61 mV E) −61 mV Điện cân cho K+ qua màng tế bào... K+của màng plasma) C) Increased plasma membrane Na+ permeability ( Tăng độ thấm với Na+ màng plasma ) D) Inhibition of the sarcoplasmic reticulum Ca++-ATPase ( Ức chế lưới tương Ca++ - ATP) E) Stimulation... AMP mạch vòng) Questions 30 and 31 The diagram illustrates the single isometric twitch characteristics of two skeletal muscles, A and B, inresponse to a depolarizing stimulus Refer to it when