Shock Management and Pharmacology

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Questions and Answers

What is the main argument against routine use of central venous monitoring for patients with septic shock in the ED?

Routine use of central venous monitoring for septic shock in the ED does not improve outcomes compared to usual care.

What are the two readily available clinical methods suggested for assessing oxygen delivery in complex patients where the adequacy is unclear?

Central venous oxygen saturation and lactate clearance.

What is the main point of the text concerning the importance of specific quantitative targets for resuscitating ED septic shock?

The importance of specific quantitative targets for the resuscitation of ED septic shock is unproven.

Describe the core concept of quantitative resuscitation as it relates to the management of shock.

<p>Quantitative resuscitation aims to restore systemic perfusion and vital organ function by resuscitating patients to predefined physiologic endpoints, such as central venous pressure (CVP) and central venous oxygen saturation.</p> Signup and view all the answers

What is the primary rationale for placing a central line in patients with septic shock in the ED?

<p>Lack of adequate peripheral access or anticipated use of high-dose vasopressor agents.</p> Signup and view all the answers

What key element of EGDT has become less common in the ED setting due to its invasiveness?

<p>Central venous oxygen saturation.</p> Signup and view all the answers

What does the term "lactate clearance" refer to in the context of shock management?

<p>Serial measurements of venous or arterial lactate levels.</p> Signup and view all the answers

Explain the critical difference between quantitative resuscitation and modern usual care in managing shock, according to the text.

<p>Modern usual care focuses on early recognition, prompt fluid resuscitation, and timely antibiotic administration, whereas quantitative resuscitation emphasizes achieving specific physiological targets through invasive measurements.</p> Signup and view all the answers

What is the main reason for the decline in using EGDT in the ED for managing shock?

<p>The lack of a proven mortality advantage over modern usual care in several large multicenter trials.</p> Signup and view all the answers

How does the text describe the optimal approach to managing shock in the ED?

<p>Early recognition and initiation of fluid and antibiotic therapy alongside close monitoring and thoughtful care are crucial for managing shock.</p> Signup and view all the answers

Explain the current consensus regarding delayed resuscitation for hemorrhagic shock, outlining the reasons behind this position.

<p>Recent consensus statements have moved away from delayed resuscitation for hemorrhagic shock, advocating for immediate transfusion and minimizing hypotension. This change is driven by the recognition that early intervention with fluids is generally beneficial for patient outcomes.</p> Signup and view all the answers

Based on the text, what type of crystalloid solution is generally recommended for treating shock in emergency settings, and explain the rational behind this choice.

<p>Balanced isotonic crystalloids, primarily lactated Ringers, are recommended for treating shock in the emergency setting. This preference stems from studies suggesting their potential to reduce the risk of acute kidney injury compared to other options.</p> Signup and view all the answers

Describe the suggested initial volume replacement strategy for a patient presenting with shock.

<p>The text suggests an initial rapid infusion of 20 to 25 mL of isotonic crystalloid per kilogram for initial volume replacement in shock.</p> Signup and view all the answers

What is the rationale behind using colloids in the management of shock, and what are the current recommendations regarding colloid use?

<p>Colloids are theoretically advantageous due to their higher osmotic pressure, potentially aiding in maintaining intravascular volume. However, current recommendations favor natural colloids like albumin over synthetic options like hydroxyethyl hetastarch due to the latter's potential to increase renal failure risk.</p> Signup and view all the answers

What is the role of vasopressors in the treatment of shock, and when are they typically introduced in the resuscitation process?

<p>Vasopressors are employed when persistent hypotension persists despite fluid resuscitation, typically after administering 30 mL/kg of intravenous fluids.</p> Signup and view all the answers

Under what circumstances are colloids generally preferred over additional isotonic crystalloid in treating shock?

<p>Colloids are recommended when a patient requires large volumes of crystalloid (&gt;4 L), especially when further volume replacement with isotonic crystalloids fails to improve hemodynamics.</p> Signup and view all the answers

Describe the recommended initial fluid resuscitation strategy for a patient in septic shock, and explain the rationale behind it.

<p>Initial fluid resuscitation for septic shock involves serial boluses of intravenous isotonic crystalloid solution, continued as long as the patient demonstrates a positive hemodynamic response. This approach is based on the fact that most patients with septic shock initially respond well to volume expansion.</p> Signup and view all the answers

What is the clinical significance of a patient exhibiting a persistent hemodynamic response to fluid loading (persistent hypotension despite fluid loading of 30 mL/kg IV fluids)in the management of shock?

<p>Persistent hypotension despite fluid loading (30 mL/kg IV fluids) signals the need for additional interventions, likely the introduction of vasopressors, to address underlying hemodynamic instability.</p> Signup and view all the answers

Compare and contrast the use of hypertonic saline and colloids in managing shock, highlighting any advantages and disadvantages associated with each.

<p>Hypertonic saline and colloids offer theoretical advantages in shock management. Hypertonic saline, aiming to improve intravascular volume and cellular hydration, has not shown consistent mortality benefits in studies. Colloids, while potentially increasing intravascular volume, can be costly, with inconclusive evidence on their impact on morbidity and mortality. Current consensus favors natural colloids over synthetic options, noting the higher risk of renal failure associated with certain synthetic colloids.</p> Signup and view all the answers

Discuss the potential risks associated with excessive crystalloid administration in shock management.

<p>While crystalloids are essential in treating shock, excessive administration carries risks. It can potentially worsen edema by shifting fluids into the interstitial space, potentially leading to organ dysfunction. This underscores the importance of carefully monitoring patients' responses to fluid resuscitation and tailoring treatment based on individual needs.</p> Signup and view all the answers

Explain why the use of central venous oxygen saturation as an endpoint of early septic shock resuscitation has been largely replaced by lactate clearance measurements and why this is not necessarily the case for other shock states.

<p>Lactate clearance is a preferred endpoint in early septic shock resuscitation because it is easily obtainable from peripheral venous blood, making it a simpler and more accessible measure compared to central venous oxygen saturation. Additionally, it has been demonstrated to be equivalent in efficacy to central venous oxygen saturation in this context.</p> <p>However, this has not been systematically studied in other forms of shock. Therefore, while lactate clearance remains a valuable indicator for managing other shock states, its equivalence to central venous oxygen saturation in these cases requires further investigation and may not be generalized.</p> Signup and view all the answers

Describe the criteria for knowing when additional steps are needed to improve systemic perfusion during the resuscitation process, highlighting the role of lactate concentration.

<p>If the lactate concentration does not decrease by 10% to 20% within 2 hours after resuscitation has begun, it indicates that systemic perfusion is not adequately improving. This signifies the need for additional measures to enhance circulatory function and improve tissue oxygenation.</p> Signup and view all the answers

Explain why CVP, while historically used to estimate right ventricular filling pressure, isn't a reliable indicator of left ventricular end-diastolic volume and has limitations in guiding volume resuscitation.

<p>CVP, a measure of right ventricular filling pressure, does not accurately reflect left ventricular end-diastolic volume, which is a more accurate indicator of preload and cardiac function. Consequently, CVP poorly predicts the hemodynamic response to fluid boluses. This emphasizes the need to rely on clinical response in addition to CVP monitoring for volume resuscitation.</p> Signup and view all the answers

Describe the preferred approach to fluid resuscitation in shock patients, highlighting the role of clinical response in managing volume replacement.

<p>Fluid resuscitation should not be based solely on CVP measurements but should incorporate assessment of clinical response, including increases in urine output, blood pressure, and decreasing lactate concentrations. This multi-faceted approach provides a more accurate picture of hemodynamic improvement and guides fluid administration more effectively.</p> Signup and view all the answers

Explain the rationale for considering dynamic variables of fluid responsiveness, such as stroke volume variation (SVV), in patients at higher risk of fluid overload. Why is routine use of these variables in the ED not yet fully recommended?

<p>In patients at higher risk of fluid overload, dynamic variables like SVV can be more beneficial than empirical fluid boluses. These variables provide a more direct assessment of hemodynamic response to volume expansion, helping to optimize fluid administration and minimize the risk of complications. However, their use in guiding therapy in the ED has not been sufficiently studied to recommend routine implementation.</p> Signup and view all the answers

How does the standard treatment for hemorrhagic shock differ in adults and children in terms of the volume of crystalloid infused?

<p>The standard treatment for adults in hemorrhagic shock involves rapidly infusing several liters of isotonic crystalloid. In children, the approach is different, with three successive 20-mL/kg boluses of crystalloid being administered. This variation in fluid volume is due to the different physiological needs and fluid requirements of adults and children.</p> Signup and view all the answers

What is the primary goal of volume replacement in shock, and why is it difficult to achieve?

<p>The primary goal of volume replacement in shock is to achieve slightly elevated left ventricular end-diastolic volume, which is an indicator of optimal preload. However, this is a challenging goal to attain in the emergency setting, as direct measurement of left ventricular end-diastolic volume is impractical.</p> Signup and view all the answers

Compare and contrast the usefulness of CVP and clinical response in guiding fluid resuscitation. What are the potential risks associated with relying solely on CVP for fluid management?

<p>CVP is a historically used measure to estimate right ventricular filling pressure, but it doesn't accurately reflect left ventricular end-diastolic volume or predict the hemodynamic response to fluid boluses. Therefore, relying solely on CVP can lead to over- or under-resuscitation. Clinical response, indicated by changes in vital signs and urine output, is a more reliable indicator of adequacy of fluid resuscitation, and should be incorporated with CVP measurements to optimize fluid management.</p> Signup and view all the answers

Why is it important to consider the potential risks of fluid resuscitation in certain patient groups?

<p>In patients with conditions like severe systolic heart failure or dialysis-dependent renal failure, excessive fluid resuscitation can worsen the situation. These conditions make them more susceptible to fluid overload, leading to potential complications like pulmonary edema or worsening of renal function. Therefore, careful consideration of fluid resuscitation strategies is crucial for these patient groups.</p> Signup and view all the answers

How do dynamic variables like SVV help to optimize fluid management in shock patients who may be at risk of fluid overload?

<p>Dynamic variables like SVV provide a more direct assessment of the circulatory response to volume expansion. They can help clinicians determine the optimal fluid volume needed to achieve adequate hemodynamic improvement while minimizing the risk of over-resuscitation. This personalized approach is especially beneficial in patients at risk of fluid overload, as it allows for more precise monitoring of the response to fluid administration.</p> Signup and view all the answers

Describe two scenarios where a triple-lumen catheter is particularly beneficial in managing shock.

<p>A triple-lumen catheter is beneficial in managing shock in patients with poor peripheral access, allowing for safe vasopressor infusion in hypotensive patients unresponsive to initial fluid bolus. It is also helpful when limited IV access requires simultaneous infusion of IV fluids and antibiotics.</p> Signup and view all the answers

Explain the rationale behind using intraosseous (IO) access in patients with shock when peripheral and central venous access are difficult to obtain.

<p>IO access provides a rapid and reliable method for administering fluids and medications in shock patients, especially when conventional venous access is challenging. It offers a temporary, yet crucial, route for resuscitation.</p> Signup and view all the answers

When might it be appropriate to use a peripheral IV catheter for administering vasoactive medications in a shock patient?

<p>Peripheral IV access can be used for vasoactive medication administration in shock patients when central venous access and IO access are both unavailable. A large-gauge peripheral catheter (18G or larger) in the antecubital fossa or more proximally is recommended.</p> Signup and view all the answers

What are some patient populations that are more likely to have indwelling catheters in place, and why is this relevant in managing shock?

<p>Patients with renal disease or cancer frequently have indwelling catheters for ongoing medical management. These catheters can be utilized for IV access in shock patients, providing a readily available route for fluid and medication administration.</p> Signup and view all the answers

Why should emergency departments establish clear policies and training protocols regarding using indwelling catheters for shock management?

<p>Clear policies and training are crucial to ensure consistent and safe utilization of indwelling catheters for shock management. This minimizes potential conflicts and delays in critical situations, prioritizing patient care over concerns about preserving the line for future use.</p> Signup and view all the answers

Explain the rationale for prioritizing rapid fluid and vasoactive medication administration in patients with shock, even if it means using an indwelling catheter originally intended for other purposes.

<p>Prompt administration of fluids and vasoactive medications is crucial in shock management, as it directly addresses the life-threatening hemodynamic instability. The potential benefits of prompt intervention outweigh concerns about preserving a catheter for future use.</p> Signup and view all the answers

Explain what "central venous pressure" (CVP) is and its clinical relevance in managing shock.

<p>CVP is measured from a central venous line and provides an assessment of the pressure in the right atrium, reflecting the preload or volume status of the heart. It can be used to guide fluid resuscitation in patients with shock.</p> Signup and view all the answers

What type of catheter is commonly used for obtaining intraosseous (IO) access in children, and what are the potential benefits of this approach?

<p>A 3- or 5-French bilumen catheter is commonly used for IO access in children. It is a relatively safe and minimally invasive procedure, offering a quick and reliable route for fluid resuscitation and medication administration.</p> Signup and view all the answers

Describe the general principle that governs the decision-making process for choosing the most appropriate IV access route in a patient with shock.

<p>The primary principle is to prioritize the most rapid and effective method of administering fluids and medications to stabilize the patient's hemodynamic status, regardless of the specific access route employed.</p> Signup and view all the answers

What are the empirical criteria for diagnosing shock according to Box 3.2?

<p>III appearance or altered mental status; heart rate &gt;100 beats/min; respiratory rate &gt;20 breaths/min or PaCO2 &lt;32 mm Hg; arterial base deficit &lt;-4 mEq/L or lactate level &gt;4 mM/L; urine output &lt;0.5 mL/kg/h; arterial hypotension lasting &gt;30 minutes.</p> Signup and view all the answers

Why may blood pressure (BP) and heart rate (HR) be unreliable indicators of shock severity?

<p>BP and HR correlate poorly with cardiac index (CI) and can underestimate systemic hypoperfusion. Children may maintain normal BP until rapid deterioration, and compensatory adrenergic reflexes can initially normalize BP.</p> Signup and view all the answers

What are the three common causes of shock and their consensus definitions?

<ol> <li><strong>Hemorrhagic Shock:</strong> Systemic hypoperfusion (lactic acidosis or base deficit &lt;-4 mEq/L) with organ dysfunction due to blood loss.</li> <li><strong>Septic Shock:</strong> Sepsis (suspected infection + SOFA score increase ≥2) plus hypotension requiring vasopressors and lactate &gt;2 mmol/L.</li> <li><strong>Cardiogenic Shock:</strong> Cardiac failure (ischemic, toxic, or obstructive) causing systemic hypoperfusion with lactic acidosis and organ dysfunction.</li> </ol> Signup and view all the answers

List the clinical management steps for septic shock.

<p>Ensure oxygenation; administer 30 mL/kg crystalloid; titrate fluids via dynamic indices/urine output; start antimicrobials/surgical drainage; transfuse PRBCs if hemoglobin &lt;7 g/dL; initiate norepinephrine (0.5 mcg/min) if perfusion remains poor.</p> Signup and view all the answers

How are lactate levels used in diagnosing and managing shock?

<p>Lactate &gt;4 mM indicates circulatory insufficiency. Serial measurements (lactate clearance) guide resuscitation efficacy; failure to decrease by 10–20% within 2 hours necessitates further intervention.</p> Signup and view all the answers

When should intraosseous (IO) access be used in shock management?

<p>IO access is indicated if rapid peripheral or central venous access is unattainable. It allows temporary administration of fluids/medications in adults and children.</p> Signup and view all the answers

What is quantitative resuscitation, and how has its approach evolved?

<p>Quantitative resuscitation targets physiologic endpoints (e.g., lactate clearance, CVP). Early goal-directed therapy (EGDT) using central venous oxygen saturation was replaced by simpler methods (e.g., lactate clearance) due to equivalent outcomes with early fluids/antibiotics.</p> Signup and view all the answers

What variables indicate tissue hypoperfusion?

<p>Hypotension, tachycardia, low cardiac output, dusky/mottled skin, delayed capillary refill, altered mental status, low urine output, low central venous oxygen saturation, elevated lactate.</p> Signup and view all the answers

How is hemorrhagic shock distinguished from simple hemorrhage?

<p>Simple Hemorrhage: Normal vital signs and normal base deficit. Hemorrhage with Hypoperfusion: Base deficit &lt; -4 mEq/L or HR &gt;100. Hemorrhagic Shock: Meets ≥4 Box 3.2 criteria (e.g., hypotension, elevated lactate).</p> Signup and view all the answers

What monitoring methods assess perfusion status in shock?

<p>Urine output (&gt;1.0 mL/kg/h = normal), mental status, lactate/base deficit trends, arterial/venous blood gases, cardiac ultrasound (e.g., stroke volume variation), and dynamic indices (e.g., CVP in select patients).</p> Signup and view all the answers

What are key interventions for hemorrhagic shock?

<p>Control bleeding (traction, direct pressure, REBOA); judicious crystalloid (10–20 mL/kg); PRBC transfusion (5–10 mL/kg) if delayed hemorrhage control; balanced transfusions (PRBCs, FFP, platelets) in massive hemorrhage.</p> Signup and view all the answers

How is cardiogenic shock managed?

<p>Provide oxygen/PEEP for pulmonary edema; start vasopressors (norepinephrine) or inotropes (dobutamine); reverse causes (e.g., thrombolysis); consider intra-aortic balloon pump for refractory cases.</p> Signup and view all the answers

What is the significance of jugular venous distention on physical exam?

<p>Suggests cardiac failure, valvular dysfunction, pulmonary embolism, or tamponade (if muffled heart sounds are present).</p> Signup and view all the answers

Why is early antibiotic administration critical in septic shock?

<p>Prompt antibiotics (with source control) reduce mortality. Treatment should not await hypotension, as delayed therapy worsens outcomes.</p> Signup and view all the answers

What are limitations of using urine output to assess perfusion?

<p>Requires 30–60 minutes for accuracy; unreliable in preexisting renal disease; does not provide real-time data.</p> Signup and view all the answers

What role does bedside ultrasound play in undifferentiated shock?

<p>Identifies cardiac tamponade, pneumothorax, hemoperitoneum, aortic aneurysm, ventricular dysfunction, or hyperdynamic heart (suggesting sepsis).</p> Signup and view all the answers

How does the Sepsis-3 definition differ from prior criteria?

<p>Sepsis-3 removes SIRS, focusing on SOFA score ≥2 with infection. Septic shock requires vasopressors + lactate &gt;2 mmol/L, emphasizing organ dysfunction over inflammatory markers.</p> Signup and view all the answers

When should vasopressors be administered via peripheral IV?

<p>If central/IO access is unavailable, use a large-gauge (≥18g) peripheral IV in the antecubital fossa or proximal site, with additional IVs for crystalloids.</p> Signup and view all the answers

What defines adequate fluid responsiveness in shock?

<p>Improved vital signs, urine output, and lactate/base deficit trends. Dynamic indices (stroke volume variation &gt;12–15%) or passive leg raise may also guide responsiveness.</p> Signup and view all the answers

Why might a hyperdynamic left ventricle on ultrasound suggest sepsis?

<p>Sepsis often causes compensatory increased cardiac output, visible as hyperdynamic contraction on ultrasound, aiding differentiation from cardiogenic shock.</p> Signup and view all the answers

What is the immediate requirement upon a patient's presentation in shock at the ED?

<p>Timely assessment and treatment, sometimes before identifying the etiology.</p> Signup and view all the answers

How can rapid recognition of shock be supported?

<p>By the presence of a worsening base deficit or lactic acidosis.</p> Signup and view all the answers

What are common physical signs of stress response in shock?

<p>III appearance, asthenic, pale, sweating, tachypneic, with a weak and rapid pulse.</p> Signup and view all the answers

How should HR, BP, and oxyhemoglobin saturation be monitored in shock?

<p>Continuously.</p> Signup and view all the answers

Why may noninvasive BP measurements be unreliable in shock?

<p>They can be inaccurate in severe hypotensive states.</p> Signup and view all the answers

What does an arterial pressure monitoring line improve?

<p>The ability to monitor the dynamic response to therapy.</p> Signup and view all the answers

What provides an excellent indicator of vital organ perfusion?

<p>Urine output via a Foley catheter.</p> Signup and view all the answers

What are concerning levels for lactate concentration and base deficit in shock?

<p>Lactate &gt;4.0 mM and base deficit more negative than −4 mEq/L.</p> Signup and view all the answers

What does a downward trend of serum lactate indicate in shock management?

<p>Adequacy of resuscitation and prognosis.</p> Signup and view all the answers

What might a rising lactate level indicate?

<p>The need for more intensive measures.</p> Signup and view all the answers

What historical factors should be considered in shock assessment?

<p>History, vital signs, and physical examination documented by prehospital providers.</p> Signup and view all the answers

What does jugular venous distention suggest?

<p>Congestive cardiac failure, severe valvular abnormality, or right ventricular strain from pulmonary embolism.</p> Signup and view all the answers

What does a loud, machine-like systolic murmur indicate?

<p>Acute rupture of a papillary muscle or interventricular septum.</p> Signup and view all the answers

What does the presence of melanic stool on rectal examination indicate?

<p>Gastrointestinal hemorrhage.</p> Signup and view all the answers

Which imaging and laboratory tests are useful in suspected shock cases?

<p>Chest radiography, electrocardiography, fingerstick glucose measurement, CBC, urinalysis, serum electrolyte levels, and kidney and liver function tests.</p> Signup and view all the answers

How soon should lactate level measurement be performed in suspected shock patients?

<p>As early as possible.</p> Signup and view all the answers

What can bedside ultrasound screen for in shock?

<p>Inadequate central venous volume, occult hemoperitoneum, abdominal aortic aneurysm, left ventricular failure, right ventricular dilation or septal bowing, cardiac tamponade, or pneumothorax/hemothorax.</p> Signup and view all the answers

What strongly suggests sepsis in patients with undifferentiated shock?

<p>Hyperdynamic left ventricular function.</p> Signup and view all the answers

What is a key indicator in children for assessing shock?

<p>Symmetry of extremity movements and appropriateness of crying.</p> Signup and view all the answers

What foundational approach is important in hemorrhagic shock treatment?

<p>Ensuring adequate ventilation and oxygenation.</p> Signup and view all the answers

Under what conditions should PRBCs be infused in hemorrhagic shock?

<p>With poor organ perfusion and anticipating a 30-minute delay to hemorrhage control.</p> Signup and view all the answers

What is the primary empirical treatment for cardiogenic shock related to increased work of breathing?

<p>Providing oxygen and positive end-expiratory pressure (PEEP) for pulmonary edema.</p> Signup and view all the answers

What should begin promptly in septic shock management?

<p>Antimicrobial therapy and potentially surgical drainage or debridement.</p> Signup and view all the answers

What are the signs of tissue hypoperfusion?

<p>Hypotension, tachycardia, low cardiac output, dusky or mottled skin, delayed capillary refill, altered mental state, low urine output, low central venous oxygen saturation, or elevated lactate level.</p> Signup and view all the answers

How is septic shock defined according to Sepsis-3?

<p>Sepsis plus hypotension requiring vasopressors after fluid loading plus lactate &gt;2 mmol/L.</p> Signup and view all the answers

What immediate step is necessary for managing inadequate peripheral or central venous access in shock?

<p>Establishing intraosseous (IO) access.</p> Signup and view all the answers

What is a practical alternative to central venous oxygen saturation for resuscitation endpoints?

<p>Lactate clearance.</p> Signup and view all the answers

According to Box 3.2, list a criterion for diagnosing shock.

<p>Heart rate &gt;100 beats/min.</p> Signup and view all the answers

When should isotonic crystalloid solution infusion be initiated in hemorrhagic shock?

<p>When there is evidence of poor organ perfusion.</p> Signup and view all the answers

Which components are administered in septic shock if volume restoration fails?

<p>Vasopressor support with norepinephrine.</p> Signup and view all the answers

What is the function of a triple-lumen catheter in shock management?

<p>Allows for safe infusion of vasopressors, fluids, and antibiotics when IV access is limited.</p> Signup and view all the answers

Why might a central line be favored over peripheral access in severe shock cases?

<p>For administering high-dose vasopressor agents.</p> Signup and view all the answers

What past study finding questions the use of invasive resuscitation measurements in septic shock?

<p>Early goal-directed therapy did not show mortality advantage over usual care.</p> Signup and view all the answers

What are the three common causes of shock covered in Box 3.3?

<p>Hemorrhagic, septic, and cardiogenic shock.</p> Signup and view all the answers

When should packed red blood cell infusion be considered in septic shock?

<p>For hemoglobin level &lt;7 g/dL.</p> Signup and view all the answers

What measurement can aid in diagnosing shock due to its correlation with oxygen delivery?

<p>Central venous oxygen saturation.</p> Signup and view all the answers

What should be done if lactate concentration does not decrease adequately after resuscitation?

<p>Additional steps to improve systemic perfusion.</p> Signup and view all the answers

What is an essential component of clinical management in cardiogenic shock according to Box 3.5?

<p>Begin vasopressor or inotropic support.</p> Signup and view all the answers

According to Box 3.2, what is a significant respiratory rate criterion for diagnosing shock?

<p>Respiratory rate &gt;20 breaths/min or Paco2 &lt;32 mm Hg.</p> Signup and view all the answers

What should be initiated if mass hemorrhage is suspected in a shock patient?

<p>Immediate packed red blood cell (PRBC) transfusion.</p> Signup and view all the answers

How does presence of muffled heart sounds with jugular venous distention suggest shock etiology?

<p>It suggests cardiac tamponade.</p> Signup and view all the answers

What should quantitative resuscitation in shock aim to achieve?

<p>Normalization of markers of volume status, perfusion, and adequate oxygen delivery.</p> Signup and view all the answers

What historical definition still used for septic shock by CMS involves which criteria?

<p>2001 definitions of severe sepsis which include 2 or more SIRS criteria plus evidence of end-organ dysfunction.</p> Signup and view all the answers

What is the role of a systematic ultrasound protocol in shock management?

<p>Improve the ability to accurately diagnose the cause of undifferentiated shock.</p> Signup and view all the answers

How should shock be managed when standard practice limits the use of indwelling catheters?

<p>Develop specific hospital policy and training sessions to make exceptions in the case of shock.</p> Signup and view all the answers

What is the base deficit threshold indicating probable shock?

<p>Base deficit less negative than –4 mEq/L.</p> Signup and view all the answers

What is the importance of early quantitative resuscitation strategy in ED?

<p>To achieve early normalization of markers within the first 6 hours.</p> Signup and view all the answers

In the context of the text, what condition could cause diffuse rhonchi in a patient?

<p>Bronchospasm, cardiac failure, or pneumonia.</p> Signup and view all the answers

Which serum concentration is strongly predictive of patient outcomes in shock?

<p>Serum lactate concentration.</p> Signup and view all the answers

What is a primary treatment strategy for refractory cardiogenic shock?

<p>Consider intra-aortic balloon pump counterpulsation.</p> Signup and view all the answers

Explain the fundamental concept of Early Goal-Directed Therapy (EGDT) in shock, highlighting how it differs from traditional approaches.

<p>EGDT is a protocol-driven, standardized method for treating shock that emphasizes rapid assessment and restoration of vital organ function through targeted interventions, unlike traditional methods, which lacked a structured, goal-oriented approach.</p> Signup and view all the answers

Describe the primary goals of EGDT in managing shock, outlining how these goals translate into improved patient outcomes.

<p>EGDT aims to resuscitate patients based on their individual needs rather than solely focusing on initial presentation; restore tissue perfusion to address the underlying cause of shock; and optimize hemodynamic parameters, striking a balance between treatment and potential complications.</p> Signup and view all the answers

Outline the key elements of clinical guidelines for EGDT, emphasizing the importance of rapid assessment, focused interventions, and continuous monitoring in managing shock.

<p>EGDT guidelines emphasize rapid assessment of the patient's physiological status, including vital signs, fluid balance, and lactate levels; implementation of targeted therapies based on the assessment and established goals; and close, ongoing monitoring and adjustment of treatment to maintain targeted physiological parameters.</p> Signup and view all the answers

Discuss the potential benefits and drawbacks associated with the implementation of EGDT in managing shock, particularly focusing on its impact on patient outcomes.

<p>EGDT has demonstrated improved patient survival rates, reduced hospital stays, and fewer complications related to aggressive fluid resuscitation. However, its effectiveness may vary based on the specific type of shock and the patient's overall health status.</p> Signup and view all the answers

Compare and contrast EGDT with traditional methods of managing shock, highlighting the key differences in approach and potential advantages of the EGDT protocol.

<p>EGDT adopts a more structured and measurable approach compared to traditional methods, which often lacked a standardized, goal-oriented plan. EGDT's emphasis on rapid assessment, targeted interventions, and continuous monitoring contributes to potentially faster and more effective treatment.</p> Signup and view all the answers

Explain the rationale behind the emphasis on rapid assessment and early goal identification in EGDT, highlighting the importance of these elements in successful shock management.

<p>Rapid assessment allows for an immediate and thorough evaluation of the patient's physiological status, providing critical information for guiding treatment decisions. Early goal identification ensures that resuscitation aligns with the patient's specific needs and helps optimize treatment effectiveness.</p> Signup and view all the answers

Describe the role of continuous monitoring and adjustments in the EGDT protocol, explaining how these elements contribute to the overall effectiveness of shock management.

<p>Continuous monitoring allows for ongoing assessment of the patient's response to treatment, enabling adjustments to the intervention strategy as needed. This dynamic approach ensures that the treatment plan remains appropriate and effective throughout the resuscitation process.</p> Signup and view all the answers

Discuss the potential challenges and limitations associated with the implementation of EGDT, recognizing that its effectiveness may vary depending on various factors.

<p>Challenges in implementing EGDT include the need for specialized training and expertise, potential for variability in protocols, and the risk of complications associated with aggressive intervention. The effectiveness of EGDT can be influenced by factors such as the specific type of shock, the patient's overall health status, and the resources available.</p> Signup and view all the answers

Explain how the pathophysiology of chronic heart failure leads to the manifestation of Jugular Vein Distension (JVD).

<p>In chronic heart failure, the heart's diminished pumping ability leads to increased central venous pressure. This elevated pressure is transmitted back into the venous system, resulting in the distension of the jugular veins.</p> Signup and view all the answers

Describe the clinical significance of observing Kussmaul's sign during a physical assessment for JVD, and what underlying condition might it indicate?

<p>Kussmaul's sign, the paradoxical increase in JVD during inspiration, suggests impaired right ventricular filling. This is often indicative of conditions such as constrictive pericarditis, restrictive cardiomyopathy, or severe right ventricular failure.</p> Signup and view all the answers

Outline the key steps in performing a reliable assessment of Jugular Venous Distention (JVD), ensuring accurate differentiation from carotid pulsations.

<p>Patient supine with head elevated to 30-45 degrees. Identify sternal angle as a reference point. Measure the vertical distance from the sternal angle to the highest point of visible jugular venous pulsation. JVD will fluctuate with respiration and is obliterated by light pressure, unlike the carotid pulse.</p> Signup and view all the answers

A patient presents with JVD, dyspnea, and lower extremity edema. After initial assessment, what are the immediate next steps in determining the underlying cause of the JVD, and how would these steps guide initial treatment strategies?

<p>Order an ECG and echocardiogram to evaluate cardiac function and rule out heart failure or structural abnormalities. Simultaneously, assess renal function with a blood urea nitrogen (BUN) and creatinine test to rule out fluid overload. Initial treatment will focus on symptom relief with diuretics while awaiting diagnostic results to address the underlying pathology.</p> Signup and view all the answers

Explain how superior vena cava syndrome causes JVD and how it differs from JVD caused by right heart failure.

<p>Superior vena cava syndrome causes JVD due to obstruction of blood flow in the superior vena cava, leading to increased pressure in the jugular veins. Unlike right heart failure, which causes JVD due to increased central venous pressure from inadequate right ventricular function, SVC syndrome causes JVD because of a physical blockage of venous return from the upper body.</p> Signup and view all the answers

Explain the primary pathophysiological mechanism that leads to Jugular Venous Distention (JVD).

<p>Elevated venous pressure inhibits venous outflow from the head and neck, causing blood to accumulate in the jugular veins.</p> Signup and view all the answers

How does right-sided heart failure contribute to the development of JVD?

<p>Right-sided heart failure impairs the heart's ability to effectively pump blood to the lungs, which increases central venous pressure and leads to JVD.</p> Signup and view all the answers

Describe how pulmonary hypertension can cause JVD, detailing the physiological connection.

<p>Pulmonary hypertension increases the resistance against which the right ventricle must pump, leading to right ventricular strain and increased right atrial pressure, ultimately causing JVD.</p> Signup and view all the answers

Explain the mechanism by which superior vena cava syndrome leads to Jugular Venous Distention (JVD).

<p>Superior vena cava syndrome involves obstruction of the superior vena cava, impeding blood flow from the head and upper extremities to the heart. This obstruction increases venous pressure, resulting in JVD.</p> Signup and view all the answers

Discuss the clinical significance of assessing the height of JVD relative to the sternal angle. What does this measurement indicate?

<p>The height of JVD relative to the sternal angle estimates central venous pressure. A higher measurement suggests elevated central venous pressure, indicative of potential heart failure or fluid overload.</p> Signup and view all the answers

Describe how cardiac tamponade can lead to JVD. Explain the underlying mechanism.

<p>Cardiac tamponade is the accumulation of fluid in the pericardial space, which compresses the heart. This compression impairs the heart's ability to fill properly. As a result, venous return is impeded, causing increased pressure in the jugular veins and leading to JVD.</p> Signup and view all the answers

What key patient positioning considerations are necessary to accurately assess Jugular Venous Distension (JVD)? Why are these considerations important?

<p>The patient should be positioned supine with the head elevated to approximately 30-45 degrees. This position allows for easier visualization of the jugular veins and helps differentiate normal venous pulsations from distension due to elevated venous pressure.</p> Signup and view all the answers

How might the presence of JVD assist in differentiating between different etiologies of dyspnea (e.g., cardiac vs. pulmonary)?

<p>JVD is more strongly associated with cardiac causes of dyspnea, such as heart failure. Its presence suggests a cardiovascular etiology as opposed to a purely pulmonary issue, though both can coexist.</p> Signup and view all the answers

In a patient with severe liver disease and active bleeding, how does the administration of FFP contribute to hemostasis, and what is the typical target range for coagulation factor levels post-transfusion?

<p>FFP provides coagulation factors to compensate for impaired liver synthesis, aiming for factor levels around 20-30% of normal to achieve hemostasis.</p> Signup and view all the answers

A patient on warfarin requires urgent reversal due to intracranial hemorrhage. Beyond FFP administration, what additional intervention should be considered, and how does it complement FFP's effects?

<p>Prothrombin complex concentrate (PCC) should be considered, as it provides a concentrated dose of vitamin K-dependent clotting factors for immediate reversal, complementing FFP's slower-acting, broader factor replacement.</p> Signup and view all the answers

A trauma patient with massive hemorrhage receives a balanced transfusion protocol, including packed RBCs, FFP, and platelets. If the patient's PT/INR remains elevated despite FFP administration, what are two potential explanations, and how would you investigate them?

<p>Potential explanations include ongoing consumption of coagulation factors due to continued bleeding or dilutional coagulopathy. Investigation should involve repeat coagulation testing, assessment of ongoing blood loss, and consideration of viscoelastic testing (TEG/ROTEM).</p> Signup and view all the answers

Describe the rationale behind using higher platelet transfusion thresholds (e.g., >50,000/µL) in patients with specific conditions such as severe sepsis, and explain the potential risks associated with this approach.

<p>Higher thresholds are used to mitigate the increased risk of bleeding due to endothelial dysfunction and platelet consumption in sepsis. Risks include transfusion-related complications, such as TRALI, TACO, and alloimmunization, as well as potential for increased thrombotic events.</p> Signup and view all the answers

A patient develops acute respiratory distress and hypotension shortly after the initiation of a transfusion. Outline a step-by-step approach to differentiate between Transfusion-Related Acute Lung Injury (TRALI) and Transfusion-Associated Circulatory Overload (TACO), including key clinical and diagnostic findings that would support each diagnosis.

<p>Assess for risk factors (e.g., multiparous females for TRALI, cardiac dysfunction for TACO). Check for fever (more common in TRALI). Obtain chest X-ray (bilateral infiltrates in TRALI, pulmonary edema in TACO). Measure BNP (elevated in TACO). Echocardiogram may show cardiac dysfunction in TACO.</p> Signup and view all the answers

A patient presents with severe sepsis and a lactate level of 4.5 mmol/L. Briefly explain the physiological processes that could contribute to this elevated lactate level beyond anaerobic metabolism.

<p>In severe sepsis, elevated lactate can result from increased glycolysis due to beta-adrenergic stimulation, impaired pyruvate dehydrogenase activity, and mitochondrial dysfunction, reducing the cells' ability to utilize oxygen effectively, even when oxygen is available.</p> Signup and view all the answers

Describe how the interpretation of a lactate level of 3.0 mmol/L would differ in a healthy athlete immediately after intense exercise compared to a critically ill patient in the ICU.

<p>In an athlete post-exercise, a lactate of 3.0 mmol/L is likely due to anaerobic metabolism in muscles and is expected to resolve quickly. In a critically ill ICU patient, the same level suggests significant tissue hypoperfusion, impaired oxygen utilization, or metabolic dysfunction, indicating a severe underlying condition that requires immediate investigation.</p> Signup and view all the answers

A patient with chronic liver disease presents with a lactate level of 2.8 mmol/L. How does liver dysfunction contribute to hyperlactatemia, and what other lab values would you want to assess to get a better clinical picture?

<p>Liver dysfunction impairs lactate clearance, leading to hyperlactatemia. Assess liver function tests (AST, ALT, bilirubin), coagulation studies (PT/INR), and ammonia levels to evaluate the extent of liver damage and its impact on metabolic processes, understanding that impaired hepatic clearance of lactate contributes to elevated levels.</p> Signup and view all the answers

A patient's lactate level is trending upwards (1.5 to 2.5 mmol/L) over 4 hours but remains within the 'normal' range (0.5-2.2 mmol/L). Outline a strategy to evaluate the clinical significance of this trend, including potential causes and immediate steps to investigate.

<p>Even within the normal range, a rising lactate trend may indicate worsening tissue perfusion or metabolic stress. Begin by reassessing the patient's vital signs, oxygenation, and fluid status. Review medications, consider occult hypoperfusion, evaluate end-organ function, check/trend an ABG, and look for signs of early sepsis or ischemia, as the trend may presage significant deterioration.</p> Signup and view all the answers

Explain how the presence of certain medications, such as metformin or antiretroviral drugs, can influence lactate levels and what specific considerations are necessary when interpreting lactate results in patients taking these drugs.

<p>Metformin and antiretroviral drugs can inhibit mitochondrial function, increasing lactate production. When elevated lactate is present in patients taking these medications, evaluate for signs of lactic acidosis, assess renal and hepatic function, and consider discontinuing the medication if there is evidence of significant metabolic compromise, understanding the drug's potential contribution.</p> Signup and view all the answers

In the context of sepsis, explain why a high ScvO2 reading might be misleading, and what physiological dysfunction it could indicate.

<p>In sepsis, a high ScvO2 can be misleading because it often results from the tissues' inability to effectively extract oxygen due to microcirculatory dysfunction or cellular metabolic abnormalities, despite inadequate tissue oxygenation.</p> Signup and view all the answers

Describe the compensatory mechanisms that might occur in the body in response to a chronically low ScvO2, and how these mechanisms could potentially mask the underlying issue.

<p>Compensatory mechanisms include increased cardiac output and oxygen extraction ratio. These adaptations can temporarily normalize oxygen delivery and consumption, masking the chronic low ScvO2 and delaying recognition of the root cause.</p> Signup and view all the answers

How does a left-to-right shunt impact ScvO2, and why might this be misinterpreted without considering the patient's complete clinical picture?

<p>A left-to-right shunt causes blood to bypass systemic circulation, resulting in a higher ScvO2 due to reduced oxygen extraction. This can be misinterpreted as adequate oxygenation if the shunt is not recognized, potentially delaying treatment for the underlying cause of the shunt.</p> Signup and view all the answers

Explain the relationship between anemia and ScvO2 levels, and how this relationship may differ in a patient with chronic anemia compared to acute blood loss.

<p>Anemia reduces oxygen-carrying capacity, typically leading to lower ScvO2 levels. In chronic anemia, compensatory mechanisms might maintain ScvO2 within a near-normal range, unlike acute blood loss where a sudden drop in hemoglobin can cause a more pronounced decrease in ScvO2.</p> Signup and view all the answers

In what clinical scenarios might a patient exhibit a normal ScvO2 despite the presence of significant regional hypoxia? Explain the underlying physiological reasons.

<p>Regional hypoxia can be masked by normal ScvO2 if overall oxygen delivery and consumption are balanced. This might occur if hypoxia is localized (e.g., limb ischemia), with unaffected areas maintaining adequate oxygenation, thereby diluting the hypoxic venous return within the central venous system.</p> Signup and view all the answers

Discuss the limitations of using a single ScvO2 measurement as the sole indicator of tissue oxygenation. What other parameters should be considered in conjunction with ScvO2 to obtain a more comprehensive assessment?

<p>A single ScvO2 provides a snapshot and doesn't reflect regional variations or trends. Other parameters to consider include arterial oxygen saturation (SaO2), cardiac output, hemoglobin levels, lactate levels, and clinical signs of tissue perfusion to provide a comprehensive assessment of tissue oxygenation.</p> Signup and view all the answers

How can the placement of the central venous catheter affect ScvO2 readings, and what precautions should be taken to ensure accurate and reliable measurements?

<p>Catheter placement can affect ScvO2 readings if positioned near areas of high oxygen extraction or infusion sites. Precautions include verifying correct placement via X-ray, avoiding placement near infusion sites, and ensuring consistent catheter position for trend monitoring.</p> Signup and view all the answers

Explain the implications of a significantly elevated ScvO2 in a post-cardiac arrest patient who has achieved return of spontaneous circulation (ROSC).

<p>In post-cardiac arrest patients with ROSC, a significantly elevated $ScvO_2$ may indicate impaired oxygen extraction due to persistent microcirculatory dysfunction or cellular damage from ischemia-reperfusion injury, rather than improved oxygen delivery.</p> Signup and view all the answers

In the context of critical care, explain why a normal SaO2 reading might not always correlate with adequate tissue oxygenation. What other parameter should be considered, and why?

<p>A normal SaO2 only indicates adequate oxygen uptake in the lungs. Despite this, oxygen delivery may be impaired, leading to inadequate tissue oxygenation. ScvO2 should also be considered as it reflects the balance between oxygen delivery and consumption at the tissue level.</p> Signup and view all the answers

How does a maldistribution of blood flow, such as in cases of regional ischemia or inflammation, affect ScvO2 levels, and why does this occur?

<p>Maldistribution of blood flow leads to increased oxygen extraction in affected tissues, resulting in a lower ScvO2. This occurs because tissues experiencing ischemia or inflammation extract a greater proportion of oxygen from the blood.</p> Signup and view all the answers

Describe the compensatory mechanisms the body might employ in response to a chronically low ScvO2, and what are the limitations of these mechanisms?

<p>The body might increase cardiac output or increase oxygen extraction. However, these mechanisms have limits; prolonged demand can lead to tissue hypoxia and organ damage if the underlying cause isn't addressed.</p> Signup and view all the answers

Explain how the use of vasopressor medications in a patient with septic shock might paradoxically affect ScvO2, considering their impact on both blood pressure and tissue perfusion.

<p>Vasopressors increase blood pressure but can impair tissue perfusion due to vasoconstriction. This can decrease oxygen delivery to tissues, leading to lower ScvO2, despite an apparent improvement in blood pressure.</p> Signup and view all the answers

In what clinical scenarios might SvO2 be preferred over ScvO2, and what are the key advantages and disadvantages of using SvO2 in these situations?

<p>SvO2 may be preferred in scenarios where a more accurate reflection of global tissue oxygenation is needed, as it reflects the oxygen saturation of venous blood after mixing in the right ventricle. However, it requires a pulmonary artery catheter, which is more invasive and has potential complications.</p> Signup and view all the answers

How do changes in metabolic rate, such as those induced by fever or hypothermia, impact ScvO2 levels, and what physiological mechanisms underlie these changes?

<p>Fever increases metabolic rate and oxygen consumption, leading to lower ScvO2, while hypothermia decreases metabolic rate and oxygen consumption, leading to higher ScvO2. These changes reflect the balance between oxygen supply and demand at the tissue level.</p> Signup and view all the answers

Describe how a significant left-to-right shunt might influence ScvO2 readings, and why this effect differs from that of a right-to-left shunt.

<p>A left-to-right shunt may cause a higher than expected ScvO2 as oxygenated blood recirculates without being fully utilized by the tissues. A right-to-left shunt would cause lower ScvO2, as deoxygenated blood bypasses the lungs..</p> Signup and view all the answers

Explain the clinical implications of a decreasing ScvO2 trend in a patient being treated for sepsis, despite seemingly adequate improvements in blood pressure and urine output.

<p>A decreasing ScvO2 trend suggests that tissue oxygen extraction is increasing, despite improvements in blood pressure and urine output. This may indicate worsening microcirculatory dysfunction or increased oxygen demand, necessitating further investigation and intervention.</p> Signup and view all the answers

How might the presence of significant peripheral edema affect the accuracy and interpretation of ScvO2 readings, particularly in patients with heart failure?

<p>Peripheral edema can lead to decreased tissue perfusion and increased oxygen extraction in the affected areas, resulting in lower ScvO2 readings. This may not accurately reflect global tissue oxygenation, as the edema can create regional variations in oxygen extraction.</p> Signup and view all the answers

Discuss the potential benefits and limitations of using ScvO2 as a goal-directed therapy parameter in the management of patients undergoing major surgery.

<p>Benefits include early detection of inadequate tissue oxygenation and guidance for optimizing hemodynamic parameters. Limitations include its global nature, which may not detect regional variations, and the potential for misinterpretation in certain clinical scenarios.</p> Signup and view all the answers

To determine if a patient has a base deficit, you can follow these steps:

<p>To determine if a patient has a base deficit, you can follow these steps:</p> <ol> <li> <p>Obtain an arterial blood gas (ABG) sample. This is a blood test that measures the levels of oxygen, carbon dioxide, and other parameters in the blood. It can provide important information about the patient's acid-base balance.</p> </li> <li> <p>Look at the bicarbonate (HCO3-) level in the ABG results. A base deficit is typically indicated by a lower-than-normal level of bicarbonate in the blood. A normal bicarbonate level is usually in the range of 22-26 mEq/L.</p> </li> <li> <p>Calculate the base deficit using the following formula: Base Deficit = 0.3 x (24 - HCO3-)</p> </li> <li> <p>Interpret the results:</p> <ul> <li>A base deficit of less than 2 mEq/L is considered normal.</li> <li>A base deficit greater than 2-5 mEq/L may indicate a mild metabolic acidosis.</li> <li>A base deficit greater than 5-10 mEq/L suggests a moderate metabolic acidosis.</li> <li>A base deficit greater than 10 mEq/L indicates a severe metabolic acidosis.</li> </ul> </li> </ol> <p>It's essential to consider the patient's overall clinical presentation and other laboratory values when interpreting the base deficit results, as it can provide valuable information about the patient's acid-base status and guide treatment decisions. Always consult with a healthcare professional for a comprehensive assessment and interpretation of the results.</p> Signup and view all the answers

What is base deficit?

<p>Base deficit is the amount of base needed to restore the blood pH to normal in the presence of excess acid (acidosis).</p> Signup and view all the answers

How is base deficit calculated?

<p>Base deficit is calculated using the formula: Base Deficit = 0.3 x (24 - HCO3-), where HCO3- represents the bicarbonate level in arterial blood gas results.</p> Signup and view all the answers

What does a higher base deficit value indicate?

<p>A higher base deficit value indicates a more severe level of metabolic acidosis in the body.</p> Signup and view all the answers

What is base excess?

<p>Base excess is the amount of acid or base needed to bring the blood pH back to normal when the bicarbonate level is abnormal.</p> Signup and view all the answers

How is base excess calculated?

<p>Base excess is calculated from the bicarbonate levels in arterial blood gas results, similar to base deficit calculation.</p> Signup and view all the answers

What does a positive base excess value indicate?

<p>A positive base excess value indicates an excess of base in the blood, suggesting alkalosis.</p> Signup and view all the answers

How are base deficit and base excess related?

<p>Base deficit and base excess provide valuable information about the acid-base balance in the body. Base deficit indicates the need for base to correct acidosis, while base excess indicates the presence of acid-base abnormalities in the blood.</p> Signup and view all the answers

What is a sign of tissue hypoperfusion?

<p>Hypotension, tachycardia, low cardiac output, dusky or mottled skin, delayed capillary refill, altered mental state, low urine output, low central venous oxygen saturation, or elevated lactate level.</p> Signup and view all the answers

Flashcards

Perfusion Status

The assessment of blood flow to tissues.

Arterial Line

A catheter placed in an artery to measure blood pressure and obtain samples.

Stroke Volume Variation (SVV)

A measure of fluid responsiveness calculated from changes in stroke volume during breathing.

Central Venous Pressure (CVP)

The pressure in the thoracic vena cava, important for assessing fluid status.

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Triple-Lumen Catheter

A catheter with three channels used for infusing fluids, medications, and measuring CVP.

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Vasopressors

Medications used to constrict blood vessels and increase blood pressure in shock states.

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Intraosseous (IO) Access

A method of delivering medication and fluids through the marrow of a bone.

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Crystalloid Infusion

Infusion of sterile water with electrolytes for volume expansion.

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Large-Gauge Catheter

A wide bore IV catheter used for fast fluid and medication administration.

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Indwelling Catheter

A catheter that remains in place for a longer time, often used for patients with chronic conditions.

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Quantitative Resuscitation

A practice aimed at resuscitating patients to set physiological endpoints.

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Early Goal-Directed Therapy (EGDT)

A strategy targeting specific volume, perfusion, and oxygen delivery endpoints early in treatment.

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Central Venous Oxygen Saturation

An indicator of oxygen delivery to oxygen consumption ratio, measured from central circulation.

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Lactate Clearance

The process of measuring lactate levels to assess tissue perfusion and oxygen delivery.

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Septic Shock

A life-threatening condition caused by sepsis leading to organ failure and low blood pressure.

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High-Dose Vasopressors

Medications used to raise blood pressure in critically ill patients.

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Volume Status

The assessment of body's fluid levels and distribution.

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Systemic Perfusion

The process of adequate blood flow to organs and tissues.

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Early Recognition

The prompt identification of a patient's deteriorating condition for timely intervention.

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Delayed resuscitation

A concept suggesting postponing fluid resuscitation in hemorrhagic shock.

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Hypotensive resuscitation

Fluid resuscitation strategy maintaining lower blood pressure during treatment.

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Isotonic crystalloids

Fluids that maintain equal osmotic pressure with blood plasma, used for resuscitation.

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Lactated Ringer's solution

A balanced isotonic crystalloid used to decrease acute kidney injury risk.

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Fluid resuscitation volume

Initial volume replacement of 20 to 25 mL per kg is recommended for shock.

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Colloids

Solutions with high osmotic pressure used to maintain intravascular volume.

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Hypertonic saline

A high-salt solution sometimes used in resuscitation but not beneficial for mortality.

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Septic shock fluid resuscitation

Consists of serial boluses of IV isotonic crystalloid to improve hemodynamic response.

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Natural vs. synthetic colloids

Natural colloids like albumin are preferred over synthetic due to better safety profile.

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Shock resuscitation endpoint

A target measurement indicating successful treatment during septic shock management.

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Volume Replacement

The process of restoring blood volume to stabilize patients in shock.

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Peripheral venous access

Access made through peripheral veins, typically safer for resuscitation.

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Right ventricular filling pressure

Pressure measurement used to infer fluid status in the right heart.

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Dynamic variables of fluid responsiveness

Measurements that help assess how well a patient will respond to fluid resuscitation.

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Crystalloids

Isotonic solutions used to treat hemorrhagic shock through rapid infusion.

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Urine output

A clinical response indicator used to assess kidney perfusion during resuscitation.

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Fluid bolus

A rapid infusion of fluid given to patients to increase their blood volume quickly.

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Criteria for Diagnosing Shock

Empirical indicators include altered mental status and tachycardia.

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Key Interventions for Hemorrhagic Shock

Control bleeding and transfuse PRBC if delayed control occurs.

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Management of Cardiogenic Shock

Provide oxygen, use vasopressors, and possibly thrombolysis.

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Significance of Jugular Venous Distention

Indicates potential cardiac failure or pulmonary embolism.

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Importance of Early Antibiotic Administration in Septic Shock

Prompt antibiotics reduce mortality risk; don't wait for hypotension.

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Limitations of Urine Output in Perfusion Assessment

Urine output requires time to be accurate; often unreliable in renal issues.

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Role of Bedside Ultrasound in Shock

Ultrasound can identify multiple potential causes of shock.

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Sepsis-3 Definition

Sepsis is now defined by SOFA score ≥2 with infection; shock needs vasopressors and lactate >2.

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When to Use Peripheral IV for Vasopressors

Use if central access isn’t available, ensuring a large-gauge IV.

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Adequate Fluid Responsiveness Indicators

Improved vital signs, urine output, and lactate trends indicate responsiveness.

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Hyperdynamic Left Ventricle and Sepsis

Suggests sepsis due to high cardiac output; helps differentiate from cardiogenic shock.

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Immediate Requirement in Shock Presentation

Timely assessment and treatment are essential even before identifying the cause.

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Monitoring Vital Signs in Shock

Heart rate, blood pressure, and oxygen saturation should be continuous.

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Noninvasive Blood Pressure Measurement Issue

These measurements can be inaccurate in extreme hypotension.

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Arterial Pressure Monitoring Line Benefit

Improves tracking of the body's response to therapy.

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Urine Output as Vital Organ Perfusion Indicator

Foley catheter urine output indicates organ blood flow efficiency.

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Lactate and Base Deficit Concern Levels

Lactate >4.0 mM and base deficit <−4 mEq/L indicate shock severity.

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Downward Trend of Serum Lactate

Indicates adequacy of resuscitation and favorable prognosis.

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Rising Lactate Level Indication

A rising level signifies the need for more aggressive treatment.

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Historical Factors in Shock Assessment

Factors including history and vital signs are crucial for evaluation.

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Jugular Venous Distention Meaning

Suggests potential for severe cardiac conditions like failure or strain.

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Indications of Tissue Hypoperfusion

Signs include low blood pressure, altered mental state, and low urine output.

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Septic Shock Definition per Sepsis-3

Septic shock is sepsis with hypotension needing vasopressors after fluids.

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Immediate Step for IV Access in Shock

Establish intraosseous access when peripheral is not available.

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Alternative to Central Venous Oxygen Saturation

Lactate clearance can serve as practical resuscitation endpoint.

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Criterion for Diagnosing Shock (Box 3.2)

Heart rate greater than 100 beats per minute is a primary criterion.

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Indications for Isotonic Crystalloid Infusion

Initiate infusion upon evidence of poor organ perfusion.

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Components for Septic Shock if Fluid Fails

If initial resuscitation fails, vasopressors like norepinephrine are needed.

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Function of Triple-Lumen Catheter

Allows simultaneous administration of vasopressors, fluids, and antibiotics.

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Advantages of Central vs. Peripheral Access in Shock

Central access is preferred for high-dose vasopressors in severe cases.

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Concerns about Invasive Resuscitation Measurements

Past studies showed no mortality advantage over usual care in septic shock.

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Common Causes of Shock (Box 3.3)

Include hemorrhagic, septic, and cardiogenic shock types.

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EGDT (Early Goal-Directed Therapy)

A protocol-driven approach to resuscitation in shock, focusing on achieving physiological targets.

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Goals of EGDT

To restore tissue perfusion, optimize hemodynamics, and tailor resuscitation to patient needs.

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Rapid Assessment in EGDT

Immediate evaluation of the patient's physiological status, including vital signs and fluid balance.

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Focused Interventions in EGDT

Targeted therapies based on assessment, like fluid resuscitation and vasopressors.

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Continuous Monitoring in EGDT

Ongoing monitoring and adjustment of treatment to maintain targeted physiological parameters.

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Outcomes of EGDT

Improved survival rates, reduced hospital stay, and lower complication rates in shock management.

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Specific EGDT Protocols

Common elements within protocols include targeting values for vital signs and lab data.

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Clinical Guidelines for EGDT

Includes rapid assessment, focused interventions, continuous monitoring, and early goal identification.

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Jugular Venous Distention (JVD)

An observable swelling of the jugular veins indicating possible heart failure or venous obstruction.

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Respiratory Fluctuation of Venous Pulsations

The variation in venous pulse with breathing, increasing during inspiration and decreasing during expiration.

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Treatment for JVD

Focuses on addressing the underlying condition, such as fluid overload or heart failure.

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Medications for JVD

Includes diuretics to decrease fluid volume and inotropes to enhance cardiac performance.

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Monitoring JVD

Regular observation of JVD alongside vital signs to evaluate treatment effectiveness.

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JVD Definition

Jugular venous distention (JVD) is visible swelling of neck veins due to increased pressure.

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Cause of JVD

JVD occurs from increased venous pressure that prevents blood outflow.

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Clinical Significance of JVD

JVD indicates potential heart issues, reflecting inability to pump blood efficiently.

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Technical Assessment of JVD

JVD is assessed by observing neck distension with the patient at a 45-degree angle.

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Cardiac Causes of JVD

Right-sided heart failure and restricted heart muscle can lead to JVD.

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Pulmonary Causes of JVD

JVD can arise from pulmonary hypertension or right ventricular issues.

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Venous Causes of JVD

Conditions like superior vena cava syndrome can cause JVD due to vessel compression.

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Other Causes of JVD

High fluid volume from conditions such as dehydration or overload can contribute to JVD.

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Balanced Transfusions

Administering FFP, platelets, and packed RBCs in specific ratios.

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FFP Indications

Patients with coagulation factor deficiencies due to liver disease, DIC, or warfarin use.

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FFP Goal

Increase coagulation factor levels to 20-30% of normal to achieve hemostasis.

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FFP Dose

Standard initial dose is 10-15 mL/kg.

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Platelet Transfusion Indications

Patients with thrombocytopenia or platelet dysfunction who are actively bleeding or at high risk of bleeding.

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Serum Lactate

A laboratory value reflecting the amount of lactate in the blood.

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Normal Serum Lactate Range

The acceptable range for lactate levels in a blood sample.

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Typical Lactate Normal Range

Often considered 0.5-2.2 mmol/L, though lab-specific.

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Lab-Dependent Lactate Values

Lactate levels differ slightly based on the testing facility.

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Check Lab Specific Lactate Ranges

Examine your lab's documentation.

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ScvO2 Definition

Reflects oxygen balance; a key indicator of tissue oxygenation in critical care.

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Normal ScvO2 Range

Generally 65-75%; indicates the saturation of venous blood returning to the right heart.

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High ScvO2 (above 75%)

Increased oxygen delivery relative to consumption or decreased oxygen extraction.

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High ScvO2 in Sepsis

Conditions like sepsis, where tissues can't extract oxygen effectively.

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Low ScvO2 (below 65%) meaning

Inadequate oxygen delivery or increased oxygen consumption by tissues.

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Anemia and ScvO2

Reduced hemoglobin concentration, limiting oxygen-carrying capacity.

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Hypoxemia and ScvO2

Limits the amount of oxygen available for delivery to tissues.

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Conditions Increasing Oxygen Consumption

Fever, shivering, seizures which increases tissue oxygen demand.

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Maldistribution of Blood Flow

Reduced blood flow to a specific area, leading to increased oxygen extraction.

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Arterial Oxygen Saturation (SaO2)

Percentage of oxygen bound to hemoglobin in arterial blood, reflecting lung oxygen uptake.

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Central Venous Oxygen Saturation (ScvO2)

The balance between oxygen delivery and consumption at the tissue level measured from the central venous system.

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Mixed Venous Oxygen Saturation (SvO2)

Reflects oxygen saturation of venous blood returning from all tissues, collected from the pulmonary artery.

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Low Central Venous Oxygen Saturation

Increased oxygen extraction by tissues relative to oxygen delivery.

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Supplemental Oxygen

Oxygen availability can be improved by delivering supplemental oxygen

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Red Blood Cell Transfusion

Oxygen carrying capacity improved by transfusing red blood cells

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Cardiac Output Optimization

Can be improved with fluids or inotropic agents.

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Hemoglobin and ScvO2

Reduced hemoglobin levels decrease the blood's ability to carry oxygen, lowering ScvO2.

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Tissue Perfusion and ScvO2

Inadequate blood provision to tissues impairs oxygen delivery, reducing ScvO2.

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Base Deficit

The amount of base needed to normalize blood pH when excess acid (acidosis) is present.

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Base Deficit Calculation

Base Deficit = 0.3 x (24 - HCO3-). HCO3- is bicarbonate level from arterial blood gas.

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Higher Base Deficit

A more severe state of metabolic acidosis.

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Base Excess

The amount of acid or base needed to bring blood pH back to normal when bicarbonate level is abnormal.

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Base Excess Calculation

Similar to base deficit calcuation, uses bicarbonate levels in arterial blood gas results.

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Positive Base Excess

An excess of base in the blood, suggesting alkalosis.

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Negative Base Excess

An excess of acid in the blood, indicating acidosis.

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Base Deficit and Excess Relation

They provide information about the acid-base balance in the body.

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Base Deficit Indicates

Indicates the need for base to correct acidosis.

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Base Excess Indicates

Indicates the presence of acid-base abnormalities in the blood.

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Acid-Base Balance

Measurement to assess the patient's acid-base imbalances.

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Acidosis

Condition where there is too much acid in body fluids.

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Alkalosis

High blood pH.

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Arterial Blood Gas

ABG

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Bicarbonate

HCO3

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Worsening Acidosis

If base deficit increases, it indicates acidosis is worsening.

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Systems That Regulate Acid-Base

Respiratory and metabolic systems.

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Causes of Abnormal Acid-Base

Conditions such as COPD.

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How to Fix Acid Base Imbalances

Ventilate and fix issues.

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Blood pH.

Normal blood acidity.

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Study Notes

  • Patients with cardiac failure or renal failure may benefit from closer measurement of dynamic variables like stroke volume.
  • A triple-lumen catheter allows safe infusion of vasopressors and simultaneous infusion of IV fluids and antibiotics when IV access is limited.
  • In children, a 3- or 5-Fr bilumen catheter can be placed in the femoral vein.
  • If peripheral or central venous access cannot not be attained, intraosseous (IO) access should be established.
  • Vasoactive medications should be given through a large-gauge (18g or larger) peripheral catheter at the level of the antecubital fossa if central venous access and IO access are unavailable.
  • In EDs where current practice limits catheter use, a specific hospital policy and training session should be developed to make an exception in the case of shock.
  • Controlling hemorrhage remains the cornerstone of treating hemorrhagic shock.
  • In the setting of traumatic shock from an injury distal to the renal arteries, Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) can maintain cardiac and cerebral perfusion while source control is obtained.
  • Gastrointestinal bleeding may require urgent endoscopy.
  • In septic shock related to an abscess, removal of the infectious stimulus through surgical intervention should proceed as soon as practical.
  • Large, acute pericardial effusions should be managed with pericardiocentesis.
  • Tension pneumothorax or hemothorax should be treated with tube thoracostomy.

Quantitative Resuscitation

  • Quantitative resuscitation aims to restore systemic perfusion and vital organ function.
  • Routine use of central venous monitoring for patients with septic shock does not improve outcomes compared to usual care.
  • Patients should be resuscitated early, within the first 6 hours, to achieve normalization of volume status, perfusion, and oxygen delivery markers.
  • Lactate clearance is a simpler and preferred endpoint of resuscitation to central venous oxygen saturation.
  • If the lactate concentration has not decreased by 10% to 20% 2 hours after resuscitation, take additional steps to improve systemic perfusion.

Pharmacology

  • Vasopressors are used to increase cardiac output and oxygen delivery if crystalloid resuscitation alone is inadequate.
  • Vasoactive medications should optimally be administered through a central venous catheter to avoid the potential for extravasation.
  • Initial fluid resuscitation should consist of serial boluses of IV isotonic crystalloid as long as the patient continues to demonstrate a positive hemodynamic response to fluid loading.
  • Persistent hypotension, despite 30 mL/kg of IV fluid, indicates the need to add vasopressors to the resuscitation.
  • Avoid synthetic colloids like hydroxyethyl hetastarch due to a higher risk of renal failure.
  • Balanced crystalloids are recommended once shock is identified.
  • Rapid infusion of 20 to 25 mL of isotonic crystalloid per kilogram is the initial volume replacement, though evidence of the superiority of a specific volume of crystalloid bolus is lacking.
  • If patients require large crystalloid volumes (>4 L), add 5- to 10-mL/kg boluses of a natural colloid like albumin.
  • Transfuse PRBCs (1 to 2 units in adults or 5 to 10 mL/kg in children) if criteria for shock persist despite crystalloid infusion and hemoglobin is <7 g/dL.
  • Transfuse PRBCs, fresh-frozen plasma, and platelets in a 1:1:1 ratio.
  • Focus on blood products and bleeding control, as vasopressors have increased mortality risk in hemorrhagic settings.
  • Norepinephrine is the vasopressor of choice for correcting hypotension in septic shock.
  • Norepinephrine should be initiated at 0.05 mcg/kg/min or 3 to 5 mcg/min for most adult patients, and titrated at 3- to 5-minute intervals until mean arterial pressure is >65 mm Hg.
  • Vasopressin may be added as a second vasopressor agent.
  • Dobutamine may be used with norepinephrine to increase cardiac output and maintain oxygen delivery in both cardiogenic and septic shock.
  • If simultaneous BP and inotropic support is necessary for septic shock, use epinephrine alone
  • Begin antimicrobial therapy and surgical drainage (Source Control) as fast as possible in septic shock, antibiotic as soon as practical.
  • Piperacillin-tazobactam and vancomycin are a rational empirical choice.
  • High-dose, short-course corticosteroid therapy in unselected patients with septic shock may decrease shock duration but does not decrease mortality.

Devices and Procedures

  • Rapid sequence intubation is the preferred method of airway control in most patients with refractory shock.
  • Positive-pressure ventilation can improve ventricular function and cardiac output up to 30%.

Septic Shock Treatments

  • Treatment involves prompt antibiotics, fluid resuscitation with crystalloids, and vasopressors.
  • Norepinephrine (or inotropes such as dobutamine) are first-line agents for cardiogenic shock.
  • In hemorrhagic shock patients, immediate PRBC transfusion should be initiated.
  • Outcomes for patients with shock depend on the underlying cause and the patient's condition.
  • Persistent refractory hypotension implies worse outcomes; the mortality rate is 20% for hemorrhagic shock and over 40% for septic and cardiogenic shock.

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