Different parts of the conduction system are capable of spontaneously discharging and generating action potentials. The part that discharges most frequently, however, determines the rate at which the heart beats and is termed the cardiac pacemaker. The atrial conduction system consists of the:

The ventricular conduction system consists of the bundle of His (BOH) and Purkinje system (◘ Fig. 17.2). The impulses after traversing the AV node travel to the BOH, which divides into a left bundle branch (LBB) and a right bundle branch (RBB) at the top of the interventricular septum. Anatomically, the AV node and BOH reside in the triangle of Koch, which is bordered by the coronary sinus, tendon of Todaro, and the TV septal leaflet. The LBB further divides into anterior and posterior fascicles, which extend to the base of the left papillary muscles. Fibers from the LBB and RBB then merge with the Purkinje system supplying all of the ventricular myocardium and this enables depolarization of ventricles in about 100 ms. Depolarization in the ventricles typically commences at the left side of the IVS, then moves across to the right side, followed by spread down the septum to the apex and culminates by returning along the ventricular walls to the AV groove.

The discharging cells that act as dominant pacemakers determine two things: the heart rate and the heart rhythm. The rate is usually determined by the rate of discharge while the rhythm is determined by which group of cells is acting as the dominant pacemaker. The SA node discharges at about 60–100 times/min in adults. As this is higher than what other cells discharge at, the SA node acts as the dominant pacemaker. This phenomenon is called cardiac overdrive suppression, wherein other cells fail to discharge in the presence of a more rapidly discharging focus. Tonic vagal discharge influences the SA node leading to a resting heart rate of about 75 beats/min. Fluctuations in parasympathetic output during respiration, especially deep breathing, lead to acceleration of heart rate during inspiration and deceleration during exhalation. This sinus arrhythmia is a normal phenomenon. If for some reason the SA node stops discharging, other cells in the conduction system, such as AV nodal cells and cells of the His Purkinje system, can take over the pacemaker function. However, these cells discharge at lower rates of 30–50 beats/min. AV nodal rhythm is generated by AV nodal cells, and ventricular escape rhythms are generated by the His Purkinje system. Myocardial cells can also act as pacemakers, but they discharge sporadically and usually lead to ectopic or extra beats. This mechanism allows the heart to have multiple fallback options in case the SA node fails due to disease or degeneration [1, 2, 5].

Ventricular myocardial cells and pacemaker cells have somewhat different electrical properties. Although both generate action potentials, the former group of cells produces a fast response action potential while the latter group demonstrates a slow response action potential. Myocardial cells have a resting membrane potential (RMP) of about −90 millivolts (mv), which is determined mainly by ion fluxes across the plasma membrane. Although K+ equilibrium potential predominantly determines the RMP, other ions such as Na+, Ca ²⁺, and Cl- play an important role in generation of the action potential. Cells are mechanically connected via intercalated discs and electrically connected through gap junctions. This allows them to act as a syncytium and ensures rapid spread of electrical impulses. Fast response action potentials have 5 phases that are generated as follows:

In contrast to the fast response action potential, the slow response action potential of pacemaker cells is characterized by a less steep Phase 0, absent Phase 1, shortening and merging of Phase 2 and 3 with repolarization occurring to firing levels (approximately −40 mV), and a Phase 4 that is characterized by spontaneous diastolic depolarization (◘ Fig. 17.3). Phase 4 in the SA node occurs predominantly due to a mixed cation current (Na + and K+). Because of its unusual activation following hyperpolarization, this channel has been termed the “funny” channel and the current I_f as the funny current. The membrane starts depolarizing because of the funny current, leading to activation of transient (T) and long (L) Ca ²⁺ channels, which generates a Ca ²⁺ influx leading to Phase 1. At the peak of the impulse, K + efflux ensues bringing about phase 3 or repolarization. When the membrane potential reaches firing levels, funny current kicks in and causes spontaneous diastolic depolarization during Phase 4, thereby ensuring automatic firing of pacemaker cells.

Action potentials generated at one region, tend to depolarize neighboring regions and as myocytes are electrically continuous; this leads to rapid spread of depolarization as an electrical signal through the heart [3, 4].

Now that we know how the heart generates and spreads an “electric” spark, let us see how this spark is translated into a contraction.

Unlike the excitatory and conducting cardiomyocytes, which function as electric generators, the primary role of contractile cardiomyocytes is to function as force generators. Both these cells are supported by extracellular connective tissue, which predominantly contains collagen, elastin, proteoglycans, and metalloproteinases. A group of cardiomyocytes supported by this distinct extracellular matrix network constitutes a myofiber.

Cardiomyocytes typically have an outer plasma membrane, called sarcolemma, that becomes highly specialized at the junction of adjoining cells to form intercalated discs (◘ Fig. 17.4). These bind adjacent cells in series and parallel, thereby creating a syncytium of cells. This enables mechanical coupling between cells and effective transmission of the force generated by the heart. Recall that electrical coupling between cells is provided by Gap junctions. The sarcolemma also invaginates into the cell to form an extensive tubular network called transverse tubules or T tubules.

Most of the contractile cardiomyocyte’s cell volume is made of myofibrils. The rest is made up of cytosol, mitochondria, nucleus, and sarcoplasmic reticulum (SR). Unlike skeletal muscle cells, cardiomyocytes have a high density of mitochondria and strategic positioning of SR in the vicinity of T tubules.

Myofibrils consist mainly of two types of contractile proteins: thin filament actin and thick filament myosin. These are arranged in a specific pattern to generate the basic unit of contraction: the sarcomere. The arrangement of sarcomeres in turn gives cardiac muscle a distinct striated appearance when examined under the electron microscope. This is due to differences in refractive properties of the elements. These striations are identified by letters and represent either specific lines or bands of refraction. Z lines (from the German word zuckung or twitch line), are dark lines present at regular intervals along the myofibril. For the sake of understanding, let us imagine the sarcomere to be a square, with two lateral pillars, a roof, and a base (◘ Fig. 17.5).

The “pillars” then represent the Z lines. Now imagine a line running through the center of this square. This is the M line, which anchors the myosin filaments. Actin filaments anchor onto Z lines via actinin and extend toward the M line, interdigitating with the myosin filaments. The region occupied by myosin filaments (with and without overlapping actin) is termed the A band (appears dark). The region occupied by actin filaments without any overlap with myosin, is called the I band (appears light). Z lines are connected to the sarcolemma via desmin. Scaffolding for the sarcomere is provided by the largest known protein, titin. Thus each sarcomere consists of two half I bands and 1 A band between 2 Z lines. Sliding of the thin filaments over the thick filaments generates contraction. Actual lengths of the filaments do not change; shortening is brought about by increasing overlap between the thin and thick filaments. This is represented by lengthening of A band and shortening of I band during contraction. The sarcomeres are arranged in series along the length of the cylindrical myofibril and adjacent sarcomeres are joined at the Z lines.

At rest, actin is covered by the troponin- tropomyosin complex. These are regulatory proteins that prevent myosin from binding to actin in the resting state. Troponin has three subunits: troponin C, which binds Ca ²⁺; troponin I, which inhibits muscle contraction; and troponin T, which binds the troponin complex to tropomyosin. The myosin protein has two heads attached to a long tail via a hinge. It rests in an extended position and is bound to a molecule of ATP.

The T tubule network is responsible for transmitting the electrical current or action potential to the myofibrils. The dihydropyridine receptors (DHPR) in the T tubules are activated by the action potential and being voltage gated L-type Ca ²⁺ channels cause an influx of Ca ²⁺ into the cell. This triggers the ryanodine receptors (RyR) in the SR, leading to Ca ²⁺ release from the SR and amplification of Ca ²⁺ concentration in the cytosol. This phenomenon is called calcium-induced calcium release.

The released Ca ²⁺ then binds troponin C, causing the troponin I-tropomyosin curtain to move and uncover the binding site on actin, thereby making it “available.” The myosin head can now interact with the “available” actin, leading to formation of a cross bridge. Cross bridge cycling in turn leads to an actual contraction. ATP bound to the myosin head gets hydrolyzed to ADP and energizes the myosin head. A conformational change occurs with release of ADP that causes the thin actin filament to move in relation to the thick myosin filament increasing their overlap, and producing a “power stroke.” The myosin head goes from a resting “extended” to an active “flexed” position, moving the actin molecule along. ATP binds to the free site on myosin, interrupting the myosin actin interaction. Rapid hydrolysis of ATP to ADP via myosin ATPase enzyme, leads to “re-extension” of the myosin head and return to the original state. This myosin head is then ready for interaction with the next “available” actin. This can be visualized as follows: Lay your left arm supine on a table with palm facing the ceiling such that your elbow and wrist are in a straight line. Now make a fist and bend your elbow, making a 120° angle between your arm and forearm. Place the palm of right hand on top of your left fist. Your left fist represents a myosin head, your left elbow is the hinge, and your right palm is an actin molecule. Flex your left elbow to bring your right hand/palm toward your left shoulder. That represents the myosin head moving the actin molecule. Now disengage your left fist from your right palm. Let your right palm stay at the level of the left shoulder and bring your left fist back to its extended 120° position. Your left fist is ready to “cross bridge” with another palm (ask a friend to lend one). This is how myosin moves actin. Two ATPs are required: one to energize the myosin head and other to disengage from actin.

This process is repetitive and depends only on the availability of Ca ²⁺ and ATP. Many myosin heads cycle almost simultaneously to produce gross muscle contraction. The sarcoplasmic or endoplasmic reticulum Ca ²⁺ ATPase (SERCA) is an ATP-dependent pump that moves cytosolic Ca ²⁺ back into the SR. Along with the Na + − Ca ²⁺ exchanger, it is responsible for the decrease in cytosolic Ca ²⁺. Calmodulin is one of the primary sensors of cytosolic Ca ²⁺. Fall in calcium levels restores the inhibitory function of the troponin-tropomyosin complex, ceasing the interaction between actin and myosin. This in turn leads to relaxation. Thus, both contraction and relaxation are ATP-dependent processes. SERCA activity is inhibited by the protein phospholamban. Once Ca ²⁺ enters back into the SR, it is stored bound to calsequestrin and calreticulin. These proteins release Ca ²⁺ when the next wave of action potential arrives. This entire process is called excitation-contraction coupling (◘ Fig. 17.6) and is responsible for the heart’s ability to act as a tireless electromechanical pump.

The cardiomyocyte also has cytoskeleton proteins: intermediate filaments, microtubules, and microfilaments. Intermediate filaments are important for mitochondrial function. Microtubules are important for cell transport mechanisms and microfilaments are important linking-anchoring proteins. Familial hypertrophic cardiomyopathy is a sarcomeric protein disease that arises from mutations in genes encoding myosin, actin, titin, tropomyosin, and troponins. Familial dilated cardiomyopathy, on the other hand, is a cytoskeleton protein disease arising from mutations in genes encoding actin, desmin, lamin, and sarcoglycan. [1–5]

Efficiency of contraction in the heart is achieved by precise timing of events during the cardiac cycle. The atria depolarize and repolarize before the ventricles. Thus at any given point of time, different parts of the heart are in different phases of depolarization and repolarization. These discrepancies are responsible for generating a fluctuating potential difference. Given that the heart is enclosed by conducting fluid, much like a battery suspended in saltwater, it generates an electrical field around it. This can be measured and displayed by appropriately placed electrodes as an electrocardiogram (ECG). The ECG is not a display of individual action potentials occurring in the myocytes; it represents the cumulative change in electrical activity over time. When the ECG is measured by electrodes placed on skin, it is typically referred to as surface ECG. Electric potentials, other than that generated by the heart, can interfere or influence the net potential measured at the level of the skin. Patients are usually instructed to breathe quietly and lay still while an ECG is being recorded to minimize interference from skeletal muscle potentials. In the perioperative setting, it is difficult to get a good ECG trace from patients who are shivering or when electrocautery is being used.

William Einthoven did pioneering work in the field of electrocardiography and was awarded the Nobel Prize in 1924. His hypothesis: The Einthoven’s triangle is used to obtain a surface ECG. According to the hypothesis, if a current source is placed in the center of an equilateral triangle, the sum of potential at the points of the triangle is zero at all times. Clinically this can be approximated by placing recording electrodes on both arms and the left leg. The heart then lies in the center of this imaginary triangle. If all these “active” electrodes are connected together, a fourth indifferent electrode with zero potential can be formulated. This indifferent electrode can hypothetically be thought to reside in the center of the triangle, just like the heart.

Two electrodes constitute a lead. Each lead has two ends: a positive potential end and either a negative or zero potential end. Current can therefore flow between an active and an indifferent electrode or between two active electrodes. The former is an example of a unipolar lead and the latter represents a bipolar lead.

There are three standard bipolar limb leads (I, II, and III) and nine unipolar leads. Originally only bipolar limb leads were used to generate a 3-lead ECG, but later with addition of nine unipolar leads (six chest leads: V1 to V6, and three augmented limb leads: aVL, aVR, and aVF), it was possible to obtain a 12-lead ECG.

In clinical practice, to generate a 12-lead ECG, 10 electrodes need to be placed on the skin as follows (◘ Fig. 17.7):

Standard limb leads would then be:

Intraoperatively, usually a 5-electrode system is used (◘ Fig. 17.8). This has the capability of monitoring standard limb leads I, II, III; the augmented limb leads aVR, aVL, and aVF; and 1 precordial limb lead (typically V5). Monitors in the operating room, however, generally display only two of these seven possible leads. Commonly, leads II and V5 are displayed, as this combination allows the clinician to diagnose arrhythmias and ischemia optimally. The monitor can be configured to display any of the aforementioned seven leads. To yield accurate information, it is imperative that the clinician places the leads in recommended anatomical positions. Ideally, the right arm, left arm, and left leg electrodes should be equidistant from the heart to accurately reflect the electrical axis of the heart.

By convention, an upward deflection on the ECG trace occurs when the active electrode becomes positive, whereas a downward deflection is generated when the active electrode becomes negative. The wave of depolarization moves from the SA node to the rest of the heart in multiple directions, but these can be summated to present a single electrical vector. The way the different leads are positioned to this vector determines if they record positive or negative deflections. These deflections give rise to the waves, segments, and intervals of the ECG. In a standard ECG strip, 1 mm square equates to 40 ms of duration on the horizontal axis and 0.1 mV of amplitude on the vertical axis. One mm square is often referred to as a “small” box. Five 1 mm squares form a 5 mm or large box (◘ Fig. 17.9).

The component waves are as follows:

Segments in ECG are the regions between two waves whereas intervals include one segment and one or more waves:

The normal value for the QTc in men is ≤0.44 s and in women is ≤0.45–0.46 s. Hypercalcemia, hyperthyroidism, hyperkalemia, digitalis toxicity, and class IB drugs shorten the interval. Myocarditis, hypokalemia, hypocalcemia, CHF, class 1A and 3 drugs prolong it. Long QT intervals predispose to development of ventricular arrhythmias, torsade, and sudden death. In the perioperative setting, use of halogenated volatile gases (sevoflurane particularly) and antiemetics (droperidol, ondansetron) has been associated with prolonged QT interval.

The sequence of electromechanical events that take place during the course of a heartbeat constitutes the cardiac cycle (CC). As outlined before, CC can be broadly divided into systole (phase of contraction) and diastole (phase of relaxation). The atria as well as the ventricles undergo contraction and relaxation. However, we shall use the terms systole and diastole to denote ventricular contraction and relaxation, unless otherwise specified. Keeping this in mind, CC then comprises broadly of six events that occur sequentially: isovolumic (ventricular) contraction, ventricular ejection (rapid and slow phases), isovolumic (ventricular) relaxation, ventricular filling (early filling), diastasis, and atrial systole.

The QRS complex of the ECG represents ventricular depolarization. This triggers ventricular contraction and an increase in ventricular intracavitary pressures. This leads to closure of the tricuspid and mitral valves, which in turn generates the first heart sound or S1. This heralds the beginning of the isovolumic contraction phase wherein ventricular pressure increases without change in volume and in this phase, all the valves are closed (beginning of R to end of S wave). The continuing increase in ventricular pressures eventually leads to opening of the pulmonary and aortic valves with rapid ejection of blood into the great arteries (rapid ventricular ejection phase). This leads to increasing pressures in the great arteries and the rate of ventricular ejection slows down (end of S wave to approximately distal portion to end of T wave represents ventricular contraction). As action potentials are time-dependent, the LV and RV start repolarizing (T wave) and eventually stop ejecting. When the ventricles stop ejecting, the PA and aortic pressures briefly exceed ventricular pressures, leading to closure of PV and AoV. This generates the second heart sound (S2) and represents end systole (approximately at around peak of T wave). The RV being crescent-shaped demonstrates peristaltic contraction and typically does not exhibit the isovolumic contraction phase like the LV.

The diastolic period has four phases: isovolumic relaxation, ventricular filling, diastasis, and atrial systole. The ventricular diastolic period (distal portion to end of T wave to beginning of QRS) starts after PV and AoV closure. The pressure in the ventricles decreases rapidly without an initial change in volume. This is called isovolumic relaxation and all the valves are closed in this phase. Atrial diastole starts and continues during ventricular depolarization (QRS) and contraction (ST). Electrically it is overshadowed by the QRS and is thus the atrial T wave or Ta (atrial repolarization wave) is not represented on the ECG. The ventricles continue to untwist and relax with continuing fall in their intracavitary pressures. On the other hand, the atrial pressures rise, given that they have been filling during atrial diastole. This pressure difference leads to opening of TV and MV, leading to rapid ventricular filling. Early filling is due to diastolic suction and contributes to about 70% of ventricular filling. It generates the third heart sound (S3). This phase is followed by diastasis, wherein rapid ventricular filling and subsequent ventricular pressure rise, impeding further filling from the atria to such an extent that the atria simply act as passive conduits for blood flow from the pulmonary veins into the left ventricle. This phase contributes about 5% to total ventricular filling and may disappear with tachycardia.

Atrial systole follows diastasis and is constituted by atrial depolarization (P wave) and contraction (PR segment) or “atrial kick.” This “kick” contributes to about 20%–30% of ventricular filling and generates the fourth heart sound (S4). When the heart is hypertrophied or has low compliance, the atrial kick may be responsible for up to 40% of ventricular filling.

Atrial contraction is followed by atrial relaxation or diastole. Following atrial contraction, the propagating impulse leads to ventricular depolarization (QRS). This marks the beginning of ventricular systole. As the ventricles fill up during diastole, the intracavitary pressures rise, leading to closure of TV and MV and beginning of isovolumic contraction completing the cardiac cycle.

Thus, atrial systole occurs during ventricular diastole and ventricular systole occurs during atrial diastole. This mechanism of sequential activation is important to ensure forward flow of blood through the pulmonary and systemic circulation. Additionally, the kinetic energy of ventricular ejection is stored as potential energy in the great arteries and released to the distal vasculature during diastole ensuring forward flow through the entire CC [3, 4].