Fundamentals of hemodynamic monitoring
It is important to monitor cardiac circulatory function in critically ill patients
Basic monitoring: ECG, noninvasive blood pressure, and pulse oximetry do not provide sufficient information for treatment. Advanced hemodynamic monitoring measures cardiac output and the relevant parameters it determines (preload, afterload, myocardial contractility) in a minimally invasive manner, while quantifying lung fluid to guide goal-directed therapy. 5
Frank-Starling 曲线
According to Frank-Starling's law, within a certain range, the higher the volume of blood entering the ventricles during diastole (end-diastolic volume), the greater the pumping volume (stroke volume) during systole. Vice versa. This is the mechanism by which the myocardium adapts to compensatory regulation of slight changes in ventricular filling.
The capacity of the heart muscle depends on the load of its initial state of contraction
At the same time, it can also increase cardiac output through volume management therapy. The force produced by any single myocardial fiber is proportional to the length of the initial sarcomere (preload), and the stretching of the individual fibers is related to the ventricular end-diastolic volume.
Within a certain range, myocardial fibers are at an optimal stretch length, and increasing preload increases stroke volume (SV). Within a certain limit, the more the sarcomere fibers of the cardiomyocyte stretch, the stronger the contractile force. On the other hand, if the capacity is overloaded, the shrinkage capacity may be reduced.
Hemodynamic parameters
PiCCO combines two technologies
The PiCCO technique works in two parts: transpulmonary thermodilution and pulse profiling. Hemodynamic parameters, obtained in both ways, have been clinically validated for more than 20 years6,7
Arterial pulse profiling techniques
Arterial pulse profiling provides continuous parameters, and transpulmonary thermodilution provides discontinuous parameters. Transpulmonary thermodilution technique is used to correct the technical parameters of pulse profiling.
Transpulmonary thermodilution technique
During the transpulmonary thermal dilution procedure, ice saline projectiles (eg, 15 ml of ice saline) are injected through a central venous catheter.
Along with the blood, the ice saline passes through the central vein→ right atrium→ right ventricle→ lung→ left atrium→ left ventricle, → femoral artery, and is monitored by the PiCCO arteriosus to detect changes in blood temperature. It is recommended to perform 3 ice saline injections within 10 minutes, and the average value is taken to calibrate the pulse profiling method.
Whenever there is a significant change in the patient's condition or treatment, the transpulmonary thermodilution parameter should be calibrated with ice saline (i.e., the transpulmonary thermodilution parameter is updated only when ice saline is administered). A minimum of 3 calibrations per day is recommended.
Pulse profile analysis
Pulse profiling was first proposed in 1899.8
The basic principle of pulse profiling is to analyze the continuous arterial pressure signal to obtain more information than systolic, diastolic, and mean arterial pressure.
From a physiological point of view, the arterial pressure curve suggests information about the onset of the aortic valve opening systolic blood pressure ascending branch and the time of aortic valve closure (aortic notch). The time from the ascending ramus to the beat-a-beat notch represents the duration of contractions, while the area under the systolic pressure curve directly reflects stroke volume (SV), which is the amount of milliliters of blood expelled by the left ventricle at each beat.
However, arterial pressure waveforms and area under the curve are not only affected by stroke volume, but also by the different vascular compliance of each patient.
This is especially true for patients in intensive care, as disease processes or medications can cause rapid changes in vascular compliance. The individualized correction factor determined at the time of the initial correction needs to be updated regularly. 6,9 In PiCCO technology, this calibration factor is derived from transpulmonary thermodilution measurements.
The basic formula for calculating the cardiac output (PCCO) of the pulse profile
The PiCCO pulse profile algorithm has been extensively validated and proven to be very reliable in clinical applications. 11-18
Comparison of PiCCO pulse profiling and pulmonary artery thermodilution flotation catheters. 11–18
Thermally diluted by the lungs
Cardiac output is calculated from the area under the thermodilution curve19-20
Cardiac output (CO) is calculated by transpulmonary thermodilution
The transpulmonary thermodilution curve was analyzed and the CO was derived using the modified Stewart-Hamilton algorithm. 19,20 This method of calculating cardiac output is also applicable to the right heart (pulmonary artery) catheter.
经肺热稀释法和肺动脉热稀释漂浮导管对比文献。
临床研究显示，经肺热稀释法测得的心输出量准确性与肺动脉漂浮导管具有良好的一致性。
10,12,21-28
In addition, because the indicator passes through the heart and lungs, intravascular and extravascular volumes in the thoracic cavity, especially preload and lung water, can be determined.
Physiological basis
Volume was assessed by pulmonary thermodilution
The shape of the transpulmonary thermodilution curve depends on the intravascular and extravascular volumes in the path from the injection start (central venous catheter) to the measurement point (ductus arteriosus). This means that the larger the volume in the chest cavity, the longer the indicator will pass. Vice versa.
Intrapleural volume can be quantified by analyzing the specific passage time of the thermal indicator. 29 The analyses and calculations are based on the analytical literature of Newman et al. At the same time, it has also been verified by many authors. 2,30-35
Average Transfer Time (MTt)
The average transit time represents half of the indicator passing through the measurement point (artery). It is determined by the median line of the area under the curve.
Time to Exponential Decline (DSt)
The exponential drop time is a function of the clearance of the indicator. It is obtained by measuring the descending branch of the transpulmonary thermodilution curve.
Both the average transmission time and the exponential drop time are used to calculate the capacity value.
Intrathoracic thermal volume
The product of mean transit time (MTt) and cardiac output (CO) represents intrathoracic thermal volume (ITTV).
ITTV: intrathoracic thermal volume
Intrapulmonary heat volume
The exponential decline time typically characterizes the volume of the largest mixing chamber in a series of mixing chambers. Thus, the product of exponential descent time (DST) and cardiac output (CO) represents the intrapulmonary thermal volume (PTV).
PTV: pulmonary thermal volume
Quantification of the preload
Subtracting the intrathoracic heat volume from the intrapulmonary heat volume yields the total end-diastolic volume (GEDV). GEDV can stand for Front Load.
GEDV: global end-diastolic volume
Cardiac output and transmission time come from the same thermodilution signal. This leads to a mathematical coupling problem34, in which several studies have shown that an increase in cardiac output does not result in a corresponding increase in GEDV.
Quantify pulmonary edema
With further calculations, the PiCCO technique also provides quantified lung water parameters, expressed as extravascular lung water (EVLW). 36–39 The only more data required to calculate this parameter is intravascular thermal volume (ITBV).
A clinical study measuring ITBV and EVLW 36 using a dual indicator dilution technique found that intrathoracic blood volume was consistently 25% higher than end-diastolic blood volume. Thus, the intrathoracic volume can be obtained by multiplying the end-diastolic volume by a factor of 1.25. Intrathoracic thermal volume (ITTV) minus the calculated intrapleural blood volume (ITBV) yields extravascular lung water (EVLW).
Several confirmatory studies comparing weighing and lung weight have shown that this method and the introduction of a fixed factor have high accuracy in calculating extravascular lung water. 36–38
The value of lung water measured by PiCCO correlate well with the measurement of lung water by weighing method and the measurement of lung weight by anatomy. 36–38
PiCCO parameters
Cardiac Output Index (CI), Stroke Volume Index (SVI)
The cardiac output index is the amount of blood pumped by the heart per minute divided by the body surface area (BSA); The cardiac output index represents the total blood flow. The PiCCO technique provides both non-continuous (transpulmonary thermodilution) and continuous (pulse profile analysis) parameters.
A decrease in cardiac output index is a clear warning sign that appropriate measures need to be taken to manage the condition.
However, knowing the cardiac output index alone is not sufficient to make a treatment decision, as the cardiac output index is influenced by a variety of factors. 31,40 First of all, it is the product of stroke volume and heart rate. Stroke volume depends on preload, afterload, and myocardial contractility.
Therefore, in addition to cardiac output index, further understanding of its determinants is needed for appropriate treatment. 31,40
Preload
全心舒张末期容积指数(GEDI)
Preload, along with afterload and myocardial contractility, is a factor that determines stroke volume and thus cardiac output. Theoretically, it can be understood as the initial stretch length of a single cardiomyocyte of the heart before contracting at the end of diastole. Since this cannot be measured in vivo, it can only be replaced with other measurements. In a clinical setting, preload is referred to as end-diastolic pressure or (more precisely) end-diastolic volume. The larger the end-diastolic volume, the greater the preload.
Higher central venous pressure (CVP) and/or higher pulmonary capillary wedge pressure (PCWP) are still often considered high indicators of preload (right-sided CVP, left-sided PCWP). However, many studies have shown that CVP and PCWP are not reliable indicators of preload. This is mainly due to the fact that pressure does not directly represent capacity. Thus, any parameter assessing the volume of end-diastolic ventricular filling 15,35,41-43 more accurately reflects the actual preload.
The clinical term for preload is usually referred to as end-diastolic pressure or, more precisely, end-diastolic volume.
Volume reactivity
Stroke volume variability (SVV) and pulse pressure variability (PPV)
In patients who are continuously mechanically ventilated and have a stable cardiac rhythm, stroke volume variability (SVV) and pulse pressure variability (PPV) may indicate whether a clinical increase in preload leads to increased cardiac output.
Mechanical ventilation causes circulatory changes in vena cava, pulmonary artery, and aortic flow. At the bedside, changes in aortic blood flow can be reflected by fluctuations in the blood pressure curve (and therefore stroke volume and blood pressure). The magnitude of these changes depends on the patient's volume responsiveness. In the setting of mechanical ventilation, an increase in intrathoracic pressure early in the inspiratory phase causes pulmonary blood to squeeze into the left ventricle. This process results in an increase in left ventricular preload. In volemically responsive patients, this will result in an increase in stroke volume or pulse pressure.
Elevated intrathoracic pressure can also result in decreased right ventricular filling. If the right heart responds to volume, this will reduce the amount of blood pumped. Thus, during the late inspiratory phase (after a few beats), the left ventricular preload decreases, along with stroke volume or pulse pressure. Changes in stroke volume and pulse pressure can be analyzed in 30 seconds.
The greater the variant, the more likely the patient is to have a volume response. In order to use parameters correctly, the following prerequisites must be met:
- Fully mechanically ventilated, tidal volume ≥ 8 ml/kg PBW (predicted body weight)
- Sinus rhythm
- Arterial pressure waveforms are normal
Afterload
Systemic vascular blocking index (SVRI)
Afterload is another factor that determines stroke volume/cardiac output. The physiological significance of SVRI refers to the tension or resistance that occurs in the left ventricular wall during left ventricular ejection. According to Laplace's law, the tension of the muscle fibers on the heart wall is the product of the intraventricular pressure and the radius of the ventricle, divided by the thickness of the ventricular wall.
Clinically, afterload is seen as the resistance of the heart to pump; The systemic vascular resistance index (SVRI) is the parameter that represents this.
- If the afterload (SVRI) increases, then the heart has to contract more forcefully to pump the same amount of blood as before
- Increasing afterload decreases cardiac output
- Decreasing afterload increases cardiac output
If the afterload exceeds the function of the heart muscle, the heart may be decompensated.
Myocardial contractility
Myocardial contractility affects cardiac output
Myocardial contractility refers to the ability of the heart to contract without being affected by preload or afterload. Substances that cause an increase in intracellular calcium ions lead to an increase in contractility. Different concentrations of calcium ions in cells result in varying degrees of binding between cardiac actin (fine) and myosin (thick) fibers.
Cardiac contractility cannot be directly measured clinically. Therefore, alternative parameters are used to evaluate or estimate the contractile force.
Whole cardiac ejection fraction (GEF)
Ejection fraction indicates the percentage of intraventral volume ejected from a single contraction. The measurement of whole cardiac ejection fraction provides a complete picture of the overall contractility of the heart.
Cardiac Function Index (CFI)
Cardiac function index can be used to assess cardiac contractility. It represents blood flow (cardiac output) as a function of preload volume (GEDV). Thus, the cardiac function index is a cardiac performance parameter associated with preload.
Cardiac Work Index (CPI)
CPI stands for Left Ventricular Cardiac Power Output. It is related to pressure (MAP) and flow rate (CO). In clinical studies, it has been found to be the strongest factor associated with independent prediction of in-hospital mortality in patients with cardiogenic shock. 44,45
Cardiac contractility cannot be directly measured clinically. Therefore, alternative parameters are used to evaluate or estimate the contractile force.
左心收缩力 Left ventricular contractility (dPmx)
Based on the arterial pressure curve, the change in systolic pressure can be analyzed and the degree of pressure increase over time can be calculated (analyzed in velocity). The steeper the ascending ramus of the curve, the stronger the left ventricular contractility.
Since the ascending branch also depends on the compliance of the aorta in a single patient, this parameter should be viewed and evaluated primarily as part of an overall trend.
Lung fluid was assessed using the PiCCO technique
Examples where chest x-ray does not reflect the degree of pulmonary edema
Extravascular Lung Fluid Index (ELWI)
Pulmonary edema is characterized by fluid accumulation in the interstitium and/or alveoli of lung tissue. This can lead to impaired gas exchange and may even lead to respiratory failure. The extent of pulmonary edema can be easily quantified by measuring the extravascular pulmonary fluid index (ELWI) at the bedside. Common clinical signs of pulmonary edema (albino on chest x-ray, low oxygenation index, decreased lung compliance) are nonspecific and are only indicative when oedema is in advanced stages. In routine intensive care, a chest x-ray is often used to evaluate patients at risk of pulmonary edema. This method is imperfect because chest x-rays can only provide black-and-white density images of all components of the chest, including gas volume, blood volume, pleural effusion, bone, muscle, lung tissue, fat, skin edema, and pulmonary edema.
A more advanced approach is the use of extravascular lung water, which provides a systematic pathway to treatment. Extravascular pulmonary water is indexed by body weight in kg, and is written as extravascular pulmonary fluid index (ELWI).
Underestimation of lung fluid can be avoided by referring to the patient's ideal body weight (PBW), especially in obese patients.
肺血管通透性指数 Pulmonary vascular permeability index (PVPI)
When pulmonary edema occurs (measured with extravascular lung fluid), the next important question is: What is the cause of pulmonary edema?
There are two main sources of pulmonary edema in general
Cardiogenic pulmonary edema
Caused by an overload of intravascular fluid, hydrostatic pressure increases. This causes fluid to leak into the space outside the blood vessels.
Permeable pulmonary edema
Increased vascular permeability is caused by an inflammatory response, such as sepsis. This results in increased transfer of fluids, electrolytes, and proteins from intravascular to extravascular spaces, even from normal to low intravascular fluid status and hydrostatic pressure.
The differential diagnosis of pulmonary edema is important because treatment varies greatly. For cardiogenic pulmonary edema, negative fluid balance is required for treatment, whereas in the case of permeable pulmonary edema, treatment of the cause of inflammation is preferred.
The pulmonary vascular permeability index (PVPI) is helpful in the differential diagnosis of cardiogenic pulmonary edema and permeable pulmonary edema. This parameter was calculated from extravascular lung fluid (EVLW) versus pulmonary blood volume (PBV). The PVPI value was between 1 ~ 3, indicating cardiogenic pulmonary edema; A PVPI value greater than 3 indicates permeable pulmonary edema.
Indications and clinical significance
PiCCO indications
Indicated in patients with haemodynamic instability, unclear volume status, and treatment conflicts.
This type of situation usually occurs in the following situations:
- Septic shock
- Cardiogenic shock
- Traumatic shock
- ARDS
- Severe burns
- pancreatitis
- High-risk surgical procedures
Clinical significance
Monitoring alone does not reduce mortality or morbidity, but it provides useful information for developing treatment plans to implement goal-directed treatment for patients as early as possible. The literature recommends early goal-directed therapy (EGDT) and points to the following advantages of early goal-directed therapy5,46
- Reduction in mechanical ventilation time47,48
- Reduce ICU length of stay 5
- Reduces complications 5
- Reduce recovery time 5
Based on validated data, goal-directed therapy improves prognosis. 49-57
Hemodynamic therapy decision trees
This decision tree does not assume any responsibility. It is not a substitute for individual treatment decisions by physicians.