NSG 430 TOPIC 10
1. cardiogenic shock results in: low CO and pulmonary edema
2. use of nitroglycerine in cardiogenic shock: used as a vasodilator to decreaseafterload
3. use of furosemide in cardiogenic shock: reduce preload
4. use of beta blockers in cardiogenic shock: reduce HR
5. treatments to restore blood flow in cardiogenic shock: Angioplasty withstenting,
emergency revascularization, valve replacement, cardiac cath
6. treatments to decrease SVR and workload of left side of heart in cardio-genic shock:
IABP, VAD, heart transplant
7. s/s of neurogenic shock: Bradycardia, warm dry skin (cant regulate body temp)
Poikilothermia
loss of sympathetic tone
8. causes of neurogenic shock: Can occur within 30 minutes of spinal injury atT5 or above
Spinal anesthesiaOpioids, benzos
Stimulation of PNS and/or inhibition of SNS
9. interventions for neurogenic shock: stabilize the spine
10. monitor for what with neurogenic shock: hypothermia
11. drugs for neurogenic shock: Phenylephrine (vasopressor), atropine
12. s/s of anaphylactic shock: Cough, dyspnea, pruritus, restless, dec. LOC,sense of
impending doom
13. SVR in anaphylactic shock: decreased
14. patho of anaphylactic shock: Massive vasodilation, increased capillary perme- ability, and
release of vasoactive mediators leads to fluid leaking into the interstitialspace
15. complications of anaphylactic shock: Respiratory distressCirculatory failure
16. drugs for anaphylactic shock: IM epi, diphenhydramine, famotidine, ranitidine
17. maintaining the airway in anaphylactic shock: Nebulized bronchodilators,aeresolized epi,
intubation, cric
18. fluids for anaphylactic shock: crystalloids
19. what should be given if hypotension persists in anaphylactic shock: IVcorticosteroids
20. s/s of septic shock: Full bounding pulse, pink warm flushed skin, fever, DIC, GI
bleeding/dysfunction
21. SVR in septic shock: decreased
, 22. what forms in the body during septic shock due to the exaggerated immuneresponse:
Microthrombi
23. the release of what causes myocardial dysfunction in septic shock: TNFand IL-1
24. what do TNF and IL-1 do: Decreases ejection fraction initially ’ resolves in 7-10days
25. high CO and low SVR beyond 24 hours during septic shock places thepatient at an
increased risk for: hypotension and MODS
26. common complication of septic shock: respiratory failureInitial hyperventilation leads to
respiratory alkalosis
ARDS
27. SIRS causes what to happen in the body: vasodilation, edema, hypermetabo-lism, and
activation of the coagulation cascade
28. SIRS can lead to: MODS
29. most common COD from MODS: sepsis
30. first body system to show signs of dysfunction: respiratory system
31. what happens to the respiratory system: alveolar edema --> collapseARDS
32. what happens to the cardiovascular system: Vasodilation results in dec. SVRand BP
33. what happens to the neurologic system: Hypoxemia ’ mental status changes,impaired
perfusion ’ dec. CR & skin mottling
34. what happens to the renal system: Decreased perfusion activates the RAASsystem which
causes sodium and water reabsorption
35. what happens to the GI system: abd. distention and paralytic ileusvulnerable to ischemic
injury
36. due to the hyper metabolic state catecholamines and glucocorticoids arereleased which
cause: hyperglycemia and insulin resistance
37. Insulin resistance causes a: catabolic state ’ body mass is lost
38. what happens to the liver: unable to make albumin
39. does administration of albumin fix the issue: no
40. what happens due to altered plasma pressure: fluid and protein leak into theinterstitial
space
41. what happens to the body as the hypermetabolic state continues: lacticacidosis
accumulates ’ metabolic acidosis
42. metabolic acidosis results in: renal dysfunction
43. DIC results from depletion of: clotting factors and platelets
1. cardiogenic shock results in: low CO and pulmonary edema
2. use of nitroglycerine in cardiogenic shock: used as a vasodilator to decreaseafterload
3. use of furosemide in cardiogenic shock: reduce preload
4. use of beta blockers in cardiogenic shock: reduce HR
5. treatments to restore blood flow in cardiogenic shock: Angioplasty withstenting,
emergency revascularization, valve replacement, cardiac cath
6. treatments to decrease SVR and workload of left side of heart in cardio-genic shock:
IABP, VAD, heart transplant
7. s/s of neurogenic shock: Bradycardia, warm dry skin (cant regulate body temp)
Poikilothermia
loss of sympathetic tone
8. causes of neurogenic shock: Can occur within 30 minutes of spinal injury atT5 or above
Spinal anesthesiaOpioids, benzos
Stimulation of PNS and/or inhibition of SNS
9. interventions for neurogenic shock: stabilize the spine
10. monitor for what with neurogenic shock: hypothermia
11. drugs for neurogenic shock: Phenylephrine (vasopressor), atropine
12. s/s of anaphylactic shock: Cough, dyspnea, pruritus, restless, dec. LOC,sense of
impending doom
13. SVR in anaphylactic shock: decreased
14. patho of anaphylactic shock: Massive vasodilation, increased capillary perme- ability, and
release of vasoactive mediators leads to fluid leaking into the interstitialspace
15. complications of anaphylactic shock: Respiratory distressCirculatory failure
16. drugs for anaphylactic shock: IM epi, diphenhydramine, famotidine, ranitidine
17. maintaining the airway in anaphylactic shock: Nebulized bronchodilators,aeresolized epi,
intubation, cric
18. fluids for anaphylactic shock: crystalloids
19. what should be given if hypotension persists in anaphylactic shock: IVcorticosteroids
20. s/s of septic shock: Full bounding pulse, pink warm flushed skin, fever, DIC, GI
bleeding/dysfunction
21. SVR in septic shock: decreased
, 22. what forms in the body during septic shock due to the exaggerated immuneresponse:
Microthrombi
23. the release of what causes myocardial dysfunction in septic shock: TNFand IL-1
24. what do TNF and IL-1 do: Decreases ejection fraction initially ’ resolves in 7-10days
25. high CO and low SVR beyond 24 hours during septic shock places thepatient at an
increased risk for: hypotension and MODS
26. common complication of septic shock: respiratory failureInitial hyperventilation leads to
respiratory alkalosis
ARDS
27. SIRS causes what to happen in the body: vasodilation, edema, hypermetabo-lism, and
activation of the coagulation cascade
28. SIRS can lead to: MODS
29. most common COD from MODS: sepsis
30. first body system to show signs of dysfunction: respiratory system
31. what happens to the respiratory system: alveolar edema --> collapseARDS
32. what happens to the cardiovascular system: Vasodilation results in dec. SVRand BP
33. what happens to the neurologic system: Hypoxemia ’ mental status changes,impaired
perfusion ’ dec. CR & skin mottling
34. what happens to the renal system: Decreased perfusion activates the RAASsystem which
causes sodium and water reabsorption
35. what happens to the GI system: abd. distention and paralytic ileusvulnerable to ischemic
injury
36. due to the hyper metabolic state catecholamines and glucocorticoids arereleased which
cause: hyperglycemia and insulin resistance
37. Insulin resistance causes a: catabolic state ’ body mass is lost
38. what happens to the liver: unable to make albumin
39. does administration of albumin fix the issue: no
40. what happens due to altered plasma pressure: fluid and protein leak into theinterstitial
space
41. what happens to the body as the hypermetabolic state continues: lacticacidosis
accumulates ’ metabolic acidosis
42. metabolic acidosis results in: renal dysfunction
43. DIC results from depletion of: clotting factors and platelets
