What are the consequences of PRR activation?
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It initiates the repair process and mobilizes antimicrobial defenses but can also lead to excessive tissue damage.
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What are the consequences of PRR activation?
It initiates the repair process and mobilizes antimicrobial defenses but can also lead to excessive tissue damage.
What role do tissue-based macrophages and mast cells play in injury response?
They act as sentinel responders, releasing histamines, eicosanoids, and cytokines.
Which receptors are important in the initiation of adaptive responses to shock?
Baroreceptors and chemoreceptors.
What is the primary source of energy for cellular metabolism?
Adenosine triphosphate (ATP) hydrolysis.
What process generates ATP in the body?
Aerobic metabolism through oxidative phosphorylation in the mitochondria.
What are some cellular processes influenced by ATP depletion?
Maintenance of cellular membrane potential, enzyme synthesis, cell signaling, and DNA repair mechanisms.
What are damage associated molecular patterns (DAMPs)?
Endogenous molecules that signal the presence of danger to surrounding cells and tissues.
What are core principles in managing patients in septic shock?
Early treatment/resuscitation, rapid identification of infection source, and initiation of broad-spectrum antibiotics within 1 hour of diagnosis.
What is the recommended amount of intravenous crystalloid fluid to be given within the first 3 hours of shock treatment?
At least 30 mL/kg.
What happens if shed blood volume is slowly returned during hemorrhagic shock?
Eventually, the injury progresses to irreversible shock, where further volume will not reverse the process and the animal dies.
What do baroreceptors do when activated during shock?
They diminish their output, disinhibiting the effect of the autonomic nervous system (ANS) to increase sympathetic output.
What is the effect of chemoreceptors being stimulated in shock?
They result in vasodilation of coronary arteries, slowing of heart rate, and vasoconstriction of splanchnic and skeletal circulation.
What is the 'vicious cycle of shock'?
Decreased tissue perfusion and shock result in a feed-forward loop that can exacerbate cellular injury and tissue dysfunction.
What are some stimuli that can produce the neuroendocrine response?
Pain, hypoxemia, hypercarbia, acidosis, infection, change in temperature, emotional arousal, or hypoglycemia.
How does the renin-angiotensin system respond to shock?
It is activated, leading to vasoconstriction and retention of sodium and water.
What is the role of pattern recognition receptors (PRRs)?
They recognize DAMPs and effect intracellular signaling that primes and amplifies the immune response.
What is ARDS and how is it related to shock?
Acute Respiratory Distress Syndrome, recognized as an early cause of death after seemingly successful surgery to control hemorrhage.
What mean arterial pressure should be achieved with vasopressors if fluid resuscitation is inadequate?
65 mmHg.
What are the primary responses in the cardiovascular system during shock?
Changes in cardiovascular function due to neuroendocrine response and autonomic nervous system response.
How does hemorrhage affect cardiac output?
It results in diminished venous return to the heart and decreased cardiac output.
How does interleukin-1 (IL-1) function in the immune response?
It modulates local cellular responses and produces a febrile response to injury, affecting various hormonal secretions.
What is the relationship between IL-2 and shock?
IL-2 is produced by activated T cells and its role in shock response is unclear, with some studies linking it to tissue injury.
How does sympathetic stimulation affect peripheral circulation?
It induces vasoconstriction and increases systemic vascular resistance and blood pressure.
What is the role of catecholamines in shock?
They stimulate glycogenolysis and gluconeogenesis to increase glucose availability.
What hormonal response is triggered by shock?
Activation of the hypothalamic-pituitary-adrenal axis leading to cortisol release.
What is 'no-reflow' phenomenon?
It is the persistence of capillary occlusion after resuscitation, leading to ischemic injury.
What is the significance of tissue injury in traumatic shock?
It leads to the activation of inflammatory cells and the release of circulating factors that modulate the immune response.
What is the 'uptake phase' or 'compensation endpoint' in hemorrhagic shock?
It is when shed blood must be returned to the animal to sustain hypotension at a set level to prevent further hypotension and death.
What is the goal of the neuroendocrine response to hemorrhage?
To maintain perfusion to the heart and brain, even at the expense of other organ systems.
What leads to the decompensation phase of shock?
Continued hypoperfusion and ongoing cellular death and injury.
What is the 'vicious cycle' of shock?
Persistent hypoperfusion leads to further hemodynamic derangements and cardiovascular collapse.
What factors can exacerbate ischemia/reperfusion injury in shock?
Microcirculatory dysfunction and inflammatory cell activation.
What is the irreversible phase of shock characterized by?
Extensive parenchymal and microvascular injury, leading to failure of volume resuscitation.
What are the cellular events that current investigations in shock focus on?
Events leading to organ dysfunction, shock irreversibility, and death.
What occurs to pyruvate under hypoxic conditions during anaerobic metabolism?
It is converted into lactate, leading to intracellular metabolic acidosis.
What role does ADH play in the body's response to hypovolemia?
It increases water permeability in the nephron, preserving intravascular volume.
What are pathogen-associated molecular patterns (PAMPs)?
Bacterial products, including lipopolysaccharide, that enter a normally sterile environment.
What are the primary physiological responses in shock driven by?
Tissue hypoperfusion and developing cellular energy deficit.
What is the Frank-Starling curve?
It describes the force of ventricular contraction as a function of its preload.
What compensatory mechanisms increase cardiac output during shock?
Increased heart rate, contractility, and vasoconstriction.
What is the consequence of decreased intracellular pH?
It influences normal enzyme activity, cell membrane ion exchange, and cellular metabolic signaling.
What is the relationship between catecholamines and shock according to Cannon?
Elevated levels of catecholamines in the bloodstream contribute to the 'fight or flight response' and shock.
What causes neurogenic shock?
Vasodilation due to acute loss of sympathetic vascular tone, often from spinal cord injury.
What is obstructive shock?
A form of cardiogenic shock caused by mechanical impediment to circulation.
What are essential prevention measures in managing hemorrhagic shock?
Prevention of hypothermia, acidemia, and coagulopathy.
What role does arginine vasopressin play in septic states?
It is stimulated by endotoxin independently of blood pressure, osmotic, or intravascular volume changes.
How does preload affect cardiac output?
Most alterations in cardiac output in the normal heart are related to changes in preload.
What is the significance of cytokines in the immune response to shock?
They have both proinflammatory and anti-inflammatory properties and are crucial in mediating the immune response.
What phase of shock occurs when the body compensates for initial blood volume loss?
Compensated phase of shock.
What is afterload?
It is the force that resists myocardial work during contraction, primarily influenced by arterial pressure.
What initiates the neuroendocrine response in hemorrhagic shock?
Loss of circulating blood volume.
How does the microcirculation respond to shock?
It regulates cellular perfusion and is influenced by sympathetic nervous system activity.
What happens to capillary flow in shock states?
Flow is heterogeneous, leading to diminished capillary perfusion.
What are damage-associated molecular patterns (DAMPs)?
Molecules released during tissue damage that can trigger an immune response.
How does TNF-alpha affect muscle during the stress response?
It contributes to muscle protein breakdown and cachexia.
What causes intracellular swelling during shock?
Dysfunction of energy-dependent mechanisms, such as the sodium-potassium pump.
What is oxygen debt?
The deficit in tissue oxygenation over time that occurs during shock.
What are the main types of shock classified in the document?
Hypovolemic, Cardiogenic, Septic (vasogenic), Neurogenic, Traumatic, Obstructive.
What does modern shock definition emphasize regarding tissue perfusion?
Inadequate tissue perfusion marked by decreased delivery of metabolic substrates and inadequate removal of waste products.
What occurs during the neuroendocrine response to hemorrhage?
Peripheral vasoconstriction occurs and fluid excretion is inhibited.
What is TNF-alpha and its role in shock?
A potent proinflammatory cytokine released by monocytes, macrophages, and T cells, it plays a key role in the development of shock and hypoperfusion.
What receptors are activated to increase heart rate and contractility?
β1-adrenergic receptors.
What happens to myocardial oxygen consumption during shock?
It increases due to increased workload, requiring maintained oxygen supply.
What is dysoxia?
A state where O2 delivery is so severely impaired that oxidative phosphorylation cannot be sustained.
What process do cells shift to when oxidative phosphorylation is insufficient?
Anaerobic metabolism and glycolysis.
How much ATP is produced from 1 mol of glucose during glycolysis?
2 mol of ATP.
What is the effect of cortisol during shock?
It induces a catabolic state, stimulates gluconeogenesis, and causes insulin resistance.
What is the role of catecholamines like epinephrine and norepinephrine during shock?
They increase hepatic glycogenolysis, gluconeogenesis, ketogenesis, and lipolysis.
What can lead to systemic inflammatory response syndrome (SIRS)?
Failure to adequately control the activation, escalation, or suppression of the inflammatory response.
What is the primary treatment for hemorrhagic/hypovolemic shock?
Volume resuscitation with blood products.
What are the hemodynamic responses to different types of shock?
Responses include variations in cardiac index, systemic vascular resistance, and venous capacitance.
What is hypovolemic shock?
The most common type of shock resulting from loss of circulating blood volume.
What is the rudimentary definition of shock?
Shock is the failure to meet the metabolic needs of the cell and the consequences that ensue.
What happens to cellular injury in shock if tissue perfusion is prolonged?
The injury becomes irreversible.
What characterizes vasogenic shock?
Decreased resistance within capacitance vessels, usually seen in sepsis.
Why are hemodynamic parameters like blood pressure and heart rate considered insensitive measures of shock?
They do not adequately reflect the early stages of shock.
Who introduced the term 'homeostasis'?
Walter B. Cannon.
What are the four initial categories of shock proposed by Alfred Blalock?
Hypovolemic, vasogenic, cardiogenic, and neurogenic.
What is shock defined as?
A failure to meet the metabolic demands of cells and tissues and the consequences that ensue.
What is a central component of shock?
Decreased tissue perfusion.
What is the mainstay of treatment for septic shock?
Fluid resuscitation, initiation of appropriate antibiotic therapy, and control of the source of infection.
What phenomenon describes the translocation of intravascular volume after major trauma?
Third spacing.
