Studies show substantially reduced brain damage and improved neurologic outcome following cardiac arrest
Mechanism unclear:
Reduction in cerebral oxygen consumption
Retardation of destructive enxymatic rxns
Suppression of free radical rxns
Protection of fluidity of lipoprotein membranes
Reduction of oxygen demand
Reduction of intracellular acidosis
Inhibition of biosynthesis, release, and uptake of excitatory neurotransmitters
Study design:
Randomized, controlled trial w/ blinded assessment at multiple hospitals
March 1996 – January 2001.
275 total patients resuscitated after cardiac arrest d/t ventricular fibrillation
Patients randomly assigned to undergo therapeutic hypothermia
136 in hypothermia group
137 in normothermia group
Results:
75/136 patients (55%) w/ hypothermia had favorable neurologic outcome compared to 54/137 (39%) in normothermia group.
Neurologic outcome defined as Pittsburgh cerebral-performance category : 1 (good recovery) – 5 (death)
Mortality at 6 months: 41% in hypothermia group and 55% in normothermia group
Conclusion: In patients who have been successful resuscitated after cardiac arrest d/t ventricular fibrillation, therapeutic mild hypothermia increased rate of favorable neurologic outcome and reduced mortality.
Cardiac arrest caused by ventricular fibrillation (VF), asystole, or pulseless electrical activity (PEA)
VF – rapid, erratic heart movements. Heart can’t pump blood
Asystole – “flat-line”, no electrical activity
PEA – lack of pulse
Requiring CPR and with Return of Spontaneous Circulation (ROSC)
GCS = glascow score
Exclusion criteria:
Pre-existing coma from other cause
Unmanageable hemodynamic instability – cooling may lead to further hemodynamic collapse
Suspected sepsis w/ systemic inflammatory response syndrome (SIRS) physiology --- hypothermia inhibits immune fxn to fight illness
Major surgery w/in 14 days – again, increased risk of infection
Active bleeding
Major head trauma
Active DNR status
Initiate cooling ASAP – w/in 6 hours after ROSC
Lie supine - flat
Monitor for dysrhythmias – bradycardia is common
Monitor for s/s of infection – greater risk of infection w/ hypothermia
Dietitian is part of the team – especially in acute care
Continue to look for signs of malnutrition risk
Typically, 25-30 kcal/kg recommended
Typically, enteral feeding is initiated to prevent malnutrition in hypercatabolic states
While initiation of enteral nutrition is often our first step in prevention of malnutrition in the critically ill patient it’s vital that we consider each of the following aspects prior to initiating nutrition support.
Critical illness severity: does the family wish to continue with care?
Age: pediatric vs. adult formula
Nutrition risk screening: is this person at risk for malnutrition
Wait for resuscitation: cannot feed until hemodynamically stable
Energy requirements: consider metabolic state, ventilation, inflammation, stress, etc.
Formula selection: based on labs, electrolytes, disease state, etc.
Enteral access: ensure access prior to initiation
Efficacy: is it in the best interest of the patient?
Determination of tolerance: monitor s/s – aspiration, abdominal distention, N/V, etc
This is what we are here to investigate today
Research is lacking under the general assumption that energy metabolism is slowed, reduced gut motility, and difficulty to manage hyperglycemia.
Most intensive care physicians will hold enteral nutrition until therapeutic hypothermia is complete.
Why the concern? – following slides to discuss
What happens during therapeutic hypothermia
Physiologic changes in almost every organ of the body
Enzymatic reactions are temperature controlled, thus any rxn is changed by hypothermia
Cardiac output decreases by 25-40% (d/t decreased HR) decrease in metabolism rate
Increased lactate levels metabolic acidosis
Risk of arrhythmias and bradycardia throughout
“Cold-diuresis” d/t decrease in ADH hypovolemia, renal electrolyte loss, and hemoconcentration
Decreased drug clearance
Decreased metabolism (7-10% per degree C below 37 degrees)
Induction counterregulatory mechanisms to decrease heat loss. Greatest instability at this phase
Risks minimized by cooling as quickly as possible
-Shivering: linked to increased risk of morbid cardiac events and adverse outcome
-Increased rate of metabolism
-Increased oxygen consumption
-Excess work of breathing
-Increased HR
-Stress like response
*Counteracted w/ sedatives, anesthetics, opiates, paralytics, etc.
-Electrolyte disorders: low electrolyte levels d/t increased renal exrection and intracellular shift
-Maintain Mg in high-normal range
-Hyperglycemia: decreased insulin sensitivity and reduce insulin secretion
-Target levels: 4-8 mmol/L
-Metabolic acidosis: increased synthesis of glyceol, FFAs, ketonic acids, and lactate
-GI problems: impaired bowel fxn and gastric emptying problems
Rewarming phase: electrolyte disorders d/t intracellular shifts
Controlled by slow rewarming
Cooling: low electrolytes d/t renal excretion (cold diuresis and tubular dysfunction) and intracellular shifts
-Increased risk of arrhythmias and mortality
-Mg depletion increases brain injury
Potassium: decreased during induction
-Rewarming opposite shift. Monitor q6h and replete to low-normal levels.
-DO NOT REPLETE K+ during rewarming phase
-Why we rewarm slowly to give kidneys time to excrete K+
Glucose: Hyperglycemia
-Reduced insulin secretion and sensitivity
-More insulin required during induction
-Maintain moderate glucose control (<180 mg/dL)
Insulin required during cooling to manage hyperglycemia
Greater threshold
Replete ALL electrolytes during induction phase
Rebound of electrolytes during rewarming – especially K+
Discuss pros and cons – investigate further
Metabolic changes – hemodynamically stable?
Wait until hyperglycemia resolves?
Early enteral feeding preserves intestinal mucosal integrity, maintains mucosal immunity, prevents increased mucosal permeability, and decreases bacterial translocation
Independent predictor of survival in post cardiac arrest and post-CPR patients
Cardiac arrest – severe intestinal ischaemia occurs translocation of bacteria and endotoxins early intestinal dysfunction
Critical illness and hypothermia delayed gastric emptying and decreased peristalsis ileus
Intolerance of feeds?
Data collected from one hospital from 2002-2008 (N=32)
Feed balance calculated by subtracting volume discarded aspirate from volume of input
Day 1 = initiation and maintenance phase (cooling)
Day 2 = 14 hours re-warming and 10 hours normothermia
Day 3 = normothermia
Sufficient GI fxn to allow some enteral feeds w/o significant increase in vomiting
Conclusion: May be appropriate to feed patients undergoing therapeutic hypothermia following cardiac arrest
Objective: determine whether patients undergoing therapeutic hypothermia tolerate early enteral feeding
N=55 patients treated w/ therapeutic hypothermia following cardiac arrest
Day 1 = initiation and maintenance phase (cooling)
Day 2 = 24h rewarming
Day 3 = normothermia
Patients fed nasogastrically
Enteral feeding (timing, success/fail, vomiting events, or increase aspirate volume)
Failure to tolerate if feeding aspirate exceeded volume administered or pt vomited
Cooling (day 1): 83% tolerated and 13% had negative gastric aspirates
-72% of feeds at 10 mL/h
-10% vomited
Rewarming (day 2): 83% tolerated and 13% had negative gastric aspirates
-95% of feeds
-19% vomited
Normothermia (day 3): 91% tolerated and 9% had negative gastric aspirates
Reduced rate during hypothermic state: 10mL/h
Increase rate when normothermia has been achieved
More research needed
