Based on instructor lecture: 265 SP26 Shock
Important/repeated instructor points are marked in red/bold.
Highest-Yield Must Know Points
Shock in 3 words: lack of tissue perfusion.
All shock types have the same core problem: cells are not being perfused; causes and interventions are
different.
MAP = mean arterial pressure. A MAP of at least 65 is needed to perfuse vital organs.
By the time blood pressure drops, cellular damage has already started.
Urine output is a major perfusion clue. Minimum goal is 30 mL/hr because it shows kidneys are
perfusing.
Progressive shock is a life-threatening emergency. Once it reaches a certain point, the instructor
emphasized there may be about one hour to rescue before refractory/irreversible shock.
Refractory shock = irreversible, multiple organ failure/MODS, very high mortality; bring family in while
still continuing care.
Sepsis: obtain cultures before antibiotics, give antibiotics, and give rapid large-volume fluids.
Sepsis bundle fluid: minimum 30 mL/kg for hypotension or elevated lactate.
Lactate above 4 is bad and indicates significant anaerobic metabolism/tissue hypoperfusion.
Vasopressors/vasoactive medications are titrated to desired effect and should never be stopped
abruptly.
Hypovolemic shock = volume/fluid problem. Cardiogenic shock = pump problem. Obstructive shock =
blockage/kink problem. Distributive shock = vessels/pipes too big and fluid shifts out of vasculature.
Shock Made Simple: IV Setup Analogy
Instructor used the IV bag/tubing/pump analogy to “Todd-proof” shock types:
Shock type IV analogy Real meaning Core intervention idea
Hypovolemic IV bag is empty or low Not enough circulating Replace volume: fluids/blood; stop
intravascular volume loss
Cardiogenic Pump is bad Heart cannot pump Fix/support pump: inotropes,
effectively cardiac meds, balloon pump, treat
MI/dysrhythmia
Obstructive Tubing to pump is Blood flow is blocked Remove obstruction: chest tube,
clamped/kinked before/through heart pericardiocentesis,
circulation anticoagulants/TPA/thrombectomy
Distributive Tubing after pump is too big Vasodilation/capillary leak; Fluids + treat cause +
fluid leaves vascular space vasopressors as needed
Perfusion Basics
Perfusion triangle: heart = pump, blood = fluid, vessels = pipes. All three must work together.
Shock causes decreased tissue perfusion. As MAP falls, perfusion decreases and the body tries to compensate.
Lack of oxygen at the cellular level causes anaerobic metabolism. Anaerobic metabolism produces lactate, which
contributes to lactic acidosis.
Kidneys are an important early clue because urine output drops when perfusion drops.
Exam Alert: MAP below 65 means poor vital-organ perfusion risk. MAP well below 60 is very dangerous and
is seen in progressive shock.
Exam 3 Shock Study Guide | ASH
, Stages of Shock
Stage MAP / perfusion Expected findings Reversibility / priority
1. Initial MAP decreased about 5–10 Slight ↑ HR, ↑ RR, possible Usually hard to see. Body is
mmHg from baseline. Often slight ↑ BP from sympathetic starting to compensate.
subtle. stimulation. Early anaerobic
metabolism begins. Urine
output may be slightly
reduced.
2. Compensatory MAP drops about 10–15 from ↑ HR, ↑ RR, BP starts Reversible if cause is found
baseline; often around 60– decreasing, moderate and interventions support
65. vasoconstriction, narrowed compensation.
pulse pressure, thirst,
anxiety, mild acidosis,
potassium can rise as urine
output drops.
RAAS/ADH/aldosterone
activate.
3. Progressive MAP well below 60 or >20 Anoxia/ischemia in non-vital Life-threatening emergency.
mmHg below baseline. Vital organs, moderate acidosis, Instructor stressed: once
organs begin losing hyperkalemia, elevated severe in this stage, may
perfusion. lactate/lactic acid, cool skin, have about 1 hour to rescue
altered mental status, before refractory stage.
impending doom, weak rapid
pulse, pallor/cyanosis, cool
moist skin, oliguria/anuria.
4. Refractory Severe sustained MODS, DIC, worsening Irreversible/point of no return.
hypoperfusion despite acidosis, rapid LOC loss, Continue treatment but get
treatment. nonpalpable pulse, dusky family with patient.
extremities, slow shallow
respirations, O2 sat may be
unreadable, kidney/liver
failure.
Clinical Manifestations of Shock: What to Watch For
Cardiovascular: ↓ cardiac output, ↑ pulse early, weak/thready pulses, ↓ blood pressure, postural hypotension,
low CVP, flat neck veins.
Respiratory: ↑ RR with shallow/fast breathing, initially ↓ PaCO2 from blowing off CO2, later worsening acidosis;
↓ PaO2, central cyanosis around lips/nail beds.
GI: ↓ motility, diminished or absent bowel sounds.
Neuro / neuromuscular: Early: anxiety, restlessness, thirst. Late: lethargy to coma, generalized weakness,
diminished/absent DTRs, sluggish pupils.
Renal: ↓ urine output. Concentrated urine. Minimum goal is 30 mL/hr.
Skin / temperature: Cold, clammy, pale, cool extremities; hypothermia can occur from poor perfusion.
Exam Alert: Do not wait for low BP to recognize shock. Instructor emphasized that once BP drops, damage
has already started at the cellular level.
Hypovolemic Shock
Problem: too little circulating intravascular volume. The fluid/blood is not in the vascular space where it needs to
be.
Can be caused by hemorrhage/trauma, GI bleed, surgery, liver disease with third spacing/ascites, dehydration
from vomiting/diarrhea, diuretic therapy, and DI-related fluid loss.
Decreased volume lowers MAP, which lowers tissue perfusion and gas exchange.
Patients can look edematous but still be intravascularly depleted because fluid is third spaced.
Exam 3 Shock Study Guide | ASH