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Cardiac cycle

Cardiac cycle is the term used to describe the sequence of events that occur as a heart works to pump blood through the body.

Every single 'beat' of the heart involves three major stages: atrial systole, ventricular systole and complete cardiac diastole. The term systole is synonymous with contraction of a muscle. Electrical systole is the electrical activity that stimulates the myocardiumof the chambers of the heart to make them contract. This is soon followed by Mechanical systole, which is the mechanical contraction of the heart.

The term diastole is synonymous with relaxation of a muscle.

Throughout the cardiac cycle, the blood pressureincreases and decreases.

Inhaltsverzeichnis

1 Atrial systole
- 1.1 Detection of atrial systole
2 Ventricular systole
- 2.1 Detection of ventricular systole
3 Complete cardiac diastole
4 Regulation of the cardiac cycle
5 Physiological mechanism of systole
6 See also

Atrial systole

Image:Heart diastole.png Atrial systole is the contraction of the heart muscle (myocardia) of the left and right atria. Both atria contract at the same time.

As the atria contract, the blood pressure in each atrium increases, forcing additional blood into the ventricles. The additional flow of blood is called atrial kick.

Atrial kick is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation, atrial flutter, and complete heart block.

Detection of atrial systole

Electrical systole of the atria begins with the onset of the P wave on the EKG.

Ventricular systole

Image:Heart systole.png Ventricular systole is the contraction of the muscles (myocardia) of the left and right ventricles.

As the ventricles contract, the blood pressure in each ventricle increases.

In the left ventricle, the pressure soon eclipses that in the left atrium, closing the mitral valve, preventing regurgitation of blood from the left ventricle back into the left atrium. Soon pressure in the left ventricle rises until it is greater than the pressure in the aorta. This causes the aortic valveto open, allowing oxygenated blood to eject into the aorta, to perfuse the end organsof the body.

At the same time, the right ventricle contracts, and the pressure inside the ventricle increases. The pressure eclipses that in the right atrium, closing the tricuspid valve, preventing regurgitation of blood from the right ventricle back into the into right atrium. The pressure in the right ventricle rises until it is greater than the pressure in the pulmonary artery. This causes the pulmonic valveto open, allowing blood to eject into the pulmonary artery, to flow to the lungsto be oxygenated.

Detection of ventricular systole

The closing of the mitral and tricuspid valves (known together as the atrioventricular valves) at the beginning of ventricular systole cause the first part of the "lub-dub" sound made by the heart as it beats. Formally, this sound is known the First Heart Tone, or S₁.

The second part of the "lub-dub" (the Second Heart Tone, or S₂), is caused by the closure of the aortic and pulmonic valves 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.

See main article Heart sounds.

In an electrocardiogram, electrical systole of the ventricles begins at the beginning of the QRS complex.

Complete cardiac diastole

Image:Heart diastole.png 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 valveopens, 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 valveopens, and the right ventricle fills with blood that was accumulating in the right atrium.

Regulation of the cardiac cycle

Cardiac muscle is myogenic, which means that it is self-exciting. This is in contrast with skeletal muscle, which requires either conscious or reflex nervous stimuli. The heart's rhythmic contractions occur spontaneously, although the frequencyor heart ratecan be changed by nervous or hormonal influences such as exercise or the perception of danger. For example, the phrenic nerveaccelerates heart rate and the vagus nervedecelerates heart rate.

The rhythmic sequence of contractions is coordinated by the sinoatrial (SA) and atrioventricular (AV) nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation (See action potential) that initiates atrial contraction. Once the wave reaches the AV node, situated in the lower right atrium, it is delayed there before being conducted through the bundles of His and back up the Purkinje fibers, leading to a contraction of the ventricles. The delay at the AV node allows enough time for all of the blood in the atria to fill their respective ventricles. In the event of severe pathology, the AV node can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the pacemaker cells in the SA node and hence is overridden.

Physiological mechanism of systole

Systole, or contraction, of the heart is induced as the sarcolemma, or thin sheath, of the myocardial cells, or heart muscle cells, of the sinoatrial node, or the cluster of cells in the heart that initiate a heart beat, slowly depolarises beyond the threshold. At this point, the voltage-gated calcium channels open and allow calcium ions to pass through, into the sarcoplasm, or interior, of the muscle cell. Some calcium ions bind to the receptors on the sarcoplasmic reticulum, or network, causing their intrinsic calcium channels to open and an influx of calcium ions into the sarcoplasm results. 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.

Noradrenaline is released by the terminal boutons of depolarised sympathetic fibres, at the sinoatrial and atrioventricular nodes. Noradrenaline 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 cyclic adenyl monophosphate (cAMP) from adenyl triphosphate (ATP) and this in turn activates the protein kinase (β-adrenoreceptor kinase). β-adrenoreceptor kinase phosphorylates the calcium ion channels in the sarcolemma, 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.