During normal conditions, the heart obtains its energy through a process called oxidative phosphorylation. In this process, each mole of glucose produces 36 mol of ATP. However, in cases of hypoxia, the heart relies on glycolysis for energy production, which only provides 2 mol of ATP per mole of glucose. Additionally, the breakdown of fatty acids through β-oxidation is reduced during hypoxia. If hypoxia persists, the heart's cellular creatine phosphate and ATP stores become depleted.

In the condition known as ischemia, the accumulation of lactic acid leads to a decrease in intracellular pH. This acidic environment inhibits glycolysis, fatty acid utilization, and protein synthesis, resulting in cellular damage and ultimately necrosis of myocardial cells.

The transmembrane action potentials recorded from cardiac myocytes can be described in five phases:
1. Phase 0: The action potential upstroke begins when a suprathreshold stimulus rapidly depolarizes the cell membrane by activating fast sodium channels.
2. Phase 1: The notch represents an early partial repolarization achieved by the efflux of K+ through channels that conduct the transient outward current (ito).
3. Phase 2: The plateau phase occurs due to a balance between the influx of Ca++ through calcium channels and the efflux of K+ through various potassium channels.
4. Phase 3: Final repolarization commences when the efflux of K+ surpasses the influx of Ca++. This leads to a partial repolarization followed by a rapid increase in K+ conductance, ultimately restoring full repolarization.
5. Phase 4: The resting potential of a fully repolarized cell is determined by the cell membrane's conductance to K+ through iK1 channels.

Fast-response action potentials are observed in atrial and ventricular myocardial fibers as well as ventricular specialized conducting (Purkinje) fibers. These action potentials exhibit a large amplitude, a steep upstroke, and a relatively long plateau. The effective refractory period of fast-response fibers begins at the upstroke of the action potential and continues until midway through phase 3. During the remaining part of phase 3, the fiber is relatively refractory, regaining full excitability shortly after complete repolarization in phase 4.

Slow-response action potentials are recorded from normal sinus (SA) and atrioventricular (AV) nodal cells, as well as abnormal partially depolarized myocardial cells. These action potentials display a less negative resting potential, a smaller amplitude, a less steep upstroke, and a shorter plateau compared to fast-response action potentials. The upstroke in slow-response fibers is triggered by the activation of calcium channels. Slow-response fibers become absolutely refractory at the beginning of the upstroke and may only regain partial excitability very late in phase 3 or after full repolarization.

Under normal circumstances, the SA node acts as the primary pacemaker of the heart, initiating the cardiac impulse. This impulse is then propagated from the SA node to the atria and eventually reaches the AV node. After a delay in the AV node, the cardiac impulse spreads throughout the ventricles. However, ectopic foci in the atrium, AV node, or the His-Purkinje system can initiate propagated cardiac impulses if the normal pacemaker cells in the SA node are suppressed or if the rhythmicity of the ectopic automatic cells is abnormally enhanced.

In certain abnormal conditions, afterdepolarizations can be triggered by an otherwise normal action potential. Early afterdepolarizations (EADs) occur during phase 3 of a normal action potential, particularly when the initiating beats have a very long basic cycle length and the cardiac action potentials are abnormally prolonged. Delayed afterdepolarizations (DADs) arise late in phase 3 or during phase 4. DADs are more likely to occur when the basic cycle length of the initiating beats is short and when the cardiac cells are overloaded with Ca++.

Reentrant arrhythmias occur when a cardiac impulse follows a loop of cardiac fibers, reentering previously excited tissue. This can happen when the impulse is conducted slowly around the loop and is unidirectionally blocked in a particular section of the loop.
Normally, the heart derives its energy by oxidative phosphorylation, in which each mole of glucose yields 36 mol of ATP. However, during hypoxia, glycolysis takes over, and 2 mol of ATP is provided by each mole of glucose; β-oxidation of fatty acids is also curtailed. If hypoxia is prolonged, cellular creatine phosphate and eventually ATP are depleted.
In ischemia, lactic acid accumulates and decreases intracellular pH. This condition inhibits glycolysis, fatty acid use, and protein synthesis, and therefore it results in cellular damage and eventually necrosis of myocardial cells.
1. The transmembrane action potentials recorded from cardiac myocytes may contain the following five phases: Phase 0: The action potential upstroke is initiated when a suprathreshold stimulus rapidly depolarizes the membrane by activating the fast sodium channels. Phase 1: The notch is an early partial repolarization that is achieved by the efflux of K+ through channels that conduct the transient outward current (ito). Phase 2: The plateau represents a balance between the influx of Ca++ through calcium channels and the efflux of K+ through several types of potassium channels. Phase 3: Final repolarization is initiated when the efflux of K+ exceeds the influx of Ca++ . The resultant partial repolarization rapidly increases K+ conductance and restores full repolarization.
Phase 4: The resting potential of the fully repolarized cell is determined by conductance of the cell membrane to K+ , mainly through iK1 channels.
2. Fast-response action potentials are recorded from atrial and ventricular myocardial fibers and from ventricular specialized conducting (Purkinje) fibers. Such an action potential is characterized by a large amplitude, a steep upstroke, and a relatively long plateau. The effective refractory period of fast-response fibers begins at the upstroke of the action potential and persists until midway through phase 3. The fiber is relatively refractory during the remainder of phase 3, and it regains full excitability soon after it is fully repolarized (phase 4).
3.
Slow-response action potentials are recorded from normal SA and AV nodal cells and from abnormal myocardial cells that have been partially depolarized. The action potential is characterized by a less negative resting potential, a smaller amplitude, a less steep upstroke, and a shorter plateau than is typical of the fast-response action potential. The upstroke in slow-response fibers is produced by the activation of calcium channels. Slow-response fibers become absolutely refractory at the beginning of the upstroke, and partial excitability may not be regained until very late in phase 3 or until after the fiber is fully repolarized.
4.
Normally, the SA node serves as the cardiac pacemaker to initiate the cardiac impulse. This impulse is propagated from the SA node to the atria and ultimately reaches the AV node. After a delay in the AV node, the cardiac impulse is propagated throughout the ventricles. Ectopic foci in the atrium, the AV node, or the His-Purkinje system may initiate propagated cardiac impulses if the normal pacemaker cells in the SA node are suppressed or if the rhythmicity of the ectopic automatic cells is abnormally enhanced.
5.
Under certain abnormal conditions, afterdepolarizations may be triggered by an otherwise normal action potential. EADs arise early in phase 3 of a normal action potential. They are more likely to occur when the basic cycle length of the initiating beats is very long and when the cardiac action potentials are abnormally prolonged. DADs appear late in phase 3 or in phase 4. They are more likely to occur when the basic cycle length of the initiating beats is short and when the cardiac cells are overloaded with Ca++ .
6.
Reentrant arrhythmias occur when a cardiac impulse traverses a loop of cardiac fibers and reenters previously excited tissue, when the impulse is conducted slowly around the loop, and when the impulse is blocked unidirectionally in some section of the loop.
7.