Hypovolemic Shock Overview

Hypovolemic Shock

• Caused by a severe loss of blood volume or body water.
• The severity depends on the amount and rate of intravascular volume loss, and individual capacity for compensation.
• Occurs when the intravascular volume is inadequate to meet the body's oxygen and metabolic needs.
• Rapid restoration of circulatory homeostasis using fluids, pharmacologic agents, and/or blood products is crucial for preventing complications and death.
• Compensatory mechanisms (increased heart rate, myocardial contractility, and systemic vascular resistance) are effective for moderate volume loss, but losses exceeding 80% can overwhelm them, leading to overt shock with hypotension and hypoperfusion.
• Clinical manifestations include arterial hypotension, signs of hypoperfusion, and metabolic acidosis.
• Metabolic acidosis results from lactic acid accumulation due to tissue hypoxia and anaerobic metabolism
• Severe and prolonged decrease in mean arterial pressure (MAP) leads to hypoperfusion and organ dysfunction.
• Regional ischemia develops as blood flow is shunted from organs like the gastrointestinal tract or kidneys to more vital organs such as the heart and brain.
• Symptoms begin with decreases in intravascular volume exceeding 750 to 1500 mL in adults.
• The body tries to maximize fluid status by decreasing water and sodium excretion through the release of antidiuretic hormone (ADH), aldosterone, and cortisol.
• MAP is maintained by peripheral vasoconstriction mediated by catecholamine release and the renin-angiotensin system.
• Cardiac output (CO) is increased by catecholamine release and fluid retention.
• Central venous catheter (CVC) placement in the superior vena cava can be used to monitor central venous pressure (CVP), offering comparable survival and fewer complications compared to pulmonary artery catheters.

Treatment

• Fluid therapy is the cornerstone of managing hypovolemic shock.
• Fluid types used include crystalloids, colloids, and blood products.
• When administering fluids, warming them to 37°C (98.6°F) is crucial to prevent hypothermia, arrhythmias, and coagulopathy.

Crystalloids

• Electrolyte-based solutions that approximate plasma (balanced solutions) like lactated Ringer’s solution (LR) or Plasma-Lyte.
• Solutions with osmolality similar to plasma like 0.9% sodium chloride (normal saline [NS] or 0.9% NaCl).
• Data on superiority of hypertonic crystalloid solutions compared with isotonic solutions is limited.

Advantages of Crystalloid Solutions:

• Readily available
• Low cost
• Equivalent outcomes compared to colloids

Side Effects of Crystalloids:

• Fluid overload
• Electrolyte disturbances (sodium, potassium, and chloride)
• Dilutional coagulopathy

Balanced Solutions vs. NS:

• Balanced solutions generally contain potassium and have lower sodium content, while NS can cause hypernatremia, hypokalemia, metabolic acidosis, and hyperchloremia.

• Balanced solutions are associated with hyponatremia and/or hyperkalemia, while hyperchloremia is a potential risk factor for acute kidney injury in critically ill patients.

• There is no consensus on selecting a balanced crystalloid solution over NS.

Initial Volume of Crystalloids:

• A reasonable initial volume of an isotonic crystalloid (0.9% NaCl, LR, or Plasma-Lyte) in adult patients is 1000 to 2000 mL, administered over the first hour of therapy.
• Ongoing bleeding requires more aggressive fluid resuscitation.
• In the absence of ongoing blood loss, administration of 2000 to 4000 mL of isotonic crystalloid typically restores baseline vital signs in adult hypovolemic shock patients.
• Some populations, like burn patients, may require more aggressive fluid resuscitation.
• Individualized therapy with well-defined endpoints is crucial to avoid excessive crystalloid administration.

Colloids

• Large molecular weight solutions that remain primarily in the intravascular space, although a small portion leaks into the interstitial space.
• Increase plasma colloid osmotic pressure, drawing fluid from the interstitial space.
• Administering 500 mL of colloid results in a 500-mL intravascular volume expansion, except for 25% albumin.
• 25% albumin has a higher oncotic pressure than normal plasma, leading to a fluid shift from the interstitial space into the intravascular space.
• 100 mL of 25% albumin can result in around 500 mL of intravascular volume expansion.
• 25% albumin should be avoided in patients needing fluid resuscitation as it can cause dehydration.
• This hyperoncotic solution is helpful for patients who don't need fluid resuscitation but need fluid redistribution (e.g., ascites, pleural effusions).

Adverse Effects of Colloids:

• Fluid overload
• Dilutional coagulopathy
• Anaphylactoid/anaphylactic reactions
• Hydroxyethyl starch and dextran products can lead to coagulopathy and kidney impairment.
• Hydroxyethyl starch is associated with increased mortality in critically ill patients and is no longer recommended.

Blood Products

• Indicated for hypovolemic shock patients with blood loss from hemorrhage exceeding 1500 mL (freshly obtained whole blood is administered).
• Packed red blood cells (PRBCs) can be transfused during ongoing resuscitation of hemorrhagic shock to increase oxygen-carrying capacity along with crystalloid solutions to increase blood volume.
• Fresh-frozen plasma (FFP) is administered for patients with documented coagulopathies to replenish clotting factors.
• Platelets are administered for patients with severe thrombocytopenia (< 20–50 × 103/mm3 [20–50 × 109/L]).
• Type O negative blood (universal donor blood) is given in emergent cases of hemorrhagic shock.
• Subsequently, blood that has been typed and cross-matched with the recipient's blood is given.

Traditional Threshold for PRBC Transfusion:

• Serum hemoglobin less than 10 g/dL and hematocrit (Hct) less than 30% (0.30).
• A more restrictive threshold of 7 g/dL appears to be safe for critically ill patients who have received appropriate fluid resuscitation and have no signs of ongoing bleeding.

Risks of Blood Product Administration:

• Transfusion reactions and transmission of blood-borne infections in contaminated blood.
• Recent research shows transfusions are linked to increased infection and higher mortality, potentially due to adverse immune and inflammatory effects.

Normalization of Laboratory Measurements:

• Expected within hours to days after fluid resuscitation.
• Normalization of base deficit and serum lactate within 24 hours is recommended and may be associated with decreased mortality.
• Pulmonary artery occlusion pressure (PAOP) should be reached to a goal of 14 to 18 mm Hg (alternatively, CVP 8–12 mm Hg).

Cardiogenic Shock

• Characterized by decreased cardiac output (CO) due to systolic or diastolic dysfunction.
• Increased central venous pressure (CVP), pulmonary wedge pressure (PAWP), decreased CO, and increased systemic vascular resistance (SVR).
• Causes include myocardial infarction, cardiomyopathy, and myocardial depression from metabolic issues.
• Management involves standard treatment for the underlying disorder (e.g., aspirin, oxygen, morphine for acute MI).
• Diuretics can be used to decrease preload or fluid if hypovolemic.
• Inotropes (dobutamine, dopamine) can be used to improve contractility and increase CO.

Obstructive Shock

• Decreased CO due to extracardiac obstruction to blood flow.

• Impaired diastolic filling:

  • Cardiac tamponade, tension pneumothorax, constrictive pericarditis.
  • Impaired delivery of blood to the heart.
  • Increased CVP, increased PAWP, decreased CO, increased SVR.
  • Managed mechanically (fluids and vasopressors have limited utility).

• Impaired systolic contraction:

  • Pulmonary embolism, severe pulmonary hypertension.
  • Increased CVP, decreased PAWP, decreased CO, increased SVR.
  • Management:
  • Disease-specific therapy
  • Inotropes and vasopressors
  • Fluids or diuretics based on fluid status

Distributive Shock

• Includes septic, anaphylactic, and neurogenic shock (e.g., spinal injury).
• All types of distributive shock are associated with tachycardia, except neurogenic shock, which is associated with bradycardia.
• Generalized vasodilation with enhanced vascular permeability, resulting in decreased preload.
• Management:
  • Fluids: Crystalloids are preferred.
  • Vasopressors:
    • Norepinephrine is preferred in septic and neurogenic shock.
    • Epinephrine is preferred for anaphylactic shock.
  • Adjuvant agents: Steroids.