Cardiac Cycle

Cardiac cycle is the term used to describe the relaxation and contraction that occur, as a heart works to pump blood through the body. Heart rate is a term used to describe the frequency of the cardiac cycle. It is considered one of the four vital signs. Usually it is calculated as the number of contractions (heart beats) of the heart in one minute and expressed as "beats per minute" (bpm). When resting, the adult human heart beats at about 70 bpm (males) and 75 bpm (females), but this rate varies between people. However, the reference range is nominally between 60 bpm (if less termed bradycardia) and 100 bpm (if greater, termed tachycardia). Resting heart rates can be significantly lower in athletes, and significantly higher in the obese. The body can increase the heart rate in response to a wide variety of conditions in order to increase the cardiac output (the amount of blood ejected by the heart per unit time). Exercise, environmental stressors or psychological stress can cause the heart rate to increase above the resting rate. The pulse is the most straightforward way of measuring the heart rate, but it can be deceptive when some strokes do not lead to much cardiac output. In these cases (as happens in some arrhythmias), the heart rate may be considerably higher than the pulse. Every single 'beat' of the heart involves three major stages: atrial systole, ventricular systole and complete cardiac diastole. Throughout the cardiac cycle, the blood pressure increases and decreases. As ventricles contract the pressure rise, causing the AV valves to slam shut.

Systole

The heart in the systole phase.

The heart in the systole phase. Systole, or contraction, of the heart is initiated by the electrical cells of the sinoatrial node, which is the heart's natural pacemaker. These cells are activated spontaneously by depolarization of their membranes beyond a certain threshold for excitation. At this point, voltage-gated calcium channels on the cell membrane open and allow calcium ions to pass through, into the sarcoplasm, or interior, of the muscle cell. Some calcium ions bind to receptors on the sarcoplasmic reticulum causing an influx of calcium ions into the sarcoplasm. The calcium ions bind to the troponin, causing a conformation change, breaking the bond between the protein tropomyosin, to which the troponin is attached, and the myosin binding sites. This allows the myosin heads to bind to the myosin binding sites on the actin protein filament and contraction results as the myosin heads draw the actin filaments along, are bound by ATP, causing them to release the actin, and return to their original position, breaking down the ATP into ADP and a phosphate group. The action potential spreads via the passage of sodium ions through the gap junctions that connect the sarcoplasm of adjacent myocardial cells. Norepinephrine (noradrenaline) is released by the terminal boutons of depolarized sympathetic fibers, at the sinoatrial and atrioventricular nodes. Norepinephrine diffuses across the synaptic cleft binds to the β1-adrenoreceptors – G-protein linked receptors, consisting of seven transmembrane domains – shifting their equilibrium towards the active state. The receptor changes its conformation and mechanically activates the G-protein which is released. The G-protein is involved in the production of adenosine 3',5'-cyclic monophosphate (cAMP) from adenosine triphosphate (ATP) and this in turn activates the protein kinase (β-adrenoreceptor kinase). β-adrenoreceptor kinase phosphorylates the calcium ion channels in the sarcolema, so that calcium ion influx is increased when they are activated by the appropriate transmembrane voltage. This will of course, cause more of the calcium receptors in the sarcoplasmic reticulum to be activated, creating a larger flow of calcium ions into the sarcoplasm. More troponin will be bound and more myosin binding sites cleared [of tropomyosin] so that more myosin heads can be recruited for the contraction and a greater force and speed of contraction results. [Phosphodiesterase catalyses the decomposition of cAMP to AMP so that it is no longer able to activate the protein kinase. AMP will of course, go on to be phosphorylated to ATP and may be recycled.] Noradrenaline also affects the atrioventricular node, reducing the delay before continuing conduction of the action potential via the bundle of HIS.

Diastole

The heart in the diastole phase.

The heart in the diastole phase. Cardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing. Together they are known as complete cardiac diastole. During ventricular diastole, the pressure in the (left and right) ventricles drops from the peak that it reaches in systole. When the pressure in the left ventricle drops to below the pressure in the left atrium, the mitral valve opens, and the left ventricle fills with blood that was accumulating in the left atrium. Likewise, when the pressure in the right ventricle drops below that in the right atrium, the tricuspid valve opens and the right ventricle fills with blood that was in the right atrium

"Lub-Dub"

The first heart tone, or S1, "Lub" is caused by the closure of the atrioventricular valves, mitral and tricuspid, at the beginning of ventricular contraction, or systole. When the pressure in the ventricles rises above the pressure in the atria, these valves close to prevent regurgitation of blood from the ventricles into the atria. The second heart tone, or S2 (A2 and P2), "Dub" is caused by the closure of the aortic valve and pulmonic valve at the end of ventricular systole. As the left ventricle empties, its pressure falls below the pressure in the aorta, and the aortic valve closes. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonic valve closes. During inspiration, negative intrathoracic pressure causes increased blood return into the right side of the heart. The increased blood volume in the right ventricle causes the pulmonic valve to stay open longer during ventricular systole. This causes an increased delay in the P2 component of S2. During expiration, the positive intrathoracic pressure causes decreased blood return to the right side of the heart. The reduced volume in the right ventricle allows the pulmonic valve to close earlier at the end of ventricular systole, causing P2 to occur earlier, and "closer" to A2. It is physiological to hear the splitting of the second heart tone by younger people and during inspiration. During expiration normally the interval between the two components shortens and the tone becomes merged.