Shock Flashcards
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What’s shock?
Shock is a life-threatening condition where the heart fails to pump enough blood, or the blood volume is insufficient, leading to inadequate tissue perfusion and cellular hypoxia. This means that tissues and organs do not get enough oxygen, which can cause severe damage and even lead to organ failure.
List the Major Types of Shock
Cardiogenic Shock
Hypovolemic Shock
Septic Shock
What’s the mechanism & examples of Cardiogenic Shock:
- Examples: Myocardial infarction (heart attack), arrhythmias (irregular heartbeats), cardiac tamponade (pressure on the heart due to fluid accumulation), pulmonary embolism (blood clot in the lungs).
- Mechanism: Failure of the heart to pump blood effectively due to intrinsic myocardial damage (damage to the heart muscle itself), extrinsic compression (external pressure on the heart), or obstruction to blood outflow.
What’s the mechanism and examples of Hypovolemic Shock:
- Examples: Blood loss (from injuries, surgery), fluid loss (from severe dehydration, vomiting, diarrhea).
- Mechanism: Inadequate blood/plasma volume due to significant loss of fluids or blood.
What’s the mechanism and examples of Hypovolemic Shock:
- Examples: Blood loss (from injuries, surgery), fluid loss (from severe dehydration, vomiting, diarrhea).
- Mechanism: Inadequate blood/plasma volume due to significant loss of fluids or blood.
What’s the mechanism and examples of Septic Shock:
Septic Shock:
Example: A patient with a severe bacterial infection develops septic shock due to the body’s overwhelming inflammatory response.
Illustration: Picture a city’s defense system (immune system) going into overdrive during an invasion (infection). The defenders (immune cells) release chemicals (cytokines) that cause chaos, damaging infrastructure (blood vessels) and making it hard for the city to function normally.
Overwhelming microbial infections (bacterial and fungal) Superantigens (e.g., toxic shock syndrome) Trauma, burns, pancreatitis Activation of cytokine cascades; peripheral vasodilation and pooling of blood; endothelial activation/injury; leukocyte-induced damage, disseminated intravascular coagulation
What’s neurogenic shock?
It’s primary & secondary cause?
Neurogenic Shock: Neurogenic shock is a type of shock resulting from a loss of vasomotor tone in the peripheral arterial beds, often due to spinal cord injury
Loss of Vasomotor Tone:
The blood vessels lose their ability to constrict, leading to inadequate tissue perfusion (blood flow to tissues).
Example: Imagine a garden hose (blood vessel) that suddenly becomes floppy and cannot direct water (blood) where it is needed.
Secondary to Spinal Cord Injury:
Typically occurs after a spinal cord injury from a vertebral fracture.
What are the symptoms of Neurogenic Shock?
Hypotension with Bradycardia: Low blood pressure accompanied by a slow heart rate.
- Warm Extremities: Unlike other forms of shock where extremities might be cold, here they remain warm due to vasodilation (widening of blood vessels).
Motor and Sensory Deficit: Loss of muscle control and sensation below the level of injury.
How does the body Compensate for Shock?
Compensation for Shock: When the body detects a decrease in oxygen delivery (DO2), it initiates several compensatory mechanisms to maintain tissue perfusion and oxygenation.
How:
- Increased Oxygen Extraction:
Tissues compensate for reduced oxygen delivery by extracting a higher percentage of the available oxygen from the blood.
Example: Imagine a sponge soaking up every last drop of water in a drying puddle.
Adrenergic Response:
Low arterial pressure triggers the release of adrenergic hormones (like epinephrine and norepinephrine), causing:
- Sympathetic-Mediated Vasoconstriction: Blood vessels constrict to increase blood pressure.
- Increased Heart Rate: The heart pumps faster to circulate blood more effectively.
- Selective Vasoconstriction: Blood is redirected to essential organs like the heart and brain, away from less critical areas like the splanchnic (intestinal) circulation.
Example: Picture a city experiencing a water shortage. The supply is rerouted to hospitals and fire stations, cutting off parks and fountains
Circulating Beta-Adrenergic Amines:
- Epinephrine and Norepinephrine: These hormones enhance heart muscle contraction and trigger the release of other crucial substances:
- Corticosteroids from the Adrenal Gland: Enhance the effects of catecholamines (epinephrine and norepinephrine).
- Renin from the Kidneys: Promotes volume retention and vasoconstriction, helping maintain blood pressure.
- Glucose from the Liver: Released to ensure energy supply, increasing pyruvate uptake in the mitochondria and leading to lactate production under low oxygen conditions.
Circulating Beta-Adrenergic Amines:
- Epinephrine and Norepinephrine: These hormones enhance heart muscle contraction and trigger the release of other crucial substances:
- Corticosteroids from the Adrenal Gland: Enhance the effects of catecholamines (epinephrine and norepinephrine).
- Renin from the Kidneys: Promotes volume retention and vasoconstriction, helping maintain blood pressure.
- Glucose from the Liver: Released to ensure energy supply, increasing pyruvate uptake in the mitochondria and leading to lactate production under low oxygen conditions.
Which Shock is Associated with Systemic Inflammation:
Septic shock
What are the effects & consequences of septic shock?
Effects:
Arterial Vasodilation: Blood vessels widen, leading to a drop in blood pressure.
Vascular Leakage: Fluids leak out of the blood vessels, causing swelling and further reducing blood volume.
Venous Blood Pooling: Blood pools in the veins, reducing the effective blood volume circulating to vital organs.
Consequences:
Tissue Hypoperfusion: Reduced blood flow to tissues.
Cellular Hypoxia: Lack of oxygen at the cellular level.
Metabolic Derangements: Disruptions in normal metabolic processes, leading to organ dysfunction.
Organ Failure and Death: If these conditions are severe and persistent, they can lead to multiple organ failure and death.
Shock Associated with Systemic Inflammation:
Causes: Can be triggered by microbial infections, burns, trauma, or pancreatitis.
How does Septic Shock actually happen?
Inflammatory and Counter-Inflammatory Responses:
Initiation of Inflammation:
The inflammatory response in sepsis is triggered when receptors on immune cells are activated by microbial cell wall products.
Example: Think of a security system (immune receptors) being triggered by an intruder (microbial products), setting off alarms (inflammatory response).
Production of Cytokines:
Activated innate immune cells produce various cytokines, including TNF (Tumor Necrosis Factor), IL-1 (Interleukin-1), IFN-γ (Interferon-gamma), IL-12, and IL-18.
These cytokines promote the expression of adhesion molecules on endothelial cells and stimulate further cytokine and chemokine production.
Example: It’s like a chain reaction where the initial alarms (cytokines) not only alert the security team (immune cells) but also activate more security measures (adhesion molecules and additional cytokines).
Endothelial Activation and Injury:
The endothelial cells lining blood vessels become activated and injured due to the intense inflammatory response.
This leads to increased vascular permeability and leakage of fluids into tissues, contributing to hypotension and edema.
Illustration: Imagine a dam (endothelium) that starts to crack and leak under intense pressure, allowing water (fluids) to escape and flood surrounding areas (tissues).
Induction of a Procoagulant State:
The inflammatory response promotes a procoagulant state, where the blood becomes more prone to clotting.
This can lead to disseminated intravascular coagulation (DIC), a condition characterized by widespread clotting and bleeding.
Example: Picture a river (blood) that suddenly starts to form clots (thrombosis) everywhere, obstructing its flow and causing chaos.
What are the metabolic abnormalities that can happen in Septic Shock
Metabolic Abnormalities:
Sepsis can cause significant metabolic changes, including insulin resistance and hyperglycemia.
These changes can impair cellular function and energy production, exacerbating organ dysfunction.
Illustration: Think of a power plant (metabolism) that becomes less efficient and starts to produce less energy, leading to blackouts (organ dysfunction) throughout the city.
Organ Dysfunction:
The combined effects of inflammation, endothelial injury, coagulation, and metabolic abnormalities lead to impaired organ function.
If not promptly addressed, this can progress to multiple organ failure and death.
Example: Imagine a complex machine (the body) where multiple components (organs) start to fail one after another due to a cascade of malfunctions.
How does septic shock induce Complement Cascade Activation
Complement Cascade Activation:
Mechanism:
Microbial components activate the complement cascade.
This leads to the production of various molecules:
Anaphylotoxins (C3a, C5a): These promote inflammation by increasing vascular permeability and attracting immune cells.
Chemotactic Fragments (C5a): These attract neutrophils and other immune cells to the site of infection.
Opsonins (C3b): These enhance the phagocytosis of microbes by marking them for destruction.
Illustration: Think of the complement system as a set of emergency signals and markers sent out by the body to call for backup (immune cells) and mark the invaders (microbes) for destruction.
Explain how septic Shock initiates Complement Cascade Activation &Counter-Regulatory Immunosuppressive Mechanisms:
Complement Cascade Activation:
Mechanism:
Microbial components activate the complement system, leading to:
- Anaphylotoxins (C3a, C5a): Increase vascular permeability and attract immune cells.
- Chemotactic Fragments (C5a): Draw neutrophils and other immune cells to infection sites.
Opsonins (C3b): Mark microbes for destruction by immune cells.
Illustration: The complement system functions like an emergency response team, marking invaders and calling for backup.
Counter-Regulatory Immunosuppressive Mechanisms:
Definition: These are processes that reduce the inflammatory response to prevent damage to the host’s own tissues.
- Mechanism:
- Shift from TH1 to TH2 Cytokines: The body moves from a pro-inflammatory state to an anti-inflammatory state.
- Production of Anti-Inflammatory Mediators: Mediators such as soluble TNF receptor, IL-1 receptor antagonist, and IL-10 are produced to reduce inflammation.
Illustration: This is akin to initiating peace talks to reduce collateral damage from an all-out war.
Counter-Regulatory Immunosuppressive Mechanisms:
Hyperinflammatory State:
While sepsis initially triggers a hyperinflammatory response, it also activates mechanisms that suppress the immune system to prevent excessive damage.
Immune Suppression Mechanisms:
Shift from TH1 to TH2 Cytokines: The body shifts from producing pro-inflammatory (TH1) cytokines to anti-inflammatory (TH2) cytokines.
Production of Anti-Inflammatory Mediators: Soluble TNF receptor, IL-1 receptor antagonist, and IL-10 are produced to counteract inflammation.
Illustration: It’s like a city launching an all-out attack (hyperinflammation) on invaders and then trying to negotiate peace and prevent collateral damage (immunosuppression).
How does sepsis induce Procoagulant State:?
Definition: This refers to the process by which sepsis shifts the body towards a state where blood clotting is promoted, often leading to the formation of clots.
Mechanism:
Proinflammatory cytokines increase the production of tissue factor and decrease the production of endothelial anti-coagulant factors (tissue factor pathway inhibitor, thrombomodulin, protein C).
Sepsis also reduces fibrinolysis (the breakdown of clots) by increasing plasminogen activator inhibitor-1.
Illustration: Picture a river that starts forming excessive barriers and dams due to miscommunication and overreaction.
Complement Cascade Activation:
Anaphylotoxins (C3a, C5a): Promote inflammation and increase vascular permeability.
Chemotactic Fragments (C5a): Attract immune cells.
Opsonins (C3b): Enhance the destruction of microbes.
Counter-Regulatory Immunosuppressive Mechanisms:
Shift to Anti-Inflammatory Cytokines (TH2): Reduces inflammation.
Production of Anti-Inflammatory Mediators: Helps moderate the inflammatory response.
How does Septic shock cause Organ Dysfunction?
- Systemic Hypotension: Low blood pressure reduces blood flow to organs.
- Interstitial Edema: Fluid leakage into tissues reduces oxygen and nutrient delivery.
- Small Vessel Thrombosis:
Blood clots in small vessels further restrict blood flow. - Cellular Hypoxia:
Even when nutrients reach tissues, they cannot be properly utilized due to lack of oxygen.
Illustration: Imagine a city’s power grid failing. Even if power lines reach the neighborhoods, the electricity can’t be used because the power plants (organs) aren’t functioning properly due to damage (hypoxia).
- Impact of Cytokines and Secondary Mediators:
What’s the Impact of Cytokines and Secondary Mediators during sepsis?
High levels of cytokines and secondary mediators decrease myocardial contractility, reducing the heart’s ability to pump blood efficiently.
Increased vascular permeability and endothelial injury can lead to acute respiratory distress syndrome (ARDS).
These factors together may cause multiple organ failures, especially in the kidneys, liver, lungs, and heart, ultimately leading to death
What are Superantigens?
Superantigens are bacterial proteins that cause a syndrome similar to septic shock, known as toxic shock syndrome.
