Week 3 - Chapter 20: Shock
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Questions and Answers

What is initially characterized by a high cardiac output (CO) and warm extremities in septic shock?

  • Reduced cellular oxygen utilization
  • Organ ischemia
  • Hypodynamic phase
  • Sympathetic activation (correct)

    • Septic shock is always characterized by decreased cardiac output and organ ischemia.

    False (B)

    What are the main therapeutic strategies for septic shock?

    Improving blood flow distribution and managing infection with antibiotics.

    Septic shock can deteriorate to a _____ phase, characterized by decreased cardiac output and organ ischemia.

    <p>hypodynamic</p> Signup and view all the answers

    Match the following hemodynamic parameters with their corresponding descriptions:

    <p>Cardiac Output = Amount of blood ejected by the heart per minute Preload = Amount of blood in the ventricle at the end of diastole Afterload = Resistance the heart must overcome to eject blood Contractility = Inherent strength of cardiac muscle contraction</p> Signup and view all the answers

    What is the primary cause of cardiogenic shock?

    <p>All of the above (D)</p> Signup and view all the answers

    Cardiogenic shock is usually the result of severe ______ dysfunction.

    <p>ventricular</p> Signup and view all the answers

    Cardiogenic shock is always caused by a heart attack.

    <p>False (B)</p> Signup and view all the answers

    What are the diagnostic features of cardiogenic shock?

    <p>Elevated left ventricular end-diastolic pressure, decreased cardiac output, low SVO2 and S3 heart sounds.</p> Signup and view all the answers

    Match the type of shock with its primary cause:

    <p>Cardiogenic Shock = Severe ventricular dysfunction Obstructive Shock = Mechanical obstruction to blood flow Hypovolemic Shock = Inadequate blood volume Septic Shock = Infection-induced systemic inflammatory response</p> Signup and view all the answers

    What condition can lead to neurogenic shock?

    <p>Spinal cord injury (B)</p> Signup and view all the answers

    Septic shock results solely from bacterial infections.

    <p>False (B)</p> Signup and view all the answers

    What is the primary treatment for neurogenic shock?

    <p>Vasopressors and fluids</p> Signup and view all the answers

    Septic shock is characterized by the release of immune mediators resulting in __________.

    <p>widespread inflammation</p> Signup and view all the answers

    Match the type of shock with its description:

    <p>Neurogenic Shock = Loss of sympathetic activation of arteriolar smooth muscle Septic Shock = Severe systemic inflammatory response to infection Anaphylactic Shock = Severe allergic reaction leading to systemic vasodilation Cardiogenic Shock = Insufficient blood flow due to heart failure</p> Signup and view all the answers

    Which of the following is a common cause of septic shock?

    <p>Fungal infections (D)</p> Signup and view all the answers

    What key systems are activated during septic shock leading to inflammation?

    <p>Clotting cascade, complement system, and kinin system</p> Signup and view all the answers

    Peripheral vasodilation is a characteristic of septic shock.

    <p>True (A)</p> Signup and view all the answers

    What is the primary goal of therapy in hypovolemic shock?

    <p>Fluid replacement and controlling the source of volume loss (A)</p> Signup and view all the answers

    Distributive shock is characterized by decreased vasodilation and reduced peripheral blood pooling.

    <p>False (B)</p> Signup and view all the answers

    Name one type of shock associated with excessive vasodilation.

    <p>Distributive Shock</p> Signup and view all the answers

    In anaphylactic shock, excessive mast cell degranulation is mediated by ______ antibodies.

    <p>IgE</p> Signup and view all the answers

    Which of the following is NOT a clinical symptom of anaphylactic shock?

    <p>Inflammation (A)</p> Signup and view all the answers

    Treatment for anaphylactic shock includes the use of epinephrine.

    <p>True (A)</p> Signup and view all the answers

    What are colloids used for in treating hypovolemic shock?

    <p>To increase serum colloid osmotic pressure</p> Signup and view all the answers

    Match the types of shock with their characteristics:

    <p>Hypovolemic Shock = Caused by blood loss Anaphylactic Shock = Mediated by IgE antibodies Septic Shock = Infection-induced vasodilation Neurogenic Shock = Loss of sympathetic tone</p> Signup and view all the answers

    What is the normal percentage of oxygen extracted from arterial blood?

    <p>25% (B)</p> Signup and view all the answers

    A lower cardiac output (CO) results in higher mixed venous oxygen saturation (SVO2).

    <p>False (B)</p> Signup and view all the answers

    What is the primary purpose of a pulmonary artery catheter?

    <p>To measure intracardiac pressures, cardiac output, and SVO2.</p> Signup and view all the answers

    Right atrial pressure is used to manage blood volume, also known as right __________.

    <p>preload</p> Signup and view all the answers

    What does left atrial pressure indicate?

    <p>Left ventricular preload (D)</p> Signup and view all the answers

    Maldistribution of blood flow leads to higher SVO2.

    <p>True (A)</p> Signup and view all the answers

    Pulmonary capillary occlusion pressure is a direct measure of __________.

    <p>left atrial pressure</p> Signup and view all the answers

    What is a primary complication of shock that affects the lungs?

    <p>Acute Respiratory Distress Syndrome (ARDS) (A)</p> Signup and view all the answers

    Reduced oxygen consumption in shock affects only the respiratory system.

    <p>False (B)</p> Signup and view all the answers

    What is the primary cause of death in Acute Respiratory Distress Syndrome (ARDS)?

    <p>Multiple organ failure</p> Signup and view all the answers

    In shock states, the body's _______ consumption is reduced, leading to multiple complications.

    <p>oxygen</p> Signup and view all the answers

    Match the following complications of shock with their descriptions:

    <p>Septic shock = Most commonly leads to ARDS Refractory hypoxemia = A result of impaired gas exchange Pulmonary edema = Radiographic evidence seen in ARDS Neutrophil activity = Promotes inflammation and capillary permeability</p> Signup and view all the answers

    What role do inflammatory cytokines play in shock?

    <p>They cause organ damage and alter metabolism. (B)</p> Signup and view all the answers

    Proteolytic enzymes released by neutrophils are beneficial for lung function.

    <p>False (B)</p> Signup and view all the answers

    What happens to pulmonary capillaries during shock states?

    <p>They become leaky.</p> Signup and view all the answers

    Flashcards

    Oxygen Delivery (DO2)

    The amount of oxygen transported to tissues per minute.

    Oxygen Consumption (VO2)

    The amount of oxygen used by tissues for metabolism.

    Mixed Venous Oxygen Saturation (SVO2)

    The percentage of oxygen in blood returning to the heart from tissues.

    Effects of Low Cardiac Output (CO)

    Lower CO leads to greater oxygen extraction and lower SVO2 values.

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    Pulmonary Artery Catheter

    A catheter used to measure pressures in the heart and lungs.

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    Right Atrial Pressure

    Pressure in the right atrium, reflects blood volume and preload.

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    Left Atrial Pressure

    Pressure in the left atrium, indicates left ventricular preload.

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    Pulmonary Capillary Occlusion Pressure

    Reflects left atrial pressure, assesses pulmonary blood flow.

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    Septic Shock

    A condition initially marked by high cardiac output but with cellular hypoxia and high SvO2.

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    High Cardiac Output (CO)

    Initial phase of septic shock characterized by increased heart activation and blood flow.

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    Cellular Hypoxia

    A state where cells are deprived of adequate oxygen despite high CO.

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    SvO2

    Mixed venous oxygen saturation, indicating the balance between oxygen delivery and consumption.

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    Hypodynamic Phase

    A later stage in septic shock with decreased cardiac output and organ ischemia.

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    Therapy for Septic Shock

    Treatment focuses on improving blood flow distribution and managing infection with antibiotics.

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    Preload

    The amount of blood in the ventricle at the end of diastole, affecting CO.

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    Contractility

    The inherent ability of cardiac muscle fibers to contract, influencing heart performance.

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    Cardiogenic Shock

    A condition characterized by severe ventricular dysfunction leading to reduced cardiac output and oxygen delivery.

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    Low Cardiac Output (CO)

    A state where the heart fails to pump sufficient blood, reducing oxygen available to tissues.

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    S3 Heart Sounds

    Abnormal heart sounds indicative of heart failure, often heard in cardiogenic shock.

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    Elevated Left Ventricular End-Diastolic Pressure

    Increased pressure in the left ventricle at the end of filling, indicating poor cardiac function.

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    Obstructive Shock

    Shock due to mechanical obstructions preventing effective heart filling and blood flow.

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    Common Causes of Obstructive Shock

    Includes pulmonary embolism, cardiac tamponade, and tension pneumothorax.

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    Hypovolemic Shock

    Shock resulting from inadequate blood volume due to bleeding, burns, or fluid loss.

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    SNS Activation in Hypovolemic Shock

    Sympathetic nervous system response leads to increased heart rate and vasoconstriction to compensate for low blood volume.

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    Neurogenic Shock

    Shock caused by loss of sympathetic activation of blood vessels.

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    Causes of Neurogenic Shock

    Includes brain injury, drug overdose, or sympathetic nerve damage.

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    Treatment for Neurogenic Shock

    Involves vasopressors, fluids, leg elevation, and pressure stockings.

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    Causes of Septic Shock

    Commonly caused by gram-negative bacteria, gram-positive bacteria, or fungi.

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    Immune Response in Septic Shock

    Characterized by release of immune mediators causing widespread inflammation.

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    Effects of Septic Shock

    Leads to vasodilation, hypotension, blood flow maldistribution, and edema.

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    SIRS

    Systemic Inflammatory Response Syndrome, a response to infection.

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    Shock States

    Conditions resulting in reduced or inadequate oxygen consumption affecting all organs and systems.

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    Complications of Shock

    Consequences that arise from shock, often inflammatory and may involve multiple organ systems.

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    Inflammatory Cytokines

    Substances that mediate organ damage, alter metabolism, and recruit immune cells.

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    Neutrophils

    Type of white blood cells that respond to inflammation and infection, altering capillary permeability.

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    Acute Respiratory Distress Syndrome (ARDS)

    Lung condition often caused by septic shock, leading to hypoxemia and pulmonary edema.

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    Refractory Hypoxemia

    Severe and persistent low oxygen levels in blood, even with oxygen treatment.

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    Pulmonary Edema

    Fluid accumulation in the lung tissue, affecting gas exchange during ARDS.

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    Type II Pneumocytes

    Cells in the lungs responsible for producing surfactant, which reduces surface tension.

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    Classes of Hypovolemic Shock

    Four classes based on blood loss: I (15%), II (15-30%), III (30-40%), IV (>40%).

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    Fluid Replacement Therapy

    Treatment for hypovolemic shock focusing on fluid and blood product administration to restore volume.

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    Colloids vs Crystalloids

    Colloids increase serum osmotic pressure; crystalloids are electrolyte solutions for fluid replacement.

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    Distributive Shock

    Characterized by excessive vasodilation and inadequate cardiac output due to reduced preload.

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    Anaphylactic Shock

    Severe shock from extensive mast cell degranulation triggered by allergens, leading to hypotension.

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    Symptoms of Anaphylactic Shock

    Manifestations include urticaria, bronchoconstriction, stridor, angioedema, wheezing, and itching.

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    Treatment of Anaphylactic Shock

    Includes airway management and medications like epinephrine, bronchodilators, and antihistamines.

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    Study Notes

    Shock Pathogenesis

    • Shock is an imbalance between oxygen supply and cellular needs.
    • It encompasses a diverse range of life-threatening conditions.
    • A common feature is hypoperfusion and impaired cellular oxygen utilization.
    • Inadequate cellular oxygenation may stem from decreased cardiac output, maldistributed blood flow, or reduced blood oxygen content.

    Shock Causes

    • Cardiogenic: Inadequate cardiac output despite sufficient vascular volume.
    • Obstructive: Circulatory blockage (e.g., pulmonary embolism, cardiac tamponade) disrupting cardiac output.
    • Hypovolemic: Loss of blood volume due to hemorrhage or fluid loss.
    • Distributive: Greatly expanded vascular space due to inappropriate vasodilation.

    Impaired Tissue Oxygenation

    • Impaired oxygen utilization by cells disrupts function, potentially leading to cell death, organ dysfunction, and inflammation.
    • Lack of oxygen results in diverse outcomes, including lactate production, cellular swelling, oxygen radical formation, and induction of inflammatory cytokines.
    • Cellular hypoxia leads to anaerobic metabolism, free radical production, macrophage induction, and potential reperfusion injury.
    • Tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) cytokines increase in septic shock.
    • They mediate vascular failure and progressive organ damage.
    • Increased nitric oxide (NO) synthase activity can lead to excess NO, impacting microcirculation autoregulation, and activating coagulation, which further impacts oxygen debt in tissues.

    Compensatory Mechanisms and Stages of Shock

    • Shock progresses through compensated, progressive, and refractory stages.
    • In the compensatory stage, homeostatic mechanisms maintain adequate tissue perfusion despite reduced cardiac output (CO).
    • Sympathetic nervous system (SNS) activation attempts to maintain blood pressure even when cardiac output falls.
    • CO and vascular resistance both increase.
    • The progressive stage is marked by hypotension and tissue hypoxia.
    • Lactate production rises with anaerobic metabolism.
    • Organ dysfunction is caused by cellular swelling and death, oxygen-free radicals, inflammatory cytokines, and clotting cascade activation.

    Types of Shock

    Cardiogenic Shock

    • Characterized by low cardiac output (CO), reducing oxygen delivery to tissues and increasing oxygen extraction.
    • Therapy focuses on improving CO, reducing workload, and optimizing myocardial oxygen delivery via inotropic, preload-reducing, and afterload-reducing agents; intra-aortic balloon counterpulsation; ventricular assist devices; and, in severe cases, heart transplantation.

    Obstructive Shock

    • Resulting from mechanical obstructions preventing adequate cardiac filling which reduce stroke volume.
    • Common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax.
    • Manifests as right-sided heart failure, necessitating rapid management of the obstruction to prevent cardiovascular collapse.

    Hypovolemic Shock

    • Results from inadequate circulating blood volume due to hemorrhage, burns, or fluid loss into interstitial spaces.
    • External hemorrhage is a frequent cause.
    • Low CO and reduced intracardiac pressures trigger SNS activation, causing increased heart rate (HR), vasoconstriction, and increased contractility.
    • Therapy involves fluid replacement and controlling the source of volume loss, using colloids and crystalloids, as well as blood products.
    • The severity of the shock correlates to the volume of blood loss.

    Distributive Shock

    • Excessive vasodilation and peripheral blood pooling, reducing preload for the heart.
    • Different types: anaphylactic, neurogenic, and septic.
    Anaphylactic Shock
    • Result of mast cell degranulation triggered by antigens (e.g., medications, insect bites).
    • Mast cells release vasodilatory mediators, leading to severe hypotension.
    • Treatment includes maintaining airway patency, using epinephrine, bronchodilators, antihistamines, vasopressors, and intravenous (IV) fluids.
    Neurogenic Shock
    • Resulting from loss of sympathetic activation of arteriolar smooth muscles.
    • Caused by medullary depression, or spinal cord injury.
    • Treatment includes vasopressors, fluids, elevation of extremities/position changes, and use of pressure stockings as needed.
    Septic Shock
    • Resulting from a severe systemic inflammatory response to infection (bacteria, fungi).
    • Characterized by the release of immune mediators resulting in widespread inflammation.
    • The clotting cascade, complement system, and kinin system are triggered leading to widespread inflammation, peripheral vasodilation, hypotension, and maldistribution of blood flow resulting in cellular hypoxia, increased capillary pressure, and edema formation.
    • Therapy involves improving blood flow distribution, managing infection with antibiotics, and administering fluids and drugs to improve cardiac/vascular performance.

    Assessment and Hemodynamic Monitoring

    • Monitoring helps evaluate cardiac output (CO), volume status, and oxygen delivery.
    • Techniques include monitoring right atrial pressure, pulmonary artery pressure, left atrial pressure, etc.
    • Used to guide management of cardiac preload, afterload, and contractility to optimize CO and minimize workload.

    Complications of Shock

    • Various complications can result from shock, including:
      • Acute Respiratory Distress Syndrome (ARDS): Characterized by refractory hypoxemia, decreased pulmonary compliance, pulmonary edema, multiple organ failure, not necessarily severe hypoxemia.
      • Disseminated Intravascular Coagulation (DIC): Immune activation of the clotting cascade, leading to microcirculation obstructions that cause ischemic tissue damage. Widespread clot formation consumes platelets and clotting factors. Fibrin degradation products (e.g., D-dimer) increase.
      • Acute Renal Failure (ARF): Kidneys undergo long periods of hypoperfusion; vasoconstriction reduces glomerular blood flow and filtration rates. Associated with acute tubular necrosis (ATN), reduced urinary excretion of waste products (creatinine and urea), possible dialysis requirement.
      • Multiple Organ Dysfunction Syndrome (MODS): When two or more organ systems are affected. It's most commonly caused by sepsis or septic shock. Immune mechanisms become overactive and destructive, cytokines affect the endothelium, recruit neutrophils, and activate inflammation resulting in tissue destruction and organ dysfunction. Inflammatory cytokines cause extensive damage, altering metabolism and recruiting neutrophils while initiating the coagulation cascade, and causing capillary permeability changes.

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    Description

    This quiz explores the pathogenesis of shock, focusing on the critical imbalance between oxygen supply and cellular needs. It covers various types of shock, including cardiogenic, obstructive, hypovolemic, and distributive causes, as well as the implications of impaired tissue oxygenation. Test your understanding of these life-threatening conditions and their effects on cellular function.

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