Upload
mervyn-ellis
View
214
Download
0
Embed Size (px)
Citation preview
Heat loss occurs through◦ Radiation◦ Conduction◦ Convection◦ Evaporation
Hypothermia results in derangement of multiple organ systems
Shivering – increases metabolic rate but only while glycogen stores last and down to temps of 30 °C
Initial tachycardia and peripheral vasoconstriction
Subsequent bradycardia (refractory to atropine), hypotension and fall in cardiac output
Osborn J waves appear < 32 °C Anti-arrythmic drugs and
inotropes/vasopressors are generally ineffective at temperatures < 30 °C
Loss of fine motors skills and co-ordination then loss of gross motor skills
Progressive decrease in GCS Cerebrovascular auto regulation is lost at 24
°C 20 °C EEG is flat and patient appears dead
as cerebral metabolism falls Temperatures at which shivering is lost
varies widely 24 °C - 35 °C Temp < 28 °C = rigidity, mydriasis, and
areflexia
Initially rise in resp rate followed by depression and basal metabolic rate slows
CO2 retention and resp acidosis can occur Significant fall in O2 consumption and CO2
production (50% at 30 °C) Apnoea can develop Initial left shift of the oxygen dissociation curve
◦ Impaired O2 delivery and tissue hypoxia
◦ Lactic acidosis If acidosis becomes severe the curve shifts
back R again
Cold induced diuresis GFR falls as CO and renal blood flow fall ARF in 40% of patients who require ICU Initial hypokalaemia due to shift of
extracellular potassium into cells Hyperkalaemia can occur with acidosis
secondary to cell death
Intestinal motility decreases below 34 °C Ileus < 28 °C Oral medication is not appropriate Hepatic impairment can occur due to
reduced CO (Raised lactate and therefore Hartmans is a bad idea)
Pancreatitis and Mesenteric Venous Thrombosis are both common
Mild (35 °C - 32 °C) Moderate (32 °C - 28 °C) Severe (<28 °C)
Temperature measurement Accurate low reading digital of mercury
thermometer Placed 15 cm rectally of oesophageally
(better as cold faeces can effect rectal temperatures)
UEC ◦ Hypo or hyperkalaemia/ARF/low HCO3
-
Glucose◦ Hypo/Hyperglycaemia
CK◦ May be elevated
FBC◦ Increased haematocrit due to cold induced diuresis and hypovolaemia◦ Thrombocytopaenia
COAG◦ Coagulopathy and DIC is common
LFT◦ Transaminitis
LIPASE◦ Pancreatitis
VBG◦ Initial respiratory alkalosis◦ Secondary respiratory and metabolic acidosis
ECG◦ Bradycardia◦ PR/QRS/QT prolongation◦ Variable ST and T wave changes◦ Osborn J waves◦ Arrythmias
AF/VT/VF/1st, 2nd, 3rd Degree HB
These waves were definitively described in 1953 by JJ Osborn
Also called J waves Delayed depolarisation Represented as ST elevation
at the QRS – ST junction < 32 °C Proportional to the degree of hypothermia Not pathognomonic
◦ SAH/Cerebral injuries/Myocardial ischaemia
ABC Remove wet clothing and insulate Gentle handling – rough handling and
invasive procedures have historically been thought to increase risk of cardiac arrythmias
Now thought these risks have been overemphasised
Consider co-existent pathology
Intubation as necessary IV Access (drugs IV only. IM SC poor absorption) Urinary catheter NGT Temperature and cardiac monitoring Fluid resuscitation
◦ Dehydration is often present◦ Warmed fluids◦ Dextrose is good
Avoid drugs until core temp 30 °C – ineffective and may accumulate until released
Rewarming – mild hypothermia Endogenous rewarming
◦ Exercise if possible Passive external warming
◦ Warm dry environment◦ Cover with warm blankets
Rewarming – moderate hypothermia Active external rewarming Warm blankets Radiant heat source Bair hugger 2°C per hour
Rewarming – severe hypothermia Includes cardiopulmonary arrest Warmed humidified inhaled oxygen Warmed IV fluids Warmed left pleural lavage Warmed Peritoneal lavage Cardiopulmonary bypass Most other methods are ineffective
Arrythmias VF may occur spontaneously in < 29 °C Sinus brady and AF with slow ventricular
response are common and can be considered physiological with hypothermia
AF usually reverts spontaneously on rewarming
Drugs and electricity are unlikely to work until temp is > 30 °C
ETT – Warmed humidified air 42 °C - 46 °C Aggressive active core warming
◦ Warmed saline/peritoneal lavage/pleural lavage/bypass VF/VT – Single defibrillation appropriate and
initial drug therapy. If no response defer further attempts or drug doses until core rises above 30 °C
PEA/Asystole – Again wait till core temp above 30°C (atropine not likely to be effective)
Many anecdotal reports of unexpected survival Not dead till they are warm and dead!!!!
Classical – Occurs due to exposure to a high environmental temperature
Exertional – Occurs in the setting of strenuous exercise
Oxidative phosphorylation stops at temperatures > 42 °C
Cell damage Loss of thermoregulatory compensatory
mechanisms Hypoxia, increased metabolic demands,
circulatory failure, coagulopathies and inflammatory response
Tachyarrythmias and hypotension Two types exist with exertional heat stroke
◦ Hyperdynamic group – high cardiac output and tachycardia
◦ Hypodynamic group – Low cardiac output, increase peripheral vascular resistance
Injured cells leak phosphate and calcium Hypercalcaemia and Hyperphosphataemia Hypokalaemia is seen early
◦ Secondary to heat induce hyperventilation leading to respiratory alkalosis
◦ Sweat and renal losses Hyperkalaemia is seen later
◦ Potassium losses from damaged cells and renal failure
Hyperuricaemia develops secondary to the release of purines from injured muscle
ARF in approx 30%◦ Direct thermal injury to kidneys◦ Pre-renal insult of volume depletion and renal
hypoperfusion◦ Rhabdomyolysis
Exertional heat stroke is associated with haemorrhagic complications
Petechial haemorrhages or eccyhmosis secondary to direct thermal injury or DIC
Consider in patients with altered mental state and exposure to heat
Classic triad of hyperthermia, neurological abnormalities and dry skin
Measure temp with rectal/oesophageal probe Sweating can still be present Hypotension and shock 25%
◦ Hypovolaemia, peripheral vasodilatation and cardiac dysfunction
Sinus tachy Hyperventilation – a universal finding in heat
stroke
UEC◦ Hypokalaemia◦ Hyperphosphataemia and hypercalcaemia◦ Hyperkalaemia and hypocalcaemia may be
present if rhabdomyolysis has occurred◦ Renal impairment
Urate – is frequently high and may play a role in the development of acute renal failure
Glucose – elevated in up to 70% LFT Almost always seen in exertional heat
stroke (AST and LDH most commonly elevated)
CK – 10000 to 1000000 in rhabdomyolysis
FBC – WCC as high as 30 -40,000 Coag – routinely abnormal and DIC may
occur Acid Base:
◦ Lactic acidosis◦ Compensatory respiratory alkalosis
Myoglobin – serum or urine myoglobin may be elevated
ECG◦ Rhythm disturbances (sinus tachy, SVT + AF)◦ Conduction defects (RBBB and intraventricular
conduction defects)◦ QT prolongation (most common secondary to low
K+ , Ca 2+ and Mg 2+)◦ ST changes (secondary to myocardial ischaemia)
If prompt effective treatment not undertaken mortality approaches 80%
A – ETT if needed◦ Consider early◦ Avoid suxamaethonium
B◦ Monitor Resp Rate and O2 sats◦ Look for evidence of aspiration if GCS decreased◦ Check for ARDS and ventilate as per lung injury
protocol C
◦ May be a large fluid deficit◦ N saline is probably best (CSL – lactate and avoid K+
containing fluids)◦ Monitor heart rate, BP, CVP and urine output◦ Picco/Swan-Ganz pulmonary artery catheter may be
indicated◦ Pressors may be needed but avoid adrenergic agents
as they can impair heat dissipation by causing peripheral vasoconstriction (dopamine)
Mainstay of therapy and must be initiated from the onset
Use prehospital may be lifesaving Initially remove patient from heat source
and remove all clothing Evaporative cooling – tepid water on the
skin with fans Ice water immersion – most effective
method but practically difficult and cant use monitors/equipment and uncomfortable for the patient
Ice packs to axilla, groin and neck Cooling blankets and wet towels Peritoneal lavage and cardiopulmonary bypass
can be considered in severe resistant cases Shivering may occur in rapid cooling – this will
increase oxygen consumption and heat production◦ Sedate◦ paralyse
Paracetamol and aspirin are ineffective and should not be used
Mortality should be less than 10% with prompt treatment
Most recover without sequalae Residual neurological defects are reported
Heat exhaustion – mild heat stroke Same physiological process Patients can still have the capacity to
dissipate heat and the CNS is not impaired Volume depletion is still a problem
Painful involuntary spasms of major muscles
Usually in heavily exercised muscle groups Dehydration and salt loss also thought to
plat a role Rest rehydrate and replace salts