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Action potentials generated in the heart by the SA node travel throughout the heart via the conduction system as described above. The mechanism of contrac- tion of cardiac muscle fi bers is described below (Fig.13.12):

1. Depolarization. As a cardiac muscle fi ber is stimu- lated by a neighboring action potential, voltage- gated fast Na+ channels open. This allows a rapid infl ux of Na+ from the extracellular fl uid, which results in depolarization of the cardiac muscle fi ber from −90 mV to +30 mV. These channels quickly become inactivated and close.

2. Plateau. As the voltage-gated fast Na+ channels close, voltage-gated slow Ca2+ channels open in the sarcolemma and sarcoplasmic reticulum (SR). The infl ux of Ca2+ from the extracellular space (20%) causes a large release (80%) of Ca2+ from the SR. Simultaneously, the membrane permeability to K+ decreases. As a result, the membrane remains depolarized at around 0 mV for about 0.25 sec, compared to about 0.001 sec in skeletal muscle. 3. Repolarization. After the relatively long plateau

phase, voltage-gated K+ channels open, allowing

potassium ions to fl ow out of the cell and the membrane to repolarize. The cell returns to its resting membrane potential of about −90 mV. 4. Refractory period. The refractory period, or time

during which the next contraction cannot be trig- gered, is relatively long in cardiac muscle com- pared to skeletal muscle. The refractory period prevents cardiac muscle from developing tetanus, and thereby it allows the heart to act as an effec- tive pump rather than developing a sustained contraction.

The mechanism of contraction of cardiac muscle fi bers is similar to that in skeletal muscle fi bers. As intracellular Ca2+ concentrations increase, Ca2+ binds to troponin, causing the tropomyosin to move and thus uncovering the myosin binding sites on the actin fi laments. Myosin then binds to actin, and the actin is pulled across the myosin fi lament. Drugs that alter the movement of calcium into the cardiac muscle fi bers can affect the strength of heart contraction.

ATP production

Cardiac muscle has little capacity for anaerobic cel- lular respiration; thus, cardiac muscle relies almost Sinoatrial (SA) node

James internodal tract

Atrioventricular (AV) node

Purkinje fibers

Right crus Left crus Bundle of His Left AV fibers

Fig. 13.11. Excitation and conducting system of the dog heart. The pacemaker of the heart is the sinoatrial (SA) node. A wave of

depolarization spreads from the SA node throughout the atria. This wave of depolarization then passes through the atrioventricular (AV) node where it is delayed from proceeding to the ventricles. From the AV node, the wave of depolarization travels down the bundle of His located in the intraventricular septum, and then into the Purkinje fi bers. (Modifi ed from Constantinescu, 2002.)

entirely on aerobic respiration. Therefore, cardiac muscle needs a continuous supply of O2, which arrives

via the coronary circulation or is released from myoglobin inside the cardiac muscle fi bers. Cardiac muscle can produce ATP from the oxidation of fatty acids, glucose, lactic acid, amino acids, and ketone bodies.

Cardiac muscle also contains creatine phosphate, which can be used to produce ATP. The enzyme cre- atine kinase can catalyze the transfer of a phosphate group from creatine phosphate to ADP to produce a new molecule of ATP. If the heart is damaged, it releases creatine kinase into the bloodstream, which is often measured as an indicator of heart damage.

Electrocardiogram

The propagation of the action potentials through the heart produces electrical currents that can be detected on the surface of the body. A recording of these elec- trical activities is called an electrocardiogram (ECG or EKG). An ECG represents all of the electrical activity

in the heart rather than a single action potential (Fig. 13.13).

Two electrodes are generally placed on each fore- limb, and one on the left hindlimb. The potential dif- ference between electrodes is measured using different combinations of electrodes. By comparing these various recordings, it is possible to determine whether there are abnormalities in the conduction system or whether the heart is damaged.

Each segment of the ECG is generated from a spe- cifi c area of the heart in sequential manner (Fig. 13.14). A typical ECG has three characteristic waves with each heart beat. The fi rst, or P wave, is a small upward defl ection refl ecting atrial depolarization (Fig. 13.13). It is generated as the SA node depolarizes, and the action potential spreads throughout the atria. The second wave, or QRS complex, begins with a down- ward defl ection, and then rises sharply and ends with a downward defl ection. The QRS complex represents ventricular depolarization. Its shape is complex because the movement of the wave of depolarization through the ventricle changes direction throughout A +30 2. Plateau phase 1. Rapid depolarization Depolarization Refractory Period Contraction Na+ _permeability Ca2+ permeability K+ permeability Time (msec) Repolarization Membr ane P o tential (mV) R elativ e Membr ane Pe rm eabilit y 3. Repolarization phase –30 –60 –90 0 B

Fig. 13.12. Action potential in cardiac muscle fi bers. A) The action potential in cardiac muscle fi bers has a plateau phase not seen in skeletal muscle fi bers. B) The infl ux of Na+ causes the rapid depolarization phase while increased Ca2+ permeability leads to the plateau phase. Effl ux of K+ results in repolarization.

364 Anatomy and physiology of domestic animals

the wave. The third wave is the T wave, and it repre- sents ventricular repolarization. Since repolarization is slower than depolarization, the T wave is longer than the QRS complex.

Within the ECG, it is also possible to examine various intervals or segments. The P–Q interval is the time between the beginning of atrial excitation and the beginning of ventricular excitation. Therefore, it rep- resents the time for the action potential to travel through the atria, the AV node, and the remainder of the conduction system. This interval can lengthen if there is coronary heart disease or scar tissue in the heart. The S–T segment begins with the S wave and ends with the beginning of the T wave. It represents the time when the ventricle is depolarized during the plateau phase. The T wave can be elevated in acute myocardial infarction. The Q–T interval is the period from the beginning of ventricular depolar- ization through ventricular repolarization. It can be lengthened by myocardial damage or myocardial ischemia.

Heart sounds

Auscultation involves listening to body sounds, usually with a stethoscope. Four sounds are created during each heart beat, and two of these sounds are clearly audible. These sounds are typically described as “lub-dup.” The fi rst sound, lub, is the AV valves closing. This occurs at the beginning of systole as the ventricular pressure increases above the atria pres- sure, causing the AV valves to close as blood begins returning to the atria. This sound is louder and longer than the second sound. The dup sound is caused by the semilunar valves closing at the beginning of ven- tricular diastole. The two other sounds, which are less audible, are due to the blood turbulence during ven- tricular fi lling and atrial systole.

Heart murmurs include clicking, rushing, or gur- gling sounds. Although not always due to a problem, heart murmurs generally indicate a valve disorder. If the valve is stenotic, meaning it has a narrowed opening, a click may be audible when the valve should be fully opened. In contrast, if a swishing sound is heard when the valve should be closed, it may indicate that blood is able to backfl ow through the valve.