2. Hypovolemic Shock Flashcards
Hypovolemic Shock is
The critical reduction in the circulating intravascular volume, leading to inadequate tissue perfusion
Most common type of shock:
-Internal causes: third-spacing or pooling in the intravascular compartment
-External causes: hemorrhage, GI or renal losses, burns, excessive diaphoresis
Hypovolemia effects on pulse pressure:
-Systolic decreases, diastolic maintains or elevates;
NARROW pulse pressure
e.g. Baseline is 130/80
Volume loss–>110/80, 100/80, 90/70
Hemodynamics
-Decreased BP
-Decreased pulse pressure
-Decreased Right atrial pressure (CVP)
-Decreased Cardiac output, O2 delivery
-decreased Left atrial pressure (PAOP)
-decreased SvO2
-Increased systemic vascular resistance (SVR)
Everything is decreased except SVR
Treatment of hypovolemic shock
-Identify the etiology and correct it, if possible
-Replace the volume appropriately: “Fill up the tank!”
-Rapid and vigorous volume loading
-Requires at least 2 large bore IV sites
(hemorrhagic); a central line is not necessary but
may assist fluid replacement.
-Use a fluid warmer if >2000 mL of fluids are
administered in 1 hour (ALL fluids for trauma pts)
-Avoid use of vasopressors
-Fluid resuscitation: goal is to maintain O2 delivery (DO2) and O2 uptake (VO2) into tissue and sustain aerobic metabolism.
Fluid resuscitate to clinical targets (e.g., decreased tachycardia, increased urine output)
-Use isotonic fluid: 0.9 NSS or lactated Ringer’s.
Which is better, 0.9 NSS or LR? Advantages and Disadvantages in Table 5-1
see pic
Normal Saline
is an isotonic crystalloid, effects last approximately 40 minutes, then leaves vascular space
Disadvantages – large volumes may lead to hyperchloremic acidosis
Do not give to those with hypernatremia or renal failure
-Has 154 mols Na+ and 154 of Cl-; does NOT contain any K+, Ca++, or lactate
Lactated Ringer’s
is an isotonic crystalloid, effects last approximately 40 minutes, then leaves vascular space
Best mimics extracellular fluid (ECF) minus proteins, recommended resuscitation fluid by the ACS Committee on Trauma
-Has the potential to correct lactic acidosis; yet in severe hypo perfusion, it may promote lactic acidosis due to lactate accumulation
DO NOT give through a blood product transfusion line or to those who should not receive K+ or lactate
-Has 130 mols of Na+, 109 Cl-, 4 K+, 2.7 Ca++, 28 lactate
Resuscitation endpoints
-MAP greater than/equal to 65 mmHg
-CVP ~ 6 mmHg (not well-defined)
-Urine output 0.5 mL/kg/hr
-HR decreased
-Hgb > 7.0 g/dL and coagulation/platelet abnormalities corrected
-Hemoglobin and hematocrit measurements are not
accurate during active blood loss.
Hemorrhagic Shock
The severity of hemorrhagic shock is categorized into 4 classes (Table 5-2)
Class I
Blood loss (mL): Up to 750
Blood loss (% blood vol): Up to 15%
Heart Rate: < 100
BP: Normal
Pulse pressure: Normal or decreased
Capillary refill: Normal
RR: 14-20
Urine output (mL/hr): > 30
Mental status: slightly anxious
Treat with crystalloids
Class II
Blood loss (mL): 750 - 1500
Blood loss (% blood vol): 15-30%
Heart Rate: > 100
BP: Normal
Pulse pressure: Decreased
Capillary refill: Decreased
RR: 20-30
Urine output (mL/hr): 20-30
Mental status: Mildly anxious
Treat with crystalloids
Class III
Blood loss (mL): 1500-2000
Blood loss (% blood vol): 30-40%
Heart Rate: > 120
BP: Decreased
Pulse pressure: Decreased
Capillary refill: Decreased
RR: 30-40
Urine output (mL/hr): 5-15
Mental status: Anxious, confused
Treat with crystalloids + blood
In which class does BP decrease?
BP does not decrease in hemorrhagic shock until Class III, a lost of 1500 - 2000 mL of blood.
Class IV
Blood loss (mL): > 2000
Blood loss (% blood vol): >40%
Heart Rate: > 140
BP: Decreased
Pulse pressure: Decreased
Capillary refill: Decreased
RR: >40
Urine output (mL/hr): scant
Mental status: Confused, lethargic
Treat with crystalloids + blood
Treatment of Hemorrhagic (hypovolemic) shock
-STOP the bleeding
-Blood transfusion
-Optimal hgb threshold remains controversial, and
hgb levels are NOT reliable during active bleeding.
-7.0 g/dL Hgb is fairly well established in the critically
ill.
-Goal may be higher in the presence of:
-active bleeding
-severe hypoxemia
-myocardial ischemia
-lactic acidosis
Treatment of Hemorrhagic (hypovolemic) shock (con’t)
-Packed red blood cells (PRBCs), unlike whole blood, do not have plasma or platelets; therefore, the pt will need a replacement of the coagulation components of blood with a transfusion of multiple units of PRBCs.
-Fresh Frozen Plasma
-Platelets
-Cryoprecipitate
Risks of blood product administration
-Hemolytic and non-hemolytic reactions
-Transfusion-mediated immunomodulation
-Viral infection transmission
-Transfusion-related acute lung injury (TRALI)
-Hypothermia – WARM blood products to prevent this
-Consequences of hypothermia
–>Impairment of red cell deformability
–>Platelet dysfunction
–>Increase in affinity of hemoglobin to hold onto
O2
-Coagulopathy: monitor coagulation status, provide plasma and platelets
**Hypocalcemia, hypomagnesemia (citrate in transfused blood binds ionized Ca++ and Mg++)
Banked Blood does not have adequate 2,3-DPG. What is the consequence?
-Shifts the oxyhemoglobin-dissociation curve to the LEFT (see Resp chapter); increases the affinity of hemoglobin to hold onto O2.
Massive Transfusion Protocols
-Designed to provide rapid infusion of large quantities of blood products to restore oxygen delivery (DO2), oxygen utilization (VO2), and tissue perfusion (blood pressure)
-Indications include traumatic injuries, ruptured abdominal aortic or thoracic aortic aneurysms, liver transplant, OB emergencies)
Definition of Massive Transfusion Protocol
10 units of RBCs in 24 hrs or 5 units in less than 3 hrs
Mortality Rate of Massive Transfusion protocol
> 50%
With Massive Transfusion Protocol: Need to prevent the “TRIAD OF DEATH”
-Hypothermia
-Acidosis
-Coagulopathy
Note: NO PRESSORS for hypovolemic shock. Why?
The SVR is already high due to compensatory mechanisms.
