NUR 445 EXAM 4 SHOCK TRAUMA &
BURNS EXAM QUESTIONS AND
ANSWERS 2025
Shock due to widespread vasodilation, includes anaphylactic, septic, and neurogenic
shock (spinal injury, spinal anesthesia) - ANSWERSWhat is distributive shock?
- Occurs when the heart is damaged and unable to pump enough blood forwards so
blood is backed up, often as a result of an acute MI, severe valve disfunction, or severe
HF
- s/s: chest pain, diaphoresis, N/V, pallor, decreased CO, lung crackles, dyspnea,
cardiac enzymes elevated, increased CVP
- dx: 12 lead EKG,
- tx: 100% o2 nonrebreather, vasopressor (dopamine, norepinephrine, phenylephrine),
inotropic (dobutamine), nitro for chest pain but careful because can lower BP, diuretics
for pulm congestion, morphine to decrease cardiac O2 demand, surgical interventions
(emergency revascularization, ventricular assist device, intra-aortic balloon pump) -
ANSWERSWhat is cardiogenic shock? s/s?
- decreased oxygen supply to vital organ tissues - ANSWERSWhat is the main issue
with shock?
- not enough blood volume in circulatory system which decreases the amount of oxygen
that can be delivered
- causes: blood loss (trauma, internal bleeds, hemothorax), secondary fluid loss
following vomiting, diarrhea, excessive urination, BURNS, excessive third spacing fluid
loss (ascites)
- s/s: start out with anxiety/restlessness, confusion, decreased peripheral extremity
perfusion, tachycardia, tachypnea (respiratory alkalosis), and increased BG; turns into
lethargy, low BP (low cardiac output), pallor, metabolic and respiratory acidosis as no
urine is being excreted and hyperventilation fails and turns into hypoventilation, may
result in coma and renal/hepatic failure
- tx: ***100% O2 non-rebreather, fluid resuscitation*** dependent on cause of
hypovolemia, monitor urine output, vitals, CVP (should increase as volume increases
and Tx works), neuro status, and peripheral perfusion; if hemorrhagic treat with 1:1:1 -
ANSWERSWhat is hypovolemic shock? causes? s/s? tx?
initial stage: hypoxia (decreased SPO2), subtle manifestations, decreased CO
compensatory stage: body attempts to compensate for hypoxia by increasing RR, HR,
peripheral vasoconstriction (pale, clammy, cold extremities, weakened peripheral
pulses, cap refil >3sec., DECREASED URINARY OUTPUT), metabolic acidosis begins
progressive stage: compensatory mechanisms fail and BP drops, severe shunting of
blood to vital organs and poor perfusion to peripheral organs, metabolic acidosis
worsens, severe electrolyte imbalance occurs, respiratory acidosis begins
, refractory stage: prolonged inadequate blood supply causes cell death, multi-system
organ failure, anaerobic metabolism occurs resulting in building of lactic acid; once this
stage is reached, it is irreversible - ANSWERS4 Stages of shock
Apply 100% O2 via non-rebreather
Prep for intubation
Insert 2 large bore IV lines (18G or larger) for fluid resuscitation - ANSWERSWhat are
nursing interventions that need to be done quickly for hypovolemic shock?
- def: ventricular filling blocked possibly from cardiac tamponade (pericarditis), tension
pneumothorax, PE (increases afterload)
- s/s: decreased CO, LOC, UO, pulse strength, poor peripheral perfusion, decreased
bowel sounds, chest pain (pleuritic if PE), n/v, muffled heart tones (cardiac tamponade)
** if cardiac tamponade is the cause, patient may require a pericardiocentesis -
ANSWERSWhat is obstructive shock?
- Caused by spinal cord injury, usually as a result of a traumatic accident or injury that
disrupts sympathetic nervous system communication
- s/s: hypotension from vasodilation, profound bradycardia, metabolic acidosis,
orthostatic hypotension, warm dry skin, oliguria
- tx: atropine (increases HR), Iv fluids, transcutaneous pacing, change bed position very
slowly, VTE prophylaxis (venous pooling increased risk for blood clots) -
ANSWERSWhat is neurogenic shock?
- Severe life threatening allergic reaction where IGE antibodies cause histamine release
results and widespread vasodilation
- s/s: SOB, tachypnea, wheezing, stridor, cyanosis, confusion, tachycardia,
hypotension, pallor, weak pulses, edema, angioedema, urticaria
- tx: remove allergen if possible, IM epi (sympathomimetic med to promote
bronchodilation and vasoconstriction), then assess airway, apply O2, and prep for
intubation if airway is compromised, insert IV, admin antihistamines, corticosteroids, and
albuterol - ANSWERSWhat is anaphylactic shock? s/s? tx?
- infection causes organ dysfunction followed by circulatory and metabolic abnormalities
- Early s/s: tachycardia, tachypnea, bounding pulses, warm/flushed skin, febrile, normal
or high BP, increased CO and PaO2
- Late s/s: pallor, weak pulses, hypothermia, tachycardia, hypotension, lethargy,
confusion, coma, anuria, decreased PVaO2 due to decreased CO, elevated lactic acid,
elevated WBC
- prevention: hand washing, cover wounds
- tx: bundle of care within 1 hr measure lactate levels (greater than 2= going into
sepsis), obtain blood (prior to antibiotics), sputum, and urine cultures, admin broad
spectrum antibiotics while awaiting culture results, admin fluids (30mL/kg) if hypotensive
or lactate above 4, admin vasopressors if BP doesn't respond to fluids, corticosteroid
therapy; small spectrum antibiotics once organism is identified - ANSWERSWhat is
septic shock? s/s? Tx?
- disseminated intravascular coagulophathy (DIC): excessive coagulation resulting in a
clotting phase (tiny blood clots everywhere blocking blood supply) then a bleeding
phase (body tries to fix issue with fibrinolysis but this results in no platelets left so
excessive bleeding occurs); treat with fresh frozen plasma and platelets
BURNS EXAM QUESTIONS AND
ANSWERS 2025
Shock due to widespread vasodilation, includes anaphylactic, septic, and neurogenic
shock (spinal injury, spinal anesthesia) - ANSWERSWhat is distributive shock?
- Occurs when the heart is damaged and unable to pump enough blood forwards so
blood is backed up, often as a result of an acute MI, severe valve disfunction, or severe
HF
- s/s: chest pain, diaphoresis, N/V, pallor, decreased CO, lung crackles, dyspnea,
cardiac enzymes elevated, increased CVP
- dx: 12 lead EKG,
- tx: 100% o2 nonrebreather, vasopressor (dopamine, norepinephrine, phenylephrine),
inotropic (dobutamine), nitro for chest pain but careful because can lower BP, diuretics
for pulm congestion, morphine to decrease cardiac O2 demand, surgical interventions
(emergency revascularization, ventricular assist device, intra-aortic balloon pump) -
ANSWERSWhat is cardiogenic shock? s/s?
- decreased oxygen supply to vital organ tissues - ANSWERSWhat is the main issue
with shock?
- not enough blood volume in circulatory system which decreases the amount of oxygen
that can be delivered
- causes: blood loss (trauma, internal bleeds, hemothorax), secondary fluid loss
following vomiting, diarrhea, excessive urination, BURNS, excessive third spacing fluid
loss (ascites)
- s/s: start out with anxiety/restlessness, confusion, decreased peripheral extremity
perfusion, tachycardia, tachypnea (respiratory alkalosis), and increased BG; turns into
lethargy, low BP (low cardiac output), pallor, metabolic and respiratory acidosis as no
urine is being excreted and hyperventilation fails and turns into hypoventilation, may
result in coma and renal/hepatic failure
- tx: ***100% O2 non-rebreather, fluid resuscitation*** dependent on cause of
hypovolemia, monitor urine output, vitals, CVP (should increase as volume increases
and Tx works), neuro status, and peripheral perfusion; if hemorrhagic treat with 1:1:1 -
ANSWERSWhat is hypovolemic shock? causes? s/s? tx?
initial stage: hypoxia (decreased SPO2), subtle manifestations, decreased CO
compensatory stage: body attempts to compensate for hypoxia by increasing RR, HR,
peripheral vasoconstriction (pale, clammy, cold extremities, weakened peripheral
pulses, cap refil >3sec., DECREASED URINARY OUTPUT), metabolic acidosis begins
progressive stage: compensatory mechanisms fail and BP drops, severe shunting of
blood to vital organs and poor perfusion to peripheral organs, metabolic acidosis
worsens, severe electrolyte imbalance occurs, respiratory acidosis begins
, refractory stage: prolonged inadequate blood supply causes cell death, multi-system
organ failure, anaerobic metabolism occurs resulting in building of lactic acid; once this
stage is reached, it is irreversible - ANSWERS4 Stages of shock
Apply 100% O2 via non-rebreather
Prep for intubation
Insert 2 large bore IV lines (18G or larger) for fluid resuscitation - ANSWERSWhat are
nursing interventions that need to be done quickly for hypovolemic shock?
- def: ventricular filling blocked possibly from cardiac tamponade (pericarditis), tension
pneumothorax, PE (increases afterload)
- s/s: decreased CO, LOC, UO, pulse strength, poor peripheral perfusion, decreased
bowel sounds, chest pain (pleuritic if PE), n/v, muffled heart tones (cardiac tamponade)
** if cardiac tamponade is the cause, patient may require a pericardiocentesis -
ANSWERSWhat is obstructive shock?
- Caused by spinal cord injury, usually as a result of a traumatic accident or injury that
disrupts sympathetic nervous system communication
- s/s: hypotension from vasodilation, profound bradycardia, metabolic acidosis,
orthostatic hypotension, warm dry skin, oliguria
- tx: atropine (increases HR), Iv fluids, transcutaneous pacing, change bed position very
slowly, VTE prophylaxis (venous pooling increased risk for blood clots) -
ANSWERSWhat is neurogenic shock?
- Severe life threatening allergic reaction where IGE antibodies cause histamine release
results and widespread vasodilation
- s/s: SOB, tachypnea, wheezing, stridor, cyanosis, confusion, tachycardia,
hypotension, pallor, weak pulses, edema, angioedema, urticaria
- tx: remove allergen if possible, IM epi (sympathomimetic med to promote
bronchodilation and vasoconstriction), then assess airway, apply O2, and prep for
intubation if airway is compromised, insert IV, admin antihistamines, corticosteroids, and
albuterol - ANSWERSWhat is anaphylactic shock? s/s? tx?
- infection causes organ dysfunction followed by circulatory and metabolic abnormalities
- Early s/s: tachycardia, tachypnea, bounding pulses, warm/flushed skin, febrile, normal
or high BP, increased CO and PaO2
- Late s/s: pallor, weak pulses, hypothermia, tachycardia, hypotension, lethargy,
confusion, coma, anuria, decreased PVaO2 due to decreased CO, elevated lactic acid,
elevated WBC
- prevention: hand washing, cover wounds
- tx: bundle of care within 1 hr measure lactate levels (greater than 2= going into
sepsis), obtain blood (prior to antibiotics), sputum, and urine cultures, admin broad
spectrum antibiotics while awaiting culture results, admin fluids (30mL/kg) if hypotensive
or lactate above 4, admin vasopressors if BP doesn't respond to fluids, corticosteroid
therapy; small spectrum antibiotics once organism is identified - ANSWERSWhat is
septic shock? s/s? Tx?
- disseminated intravascular coagulophathy (DIC): excessive coagulation resulting in a
clotting phase (tiny blood clots everywhere blocking blood supply) then a bleeding
phase (body tries to fix issue with fibrinolysis but this results in no platelets left so
excessive bleeding occurs); treat with fresh frozen plasma and platelets
