Week 4 ICU: Hypermetabolism: Trauma/ICU and Metabolic Phases of Stress Flashcards
Common Medical Issues contributing to Hypermetabolism in the ICU
- Trauma: multiple sites in body.
- Sepsis/Infection
- Burns (extreme case of hypermetabolism)
- Acute Respiratory Distress Syndrome (ARDS)
- End-stage organ failure (e.g liver, heart, lungs)
Physiological responses to metabolic stress
Extent depends on EBB vs. FLOW phase
* Hypermetabolism: ↑ O2 consumption
* Hyperglycemia (krebs cycle overwhelmed by AA converting to glucose)
* Hyperlactemia (excess pyruvate converting to lactate)
* Protein catabolism (contributes to hyperglycemia)
* Cardiovasular response (↑ blood flow, tachycardia, tachypnea)
* Perfusion to Gut decreased
* Increase in aldosterone & ADH-promotes fluid & sodium re-absorption in kidneys - protects microvascular volume (important in trauma where hemorrhage possible)
* Get electrolyte disturbances
* If GI trauma; may have losses of GI fluids; important to replace these losses with fluid and electrolytes to ensure hemodynamic stability
Common electrolytes disturbances
- sodium
- potassium
- chloride
- calcium
- magnesium
- phosphorous
What electrolytes are CRITICAL for normal organ function
- sodium
- potassium
- chloride
How are changes in intracranial pressure controlled for?
MD will set a tight TFI to prevent massive edema due to change in organ function
* patients with massive trauma (esp closed head injuries
Hormone response disturbances to metabolic stress
Fight or flight response: elevations in glucocorticoids (cortisol); catecholamines (epinephrine ) + increase in insulin & glucagon
* Rise in glucagon supercedes rises in insulin – ie lower insulin to glucagon ratio
* Insulin resistance develops resulting in hyperglycemia (not diabetes, but worse with diabetes)
* High catecholamine + cortisol: favors protein breakdown
Carbohydrate metabolism disturbances to stress response
↑ glycolysis, ↓ glycogen production, ↑ insulin resistance, ↑ lactate production, ↑ glucagon + ↑ epinephrine, ↑ gluconeogenesis + ↑ recycling of alanine to pyruvate (via transamination) results in hyperglycemia
* Enhanced peripheral glucose uptake & utilization
* Hyperlactemia
* Increased glucose production with depressed glycogen production, glucose intolerance, and insulin resistance
GIR recommendations for stressed adult
GIR: 4-7 mg/kg/min; Recommend 2-4 mg/kg/min due to risk of hyperglycemia esp if pt already has high Blood sugars
Protein metabolism disturbances to stress response
- Increase in protein turnover; predominantly protein degradation to supply AA for gluconeogenesis \ Increased need for protein
- Some increase in protein synthesis; diverted towards production of acute phase reactants eg coagulation proteins, immune system proteins
- Laboratory consequences: may see ↑ serum levels of acute phase reactants (eg C-reactive protein), and ↓ serum levels of protein such as albumin, pre-albumin
Fat metabolism disturbances to stress response
- lipolysis resulting in ↑ serum concentrations of triglycerides (this is via hormone sensitive lipase; hormones such as glucagon, epinephrine, norepinephrine and adrenocorticotropic hormone (ACTH) stimulate activity of this enzyme)
- Lipid oxidation is not increased (likely due to higher insulin levels and insulin resistance)
- Ketogenesis is inhibited \ gluconeogenesis becomes major energy pathway (resulting in lean body depletion)
Nutrient utilization during starvation
- Increase in Fat oxidation and gluconeogenesis
- Decrease protein synthesis
- Liver: get synthesis of ketone bodies (3-OH-butyrate) within 2-3 days
- Brain adapts to use of ketone bodies after levels sufficiently high
- During starvation individuals experience a down regular in REE; and become hypometabolic
Different from metabolic stress response
Definition of Trauma
Characterized by Blunt vs Penetrating Injury (with thermal or electrical injuries)
* Blunt Trauma; Severity determined by force of injury (eg MVA)
* Penetrating Trauma (eg stabbing)
* Combination of Both
When is nutritional support NOT indicated for trauma patient?
Patients who are able to resume oral intake within 3-5 days of injury do NOT need nutritional support
* unlikely to be those admitted to an ICU; although it is always possible
Phases of Metabolic Stress Following Trauma
- Ebb or Shock Phases; decreased metabolic rate
- Flow Phase: Regeneration and repair with increased metabolic rate
[Important to understand as one phase is a hypometabolic/catabolic state which may be influenced by the need for ventilatory support; the other phase is a hypermetabolic/catabolic state which maybe influenced by the need for ventilatory support]
Effects of trauma on blood flow to GI
Get ↓ splanchnic blood flow (abdomen organs) and relatively high metabolic demand of the GI tract during stress
* In non-stressed state: viscera (eg GI tract) responsible for about 30% of total circulating blood volume (receive 25% of cardiac output)
* In post-prandial state: have increase of blood flow to viscera (upwards 50%) so very sensitive to ischemic injury
Immediate goals following major trauma
- Restore and maintain oxygen delivery; ventilatory support
- Ensure organ function by appropriate fluid and electrolyte rescusitation; goal is to establish hemodynamic stability
What is hemodynamic instabilty
A state requiring pharmacologic or mechanical support to maintain a normal blood pressure or adequate cardiac output
* the cardiovascular system is not working.
* Being on mechanical respiratory support does NOT necessarily mean the patient is UNSTABLE
Physical signs of hemodynamic instability
Cannot get lab values into equilibrium
* Typical of acute circulatory failure constitute primary references for shock, including hypotension, abnormal heart rates, cold extremities, peripheral cyanosis and mottling together with bedside measurements of right-sided filling pressure and decreased urine flow.
* Need to consider overall perfusion to organs like the GI tract and kidneys severely diminished.
What phase is hemodynamic instability typically seen?
Most patients experiencing hemodynamic instability are in the Ebb Phase of the metabolic stress response. However, it is possible for this to occur later in the Flow Phase as well.
* Flow phase: acute insult occurs such as bleeding during operation
Hormone response during ebb phase
- Get some surges of counter-regulatory hormones such as cortisol, catecholamines, glucagon: all result in lean body tissue breakdown.
- Insulin resistance may occur due to changes in insulin secretion. Hyperglycemia often occurs as a result.
- May have low levels of TSH, lower body temperature (due to hypo-perfusion)
- CRP increased (but not as high as flow)
How long does the Ebb phase last?
Typically shorter phase; but if prolonged due to major organ damage; then patient at high risk for ++ inflammation.
* Ebb response to metabolic stress; 1-7 days but usually under 48 hrs
* Body trying to respond to a ‘physiological shock’; get major shifts in cardiovascular function. Patient may be hemodynamically unstable
Metabolic response during ebb phase
Hypometabolism
* Period of Hypoperfusion
* Decrease blood perfusion to other organs may be due to sustained organ damage.
* Medical therapy during Ebb Phase may contribute to hypometabolism
Energy requirements during ebb phase
80-90% of basal metabolic rates OR 10-20 kcal/kg
* Period of Hypoperfusion of organs results in ↓ energy requirements
How does medical therapy contribute to hypometabolism in the ebb phase?
- Ventilation
- Medications (barbituates) may inhibit Central nervous system (sedatives, analgesics, narcotics, hypnotics) and lead to hypometabolism → e.g Codeine, morphine, propofol, haldol
- Autonomic agents (neuromuscular blocking agents that are needed for optimal ventilation) or cardiovascular agents (eg B-adrenergic receptor antagonists such as propranolol).
How do energy requirements change transitioning from ebb to flow phase?
- ebb: 0.8-0.9 x REE
- transition: REE
- flow: REE x AF
Energy requirements in flow phase with REE
BMR x SF: To predict TEE add on activity/injury factor of 1.2-1.8 (depending on severity and nature of injury)
* Multiple Injuries
* Degree of Injury & Inflammation
* Body Temperature
* Ventilation
Energy requirements in flow phase with kcal/kg
- ≤ 25 kcal/kg for patients on propofol infusion (or rocuronium/pancuronium)
- 25 kcal/kg for single system organ failure
- 25-30 kcal/kg for double system organ failure
- 30-35 kcal/kg for multisystem organ failure
- 27-30 kcal/kg for CRRT
protein needs in flow phase
1.5-2.5 g/kg/d
* most patients 1.5-2 g/kg for protein.
Describe what happens in the flow phase
Period of hypermetabolism; catabolism
* lean body tissue breakdown due to high levels of catecholamines, glucagon, etc (can be higher than in Ebb Phase). Insulin resistance ++ /++ CRP (due to inflammation)
* Wound healing is the number one priority
* Increase in cardiac output, BMR, body temperature, muscle wasting, weight loss
* ++ gluconeogenesis/++ lipolysis/++ proteolysis; increases in urinary nitrogen excretion; ++ insulin resistance (caused by +++ up regulation of counter regulatory hormones).
* Increased synthesis of acute phase reactants; such as CRP; down regulation of hepatic proteins such as albumin
Summary of Metabolic Changes in Ebb vs Flow Phase
