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NURS 319: Shock
Chapter 46 Shock
| Question | Answer |
|---|---|
| purpose of perfusion | provides nutrients and removes cellular waste |
| describe of SIRS and the symptoms we use to diagnose it | inflammatory and cytokine reaction/ response SNS and endocrine response similar to alarm stage of stress increase: heart rate, cardiac output, respiratory rate decrease: GI activity and urine output |
| progression of SIRS can lead to | CARS (decrease in the immune system) |
| the SIRS patient can then develop an overwhelming infection in the blood or | sepsis |
| sepsis can further progress into | septic shock |
| septic shock is when | body is not receiving adequate perfusion |
| if more than 2 organs start to dysfunction, it can lead to | MODS |
| MODS leads to | death |
| CARS; how does this lower the immune system | period of reduced immunity; body is focusing on one area so rest of body is vulnerable to attack |
| sepsis | body-wide infection |
| how does sepsis lead to septic shock | persistent hypertension that does not alleviate with fluids |
| key manifestations that will alert the nurse to the presence of sepsis | confusion hypoxemia oliguria |
| 1st phase of MODS | increase volume requirements, mild respiratory alkalosis, oliguria, hyperglycemia, increased insulin requirements |
| 2nd phase of MODS | tachypnea, hypocapnea, hypoxemia, moderate liver dysfunction with possible hematological changes |
| 3rd phase of MODS | shock with azotemia and acid-base disturbances, significant coagulation abnormalities |
| 4th phase of MODS | vasopressor dependent, oliguric/anuric, ischemic colitis, lactic acidosis |
| shock | inability of heart and lungs to satisfy needs of peripheral tissues |
| 5 types of shock | cardiogenic, hypovolemic, obstructive, anaphylactic, neurogenic |
| 1st phase of shock | initial; change at cellular level; activation of SNS and RAAS; goal is competition to maintain perfusion |
| 2nd phase of shock | progressive; impacting several areas; decreased perfusion, signs of MODS; goal is to conserve blood for heart and brain |
| 3rd phase of shock | irreversible; body is in downward spiral; perfusion cannot maintain heart and brain |
| how does GI system respond to shock | severe vasoconstriction, ascites, hormone release in shock |
| septic: causes, symptoms, compensatory mechanisms, what makes it unique | exotoxins/ endotoxins; increased glucose, hypotension, decreased organ perfusion; hypermetabolic state; toxins involved |
| cardiogenic: causes, symptoms, compensatory mechanisms, what makes it unique | MI, severe hypotension/ low urine output, RAAS activates, cardiac tamponade and arrythmias |
| hypovolemic: causes, symptoms, compensatory mechanisms, what makes it unique | low blood volume and low blood pressure, severe dehydration + low urine output + ascites + burns + vomitting, RAAS/SNS activated, can induce renal tubular necrosis |
| anaphylactic: causes, symptoms, compensatory mechanisms, what makes it unique | overwhelming immune response, urticaria + bronchospasm + angiospasm, BP/ perfusion tanks, caused by IgE stimulating eosinophils |
| neurogenic: causes, symptoms, compensatory mechanisms, what makes it unique | SNS is disrupted- spinal cord injury (above T6) + brain injury + anesthesia, hypotension/ bradycardia, immediate medical treatment, RAAS not activated |
| what type of organ dysfunction does shock lead to? | multiple organ dysfunction |
Created by:
lcorlew1
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