The impulse initiated by the SA node travels along the con duction system and spreads out to excite the “working” atrial and ventricular muscle fibers, which are called con tractile fibers. The contractile fibers have a resting mem brane potential close to -90 mV. When they are brought to threshold by excitation in neighboring fibers, certain sodium ion (Na+) channels open very rapidly; these are called voltage-gated fast Na channels. This increase in membrane permeability allows an inflow of Na down its concentration gradient and produces a rapid depolarization
During the next phase, called the plateau, voltage-gated slow Ca channels open, allowing calcium ions (Ca**) to enter the cytosol. Some Ca passes through the sarco lemma (plasma membrane) from the extracellular fluid (which has a higher Ca concentration) while other Ca pours out of the sarcoplasmic reticulum within the fiber. The combined buildup of Na* and Ca in the cytosol maintains the depolarization for about 0.25 sec (250 msec),
By comparison, depolarization in a neuron or skeletal mus cle fiber lasts about 1 msec.
The next steps are similar in skeletal and cardiac muscle fibers. Ca binds to troponin, which allows the actin and myosin filaments to begin sliding past one another, and ten sion starts to develop. Substances that alter the movement of Ca through slow Ca channels influence the strength of heart contractions. Epinephrine, for example, increases con traction force by enhancing Ca inflow, Certain drugs, appropriately called calcium channel blockers, such as verapamil, reduce Ca inflow and diminish the strength of the heartbeat.
The repolarization (recovery of resting membrane potential) phase of the impulse in a cardiac muscle fiber resembles repolarization in other excitable tissues: after a delay (which is particularly prolonged in cardiac muscle), voltage-gated K channels open, and potassium ions (K) diffuse out along their concentration gradient. At the same time, the Na and Ca channels are closing, which slows and then almost stops further inflow of these two ions. As more K leaves the fiber and fewer Na and Ca* enter, the negative resting membrane potential (-90 mV) is restored and the muscle fiber relaxes.
In muscle, the refractory period is the time interval when a second contraction cannot be triggered. The refrac tory period of a cardiac fiber is longer than the contraction itself (Fig. 20.7). As a result, another contraction cannot begin until relaxation is well underway and tetanus (main tained contraction cannot occur. The advantage is apparent if you consider how the ventricles work. Their pumping function depends on alternating contraction, when they eject blood, and relaxation, when they refill. If tetanus could occur, blood flow would stop.
Impulse conduction through the heart generates electrical currents that can be detected at the surface of the body. A recording of the electrical changes that accompany each cardiac cycle (heartbeat) is called an electrocardiogram (e-lek’-tro-KAR-dē-7-gram), abbreviated either ECG or EKG (from the German word for heart, kardia). The ECG is a composite of action potentials produced by all the heart muscle fibers during each heartbeat. The instrument used to record the changes is an electrocardiograph. In clinical practice, the ECG is recorded by placing electrodes on the arms and legs (the limb leads) and at six positions on the chest. As the person lies still, the electrocardiograph amplif es the heart’s electrical activity and produces 12 dif ferent tracings from different combinations of limb and chest leads. This takes about a minute. Each limb and chest electrode records slightly different electrical activity because it is in a different position relative to the heart. By comparing these records with one another and with normal records, it is possible to determine
(1) if the conduction
The P-Q (PR) interval is measured from the beginning of the P wave to the beginning of the QRS complex. It rep- resents the conduction time from the beginning of atrial excitation to the beginning of ventricular excitation. The PQ interval is the time required for an impulse to travel through the atria, atrioventricular node, and the remaining fibers of the conduction system. In coronary artery disease and rheumatic fever, scar tissue may form in the heart. As the impulse detours around scar tissue, the P-Q interval lengthens.
The S-T segment begins at the end of the S wave and ends at the beginning of the T wave. It represents the time when the ventricular contractile fibers are fully depolarized, during the plateau phase of the impulse. The S-T segment is elevated (above the baseline) in acute myocardial infarction and depressed (below the baseline) when the heart muscle receives insufficient oxygen.
The T wave represents ventricular repolarization. It is flatter than normal when the heart muscle is receiving insufficient oxygen, for example, in coronary artery disease. It may be elevated in hyperkalemia (increased blood K level).
Sometimes it is necessary to evaluate the heart’s re sponse to the stress of physical exercise. Such a test is called a stress electrocardiogram, or stress test. It is based on the principle that narrowed coronary arteries may carry adequate oxygenated blood while a person is at rest, but during exercise will be unable to meet the heart’s Increased need for oxygen, creating changes that can be noted on an electrocardiogram. pathway is normal,
(2) if the heart is enlarged
(3) if certain regions are damaged. In a typical Lead II record (right arm to left leg three clearly recognizable waves accompany each heartbeat. The first, called the P wave, is a small upward wave. It represents atrial depolarization, which spreads from the SA node throughout both atria. About 0.1 sec after the P wave begins, the atria contract.
The second wave, called the QRS complex, begins as a downward deflection, continues as a large, upright, triangular wave, and ends as a downward wave. The QRS complex represents the onset of ventricular depolarization, the spread of the wave of electrical excitation through the ventricles. Shortly after the QRS complex begins, the ventricles start to contract. The third wave is a dome-shaped upward deflection called the T wave.
It indicates ventricular repolarization and occurs just before the ventricles start to relax. The T wave is smaller and more spread out than the QRS complex because repolarization occurs more slowly than depolarization. Usu ally, repolarization of the atria is not evident in an ECG because it is buried in the larger QRS complex.
In reading an electrocardiogram, it is important to note the size and timing of the waves. Larger P waves, for exam ple, indicate enlargement of an atrium, as may occur in mitral stenosis. In this condition, the mitral valve narrows, blood backs up into the left atrium, and there is expansion of the atrial wall. An enlarged Q wave may indicate a myocardial infarction (heart attack). An enlarged R wave generally indicates enlarged ventricles.