Is the patient in shock?
Reliance on BP alone may cause delay.
Compensatroy mechanisms may preclude a measurable fall in systolic bp until up to 30% of the patient’s blood volume is lost.
Pulse rate
Respiratory rate
Skin circulation
Pulse pressure
Tachycardia and cutaneous vasoconstriction (typical early physiologic responses to volume loss)
Any injured patient who is cool and has tachycardia is considered to be in shcok until proven otheriwse.
Elderly patients may not exhibit tachycardia
Limited cardiac response to catecholamine sitmulation
use of B bloers
Pacemaker
Normal hemaocrit does not exclude significant blood loss.
Base deficit and lactate levels are useful to determine presence and severity of shock.
What is the casue of hte shock state?
Haemorrhagic or
Non hemorrhagic
Cardiogenic
Cardiac injury, tamponade, air embolus, myocaridal infarction.
Investigations: ECG, CK, Echo, FAST.
Signs: Tachycardia, muffled heart sounds, and dilated engorged neck veins with ypotension resistant to fluid therapy.
Tension Pneumothorax
Mediastinal shift, impaired venous return, fall cardiac output.
Signs: Acute respiratory distress, subcutaneous emphysema, absent breath sounds, hyperresonance to percussion, tracheal shift.
Neurogenic
Intracranical injureis do not cause shock
Signs: hypotension without tachycarida or cutanrous vasoconstriction
should be treated first as hypovolemic shock, but failure to restor organ perfusion suggests either continuing hemorrhage or neurogenic shock.
Septic shock
might be confused with hypovolemic shock both present
tachycardia, cutanerous vasocontriction, impaired urinary output, decresased systolic pressure and narrow pulse pressure.
Haemorrhagic shock in injured patients.
Classification of haemorrhage
Class I
Individual who has donated a unit of blood.
Class II
uncomplicated hemorrhage, crystalloid fluid resuscitation is requried.
Class III
Complicated hemorrhage, at least crystalloid infusion is required and perhaps blood replacement
Class IV
preterminal event
Class I hemorrhage (15% blood volume loss)
750 ml
PR <100
BP Normal
PP Normal or increased
RR 14-20
UO > 30
CNS Slightly anxious
Fluid replacement Crystalloid
Class II hemorrhage (15-30% blood loss)
750-1500
PR 100-120
BP Normal
PP Decreased
RR 20-30
UO 20-30
CNS Mildly anxious
Fluid replacement Crystalloid
Class III (30-40% blood loss)
1500-2000
PR 120-140
BP Decreased
PP Decreased
RR 30-40
UO 5-15
CNS Anxious, confused
Fluid replacement Crystalloid and blood +_ SURGICAL INTERVENTION
Class IV (>40%)
>2000
PR >140
BP Decreased
PP Decreased
RR >35
UO Negligible
CNS confused, lethargic=
Fluid replacement Crystalloid and blood. + SURGICAL INTERVENTION
Initial management of haemorrhagic shock
What can I do about shock?
Stop bleeding and replace volume loss
ABCDEs
Vital signs, urinary output, and level of consciousness are essential
Airway and breathing
Establish a patent airway with adequate ventilation and oxygenation
Supplementary oxygen is supplied
Circulation - hemorrhage control
Controlling obvious hemorrhage
Obtaining adequate intravenous access
Assessing tissue perfusion
Bleeding from external wounds —— direct pressure
Rapid intravenous fluid infusion
Neurological exam
assess cerebral perfsuion
Exposure
Decompression of gastric dilatation
Urinary catheterisation
Vascular access
Two large caliber peripheral intravenous catheters
Fluid warmers and rapid infusion pumps are used in the presence of massive hemorrhage.
Forearms anticubital veins most desirable.
Central venous access (femoral, jugular, subclavian) if no peripheral access possible.
Blood drawn for type and crossmatch, lab analysis, toxicology, preganncy.
ABG
Chest xray document position of central line.
Initial fluid therapy
Warmed isotonic solutions.
Normal saline, ringer lactate
Alternative is hypertonic saline, although there is no evidence of sruvival advantage.
Initial warmed flid bolus is given as rapidly as possible 1-2 litres for adults and 20ml/kg for paediatric patients.
3-1 rule, each 1 ml of blood loss with 3 ml o fcrystalloid fluid.
monitor patient response
Urinary outpaut
Level of consciousness
Peripheral perfusion
blood pressure
Aware that fluid resuscitation is not substitute for definitive control of bleeding.
What is the patient’s response?
Good response
Return to normal blood pressure,
pulse pressure
pulse rate
Improvement in CVP status (if central line is in place)
Urine output (renal perfusion)
Urinary output
0.5ml/kg/hr in adults
1mg/kg/hr in paediatrics
Acid base balance
Respiratory alkalosis due to tachypnoea
mild metablic acidosis early phases
anaerobic metabolism due to inadequate tissue perfusion, production of lactic acid
persistent metabolic acidosis should be treated with fluid blood and operative intervention
(base deficit and lactate determines severity of shock)
Rapid response
respond rapidly and remain hemodynamically normal aftehr initial fluid bolus.
surgical consultation and evaluation are necessary
Transient response
show deterioration of perfusion indices as the intial fluids are slowed to maintenance levels. either on-going blood loss or inadequate resuscitation.
most of these patients lost 20-40% of their blood volume
continued fluid administratoin and initiation of blood transfusion is indicated.
rapid surgical intervention is needed
Minimal or no response
Immediate, definitive intervention
Remember nonhemorrhagic shock ( blunt caridac injury, cardiac tamponade, tension pneumothorax)
CVP monitoring and cardiac ultrasonography helps differentiate between the various causes of shock.
Crossmatched, type-specific and type o blood
Fully crossmatched blood is preferable, however it takes 1 hour.
Type specific blood can be provided within 10 minutes
Compatible with ABO and Rh blood types (preferred for transient responders)
Complete cross match should be performed
Type O paced cells are used if Type specific blood is not available
Rh negative preferred for females of childbearing age.
Warming fluids plasma and crystalloid
heat crystaloid to 39C before using it.
warmer or microwave oven (blood products cannot bewarmed in micrwave oven)
Autotransfusion
should be considered for any patient with a major hemothroax
Coagulopathy
PT, PTT, Platelets should be measured in the first hour
Transfusion of platelets, cryoprecipitate and FFP should be guided by coagulation parameters including fibrogen levels
consideration of early blood component therapy should be given to class IV hemorrhage pts.
Calcium administration
mostly not needed. maybe harmful
Special consdierations in the diagnosis and treatment of shock
Equating blood pressure with cardiac output
unrelated, an increase in peripheral resistance for example with vasopressor therapy with no change in caridac output results in increased blood pressure but no improvement in tissue perfusion or oxygenation.
Advanced age
Decrease in sympathetic activity, deficit in response to catecholamines
caridac complliance decresease
unable to increase hart rate or efficiency of contraction
atherosclerosis and occlusive disease makes vital organs sensitive to bp reduction
preexisting volume depletion (diuretic use, malnutrition)
b-blockers may mask tachycardia
consider early invasive monitoring
reduction in pulmonary compliance compounds cellular hypoxia
glomerular and tubular ageing
Athletes
blood volume increase 15-20%
cardiac output sixfold
storke volume 50%
resting pulse 50
remarkable ability to compensate for blood loss
pregnancy
physioloigc hypervolemia, greater blood loss to manifest perfusion abnormalities
Medications
B blockers calcium channel blockers alters hemodynamic response to hemorrhage.
Insulin overdose
long term diuretic hypokalemia
NSAIDS platelet function
Hypothermia
unresponsive to fluid resuscitation
coagulopathy
Pacemaker
unable to respond to blood loss
CVP monitoring is invaluable
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