Hypovolemic Shock


Hypovolemic shock occurs when one of either intravascular or total body volume is depleted. The former is seen with acute hemorrhage (hemorrhagic shock) while the latter is seen in cases where there is an imbalance between
intake and output (nonhemorrhagic hypovolemic shock).

Hemorrhagic Shock

CAUSES
  • External bleeding, usually due to trauma
  • Internal bleeding including AAA, GI sources, blunt trauma, fractures, arterial or venous injury, ectopic pregnancy

DIAGNOSIS

  • Diagnosis is mostly clinical.
  • Labs may be normal at presentation.
  • With time and volume resuscitation hemoglobin and hematocrit will fall.

TREATMENT

  • Ensure adequate oxygenation and ventilation.
  • Volume resuscitation
    • NS or Ringer's lactate boluses through large peripheral intravenous lines, central lines, or intraosseous lines.
      • 1-2 L in adults
      • 10-20 cc/kg in neonates, infants, and young children
  • Blood products if no response to two fluid boluses, ongoing hemorrhage, or if impending cardiovascular collapse
    • Indications for PRBC tranfusion in hemorrhagic shock:
      • No response to two fluid boluses
      • Ongoing hemorrhage
      • Impending CV collapse
    • When time is critical, the use of O-negative blood is standard (O-positive in men is also acceptable).
    • 2 units PRBC in adults  (1U PRBC = 1g/dg Hgb)
    • 10-15 mL/kg PRBC in neonates, infants, and young children
  • Hemorrhage control
    • Control source of bleeding.
    • Fix hereditary or acquired bleeding diatheses:
      • Platelets when platelet count is <50,000/μL
      • Fresh frozen plasma (FFP), prothrombin complex concentrate, or recombinant factor VIIa for patients on warfarin with an elevated INR
      • FFP and/or cryoprecipitate and specific factors for hemophiliacs

Non-Hemorrhagic Shock

NON-HEMORRHAGIC HYPOVOLEMIC SHOCK
Non-hemorrhagic hypovolemic shock arises when volume intake is insufficient to make up for volume losses. Laboratory analyses are almost always abnormal in these cases since they generally occur over a period of time.

CAUSES

Causes include:

  • Inadequate intake
  • Excessive output: Respiratory, renal diuresis, GI losses, skin losses
  • Metabolic derangement (inborn error of metabolism)

DIAGNOSIS

  • Hematocrit and hemoglobin levels are high due to hemoconcentration.
  • BUN rises in relation to creatinine secondary to decreased tubular flow.
  • Sodium is usually elevated secondary to free water loss.
    • In DKA and hyperosmolar states, sodium may be factitiously low.

TREATMENT

  • Ensure adequate ventilation and oxygenation.
  • Immediate isotonic intravascular volume resuscitation
    • NS or Ringer's lactate boluses
      • 1-2 L in adults
      • 20 cc/kg over 5-20 minutes in neonates and pediatrics
  • Restore total body water and sodium.
    • Adults: 0.45 NS with or without 5% dextrose at a rate of 100-200 cc/hr
    • Pediatrics
      • Deficit fluids: Percent fluid loss x weight (kg) = L deficit. (ie, 10% loss in 20 kg child = 2 L fluid deficit). Replace one-half the deficit over first 8 hours and remainder over next 16 hours.
      • Maintenance fluids: Calculate maintenance fluids (see Table 1.15) and add to deficit replacement.
      • Solution: Use D5.25 NS (D51/4 NS) for infants and D5.45 NS (D51/2 NS) in children.
    • Treatment of the underlying cause should be simultaneous.

Calculating Maintenance Fluids
PATIENT WEIGHT DAILY MAINTENANCE FLUIDS
For the first 0-10 kg 100 mL/kg/day
For the next 10-20 kg 50 mL/kg/day
From 20-70 kg 20 mL/kg/day
Add up total mL and divide by 24 to obtain hourly rate.


 
Agent Receptor Activity Effects Indication
a1 b1 b2 DA
(Levophed)
Norepinephrine
1-30 mcg/min
+++

 

++ 0 0 SVR ↑↑
CO ↔↓↑
Sepsis
Phenylephrine
(Neo-synephrine)
40-180 mcg/min
+++

 

0

 

0

 

0

 

SVR ↑↑
CO ↔/↑
Sepsis,
Neurogenic shock
Epinephrine +++

 

+++ ++ 0

 

CO ↑↑
SVR ↓ (L)
SVR ↔/↑ (H)
Anaphylaxis,
ACLS,
Sepsis
Dopamine (mcg/kg/min)
Low-dose (0.5-2) 0 + 0 ++ CO ↑
SVR ↑↓
Sepsis,
Cardiogenic shock
Mid-dose(5-10) + ++ 0 ++ CO ↑
High-dose(10-20) ++ ++ 0 ++ SVR ↑↑
Doubutamine
2.5-20 mcg/kg/min
0/+ +++ ++ 0 CO ↑
SVR ↓
Cardiogenic shock
Isoproterenol
2-10 mcg/min
0

 

+++ +++ 0 CO ↑
SVR ↓
Cardiogenic shock w/
bradycardia
Vasopressin
(Adjunct)
0.01-0.04 U/min
        V2 receptors Vasoconstriction
Augments catecholamine

Receptor Functions
Receptor Function
α1  vascular smooth muscle contraction
pupillary dilator muscle contraction (mydriasis), 
intestinal and bladder sphincter muscle contraction
α2 sympathetic outflow, 
Insulin release
 lipolysis, 
platelet aggregation
β1 Heart rate
Contractility
Renin release
Lipolysis
β2 Vasodilation
Bronchodilation 
Heart rate
 Contractility
lipolysis
 Insulin release
 Uterine tone (tocolysis)
Ciliary muscle relaxation
 Aqueous humor production
M1 CNS, enteric nervous system
M2  Heart rate and contractility of atria
M3  exocrine gland secretions (e.g., lacrimal, salivary, gastric acid), 
gut peristalsis, 
bladder contraction,
Bronchoconstriction, 
pupillary sphincter muscle contraction (miosis),
Ciliary muscle contraction (accommodation)
D1 Relaxes renal vascular smooth muscle
D2 Modulates transmitter release, especially in brain
H1 nasal and bronchial mucus production, 
vascular permeability
Contraction of bronchioles
Pruritus
Pain
H2 gastric acid secretion
V1 vascular smooth muscle contraction
V2 H2O permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)