According to the graph in Figure 24-6, what happens to cardiac output immediately after a transfusion is given during the irreversible stage of shock?
Explanation
Figure 24-6 illustrates the futility of therapy in irreversible shock. A transfusion can temporarily restore cardiac output, but the underlying systemic damage prevents sustained recovery, and the cardiac output inevitably declines again, leading to death.
Other questions
What is the defining characteristic of irreversible shock?
What is described as one of the most devastating and significant end results for the development of the final state of irreversibility in shock?
What is the approximate rate at which new adenosine can be synthesized by cells after the high-energy phosphate stores have been depleted during severe shock?
What is the primary cause of hypovolemic shock resulting from severe burns?
Besides hemorrhage, how can extensive bodily contusion during trauma lead to hypovolemic shock?
What is a key characteristic of hypovolemic shock caused by plasma loss that distinguishes it from shock caused by hemorrhage?
What is the primary mechanism that causes neurogenic shock?
Which of the following conditions is listed as a potential cause of neurogenic shock due to vasomotor paralysis?
While brief brain ischemia causes extreme vasomotor stimulation, what is the effect of prolonged brain ischemia lasting more than 5 to 10 minutes?
In anaphylactic shock, which substance is released by basophils and mast cells in response to an antigen-antibody reaction?
Which of the following is NOT described as a primary effect of histamine release during anaphylactic shock?
Excluding cardiogenic shock, what is the most frequent cause of shock-related death in the hospital setting?
Which of the following features is often observed in patients with septic shock, particularly in about half of the cases?
What is disseminated intravascular coagulation, a condition that can develop in septic shock?
What is identified as the best possible therapy for a person in shock caused by hemorrhage?
Why is plasma transfusion considered an adequate substitute for whole blood in the emergency treatment of hemorrhagic shock?
What is the principal requirement for a substance, such as dextran, to be an effective plasma substitute?
In which type of shock are sympathomimetic drugs like epinephrine considered particularly lifesaving?
Why have sympathomimetic drugs proven to be not very valuable in the treatment of hemorrhagic shock?
What is the recommended initial 'head-down' position for treating a patient in hemorrhagic or neurogenic shock?
What is the primary limitation of oxygen therapy in treating most types of shock, making it less beneficial than might be expected?
What is one of the reasons glucocorticoids are sometimes given to patients in severe shock?
What is the maximum duration of total circulatory arrest that more than half of patients can withstand before incurring some degree of permanent brain damage?
What is the typical consequence for a person's mental capacity following a circulatory arrest that lasts for 10 to 15 minutes?
In addition to acute cerebral hypoxia, what other factor has been shown by experiments to prevent much of the early brain deterioration during circulatory arrest?
In animal experiments, what was the effect of administering heparin or streptokinase before cardiac arrest?
What happens to the actions of the hormone insulin during the last stages of shock?
In cases of shock, where in a capillary bed does more nutritive deficiency and subsequent tissue necrosis tend to occur?
What is the term for the condition where deterioration of the lungs following shock leads to respiratory distress and death several days later?
What is the primary reason that metabolic acidosis develops in shock?
During shock, when cells switch to the anaerobic process of glycolysis for energy, what substance accumulates in the blood?
How does the poor blood flow through tissues in shock contribute to the formation of intracellular carbonic acid?
The deteriorative factors in shock, where each increase in the degree of shock causes a further increase, are an example of what type of mechanism?
What is the ultimate fate of much of the adenosine that diffuses out of cells during severe shock?
A patient with a severe intestinal obstruction develops shock. This is a form of hypovolemic shock caused by what mechanism?
What is the main conclusion from cross-transfusion experiments with normal animals regarding the cause of shock after trauma?
In neurogenic shock, what is the physiological term for the diminished venous return caused by widespread vascular dilation?
Which statement accurately describes the state of cardiac output in patients with septic shock?
In the context of septic shock, what causes the phenomenon known as 'sludging of the blood'?
What is the primary reason it is considered reasonable to use plasma instead of whole blood for the emergency treatment of most types of hypovolemic shock?
Which type of shock results primarily from an allergic antigen-antibody reaction?
What is the effect of deep general anesthesia on the vasomotor center of the brain?
How can spinal anesthesia become a potent cause of neurogenic shock?
Which of the following conditions is a cause of hypovolemic shock due to dehydration and loss of aldosterone secretion?
During the progression of shock, what happens to the mitochondrial activity in liver cells and many other tissues?
What is the consequence of lysosomes breaking open in cells during widespread tissue shock?
According to the text, which three organs are listed as being especially affected by the further deterioration that occurs during shock?
As depicted in the graph of Figure 24-6 showing the progression of shock, what happens to cardiac output after hemorrhage?
What is the key difference between circulatory shock and circulatory arrest?