Multisystem Part 1 Flashcards
Stages of shock - Compensatory
3 stages of shock: compensatory, progressive, refractory
During the COMPENSATORY stage, the B/P IS MAINTAINED as a result of 2 mechanisms: stimulation of the sympathetic nervous system and activation of the renin-angiotensin-aldosterone system (RAAS).
decrease in CO and stroke volume or increased O2 utilization ->
sympathetic stimulation ->
vasoconstriction, increased HR, increased contractility ->
B/P maintained
decrease in CO and stroke volume or increased O2 utilization ->
RAAS activation ->
renin secretion -> vasoconstriction
AND
aldosterone -> Na and H2O retention
->
B/P maintained
Stages of shock - Progressive
3 stages of shock: compensatory, progressive, refractory
The progressive stage of shock occurs when compensatory mechanisms fail.
s/s:
HYPOTENSION (remember the patient is unable to compensate),
worsening tachycardia, tachypnea, oliguria,
metabolic acidosis,
decreased PaO2,
clammy, mottled skin,
further changes in LOC,
possible nausea
Stages of shock - Refractory
3 stages of shock: compensatory, progressive, refractory
The refractory stage occurs when the patient is not responsive to interventions. MODS occurs. The patient may survive shock, but die from failure of one or more organs.
s/s:
Severe systemic hypoperfusion,
MODS (multiple organ dysfunction syndrome): pulmonary (ARDS), Kidney (acute tubular necrosis), Heart (failure, ischemia), hematologic (DIC), neuro (encephalopathy, stroke), liver (failure)
Shock
3 stages of shock: compensatory, progressive, refractory
Types of shock:
hypovolemia,
septic,
anaphylactic,
neurogenic,
cardiogenic,
obstructive (tension pneumothorax, massive PE, cardiac tamponade)
hypovolemic shock
critical reduction in the circulating intravascular volume, leading to inadequate tissue perfusion
common causes include: internal (third-spacing or pooling) and external (hemorrhage, burns, diaphoresis)
What it looks like: NARROW PULSE PRESSURE (SBP decrease, DBP stays or increases)
decrease B/P, decrease pulse pressure, decrease Right atrial pressure (CVP), decrease CO and O2 delivery, INCREASE SVR
(everything decreases except SVR)
Treatment:
ID cause and treat if possible,
Replace volume (rapid and vigorous), fluid resuscitation goal is to maintain O2 delivery and O2 uptake and sustain aerobic metabolism, use isotonic fluid (NS or LR)
Resuscitation goals:
MAP >65, CVP-6, Urine OP 0.5mL/kg/hr, heart rate decreased, Hgb >7 and coag/platelets corrected
Normal Saline vs Lactated Ringer’s
Both are isotonic crystalloids, effects last approximately 40 mins, then leave vascular space
NS:
disadvantage- large volumes may lead to hyperchloremic acidosis
* Do not give to those with hypernatremia or renal failure
LR: Best mimics extracellular fluid (ECF) minus proteins, recommended resuscitation fluid by ACS Committee on Trauma
Has potential to correct lactic acidosis; yet in severe hypoperfusion, it may promote lactic acidosis d/t lactate accumulation
Do not give through a blood product transfusion line or to those who should not receive K+ or lactate
Hemorrhagic Shock
classified into 4 classes
Class I: blood loss up to 750mL, up to 15%; treat with crystalloids
Class II: blood loss 750-1500mL, 15-30%; treat with crystalloids
Class III: blood loss 1500-2000mL, 30-40%; treat with crystalloids and blood
Class IV: blood loss >2000mL, >40%; treat with crystalloids and blood
Treatment:
1. STOP the bleeding
2. Blood transfusion;
PRBC’s, unlike whole blood, do not have plasma or platelets; therefore, the patient will need a replacement of these with FFP, Platelets, cryoprecipitate
Risks of blood product administration
hemolytic and nonhemolytic reactions
transfusion-mediated
immunomodulation
viral infection transmission
TRALI (transfusion-related acute lung injury)
hypothermia - WARM blood products to prevent this
coagulopathy
hypocalcemia, hypomagnesemia - citrate in transfused blood
banked blood shifts the oxyhemoglobin-dissociation curve LEFT (increases affinity of hemoglobin to O2)
Massive Transfusion Protocols
Designed to provide rapid infusion of large quantities of blood products to restore oxygen delivery, oxygen utilization, and tissue perfusion
indications include traumatic injuries, ruptured abdominal aortic or thoracic aortic aneurysms, liver transplant, OB emergencies
definitions: 10 units of RBCs in 24 hours or 5 units < 3 hours
mortality > 50%
need to prevent the triad of death:
hypothermia
acidosis
coagulopathy
Systemic Inflammatory Response Syndrome (SIRS)
a systemic inflammatory response to a wide variety of severe clinical insults, manifested by 2 or more of the following:
Temp > 39C or <36C
Heart Rate >90 bpm
Respiratory rate > 20 breaths/minute or PaCO2 < 32 mmHg
WBC >12,000 or <4000 or band >10%
A patient may have SIRS WITHOUT SEPSIS; not a good indicator of sepsis
Sepsis
infection + organ dysfunction
A life-threatening organ dysfunction that is caused by an abnormal host response to an infection. The infection may be “suspected” rather than “proven”
suspected infection presentation:
positive culture, receiving antibiotics, antifungal, or anti-infective therapy, AMS in the elderly, infiltrates on chest radiograph (pneumonia), nursing home pt with indwelling catheter, pressure ulcer
organ dysfunction may be identified by assessing the patient’s qSOFA or SOFA score
organ dysfunction: hypotension, acute hypoxemia, drop in Urine OP, lactate high, AMS, platelets < 100, coagulopathy
Risk factors:
extremes of age, chronic health problems, invasive procedures and devices, surgical wounds, GI infections, prolonged hospitalizations, NPO, AIDS, use of cytotoxic and immunosuppressive agents,
alcoholism, malignant neoplasm, transplantation, hx of splenectomy
Septic Shock
hypotension d/t an infection; includes markers of hypoperfusion, which persists despite adequate fluid resuscitation; requires the administration of pressors
qSOFA
quick sepsis-related organ failure assessment
3 criteria, assigning 1 point for each of the following:
SBP <= 100
Respiratory Rate >= 22 bpm
GCS < 15 (AMS)
a score of 2 or 3 indicates a high probability of organ dysfunction
Pathophysiology of Sepsis/Septic Shock
infecting organism -> Uncontrolled inflammatory response d/t release of mediators which includes:
vasodilators -> decreased SVR
increased capillary permeability and significant leak -> decreased vascular volume
impaired O2 extraction, utilization, and maldistribution of blood flow -> anaerobic metabolism (lactic acid)
accelerated coagulation and microemboli formation -> DIC
myocardial dysfunction -> decreased cardiac output (late)
pulmonary dysfunction -> ARDS
Early vs Late Septic Shock
Early s/s:
tachycardia, bounding pulse
BP low, responsive to pressors
skin is warm, flushed
deep, somewhat fast respirations
lactate > 2 mmol/L
confusion (esp in elderly)
oliguria
fever
Late s/s:
BP low, may not respond to pressors
tachycardia, weak and thread pulse
lactate > 4 mmol/L
skin is cool, pale
respirations rapid or may be slow
lethargy, coma
anuria
hypothermia