Shock, Sepsis &

MODS

Shock
Shock-clinical syndrome notable for inadequate tissue
perfusion that causes profound metabolic derangement
Results from inadequate cardiac function, vascular tone or
low blood volume

Classifications of shock
Hypovolemic-hemorrhage, ascites, diarrhea, burns,

hemothorax
Cardiogenic-pump failure
Obstructive-cardiac tamponade, PE, tension pneumo,
aortic dissection
Anaphylactic
Neurogenic
Distributive
Septic

 ANAPHYLACTIC SHOCK
SHOCK

NEUROGENIC

Pathophysiology
CV system failure in one of the 4 circulatory
components
Blood volume
Myocardial contractility
Blood flow
Vascular resistance
Compensation occurs when one component fails,
however

Stages of Shock
1. Initiation-sub clinical hypoperfusion, hard to pick up unless
monitored
2. Compensatory stage-neural, endocrine and chemical mechanismsdiscuss
3. Progressive stage- profound hypoperfusion, vasoconstriction,
anaerobic metabolism,
lactic acid, capillary fluid & protein shifts,
edema, blood becomes sludgy leading to clots, CO is decreased
4. Refractory stage-no functional systemic response to the insult
leading to MODS Review Table 11-2, p. 254

Systemic Inflammatory Response Syndrome-(SIRS)

Associated with sepsis

Widespread inflammation-inflammation is normally localized
Inflammatory cascade tries to stay balanced-proinflammatory vs
anti-inflammatory
Occurs with infection, trauma, shock, pancreatitis, or ischemia

Assessment

Clinical presentation-dependent on type of shock

CNS- most sensitive to changes in perfusion-may be agitation, restless, anxious
Cardiovascular-establish baseline B/P!! Check pulses, palpate for weak, thready
Medications, i.e. BB, may mask tachycardic changes that would occur
JVD-up in cardiogenic & early septic shock, down in hypovolemic & late septic
shock
CVC may be helpful for following hemodynamic changes, Table 11-3, p. 259
Respiratory-early-rapid & deep, late-poor gas exchange, O2 sat may not be
accurate

Assessment
Renal- hypoperfusion leads to oliguria. RAA system kicks in-retain Na, H2O
Prerenal cause of AKI-conc. urine, elevated BUN. If low perfusion persists

ATN intrarenal failure w/elevated Cr

GI system-slows down ileus, ulcers.
Liver hypoperfusion elevated enzymes, clotting problems, drug toxicity,
infection
Hematological system-clotting increases, cyanosis, consumptive coagulopathy
DIC
Integument-cyanosis may be present, usually late. Skin may be warm early, then
cool
Lab values-based on stage of shock, closely monitor

Management of shock
FLUIDS- crystalloids, colloids, blood, blood
products
Antibiotics if sepsis is suspected
Maintain O2, and ventilation
Pharmacological support-p. 265-7

Septic shock
One component of a series of insults that include:
1. Infection
2. SIRS
3. Sepsis
4. Severe sepsis
5. Septic shock
6. MODS
P. 279

Stages of septic shock

Late

Early

Pulses weak, thready

Normal or low B/P

AMS

CO up; ABGs-resp alk

Low B/P

Oliguria

Hyperthermia, warm flushed skin

Tachycardia, bradypnea or tachypnea

Bounding pulses

Tachycardia, tachypnea

Anuria

Cool, pale skin

Lethargy, coma

CO down, ABGs resp acidosis

p. 281

Treatment for sepsis

Prevent infections-pulmonary, urinary, GI, wounds,

CLABSI, CAUTI
Toxic shock syndrome
Treat with appropriate antibiotics, treat empirically
initially until BC results
Discuss blood cultures
FLUIDS
Prevent DIC-most common cause is sepsis

Other Nursing Interventions

Early nutritional support
PUP prevention and management p. 261
Nursing care plan-review pp-268-9

Multiple organ dysfunction syndrome

(MODS)
Clinical presentation caused by inflammation,

tissue hypoxia, hypermetabolism

Organ damage is sequential
Pulmonary issues are usually the 1st system
affected
Coagulopathy develops
Treatment focuses on prevention and treatment

 P. 278