Basics of Hemodynamics in Shock

• Hemodynamics refers to blood circulation and the forces involved in controlling blood flow throughout the body. Understanding hemodynamic parameters and how they are altered in various disease states is essential for effectively managing shock syndromes.
• Key hemodynamic parameters include:
  • Blood pressure (systolic, diastolic, mean arterial pressure)
    • Reflects the pressure exerted by blood on the arterial vessel walls
    • Mean arterial pressure (MAP) represents the average pressure during the cardiac cycle and determines organ perfusion
    • MAP = Diastolic BP + 1/3 (Systolic BP – Diastolic BP)
    • Normal MAP is 70-105 mmHg
  • Heart rate
    • The number of heart beats per minute
    • Determines cardiac output together with stroke volume
    • Normal resting heart rate is 60-100 beats/minute
  • Cardiac output (CO)
    • The volume of blood pumped by the heart per minute
    • Measured in L/min, normal is 4-8 L/min
    • CO = Stroke Volume x Heart Rate
    • Low CO indicates pump failure in shock
    • High CO can indicate distributive/vasodilatory shock

Physiological Concepts

• Preload is the load present before ventricular contraction and reflects ventricular filling.
  • Preload stretches myocardial muscle fibers, leading to increased force of contraction through the Frank-Starling mechanism.
  • Preload correlates with ventricular end-diastolic volume and pressures like pulmonary capillary wedge pressure.
  • Shock can cause low preload from intravascular volume loss (e.g. hemorrhagic shock).
• Afterload is the load present during ventricular ejection reflecting the pressure the ventricle must overcome to eject blood.
  • Afterload predominantly reflects vascular resistance.
  • Increased afterload makes it harder for the ventricle to eject blood.
  • Elevated afterload occurs in cardiogenic shock from left ventricular systolic dysfunction.
• Contractility refers to the intrinsic ability of cardiac muscle to contract and is influenced by:
  • Adrenergic tone
  • Heart rate
  • Preload
  • Ischemia/infarction
  • sepsis and inflammation (depressed contractility)
  • Impaired contractility reduces cardiac output and underlies cardiogenic shock.
• Stroke volume (SV) is the volume of blood ejected by the ventricle per beat. It is determined by:
  • Preload – influences ventricular filling
  • Afterload – must be overcome to eject blood
  • Contractility – intrinsic ability of myocardium to contract
  • Heart rate – higher rates shorten diastolic filling time
  • Autonomic tone – enhances contractility through adrenergic receptors
• Cardiac output (CO) is the volume of blood ejected by the ventricle per minute. It is calculated as:
  • CO = Stroke Volume x Heart Rate
  • Determinants are the same as those for stroke volume.
  • Low CO can indicate pump failure shock like cardiogenic shock.
  • High CO is characteristic of distributive/vasodilatory shock states.

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Hemodynamic Derangements in Shock

• Low cardiac output states:
  • Reduced preload is characteristic of hypovolemic shock due to intravascular volume depletion from hemorrhage, fluid losses, etc. This impairs ventricular filling and stroke volume.
  • Increased afterload occurs in cardiogenic shock where left ventricular systolic dysfunction impedes ejection. The impaired ventricle cannot overcome elevated vascular resistance.
  • Depressed myocardial contractility can result from myocardial ischemia/infarction or cardiomyopathies. The weakened heart muscle reduces stroke volume and cardiac output.
• High cardiac output states:
  • Hyperdynamic septic shock often presents with increased cardiac output and low systemic vascular resistance due to nitric oxide induced vasodilation.
  • Anaphylactic shock also presents with high output and low vascular resistance due to histamine-mediated vasodilation.
  • High output shock relies on vasoconstriction to maintain blood pressure. This state is more dependent on preload.
• Both low and high cardiac output states can result in shock through inadequate oxygen delivery. Treatment involves optimizing preload, afterload, contractility, and heart rate to improve cardiac performance.

Oxygen Delivery and Consumption

• Oxygen delivery (Do2) refers to the amount of oxygen transported to tissues per minute. It is calculated as:

Do2 = Cardiac Output x Arterial Oxygen Content

• Cardiac output determines blood flow
• Arterial oxygen content is the amount of oxygen carried in the blood (largely bound to hemoglobin)
• Oxygen consumption (Vo2) is the amount of oxygen extracted and used by tissues per minute. It is calculated as:

Vo2 = Cardiac Output x (Arterial Oxygen Content – Venous Oxygen Content)

• Represents the difference in oxygen content between arterial and venous blood
• In shock, Do2 can become inadequate to meet tissue Vo2, leading to tissue hypoxia, anaerobic metabolism, and lactate production.
• Vo2 depends on cellular metabolic activity and is relatively constant. Do2 varies based on hemodynamic factors.
• When Do2 decreases, Vo2 is initially maintained by increased oxygen extraction. However, below a critical Do2 threshold, Vo2 becomes supply dependent and cellular dysfunction occurs.
• Resuscitation goals in shock aim to optimize Do2 by improving cardiac output, hemoglobin/oxygen carrying capacity, and arterial oxygen saturation.
• Monitoring Do2, Vo2, and lactate levels helps gauge the adequacy of resuscitation. Persistent lactate elevation indicates ongoing tissue hypoxia.
• In distributive shock like sepsis, microcirculatory shunting can also impair oxygen delivery even when macrocirculatory parameters appear normal. This represents another mechanism of oxygen delivery failure.

Lactate as a Marker of Perfusion

1. Overview:
   • Definition: Lactate is a byproduct of anaerobic metabolism, produced when cells receive inadequate oxygen.
   • Relevance in Shock: Elevated lactate levels indicate impaired tissue perfusion and oxygenation, commonly seen in shock states.
2. Mechanism:
   • In shock, reduced oxygen delivery (Do2) limits aerobic metabolism, forcing cells to switch to anaerobic pathways, leading to lactate production.
3. Clinical Significance:
   • Indicator of Severity: Higher lactate levels correlate with increased severity of shock and poorer outcomes.
   • Monitoring and Trends: Serial measurement of lactate levels helps in monitoring the response to resuscitation efforts. A decreasing trend is indicative of improved perfusion and oxygenation.
4. Literature
   • Lactate as a Perfusion Marker in Blunt Multi-Trauma Patients: A study by Ozakın et al. (2021) in the “Turkish Journal of Trauma and Emergency Surgery” found that lactate values are a useful marker of perfusion in shock patients. The study revealed a positive correlation between lactate levels and shock index and heart rate, as well as a negative correlation with base deficit values, indicating its utility in predicting blood transfusion needs in trauma patients (Ozakın et al., 2021).
     1. Özakın E, et al. Lactate and base deficit combination score for predicting blood transfusion need in blunt multi-trauma patients. Ulus Travma Acil Cerrahi Derg. 2022 May;28(5):599-606. doi: 10.14744/tjtes.2021.02404. PMID: 35485459; PMCID: PMC10442980.
   • Lactate in Shock-Trauma Patients: Research by Deitch et al. (2007) in the “Annals of Surgery” emphasized that lactate is an excellent and accurate indicator of inadequate tissue perfusion in shock patients. This study provides substantial evidence supporting the clinical use of lactate levels as a reliable marker for assessing the severity and management of shock states (Deitch et al., 2007).
     1. E. Deitch et al. “Hormonally Active Women Tolerate Shock-Trauma Better Than Do Men: A Prospective Study of Over 4000 Trauma Patients.” Annals of Surgery, 246 (2007): 447-455.
   • Lactate Clearance in Septic Shock: A study by Coen et al. (2014) published in “The American Journal of Emergency Medicine” explored the role of lactate clearance as a marker of tissue perfusion in patients with septic shock. The study suggests that lactate clearance can be used effectively in this context, potentially reducing the need for central venous catheters in the early goal-directed treatment of septic shock. This finding is significant as it highlights the possibility of using less invasive methods to monitor and manage patients with septic shock (Coen et al., 2014).
     1. D. Coen et al. “Towards a less invasive approach to the early goal-directed treatment of septic shock in the ED..” The American journal of emergency medicine, 32 6 (2014): 563-8 .
        
        

Capillary Refill as a Marker of Perfusion

1. Overview:
   • Definition: Capillary refill time is the time taken for color to return to an external capillary bed after pressure is applied.
   • Application: A simple, rapid bedside assessment to gauge peripheral perfusion.
2. Clinical Application:
   • Normal vs. Prolonged Refill Time: Normal refill time is usually less than 2 seconds. Prolonged refill time can indicate poor peripheral perfusion, often seen in various shock states.
   • Limitations: External factors like ambient temperature and patient age can affect capillary refill time.
3. Relevance in Shock:
   • Initial Assessment: Provides quick initial assessment of circulatory status in patients with suspected shock.
   • Resuscitation Monitoring: Changes in capillary refill time can reflect response to resuscitative measures, although it should be used in conjunction with other hemodynamic assessments.
4. Literature
   • Capillary Refill Time in Pediatric Shock Patients: A study by Bumke and Maconochie (2001) titled “Paediatric capillary refill times,” published in “Trauma,” discusses the role of CRT in assessing peripheral perfusion in combination with other markers like heart rate, respiratory rate, and level of consciousness in shock patients. This highlights the utility of CRT in pediatric settings and its integration with other clinical signs for a comprehensive assessment of shock (Bumke & Maconochie, 2001).
     1. Bumke K, Maconochie I. Paediatric capillary refill times. Trauma. 2001;3:217-220. doi:10.1177/146040860100300404
   • Capillary Refill in Septic Shock Patients: Hernández et al. (2012) conducted a study titled “Evolution of peripheral vs metabolic perfusion parameters during septic shock resuscitation. A clinical-physiologic study,” published in the “Journal of Critical Care.” This study found that capillary refill time (CRT) is effective in assessing peripheral perfusion in septic shock patients. It was observed that early recovery of CRT anticipates successful resuscitation compared to traditional metabolic parameters (Hernández et al., 2012).
     1. Hernández G, Pedreros C, Veas E, et al. Evolution of peripheral vs metabolic perfusion parameters during septic shock resuscitation. A clinical-physiologic study. J Crit Care. 2012;27(3):283-288. doi:10.1016/j.jcrc.2011.05.024
   • Capillary Refill Time in Septic Shock Resuscitation: The study “Effects of capillary refill time-vs. lactate-targeted fluid resuscitation on regional, microcirculatory and hypoxia-related perfusion parameters in septic shock: a randomized controlled trial” by Castro et al., published in “Annals of Intensive Care” in 2020, compared the impact of CRT-targeted vs. lactate-targeted fluid resuscitation strategies in septic shock patients. The study found that while CRT-targeted fluid resuscitation was not superior in terms of fluid administration or balances, it was associated with comparable effects on regional and microcirculatory flow parameters and hypoxia surrogates. This study underscores the utility of CRT as a resuscitation target, offering a potentially safer approach in terms of tissue perfusion when compared to lactate-targeted strategies (Castro et al., 2020).
     1. Castro R, Kattan E, Ferri G, Pairumani R, Valenzuela ED, Alegría L, Oviedo V, Pavez N, Soto D, Vera M, Santis C, Astudillo B, Cid MA, Bravo S, Ospina-Tascón G, Bakker J, Hernández G. Effects of capillary refill time-vs. lactate-targeted fluid resuscitation on regional, microcirculatory and hypoxia-related perfusion parameters in septic shock: a randomized controlled trial. Ann Intensive Care. 2020 Nov 2;10(1):150. doi: 10.1186/s13613-020-00767-4. PMID: 33140173; PMCID: PMC7606372.
   • Capillary Refill in Assessing Peripheral Perfusion in Children: In 2022, Nickel et al. published “Comparison of Bedside and Video-Based Capillary Refill Time Assessment in Children” in “Pediatric Emergency Care.” This study explored the consistency of bedside and video-based capillary refill time observations in assessing peripheral perfusion in children with suspected shock. The findings indicated moderate consistency, suggesting the potential usefulness of CRT in pediatric shock assessment (Nickel et al., 2022).
     1. Nickel A, Hunter R, Jiang S, et al. Comparison of Bedside and Video-Based Capillary Refill Time Assessment in Children. Pediatr Emerg Care. 2022;38:506-510. doi:10.1097/PEC.0000000000002836

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Advanced Hemodynamic Monitoring

Pulmonary Artery Catheterization

• Involves placing a catheter into the pulmonary artery to directly measure pressures and cardiac output.
• Indications:
  • Differentiate causes of undifferentiated shock (cardiogenic, hypovolemic, etc)
  • Monitor response to interventions in complex critically ill patients
  • Manage severe hemodynamic instability that is difficult to manage with less invasive tools
  • Quantify ventricular filling pressures and pulmonary pressures in settings like heart failure
• Limitations:
  • Risks of placement (arrhythmias, infection, thrombosis, pulmonary infarction, mechanical complications)
  • No clear mortality benefit demonstrated from routine use in ICU patients
  • Pressure values affected by mechanical ventilation, mitral valve disease, pulmonary hypertension
• Key measurements:
  • Pulmonary artery pressures (systolic, diastolic, mean)
    • Elevated in pulmonary hypertension, right heart dysfunction
  • Pulmonary capillary wedge pressure (PCWP)
    • Estimate of left ventricular filling pressure
    • Reflects left ventricular preload
    • Elevated in cardiogenic shock, normal/low in hypovolemic shock
  • Continuous right heart pressures
    • Allow real-time monitoring of filling pressures to guide fluid/diuretic management
  • Cardiac output and cardiac index
    • Measured by thermodilution – injecting cold saline and measuring temperature change to calculate flow
    • Requires proper positioning (zone 3 of pulmonary artery)
    • Lower in cardiogenic shock, higher in distributive shock
  • Mixed venous oxygen saturation (SvO2)
    • Reflects global oxygen extraction ratio
    • Low levels indicate supply-dependent oxygen consumption and impaired perfusion
    • Can be used to guide shock resuscitation (e.g. early goal directed therapy protocols)

Echocardiography

• Uses ultrasound to visualize cardiac structure and function in real time
• Two main types:
  • Point-of-care – focused exam at bedside to answer specific clinical questions
  • Comprehensive – complete assessment of cardiac and valvular structure and function
• Key measurements:
  • Ejection fraction – index of left ventricular systolic function
    • Reduced in cardiogenic shock from systolic heart failure
  • Size of cardiac chambers
    • Enlarged ventricles in volume overload states like valvular disease
  • Valvular structure and flow patterns
    • Regurgitation or stenosis that can precipitate cardiogenic shock
  • Diastolic dysfunction parameters
    • Impaired relaxation indicates poor ventricular compliance
  • Inferior vena cava size and collapsibility
    • Estimates right atrial pressure and fluid responsiveness
  • Right ventricular size and function
    • Enlarged, hypokinetic right ventricle suggests acute pulmonary embolism
• Advantages:
  • Rapid bedside assessment of cardiac function and anatomy
  • Doppler allows evaluation of valve hemodynamics
  • Can diagnose underlying causes of shock like tamponade
• Limitations:
  • Operator dependent – requires specialized training
  • Image quality affected by patient factors like obesity, dressings

Arterial and Venous Blood Gases

• Analyze partial pressures of oxygen and carbon dioxide plus acid-base status
• Arterial blood gas indicates gas exchange and ventilation/perfusion adequacy
• Venous blood gas reflects global tissue oxygen extraction and perfusion
• Key parameters:
  • pH, pCO2, pO2
    • Determine acid-base disturbances like lactic acidosis in shock
  • Oxygen saturation
    • Low arterial saturation indicates impaired oxygenation
  • Lactate, base excess
    • Markers of anaerobic metabolism and hypoperfusion
  • SvO2 from venous sample
    • Indicator of balance between oxygen delivery and consumption
    • Low SvO2 suggests supply dependence and impaired perfusion
• Advantages:
  • Rapid analysis of acid-base and oxygenation status
  • Venous blood gas avoids risks of arterial puncture
• Limitations:
  • Represents single point in time versus continuous monitoring

Central Venous Catheterization (CVC)

Central Venous Catheterization (CVC) is a fundamental procedure in the management of shock, offering valuable hemodynamic insights and therapeutic options. Recent advances and best practices in CVC focus on patient preparation, catheterization techniques, and monitoring to optimize patient outcomes.

Indications and Techniques

• Indications: CVC is routinely used in critical care and emergency departments for monitoring patients and administering parenteral medications under special conditions, such as shock (Almaghraby, 2016). It is particularly beneficial for central venous pressure monitoring, transvenous cardiac pacing, hemodialysis, drug administration, rapid fluid infusion, and aspiration of air embolisms.
• Techniques: The latest techniques emphasize aseptic procedures, the use of ultrasound guidance to enhance safety and efficacy, and accurate depth insertion prediction to minimize complications (Farooq, 2007; Zujeva et al., 2022). Ultrasound guidance, in particular, has shown to reduce mechanical complications and improve success rates compared to the anatomical landmark technique (Cajozzo et al., 2004).

Key Measurements

• Central Venous Pressure (CVP): CVP is a critical measurement for guiding fluid management and vasopressor therapy. It reflects intravascular fluid status and right heart function. The correct interpretation of CVP values aids in determining fluid responsiveness and guiding resuscitation strategies (Vinson et al., 2014).
• Oxygen Saturation (ScvO2): ScvO2 measurement from the central venous catheter indicates tissue oxygen extraction and can be pivotal in guiding the management of shock, especially in septic conditions. Low ScvO2 suggests inadequate oxygen delivery and may prompt interventions to improve cardiac output and oxygenation.
• Temperature: Continuous temperature monitoring via CVC helps in identifying fever, which can be a sign of infection or inflammation. Temperature monitoring is vital in managing patients with sepsis, where fever management is a crucial part of therapy.

Limitations and Complications

• Limitations: Despite its utility, CVC is associated with risks such as infection, thrombosis, arterial puncture, and mechanical complications (Lin et al., 2009). The routine use of CVC in ICU settings has not shown a clear mortality benefit, and its usage should be weighed against potential risks.
• Complications: Complications can range from minor issues like malposition and catheter malfunction to more severe problems like tricuspid valve endocarditis, arrhythmias, and vascular perforation (Kim et al., 2017; Kale & Raghavan, 2013).

Best Practices

• Infection Control: Implementing strict infection control measures and considering antimicrobial/antiseptic-impregnated or heparin-impregnated CVCs can reduce catheter-related infections (Schiffer et al., 2013).
• Emergency Use: The use of CVC in emergency settings should be carefully considered, given the potential for serious complications (Abraham et al., 1983).
• Site Selection: The choice of insertion site (jugular vs. femoral) should consider the risk of catheter colonization and catheter-related bloodstream infections (Silvetti et al., 2018).

References

• Almaghraby, A. (2016). A Catastrophe Caused by Central Venous Catheter Insertion – A Case Report. Cardiology: Open Access.
• Farooq, M. (2007). Bedside prediction of central venous catheter insertion depth. British journal of anaesthesia.
• Zujeva, O., Gierasimovič, Z., & Giedrimė, L. (2022). Nursing needs and prevention of complications after central venous catheterisation. Slauga. Mokslas ir praktika.
• Cajozzo, M., Cocchiara, G., Greco, G., Vaglica, R., Bartolotta, T., Platia, L., & Modica, G. (2004). Ultrasound (US) guided central venous catheterization of internal jugular vein on over 65‐year‐old patients versus blind technique. Journal of Surgical Oncology.
• Vinson, D., Ballard, D., Stevenson, M., Mark, D., Reed, M., Rauchwerger, A., Chettipally, U., & Offerman, S. (2014). Predictors of Unattempted Central Venous Catheterization in Septic Patients Eligible for Early Goal-directed Therapy. Western Journal of Emergency Medicine.
• Lin, J. Y., Kuo, P., & Chen, J. S. (2009). Malpositioned Central Venous Catheter in the Main Pulmonary Artery Trunk-A Case Report.
• Kim, Y. J., & Kim, W. (2017). Sudden hypotension occurring after 4 days of left-sided central catheter placement. Journal of thoracic disease.
• Schiffer, C., Mangu, P., Wade, J., Camp-Sorrell, D., Cope, D., El-Rayes, B., Gorman, M., Ligibel, J., Mansfield, P., & Levine, M. (2013). Central venous catheter care for the patient with cancer: American Society of Clinical Oncology clinical practice guideline. Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
• Abraham, E., Shapiro, M., & Podolsky, S. (1983). Increased rate of central venous catheterization procedures in community EDs. The American journal of emergency medicine.
• Silvetti, S., Aloisio, T., Cazzaniga, A., & Ranucci, M. (2018). Jugular vs femoral vein for central venous catheterization in pediatric cardiac surgery (PRECiSE): study protocol for a randomized controlled trial. Trials.
• Kale, S. B., & Raghavan, J. R. (2013). Tricuspid valve endocarditis following central venous cannulation: The increasing problem of catheter related infection. Indian Journal of Anaesthesia.

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VOLUME Status and Responsiveness

Fluid Bolus Challenge

Indications and Contraindications

Fluid bolus therapy (FBT) is a critical component in the management of various critical conditions but requires careful consideration of its indications and contraindications. While FBT transiently improves renal function and medullary oxygenation in early septic acute kidney injury, these effects dissipate after subsequent boluses, limiting its long-term effectiveness (Lankadeva et al., 2019). In pediatric patients, particularly in cases of sepsis, FBT may lead to increased extravascular lung water and respiratory dysfunction (Long et al., 2018). Additionally, bolus fluid therapy for severe infections in African children has been associated with higher mortality rates, questioning the routine use of such regimes in sepsis treatment (Riste & Ford, 2012; Myburgh & Finfer, 2013). Therefore, while FBT can be beneficial in certain scenarios, its application needs to be judicious, considering the potential risks and patient-specific factors.

Monitoring Response to Fluid Bolus Challenge

Monitoring the response to fluid bolus therapy is crucial for optimizing patient outcomes. Techniques such as changes in pulse pressure variation and stroke volume variation after a tidal volume challenge have been shown to predict fluid responsiveness reliably during low tidal volume ventilation (Myatra et al., 2017). Non-invasive methods like stroke volume measurement and passive leg raising can predict volume responsiveness in medical ICU patients, with less than 50% being responsive to fluid boluses (Thiel et al., 2009). Furthermore, mini-fluid challenges using minimal invasive pulse contour cardiac output measurements have been proposed to improve fluid management in post-cardiac surgery patients (Smorenberg et al., 2018). These monitoring techniques aid in assessing the efficacy of fluid therapy and adjusting treatment strategies accordingly.

References:

1. Lankadeva YR, Kosaka J, Iguchi N, et al. Effects of Fluid Bolus Therapy on Renal Perfusion, Oxygenation, and Function in Early Experimental Septic Kidney Injury. Crit Care Med. 2019;47:e36–e43.
2. Long E, O’Brien A, Duke T, et al. Effect of Fluid Bolus Therapy on Extravascular Lung Water Measured by Lung Ultrasound in Children With a Presumptive Clinical Diagnosis of Sepsis. J Ultrasound Med. 2018;38.
3. Riste M, Ford S. Mortality after Fluid Bolus in African Children with Severe Infection. J Intensive Care Soc. 2012;13(4):356-357.
4. Myburgh J, Finfer S. Causes of death after fluid bolus resuscitation: new insights from FEAST. BMC Med. 2013;11:67.
5. Fielding CL, Magdesian KG. A comparison of hypertonic (7.2%) and isotonic (0.9%) saline for fluid resuscitation in horses: a randomized, double-blinded, clinical trial. J Vet Intern Med. 2011;25(5):1138-1143.
6. Younes RN, Aun F, Accioly CQ, et al. Hypertonic solutions in the treatment of hypovolemic shock: a prospective, randomized study in patients admitted to the emergency room. Surgery. 1992;111(4):380-385.
7. Myatra SN, Prabu NR, Divatia JV, et al. The Changes in Pulse Pressure Variation or Stroke Volume Variation After a “Tidal Volume Challenge” Reliably Predict Fluid Responsiveness During Low Tidal Volume Ventilation. Crit Care Med. 2017;45:415–421.
8. Thiel SW, Kollef M, Isakow W. Non-invasive stroke volume measurement and passive leg raising predict volume responsiveness in medical ICU patients: an observational cohort study. Crit Care. 2009;13:R111.
9. Smorenberg A, Cherpanath TGV, Geerts BF, et al. A mini-fluid challenge of 150mL predicts fluid responsiveness using ModelflowR pulse contour cardiac output directly after cardiac surgery. J Clin Anesth. 2018;46:17-22.

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Passive Leg Raising in Shock

Passive leg raising (PLR) is a valuable maneuver in the management of patients with shock. It involves elevating the patient’s legs, which can transiently increase venous return to the heart, potentially improving cardiac output and blood pressure. This simple, non-invasive maneuver has been found effective in various shock states, including hypovolemic shock (Rahmawati et al., 2021) and undifferentiated shock (Toppen et al., 2020).

Hemodynamic Effects

The primary hemodynamic effect of PLR is an increase in cardiac preload, which can improve blood pressure and cardiac output without significant changes in heart rate (Caillé et al., 2008). This effect is particularly beneficial in hypovolemic shock, where it can transiently simulate the effect of fluid administration, thus helping to assess fluid responsiveness. Passive leg raising (PLR) is an effective way to assess fluid responsiveness in shock patients by transiently increasing cardiac preload. This maneuver transfers blood from the lower extremities to the central circulation, effectively increasing preload. While specific volume measurements can vary, the hemodynamic changes induced are equivalent to a fluid bolus of approximately 300-500 mL (Monnet & Teboul, 2007). This transient increase in preload is useful in assessing the heart’s ability to handle additional volume, making PLR a valuable tool in fluid management in shock patients.

Predicting Fluid Responsiveness

PLR is a reliable predictor of volume responsiveness in shock patients, especially those with severe sepsis or septic shock. Studies have shown a high sensitivity and specificity of PLR in predicting volume responsiveness (Huang et al., 2011; Liu et al., 2011). The maneuver, when combined with echocardiography, can further refine the assessment of volume responsiveness (Hu et al., 2019).

Safety and Feasibility

PLR is generally safe and feasible, but it can impact patient comfort and nursing workload. It is important to perform PLR carefully, especially in patients with spinal injuries or other conditions where leg movement might be contraindicated (Toppen et al., 2020). Additionally, the maneuver should be executed properly, starting from a semi-recumbent position and detecting short-term changes in cardiac output during the test for the best results (Monnet & Teboul, 2015).

1. Rahmawati I, Dilaruri A, Sulastyawati, Supono. The Role of Passive legs Raising Position in Hypovolemic Shock: A Case Report and Review of the Literature. [Publication Title]. 2021;4:177-184.
2. Toppen W, Montoya EA, Ong S, et al. Passive Leg Raise: Feasibility and Safety of the Maneuver in Patients With Undifferentiated Shock. J Intensive Care Med. 2020;35:1123-1128.
3. Caillé V, Jabot J, Belliard G, et al. Hemodynamic effects of passive leg raising: an echocardiographic study in patients with shock. Intensive Care Med. 2008;34:1239-1245.
4. Huang L, Zhang W, Cai W, et al. [Passive leg raising predicts volume responsiveness in patients with severe sepsis and septic shock]. Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue. 2011;23(3):154-7.
5. Liu Y, Lu YH, Xie JF, et al. [Passive leg raising predicts volume responsiveness in patients with septic shock]. Zhonghua wai ke za zhi [Chinese journal of surgery]. 2011;49(1):44-8.
6. Hu XY, Li L, Hao XY, et al. [Passive leg raising combined with echocardiography could evaluate volume responsiveness in patients with septic shock]. Zhonghua wei zhong bing ji jiu yi xue. 2019;31(5):619-622.
7. Lakhal K, Ehrmann S, Benzékri-Lefèvre D, et al. Brachial cuff measurements for fluid responsiveness prediction in the critically ill. Critical Care. 2011;15:P73 – P73.
8. Monnet X, Teboul JL. Volume responsiveness. Curr Opin Crit Care. 2007;13:549–553.

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Inferior Vena Cava (IVC) Assessment in Clinical Practice

Ultrasound Assessment of IVC

Ultrasound assessment of the Inferior Vena Cava (IVC) is a widely used non-invasive technique to evaluate a patient’s volume status and fluid responsiveness. This method involves measuring the diameter of the IVC and its respiratory variability using ultrasound, which provides real-time and bedside information about intravascular volume status.

Recent studies highlight the utility and limitations of IVC ultrasound. For instance, Tan, Wijeweera, and Onigkeit (2015) noted its potential usefulness in guiding fluid resuscitation in critically ill patients, though a consensus on its application is still evolving. Spiliotaki et al. (2022) emphasized its value in emergency and intensive care settings, acknowledging its limitations and technical considerations.

Correlation with Volume Status and Fluid Responsiveness

The IVC ultrasound’s ability to correlate with a patient’s volume status and fluid responsiveness has been a subject of significant interest. However, its accuracy and reliability have been questioned. Millington and Koenig (2021) argue that while it’s an easy-to-perform tool, its utility in bedside situations may not be as robust as previously thought. Xavier Filho et al. (2021) suggest that while it’s effective for assessing intravascular volume and fluid responsiveness, standardization of value cutoffs is needed due to divergences in findings.

Studies like that by Yıldızdaş and Aslan (2020) demonstrate its utility in critically ill pediatric patients, where noninvasive, bedside methods for assessing fluid status are particularly valuable. Basu et al. (2020) further support its effectiveness in mechanically ventilated pediatric patients.

Basu S, Sharron M, Herrera N, Mize M, Cohen J. Point-of-Care Ultrasound Assessment of the Inferior Vena Cava in Mechanically Ventilated Critically Ill Children. J Ultrasound Med. 2020 Aug;39(8):1573-1579. doi: 10.1002/jum.15247. Epub 2020 Feb 20. PMID: 32078174.

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Dynamic Indicators of Fluid Responsiveness

Pulse Pressure Variation (PPV)

Principles and Measurement Techniques

Pulse Pressure Variation (PPV) is a dynamic indicator that measures the variations in arterial pulse pressure during the respiratory cycle. It is most effective in patients receiving controlled mechanical ventilation. The principle behind PPV is based on heart-lung interactions; during mechanical ventilation, the increase in intrathoracic pressure during inspiration decreases venous return, reducing left ventricular stroke volume and thus arterial pulse pressure. Techniques for measuring PPV include using arterial catheters and advanced hemodynamic monitoring systems that can analyze the arterial waveform (Kim et al., 2013). Non-invasive methods like photoplethysmography (PPG) are also being explored for their simplicity and potential for large-scale application (Loukogeorgakis et al., 2002).

Clinical Applicability and Limitations

PPV is a valuable tool for predicting fluid responsiveness in mechanically ventilated patients. However, its applicability is limited by certain conditions such as arrhythmias, spontaneous breathing activity, low tidal volume ventilation, and open chest conditions. These factors can affect the accuracy of PPV measurements, making it less reliable under certain clinical situations (Mahjoub et al., 2014; Liu et al., 2016). Despite these limitations, PPV remains a useful indicator for guiding fluid therapy in selected patient populations.

Stroke Volume Variation (SVV)

Understanding the Concept and Clinical Relevance

SVV, like PPV, is based on heart-lung interactions during mechanical ventilation. It measures the variation in stroke volume (the amount of blood ejected by the left ventricle in one beat) over the respiratory cycle. SVV is a sensitive indicator of a patient’s volume status and fluid responsiveness, particularly in settings of controlled mechanical ventilation (Chen & Yao, 2012; Cannesson et al., 2012). It is particularly useful in guiding fluid therapy, optimizing cardiac output, and improving tissue oxygenation.

Techniques for Measurement and Interpretation

SVV is typically measured using advanced hemodynamic monitoring systems that analyze the arterial waveform or by echocardiographic assessment. Technologies like the PiCCO system or the FloTrac sensor are commonly used for this purpose (Reuter et al., 2003; Rex et al., 2004). The interpretation of SVV must consider factors such as the patient’s ventilatory settings and clinical condition. For example, SVV may be less reliable in patients with spontaneous breathing efforts or with arrhythmias. It is also crucial to recognize that SVV is only one component of a comprehensive hemodynamic assessment and should be interpreted in the context of other clinical information (Marx et al., 2004; Berkenstadt et al., 2001).

Accuracy of SVV and PPV
A study found a diagnostic odds ratio of 18.4 for SVV to predict fluid responsiveness, with a sensitivity of 0.81 and a specificity of 0.80. This indicates that SVV is of diagnostic value for fluid responsiveness in operating room (OR) or Intensive Care Unit (ICU) patients monitored with systems like PiCCO or FloTrac/Vigileo, and in patients ventilated with a tidal volume greater than 8 liters( Jeong, 2017.) In mechanically ventilated septic patients in sinus cardiac rhythm, optimal threshold values for discrimination between volume responders and nonresponders were determined as 10% for SVV (sensitivity 96.15%, specificity 100%) and 12% for PPV (sensitivity 100%, specificity 100%). This indicates extremely high sensitivity and specificity for both SVV and PPV in this specific patient group when measured by the LiDCO plus system. (Biais, 2010)

PPV and SVV are valuable dynamic indicators for assessing fluid responsiveness in critically ill patients, particularly those under controlled mechanical ventilation. While they offer significant insights into a patient’s volume status and guide fluid therapy, their limitations and the need for careful interpretation must be acknowledged in clinical practice.

References

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