Diastole (/daɪˈæstəli/dy-AST-ə-lee) is the relaxed phase of thecardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase issystole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.
The term originates from the Greek wordδιαστολή (diastolē), meaning "dilation",[1] fromδιά (diá, "apart") +στέλλειν (stéllein, "to send").
A typical heart rate is 75 beats per minute (bpm), which means that the cardiac cycle that produces one heartbeat, lasts for less than one second. The cycle requires 0.3 sec in ventricular systole (contraction)—pumping blood to all body systems from the two ventricles; and 0.5 sec in diastole (dilation), re-filling the four chambers of the heart, for a total of 0.8 sec to complete the cycle.[2]
During early ventricular diastole, pressure in the two ventricles begins to drop from the peak reached during systole. When the pressure in the left ventricle falls below that in the left atrium, themitral valve opens due to a negative pressure differential (suction) between the two chambers. The open mitral valve allows blood in the atrium (accumulated during atrial diastole) to flow into the ventricle (see graphic at top). Likewise, the same phenomenon runs simultaneously in the right ventricle and right atrium through thetricuspid valve.
The ventricular filling flow (or flow from the atria into the ventricles) has an early (E) diastolic component caused by ventricular suction, and then a late one created byatrial systole (A). TheE/A ratio is used as a diagnostic measure as its diminishment indicates probablediastolic dysfunction, though this should be used in conjunction with other clinical characteristics and not by itself.[3][4]
Early diastole is a suction mechanism between the atrial and ventricular chambers.[5] Then, in late ventricular diastole, the two atrial chambers contract (atrial systole), causing blood pressure in both atria to increase and forcing additional blood flow into the ventricles. This beginning of the atrial systole is known as theatrial kick—see Wiggers diagram. The atrial kickdoes not supply the larger amount of flow (during the cardiac cycle) as about 80 percent of the collected blood volume flows into the ventricles during the active suction period.[6]
At the beginning of the cardiac cycle the atria, and the ventricles are synchronously approaching and retreating from relaxation and dilation, or diastole. The atria are filling with separate blood volumes returning to the right atrium (from thevena cavae), and to the left atrium (from the lungs). After chamber and back pressures equalize, the mitral and tricuspid valves open, and the returning blood flows through the atria into the ventricles. When the ventricles have completed most of their filling, the atria begin to contract (atrial systole), forcing blood under pressure into the ventricles. Now the ventricles start to contract, and as pressures within the ventricles rise, the mitral and tricuspid valves close producing thefirst heart sound (S1) as heard with a stethoscope.
As pressures within the ventricles continue to rise, they exceed the "back pressures" in theaorta, and thepulmonary trunk. The aortic and pulmonary valves known as thesemilunar valves open, and a defined fraction of blood within the heart is ejected into the aorta and pulmonary trunk. Ejection of blood from the heart is known assystole. Ejection causes pressure within the ventricles to fall, and, simultaneously, the atria begin to refill (atrial diastole). Finally, pressures within the ventricles fall below the back pressures in the aorta and the pulmonary arteries, and the semilunar valves close. Closure of these valves give thesecond heart sound (S2). The ventricles then start to relax, the mitral and tricuspid valves begin to open, and the cycle begins again.[7]
In summary, when the ventricles are in systole and contracting, the atria are relaxed and collecting returning blood. When, in late diastole, the ventricles become fully dilated (understood in imaging as LVEDV and RVEDV), the atria begin to contract, pumping blood to the ventricles. The atria feed a steady supply of blood to the ventricles, thereby serving as a reservoir to the ventricles and ensuring that these pumps never run dry.[8] This coordination ensures that blood is pumped and circulated efficiently throughout the body.[9]
Blood pressure is usually written with the systolic pressure expressed over the diastolic pressure or separated by aslash, for example, 120/80 mmHg. This clinical notation is not a mathematical figure for a fraction or ratio, nor a display of a numerator over a denominator, rather it is a medical notation showing the two clinically significant pressures involved. It is often shown followed by a third value, the number of beats per minute of theheart rate.
Mean blood pressure is also an important determinant in people who have had certain medical interventions likeLeft Ventricular Assist Devices (LVAD) andhemodialysis that replace pulsatile flow with continuous blood flow.
Examining diastolic function during acardiac stress test is a good way to test forheart failure with preserved ejection fraction.[10]
Classification ofblood pressure in adults:[11]
| Blood Pressure Classification | Systolic BP (mmHg) | Diastolic BP (mmHg) |
|---|---|---|
| Optimal | <120 | and <80 |
| Prehypertension | 120–139 | or 80–89 |
| Stage 1 Hypertension | 140–159 | or 90–99 |
| Stage 2 Hypertension | ≥160 | or ≥100 |
Brain natriuretic peptide (BNP) is a cardiacneurohormone secreted from ventricular myocytes (ventricular muscle cells) at the end of diastole—this in response to the normal, or sub-normal (as the case may be), stretching of cardiomyocytes (heart muscle cells) during systole. Elevated levels of BNP indicate excessivenatriuresis (excretion of sodium to the urine) and decline of ventricular function, especially during diastole. Increased BNP concentrations have been found in patients who experiencediastolic heart failure.[12]
Impaireddiastolic function can result from thedecreased compliance of ventricular myocytes, and thus the ventricles, which means the heart muscle does not stretch as much as needed during filling.[2] This will result in a reducedend diastolic volume (EDV) and, according to theFrank-Starling mechanism, a reduced EDV will lead to a reducedstroke volume, thus a reducedcardiac output. Over time, decreased cardiac output will diminish the ability of the heart to circulate blood efficiently throughout the body. Degradation of compliance in the myocardium is a natural consequence of aging.
