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| Detailed cardiovascular assessment of shock patients |
1. Is the patient shocked?
2. What type of shock is it?
3. What is the tissue perfusion? If there is insufficient perfusion, what should I do next?
4. Is there any heart failure?
This article will focus on the analysis of these four important issues.
Shock recognition
Shock is the circulatory failure that causes oxygen delivery to fail to meet tissue needs, which in turn causes cellular hypoxia, which can be life-threatening in severe cases. To identify shock, we can detect VO2 / DO2 by the bedside, but it is very cumbersome, so we use other methods instead, such as blood lactate levels. When DO2 is below a certain threshold, blood lactate levels rise sharply. In addition, shock can be identified by tissue hypoperfusion (eg, cutaneous vasoconstriction or plaque, limb extremity, prolonged capillary refill time, impaired microcirculation, increased static-arterial carbon dioxide partial pressure difference) These performances may often exist early in the VO2 / DO2 mismatch.
It should be noted that it is not possible to judge whether there is shock based on hypotension, especially in patients with high blood pressure. If the patient has tissue hypoperfusion and blood lactate levels are elevated, then shock should be thought of.
Type of shock
Defining the patient's type of shock not only guides treatment, but also helps manage it from the cause. Shock is mainly divided into four types: hypovolemia, cardiogenic, obstructive and distributed shock. Among the many hemodynamic monitoring methods, the most convenient is cardiac color Doppler ultrasound, which can be used as the preferred method to directly diagnose the type of shock (some studies have shown that the time required is 4.9 ± 1.3 min). Therefore, the newly diagnosed patients are mainly evaluated by "central catheter-cardiac color ultrasound-arterial catheter" (Fig. 1). When the patient is ineffective or complicated in the initial treatment, consider using pulmonary artery floating catheter or transpulmonary thermodilution technique. . Intravascular pressure can be monitored using a pulmonary artery floating catheter, and the amount of vascular content can be determined by a pulmonary thermodilution technique. In some extreme cases, these two invasive monitoring methods can provide us with accurate cardiac output and help us understand the patient's circulatory state and shock type (Figure 2).
Evaluation and treatment of tissue hypoperfusion
1.Lactic acid
Under normal circumstances, the ratio of lactic acid / pyruvic acid is about 10, when circulatory failure leads to tissue hypoxia, a large amount of lactic acid is formed, and the ratio of lactic acid / pyruvic acid can be increased to 20. The energy produced by anaerobic metabolism is much lower than that of aerobic metabolism, so long-term hypoxia can cause cell death.
It is worth noting that if a hemodynamically stable sepsis patient with mild lactic acid elevation is not necessarily associated with tissue hypoxia. Sepsis inflammatory cytokines accelerate the metabolism of aerobic sugars and increase the availability of pyruvate, which, to a certain extent, increases the production of lactic acid, albeit without hypoxia. When hyperlactemia occurs, the rate of lactic acid clearance also decreases. In patients with shock, if there is hyperlactosis, it is usually due to hypoxia, but if it lasts for more than 1 day, other reasons need to be considered.
2. Static-arterial carbon dioxide partial pressure difference (PvaCO2)
According to the Fick formula, PvaCO2 is related to cardiac output CO, with a normal value ≤ 6 mmHg. When ScvO2 decreased and PvaCO2 increased, it indicated that cardiac output decreased; when ScvO2 was normal and PvaCO2 was elevated, it suggested microcirculatory metabolic disorder. In addition, elevated PvaCO2 can also reflect the presence of anaerobic metabolism, and CO2 production is higher than VO2, in which case the respiratory quotient is >1. The respiratory quotient can be approximated by PvaCO2 divided by the arteriovenous oxygen partial pressure difference, and the ratio of 1.3 is indicative of anaerobic metabolism. Because of the potential interference of the Haldane effect, a ratio greater than 1 suggests anaerobic metabolism. Ospina-Tascon et al.'s study of patients with septic shock showed that if the static-arterial carbon dioxide partial pressure difference / arteriovenous oxygen partial pressure difference > 1 indicates a poor prognosis.
3. How do the above indicators work together?
Using the tree diagram in Figure 3 below, the combination of lactic acid, PvaCO2, and ScvO2 can help identify abnormalities and identification of causes (such as decreased cardiac output or microcirculation changes).
4. Evaluation of microcirculation
In patients with circulatory failure, cardiac output and perfusion pressure decrease, resulting in insufficient organ perfusion. However, after the arterial pressure and cardiac output of such patients are improved, tissue hypoperfusion often persists. Microcirculation is an important part of regulating the distribution of blood flow at the organ level. Microcirculation perfusion changes during sepsis, septic shock, and cardiogenic shock, and this change is associated with the incidence of organ disorders and the risk of death. The mechanism of this microcirculation change mainly involves the loss of contact between vascular segments, vascular reactive damage of endothelial cells, hemorheological changes of erythrocytes and leukocytes, changes of endothelial glycocalyx, platelet aggregation and microthrombosis. In addition to microcirculatory perfusion abnormalities, changes in microcirculatory vascular endothelial cells are also associated with activation of the coagulation system, inflammatory response, oxygen free radical production, and changes in permeability.
There are many ways to evaluate microcirculation perfusion, but the most direct and appropriate method is video microscopy, which can directly detect perfusion heterogeneity. Under normal conditions, microvascular perfusion is very uniform and vascular density increases or decreases in direct proportion to metabolic requirements. Microvascular perfusion during septic shock is characterized by not only a reduction in vascular density, but also a heterogeneity of perfusion, that is, a non-perfused vessel that abuts the perfused vessel. The density of the perfused blood vessels and the microcirculation shunt are reduced, resulting in hypoxia in the case of an increase in venous oxygen saturation.
5. Treatment
We guide treatment based on hemodynamic monitoring parameters, but it is worthwhile to explore whether the treatment should be standardized or individualized. The standardized hemodynamic resuscitation is based on the theory that similar treatment targets can be achieved in all patients, and that reaching a target value in most patients can improve clinical outcomes. However, some patients have the opposite effect after reaching the target value, which is sufficient for such patients with lower treatment goals.
6. Liquid therapy
Fluid therapy can improve tissue perfusion by increasing cardiac output, and thus plays an important role in the treatment of resuscitation in patients with sepsis. During the primary resuscitation phase, patients responded to fluid resuscitation, but it has now been found that the goal of subsequent fluid resuscitation treatment is highly controversial because many patients show no response to fluid resuscitation later, and fluid positive balance usually has a poor prognosis. Therefore, clinical attempts have been made to predict the patient's fluid therapy response. Usually, static indicators of cardiac preload, such as CVP, can only be analyzed from the population level. Nearly 2/3 of the patients have a response below 8 mmHg, and more than 12 mmHg suggest no response. Using dynamic parameters, it is possible to predict patient fluid therapy responsiveness from an individual level. Prerequisites need to meet several pre-requirements including no arrhythmia, tidal volume greater than 8ml/kg body weight, no spontaneous breathing exercise, etc., can apply the respiratory variability of stroke volume (via different pulse waveform analysis techniques or Doppler ultrasound) Direct measurement) or pulse pressure changes to accurately predict whether a patient has a liquid therapy response. The passive leg lift test is another reliable method, but because of the need to repeatedly apply it, there must be a cardiac output monitoring tool that can respond quickly and accurately. These dynamic tests have been included in the recommendations by the latest guidelines.
Another alternative is the minimal rehydration test, which is a rapid infusion of less than 100 ml of fluid to predict the patient's fluid resuscitation reactivity. If the patient does not change after the rapid rehydration, the patient is predicted to be unresponsive to a large amount of fluid therapy. However, a positive minimum rehydration test does not imply a response to further fluid therapy (due to the first volume reactivity being integrated into the assessment of the total amount of liquid, there is a bias in the assay). If anything, it should be the opposite, because patients with preload reactions (rising part of the Starling curve) are more responsive to fluid therapy in the initial rehydration than the subsequent rehydration. Therefore, we can predict the patient's volume reactivity by giving a small dose rehydration test, evaluate its effect, and predict the response to the liquid before the next rehydration, rather than directly giving a large dose of rehydration test. The decision flow chart for liquid therapy can be seen in Figure 4.
7. Blood pressure
The guidelines recommend fluid resuscitation to achieve an average arterial pressure of 65 mm Hg, and some may need to achieve higher blood pressure. Observational studies have shown that patients with blood pressure who do not reach the target of recovery have an increased case fatality rate, but higher blood pressure does not mean better clinical outcomes. Many studies have attempted to confirm that patients can improve clinical outcomes by increasing mean arterial pressure. A study of 776 patients with septic shock showed that mean arterial pressure of 65 or 85 mm Hg had no effect on 28-day mortality, but if patients with a history of hypertension achieved higher blood pressure goals after resuscitation, acute The incidence of kidney damage will decrease. The study also found that patients with high-dose norepinephrine to achieve higher blood pressure goals also had an increased incidence of atrial fibrillation. Therefore, all patients cannot be required to achieve higher blood pressure goals. Higher blood pressure target values are only suitable for some patients, and it is also necessary to assess whether the patient responds to the treatment and to monitor if the parameters are corrected.
8.EGDT and individualized treatment
The concept of early goal-directed therapy (EGDT) was first derived from a study by Rivers et al. in patients with septic shock. The results showed that patients with EGDT had a 28-day mortality rate lower than that of the control group (33% and 49%). EGDT is one of the treatment goals of patients with septic shock, but there are now studies that explain EGDT from multiple directions, often losing its original meaning. For some people, EGDT represents CVP-based active fluid resuscitation treatment, or early optimal hemodynamic resuscitation treatment, while others believe that its significance is to use broad-spectrum antibiotics as early as possible. The EGDT content includes ScvO2-based maximal oxygen delivery, as well as fluid resuscitation, infusion of red blood cells, and positive inotropic drug therapy. The results of the EGDT study are a boon for early resuscitation treatment, but at the same time there is controversy, especially the concept is sublimated into a cluster treatment strategy, and the law is mandatory, requiring difficult conditions such as no serious care physicians. Early resuscitation treatment for patients with sepsis. This is of course criticized by many people, because some parameters in cluster therapy (such as CVP / MAP) exist in both test groups and cannot be used to explain the difference in results between the two groups.
However, several other large randomized controlled trials that followed did not yield similar results. Does this mean that the concept of EGDT is coming to an end? This may not be the case because there are many different influencing factors between different trials. First, the cases included in these recent studies have already met ScvO2 greater than 75% from the outset, while the patient population ScvO2 studied by Rivers et al. is abnormal. Second, patients in recent studies have a much lower disease severity, as reflected in the case fatality rate, and up to 20% of patients do not stay in the ICU, although the inclusion criteria baseline is the same. Based on the above, the most reasonable approach may be that EGDT is not recommended for all patients with sepsis, but in the most severe cases it can (should) be performed, especially when ScvO2 is significantly reduced. However, it is worth noting that the occurrence of ScvO2 elevation in patients with insufficient tissue perfusion and organ dysfunction is also a good thing, because patients with high ScvO2 usually have poor prognosis, suggesting microcirculation abnormalities and mitochondrial dysfunction.
Another important concept in cluster therapy is the use of CVP to guide fluid resuscitation. The recommended CVP is maintained at 8-12 mmHg. Based on statistical results, patients with CVP less than 8 mm Hg will respond to fluid therapy, while most patients with greater than 12 mm Hg will have no capacity reactivity. Although CVP is widely used, CVP is not the best parameter for predicting capacity reactivity. The latest rescue sepsis exercise guide incorporates this notion into the guidance of fluid resuscitation: "We recommend guiding the next step in fluid therapy (best practice statement) by continuously reassessing hemodynamic status after initial fluid resuscitation." It is recommended that we repeatedly estimate the predicted volume reactivity based on clinically relevant variables, hemodynamic monitoring, and dynamic changes in static parameters. This updated concept has made EGDT more individual and an important advancement in the treatment of patients with sepsis.
9. Treatment of abnormal microcirculation
How to regulate microcirculation? Simply increasing blood flow without improving microcirculation is useless. In the early stages of fluid therapy, not only can the microcirculation be improved, but also the score of organ dysfunction can be quickly reduced, but in the later stage, the effect of liquid therapy is greatly diminished. Dobutamine can increase microcirculation perfusion, but the effect is limited. It has also been suggested that vasodilators can be used, but there is still insufficient evidence to support them. Because of the lack of selectivity of these vasodilators, it may cause the already filled blood vessels to continue to relax and steal blood. Recently, it has been found that the regulation of endothelial nitric oxide synthase may have therapeutic potential. We need more research data before using microcirculation as a therapeutic goal. In any case, it is necessary to assess the potential impact of interventions on the microcirculation.
Assessment and management of cardiovascular dysfunction
Although the measurement of cardiac output can only provide partial information, it is also important to determine whether the cardiac output is normal. The determination of cardiac output is mainly dependent on ScvO2 or SvO2, combined with the determination of tissue perfusion. In addition, the measurement of ventricular filling pressure or volume is also helpful in assessing cardiovascular conditions.
When making treatment decisions or not changing myocardial contractility, it is important to assess the consequences of decreased contractility: insufficient cardiac output, is it associated with tissue perfusion disorders? The relationship between cardiac contractility and cardiac output is indeed relatively weak, so patients who may have experienced decreased myocardial contractility but still maintain normal cardiac output do not need to use positive inotropic drugs. Other patients with decreased cardiac output may not need to use it. Only those patients with decreased cardiac output due to decreased myocardial contractility may benefit from positive inotropic drug therapy.
Recently, in the trial of levosimendan treatment in patients with septic shock, it has been found that the addition of levosimendan to standard treatment has nothing to do with the reduction of organ dysfunction or mortality caused by sepsis. On the contrary, it is related to the increased risk of developing a rapid arrhythmia. Of course, the design of this trial may be problematic. For example, cardiac output and cardiac function are not included in the test. Therefore, patients with increased cardiac output and/or myocardial contractility may be accepted even if they do not need or even have contraindications. Treatment of levosimendan. In fact, one in five patients with septic shock may present with a left ventricular outflow tract or a middle left ventricular obstruction, and these patients are contraindicated with positive inotropic drugs. Therefore, individualized treatment based on hemodynamic monitoring should be preferred in these patients.
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