NSG 430 EXAM 4
1. Septic shock criteria: Severe sepsis with persistent Hypotension: SBP <90,Lactate >4
mmol, and signs of end organ damage
2. Organs that are most venerable to damage: Lungs and kidneys
3. Which organisms are the most common cause of sepsis: Bacteria
4. Clinical manifestations of septic shock: Formation of microthrombi (DIC)
Tachypnea/hyperventilation
Respiratory failure Decreased Urine output Altered neurologic status
GI dysfunction, GI bleeding, paralytic ileus
5. What kind of pH imbalance will septic shock patients be in initally?: Res-piratory
alkalosis
6. Once the patient's respiratory system can no longer compensate, whatkind of pH
imbalance will septic shock patients be in?: Respiratory alkalosis
7. Causes of obstructive shock: Superior Vena Cava syndrome or Abdominalcompartment
syndrome
Cardiac Tamponade Tension pneumothorax
Pulmonary embolism and right ventricular thrombi
8. Clinical manifestations of obstructive shock: Decreased CO, Increased af-terload
jugular vein distention and pulsus paradoxus
9. Abnormally large decrease in blood pressure during inspiration.: pulsusparadoxus
10. 4 stages of shock: InitialCompensatory
ProgressiveRefractory
11. Usually not clinically apparent
Lactic acid building up: Initial stage of shock
12. Impaired GI motilityRisk for paralytic ileus
Cool, clammy skin except if septic patient
RAAS system activated: Compensatory stage of shock
13. Effects of RAAS system activation: Vasoconstriction (increased CO and BP)Increased
sodium reabsorption and potassium secretion
14. Mental status changesAnasarca
Sustained hypoperfusionWeak peripheral pulses
,Ischemia of distal extremities: Progressive stage of shock
15. diffuse profound edema: Anasarca
16. Cardiac effects of progressive stage of shock: DysrhythmiasMyocardial ischemia possible
infarction
17. Respiratory effects of progressive stage of shock: Pulmonary EdemaWorsening V/Q
mismatch
TachypneaCrackles
Increased work of breathing
18. Renal effects of progressive stage of shock: May result in AKIDecreased urine output
Elevated BUN and serum creatinineMetabolic acidosis
Worsened by nephrotoxic drugs
19. Hepatic effects of progressive stage of shock: Liver fails to metabolize drugsand waste
Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
20. The failure of one organ system affects several other organ systems. Recovery is unlikely
in this stage. The organs are in failure and the body's compensatory mechanisms are
overwhelmed; profound hypotension, hypox-emia, and tachycardia worsens: Refractory stage
of shock
21. Diagnostics studies that point to shock: Elevation of lactate (>2)Base deficit, Electrolytes,
BNP
12-lead ECG, continuous ECG monitoring, cardiac enzymesChest x-ray, ABGs, O2 Sats, VQ
scan
Hemodynamic monitoringEchocardiogram
22. Treatment to improve ventilation in shock patients: Optimize CO with fluidreplacement or
drugs
Increase hemoglobin by transfusion
Increase arterial oxygen with supplemental oxygen and mechanical ventilationSpace activities
that increase oxygen consumption
Intermittent or continuous monitoring of ScvO2 by a central venous catheter or mixedvenous
oxygen saturation (SvO2)
23. Volume expansion is the cornerstone of therapy for which types of shock?-
, : septic, anaphylactic, hypovolemic
24. Fluids given for fluid resuscitation: Isotonic crystalloids- normal saline, lac-tated Ringers
colloids- albumin
25. Complications of volume expansion and how to avoid them: Hypothermia-warm fluids
Coagulopathy- replace clotting factors
26. If hypotension persists after adequate volumes of fluid have been given, what should be
prescribed?: Vasopressors- norepinephrine, dopamine, phenyle-phrine
Inotropes- dobutamine
27. Syndrome characterized by decreased tissue perfusion and impaired cellu-lar metabolism:
Shock
28. Types of "Cold" shocks: Hypovolemic and cardiogenic
29. Types of "Warm" shocks/distributive shocks: Neurogenic, Anaphylactic, andSeptic
30. Cold shocks are characterized by...: high SVR, vasoconstriction
31. Warm shocks are characterized by: low SVR, massive vasodilation
32. Myocardial infarctionCardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertensionCardiac tamponade
Myocardial depression from metabolic problems: precipitating causes of cardio-genic shock
33. #1 cause of cardiogenic shock: MI
34. Early signs of cardiogenic shock: TachycardiaHypotension
Narrowed pulse pressure ‘Myocardial O2 consumption
35. Other signs of cardiogenic shock: Tachypnea, pulmonary congestionPallor and cool,
clammy skin
Decreased capillary refill time Anxiety, confusion, agitation ‘Pulmonary artery wedge
pressure
Decreased renal perfusion and urinary output
36. Hemorrhage
GI loss (e.g., vomiting, diarrhea)Fistula drainage
Diabetes insipidusHyperglycemia Diuresis
Vomiting
Diarrhea: Absolute hypovolemia
37. Fluid shifts: Burn injuries, ascites
Internal bleeding: Fracture of long bones, ruptured spleen, hemothorax, se-vere pancreatitis
1. Septic shock criteria: Severe sepsis with persistent Hypotension: SBP <90,Lactate >4
mmol, and signs of end organ damage
2. Organs that are most venerable to damage: Lungs and kidneys
3. Which organisms are the most common cause of sepsis: Bacteria
4. Clinical manifestations of septic shock: Formation of microthrombi (DIC)
Tachypnea/hyperventilation
Respiratory failure Decreased Urine output Altered neurologic status
GI dysfunction, GI bleeding, paralytic ileus
5. What kind of pH imbalance will septic shock patients be in initally?: Res-piratory
alkalosis
6. Once the patient's respiratory system can no longer compensate, whatkind of pH
imbalance will septic shock patients be in?: Respiratory alkalosis
7. Causes of obstructive shock: Superior Vena Cava syndrome or Abdominalcompartment
syndrome
Cardiac Tamponade Tension pneumothorax
Pulmonary embolism and right ventricular thrombi
8. Clinical manifestations of obstructive shock: Decreased CO, Increased af-terload
jugular vein distention and pulsus paradoxus
9. Abnormally large decrease in blood pressure during inspiration.: pulsusparadoxus
10. 4 stages of shock: InitialCompensatory
ProgressiveRefractory
11. Usually not clinically apparent
Lactic acid building up: Initial stage of shock
12. Impaired GI motilityRisk for paralytic ileus
Cool, clammy skin except if septic patient
RAAS system activated: Compensatory stage of shock
13. Effects of RAAS system activation: Vasoconstriction (increased CO and BP)Increased
sodium reabsorption and potassium secretion
14. Mental status changesAnasarca
Sustained hypoperfusionWeak peripheral pulses
,Ischemia of distal extremities: Progressive stage of shock
15. diffuse profound edema: Anasarca
16. Cardiac effects of progressive stage of shock: DysrhythmiasMyocardial ischemia possible
infarction
17. Respiratory effects of progressive stage of shock: Pulmonary EdemaWorsening V/Q
mismatch
TachypneaCrackles
Increased work of breathing
18. Renal effects of progressive stage of shock: May result in AKIDecreased urine output
Elevated BUN and serum creatinineMetabolic acidosis
Worsened by nephrotoxic drugs
19. Hepatic effects of progressive stage of shock: Liver fails to metabolize drugsand waste
Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
20. The failure of one organ system affects several other organ systems. Recovery is unlikely
in this stage. The organs are in failure and the body's compensatory mechanisms are
overwhelmed; profound hypotension, hypox-emia, and tachycardia worsens: Refractory stage
of shock
21. Diagnostics studies that point to shock: Elevation of lactate (>2)Base deficit, Electrolytes,
BNP
12-lead ECG, continuous ECG monitoring, cardiac enzymesChest x-ray, ABGs, O2 Sats, VQ
scan
Hemodynamic monitoringEchocardiogram
22. Treatment to improve ventilation in shock patients: Optimize CO with fluidreplacement or
drugs
Increase hemoglobin by transfusion
Increase arterial oxygen with supplemental oxygen and mechanical ventilationSpace activities
that increase oxygen consumption
Intermittent or continuous monitoring of ScvO2 by a central venous catheter or mixedvenous
oxygen saturation (SvO2)
23. Volume expansion is the cornerstone of therapy for which types of shock?-
, : septic, anaphylactic, hypovolemic
24. Fluids given for fluid resuscitation: Isotonic crystalloids- normal saline, lac-tated Ringers
colloids- albumin
25. Complications of volume expansion and how to avoid them: Hypothermia-warm fluids
Coagulopathy- replace clotting factors
26. If hypotension persists after adequate volumes of fluid have been given, what should be
prescribed?: Vasopressors- norepinephrine, dopamine, phenyle-phrine
Inotropes- dobutamine
27. Syndrome characterized by decreased tissue perfusion and impaired cellu-lar metabolism:
Shock
28. Types of "Cold" shocks: Hypovolemic and cardiogenic
29. Types of "Warm" shocks/distributive shocks: Neurogenic, Anaphylactic, andSeptic
30. Cold shocks are characterized by...: high SVR, vasoconstriction
31. Warm shocks are characterized by: low SVR, massive vasodilation
32. Myocardial infarctionCardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertensionCardiac tamponade
Myocardial depression from metabolic problems: precipitating causes of cardio-genic shock
33. #1 cause of cardiogenic shock: MI
34. Early signs of cardiogenic shock: TachycardiaHypotension
Narrowed pulse pressure ‘Myocardial O2 consumption
35. Other signs of cardiogenic shock: Tachypnea, pulmonary congestionPallor and cool,
clammy skin
Decreased capillary refill time Anxiety, confusion, agitation ‘Pulmonary artery wedge
pressure
Decreased renal perfusion and urinary output
36. Hemorrhage
GI loss (e.g., vomiting, diarrhea)Fistula drainage
Diabetes insipidusHyperglycemia Diuresis
Vomiting
Diarrhea: Absolute hypovolemia
37. Fluid shifts: Burn injuries, ascites
Internal bleeding: Fracture of long bones, ruptured spleen, hemothorax, se-vere pancreatitis
