The most common type of shock resulting from loss of circulating blood volume.
Elevated levels of catecholamines in the bloodstream contribute to the 'fight or flight response' and shock.
Shock is the failure to meet the metabolic needs of the cell and the consequences that ensue.
The injury becomes irreversible.
Walter B. Cannon.
Hypovolemic, vasogenic, cardiogenic, and neurogenic.
Decreased resistance within capacitance vessels, usually seen in sepsis.
Vasodilation due to acute loss of sympathetic vascular tone, often from spinal cord injury.
A form of cardiogenic shock caused by mechanical impediment to circulation.
They do not adequately reflect the early stages of shock.
Decreased tissue perfusion.
It initiates the repair process and mobilizes antimicrobial defenses but can also lead to excessive tissue damage.
They act as sentinel responders, releasing histamines, eicosanoids, and cytokines.
Third spacing.
Baroreceptors and chemoreceptors.
Early treatment/resuscitation, rapid identification of infection source, and initiation of broad-spectrum antibiotics within 1 hour of diagnosis.
Adenosine triphosphate (ATP) hydrolysis.
Aerobic metabolism through oxidative phosphorylation in the mitochondria.
Maintenance of cellular membrane potential, enzyme synthesis, cell signaling, and DNA repair mechanisms.
Endogenous molecules that signal the presence of danger to surrounding cells and tissues.
At least 30 mL/kg.
Eventually, the injury progresses to irreversible shock, where further volume will not reverse the process and the animal dies.
Acute Respiratory Distress Syndrome, recognized as an early cause of death after seemingly successful surgery to control hemorrhage.
They diminish their output, disinhibiting the effect of the autonomic nervous system (ANS) to increase sympathetic output.
They result in vasodilation of coronary arteries, slowing of heart rate, and vasoconstriction of splanchnic and skeletal circulation.
Decreased tissue perfusion and shock result in a feed-forward loop that can exacerbate cellular injury and tissue dysfunction.
Pain, hypoxemia, hypercarbia, acidosis, infection, change in temperature, emotional arousal, or hypoglycemia.
It is activated, leading to vasoconstriction and retention of sodium and water.
They recognize DAMPs and effect intracellular signaling that primes and amplifies the immune response.
A failure to meet the metabolic demands of cells and tissues and the consequences that ensue.
65 mmHg.
Changes in cardiovascular function due to neuroendocrine response and autonomic nervous system response.
It results in diminished venous return to the heart and decreased cardiac output.
It leads to the activation of inflammatory cells and the release of circulating factors that modulate the immune response.
It modulates local cellular responses and produces a febrile response to injury, affecting various hormonal secretions.
IL-2 is produced by activated T cells and its role in shock response is unclear, with some studies linking it to tissue injury.
It induces vasoconstriction and increases systemic vascular resistance and blood pressure.
They stimulate glycogenolysis and gluconeogenesis to increase glucose availability.
Activation of the hypothalamic-pituitary-adrenal axis leading to cortisol release.
It is the persistence of capillary occlusion after resuscitation, leading to ischemic injury.
It is when shed blood must be returned to the animal to sustain hypotension at a set level to prevent further hypotension and death.
To maintain perfusion to the heart and brain, even at the expense of other organ systems.
Continued hypoperfusion and ongoing cellular death and injury.
Persistent hypoperfusion leads to further hemodynamic derangements and cardiovascular collapse.
Microcirculatory dysfunction and inflammatory cell activation.
Extensive parenchymal and microvascular injury, leading to failure of volume resuscitation.
Events leading to organ dysfunction, shock irreversibility, and death.
It is converted into lactate, leading to intracellular metabolic acidosis.
It increases water permeability in the nephron, preserving intravascular volume.
Bacterial products, including lipopolysaccharide, that enter a normally sterile environment.
Prevention of hypothermia, acidemia, and coagulopathy.
Tissue hypoperfusion and developing cellular energy deficit.
It describes the force of ventricular contraction as a function of its preload.
Increased heart rate, contractility, and vasoconstriction.
It influences normal enzyme activity, cell membrane ion exchange, and cellular metabolic signaling.
Hypovolemic, Cardiogenic, Septic (vasogenic), Neurogenic, Traumatic, Obstructive.
It is stimulated by endotoxin independently of blood pressure, osmotic, or intravascular volume changes.
Most alterations in cardiac output in the normal heart are related to changes in preload.
They have both proinflammatory and anti-inflammatory properties and are crucial in mediating the immune response.
Compensated phase of shock.
It is the force that resists myocardial work during contraction, primarily influenced by arterial pressure.
Loss of circulating blood volume.
It regulates cellular perfusion and is influenced by sympathetic nervous system activity.
Flow is heterogeneous, leading to diminished capillary perfusion.
Molecules released during tissue damage that can trigger an immune response.
It contributes to muscle protein breakdown and cachexia.
Dysfunction of energy-dependent mechanisms, such as the sodium-potassium pump.
The deficit in tissue oxygenation over time that occurs during shock.
Volume resuscitation with blood products.
Inadequate tissue perfusion marked by decreased delivery of metabolic substrates and inadequate removal of waste products.
Fluid resuscitation, initiation of appropriate antibiotic therapy, and control of the source of infection.
Peripheral vasoconstriction occurs and fluid excretion is inhibited.
A potent proinflammatory cytokine released by monocytes, macrophages, and T cells, it plays a key role in the development of shock and hypoperfusion.
β1-adrenergic receptors.
It increases due to increased workload, requiring maintained oxygen supply.
A state where O2 delivery is so severely impaired that oxidative phosphorylation cannot be sustained.
Anaerobic metabolism and glycolysis.
2 mol of ATP.
It induces a catabolic state, stimulates gluconeogenesis, and causes insulin resistance.
They increase hepatic glycogenolysis, gluconeogenesis, ketogenesis, and lipolysis.
Failure to adequately control the activation, escalation, or suppression of the inflammatory response.
Responses include variations in cardiac index, systemic vascular resistance, and venous capacitance.
