In simple terms, systole is the time during which the ventricles contract and eject blood. It is followed by diastole (a period of relaxation), and a set of these events in both the atria and ventricles comprises a cardiac cycle.
The sino-atrial (SA) node, also known as the cardiac pacemaker, spontaneously and rhythmically initiates each cardiac cycle. The action potential at the SA node is propagated through both atria (atrial contraction – P wave on EKG) and then through the atrio-ventricular node (PR interval on EKG), His bundle and Purkinje system to both ventricles (QRS complex on EKG). Ventricular repolarization is seen as the T wave on the EKG.
Isovolumic contraction. During the first phase of left ventricular (LV) systole, the ventricle begins contraction with the mitral and aortic valve closed leading to a rapid increase in intraventricular pressure but no change in volume.
Ejection phase: The second phase of systole begins with the opening of the aortic valve (ventricular pressure exceeds the aortic pressure) and ends when the ventricle has stopped contracting, although ejection is still taking place (the aortic valve is still open).
Diastole: Marks the onset of ventricular relaxation. Ejection into the aorta continues until the left ventricular pressure drops below the aortic pressure and the aortic valve closes.
Physiologic systole begins at the start of isovolemic contraction and ends at the peak of ventricular ejection. Clinical systole (by echocardiography) begins with mitral valve closure and ends with aortic valve closure.
Systole and diastole require energy. During diastole, ventricular relaxation occurs by the removal/uptake of calcium from troponin C and into the sarcoplasmic reticulum. The factors that affect systolic function, preload, afterload, heart rate and contractility overlap the effects of calcium on the ventricle.
Physiology Principles
The amount of blood ejected by the ventricle with each contraction is the stroke volume (SV). Normal SV in an adult man is 70–80 mL. SV is determined by preload, afterload, and contractility. The description below pertains to LV systolic function. The amount of blood ejected by the heart per minute is the cardiac output (CO).
Preload
Is the load on the ventricle before contraction and is determined by ventricular volume.
It is the end-diastolic myocardial fiber length and is represented by the end-diastolic volume (EDV); normally around 120 mL.
Cardiac muscle develops most of its force over a small range of shortening near its maximal length. Thus, within limits, increases in preload (rise in EDV) will increase the SV and systolic pressure.
Factors affecting preload include venous return (including venous tone), total blood volume, intrathoracic pressure, body position, and atrial contraction.
Surrogate measures of LV volume used to estimate EDV are pulmonary capillary wedge pressure (PCWP) or central venous pressure (CVP).
Afterload
Is the load on the ventricle at the start of a contraction. In simple terms, afterload is the impedance to ejection of blood.
Most of the resistance to ejection is from the systemic vascular resistance (SVR).
An increase in afterload decreases ventricular ejection.
Ventricular wall stress (tension) is a concept that incorporates both preload and afterload. Arterial blood pressure, vascular compliance and volume, and wall thickness all factor into tension. It can be calculated by LaPlace's law: Tension = (change in pressure) (ventricular radius)/(wall thickness ×2).
Contractility
Is the muscle's ability to generate work (contract, develop pressure, generate a contractile force) from a set end-diastolic fiber length.
Increased contractility refers to a greater velocity of contraction (Vmax) reaching a higher peak force. This definition is useful at the subcellular level to measure contractility in isolated papillary muscle.
Another measure of contractility, the rate of pressure development (dP/dt), is not used clinically.
Ejection fraction (EF) is a clinically useful index of contractility.
Both systolic and diastolic function can be assessed using pressure-volume curves that can be obtained during cardiac catheterization.
Coronary blood flow
75% of total coronary blood flow occurs during diastole. During systolic contraction, there is an increase in tissue pressure that impedes arterial flow; blood is redistributed from the subendocardial to the subepicardial layer of the LV. Systole has minimal impact on coronary flow to the right ventricle (RV).
Coronary blood flow at rest is about 250 mL/min (4–5% of CO) or 75 mL/100 g/min, assuming the adult heart weighs 300 g and the CO is 5 L/min.
The myocardial oxygen consumption at rest is 8–10 mL/100 g/min, about 10% of the total body consumption of oxygen.
In the coronary circulation, near maximum oxygen extraction (75% of arterial oxygen content) occurs during rest. Hence, an increase in coronary blood flow is necessary when myocardial oxygen consumption occurs.
The heart consists of two atria and two ventricles that circulate blood in series; the RV pumps through the low-resistance pulmonary circulation, while the LV pumps through the high-resistance systemic circulation.
The RVs and LVs differ in their shape, size, and pressure against which they contract.
The LV is ellipsoidal in shape with the muscle fibers arranged longitudinally in the subepicardium and subendocardial layers, and circumferentially in between these two layers. The LV ejects blood with a corkscrew type of motion with the apex moving toward the base. Wall motion of regions supplied by branches of the coronary artery can be individually assessed semi-quantitatively by echocardiography.
The RV is crescent-shaped with an inflow and outflow region that contract sequentially to eject blood into the low-pressure pulmonary circulation. 3-D echocardiography is becoming useful in quantifying RV systolic function.
The atrial systole contributes 25–30% of the volume toward ventricular filling, and the SV could significantly decrease in the absence of this atrial contraction during cardiac dysrhythmias and could also be compounded by impaired relaxation of the ventricles, for example, during atrial fibrillation in older patients.
Perioperative Relevance
Electrical activity of the heart is monitored using the ECG, while the mechanical events are monitored using the arterial and pulmonary BP or echocardiography.
A pulmonary artery catheter has been traditionally used to estimate CO by thermal dilution. Assuming a normal LV systolic and diastolic function, EDV is estimated from left ventricular end-diastolic pressure (LVEDP). In disease states where ventricular compliance is abnormal, LVEDP correlates poorly with CVP/PCWP.
With transesophageal echocardiography (TEE), EDV can be directly measured, as well as estimate the EF.
The majority of intravenous induction agents decrease BP via venodilation (decreased preload) and/or vasodilation (decreased afterload).
Isoflurane, desflurane, and sevoflurane used for maintenance of anesthesia (1–1.5 MAC), decrease SV by 15–30%. An increase in heart rate caused by these inhaled agents may minimize the decrease in CO.
Positive-pressure ventilation (PPV) leads to raised intrathoracic pressure leading to reduced venous return, in turn reducing SV and thereby BP. The onset of positive pressure ventilation is associated with a greater decrease in RV function compared to LV function; however, with time, the reduction in RV output will decrease LV output. During PPV, the SV varies with inspiration and exhalation. When this variation is >15%, it may be indicative of relative hypovolemia and volume responsiveness.
Newer pulse contour analysis monitors allow estimation of LV SV from systemic arterial pressure waveforms.
Stand-alone monitors exist that use esophageal Doppler probes to estimate SV. These probes measure the velocity (peak and mean) of blood in the descending thoracic aorta, and by integrating it over the ejection time, obtain the velocity time integral (VTI). VTI multiplied by the cross-sectional area of the aorta (assuming a diameter, given the patient's age, gender, and height and weight) provides the SV with every beat. A similar method may be used to estimate SV using TEE.
Equations
In a normal-sized human with a heart rate (HR) of 70–80 beats per minute, cardiac output (CO) is 5–6 L/min.
CO = SV × HR
Cardiac index (CI) is CO indexed to bodies of varying sizes, expressed using body surface area (BSA)
Systole and diastole are both energy-requiring processes.
Adequate and judicious IV hydration before induction of anesthesia is recommended, especially in the older patient, to minimize the cardiovascular effects of the induction drugs and PPV.
When compared to other methods, an increase in CO achieved by optimizing intravascular volume that increases venous return (preload) is the most efficient method, as it does not lead to increased oxygen consumption.
A dilated, thin-walled ventricle (failing ventricle) has greater wall stress than a thicker-walled, smaller ventricle. When hydrating patients with heart failure, reducing afterload is important.
Hypoxia, acidosis, ischemia, calcium-channel blockers and beta-blockers decrease contractility.