2. Shock
• Shock is the clinical syndrome that results from
inadequate tissue perfusion which leads to hypoxia
and ultimately cellular dysfunction.
• The cellular dysfunction is manifested as aerobic to
anaerobic leading to lactic acidosis.
3. Principle mechanisms
• Not enough blood volume
• Pump failure
• Abnormalities of peripheral circulation (when all
small blood vessels dilate)
• Mechanical blockage of outflow from the heart
4. • Most common type of shock
– Insufficient circulating volume
• Primary cause = loss of blood or body fluids from an
internal or external source
• Hemorrhage, severe burns, severe dehydration
4
Hypovolemic shock
Scalp laceration 3rd degree/full thickness burn
5. • Failure of the heart to pump effectively
1. Due to damage to the heart muscle
2. Large myocardial infarction
3. Arrhythmias (too fast or too slow)
4. Cardiomyopathy
5. Congestive heart failure (CHF)
6. Cardiac valve problems
5
Cardiogenic Shock
6. • Similar to hypovolemic shock - insufficient
intravascular volume of blood or “relative"
hypovolemia
– result of dilation of all blood vessels so the “tank”
is much larger
6
Distributive shock
Urticaria/anaphylaxis Meningococcic sepsis
7. • Septic shock
– Overwhelming infection leading to profound
systemic vasodilation
• Anaphylactic shock
– Severe reaction to an allergen, antigen, drug or
foreign protein, releasing histamine causing
widespread vasodilation, hypotension and
increased capillary permeability
• Neurogenic shock
– Rarest form of shock.
– Trauma to spinal cord resulting in loss of
autonomic and motor reflexes below injury level.
Vessel walls relax uncontrolled, decreasing
peripheral vascular resistance, result =
vasodilation and hypotension
7
Distributive shock examples
11. Haemorrhagic shock
• It is one of the commonest form of hypovolemic shock
• Hypovolemia leads to decreased preload which leads to
increased sympathetic activity and vasoconstriction
• Vasoconstriction leads to decreased mean arterial
pressure and ischemia which ultimately leads to
multiorgan failure-ARDS,HEPATIC FAILURE,STRESS,GI
BLEEDING.RENAL FAILURE .
• Ischemia leads to myocardial insufficiency and severe
decrease in Systemic Vascular Resistance and finally
death
13. External Hemorrhage
• Results from soft tissue injury.
• Most soft tissue trauma is accompanied by mild hemorrhage
and is not life threatening.
– Can carry significant risks of patient morbidity and disfigurement
• The seriousness of the injury is dependent on:
– Anatomical source of the hemorrhage (arterial, venous,
capillary)
– Degree of vascular disruption
– Amount of blood loss that can be tolerated by the patient
14. Internal Hemorrhage
• Can result from:
– Blunt or penetrating trauma
– Acute or chronic medical illnesses
• Internal bleeding that can cause hemodynamic
instability usually occurs in one of four body cavities:
– Chest
– Abdomen
– Pelvis
– Retroperitoneum
15. Internal Hemorrhage
• Signs and symptoms that may suggest significant
internal hemorrhage include:
– Bright red blood from mouth, rectum, or other
orifice
– Coffee-ground appearance of vomit
– Melena (black, tarry stools)
– Dizziness or syncope on sitting or standing
– Orthostatic hypotension
• Internal hemorrhage is associated with higher
morbidity and mortality than external hemorrhage
16. Compensated shock
– 0-20% of blood loss
– Blood pressure is maintained via increased
vascular tone and increased blood flow to vital
organs
18. The Organs which well perfused :
• Brain
• Heart
• Kidneys
• Liver
The Organs which are less perfused:
• Skin
• GI tract
• Skeletal Muscle
19. But why
• The body will make whatever adjustments it can to
maintain….
Adequate
Cardiac
Output
• Brain and heart perfusions remain near normal while other
less critical organ systems are, in proportion to the blood
volume deficit, stressed by ischemia.
21. The body’s response
Uncompensated shock
• The intravascular volume deficit exceeds the capacity
of vasoconstrictive mechanisms to maintain systemic
perfusion pressure.
• Increased cardiac output
• Increased respiration
• Sodium retention
22. Classification
Class I
A. Loss of up to 15% of total blood volume (0 to 750
ml in 70 kg person).
B. Characterized by normal blood pressure, urine
output, slight tachycardia, tachypnea, slight anxiety.
23. Class II
A. Loss of 15 % to 30% of total blood volume
(750 to 1,500 ml )
B. Characterized by normal blood pressure,
tachycardia, mild tachypnea, decrease urine
output and mild anxiety.
24. Class III
A. Loss of 30% to 40% of total blood volume
(1,500 to 2,ooo)
B. Characterized by hypotension, tachycardia,
tachypnea, decreased urine output , anxiety and
confusion.
25. Class IV
A. Loss of > 40% of total blood volume (>2,ooo)
B. Characterized by severe hypotension and
tachycardia, tachypnea, negligible urine output
and lethargy
26. Class 4
Class 3
Class 2
Class 1
>2000
1500-2000
750-1500
<750 ml
Blood loss (in
ml)
>40
30-40
15-30
<15
Blood volume
(in%)
>140
>120
>100
<100
Heart rate
decreased
Decreased
mean arterial
pressure<60
Normal (+tilt )
Normal or
increased
Blood pressure
decreased
Decrease
Decreased
Normal
Pulse
pressure
Always delayed
Usually
delayed
May be
delayed
Normal
Capillary refill
Always delayed
Usually
delayed
Mildly delayed
normal
Respirations
Essentially
anuric
5-15
20-30
>30
Urinary output
(ml/hr)
Lethargic,obtu
nded
confused
Anxious
Normal or
anxious
Mental status
27. Concomitant Factors
• Pre-existing condition
– eg Anaemia, HTN etc
• Rate of blood loss
• Patient Types
– Pregnant
• >50% greater blood volume than normal
• Fetal circulation impaired when mother compensating
– Athletes
• Greater fluid and cardiac capacity
– Obese
• CBV is based on IDEAL weight (less CBV)
28. • Children
– CBV 8–9% of body weight
– Poor compensatory mechanisms
– TREAT AGGRESSIVELY!
• Elderly
– Decreased CBV
– Medications
• BP
• Anticoagulants
29. Hemorrhage Assessment
• Blood loss at the scene
• Mechanism of Injury/Nature of Illness
• Should only be used in conjunction with vital signs and
other clinical signs of injury to determine the
probability of injury
• Need for Additional Resources
30. • Initial Assessment
– General Impression
• Obvious bleeding
– Mental Status
– Interventions
• Manage as you go
– O2
– Bleeding control
– Shock
– BLS before ALS!
31. • Focused History & Physical examination
– Rapid Trauma Assessment
• Full head to toe
• Consider air medical if stage 2+ blood loss
– Focused Physical Exam
• Guided by c/c
– Vitals, SAMPLE, and OPQRST
– Additional Assessment
• Orthostatic hypotension
• Tilt test: 20
– BP or P from supine to sitting
32. Fractures and Blood Loss
• Pelvic fracture:
• Femur fracture:
• Tibia/fibula fracture:
• Hematomas and contusions:
2,000 mL
1,500 mL
500–750 mL
500 mL
33. • Ongoing Assessment
– Reassess vitals and mental status:
• Q 5 min: UNSTABLE patients
• Q 15 min: STABLE patients
– Reassess interventions:
• Oxygen
• ET
• IV
• Medication actions
– Trending: improvement vs. deterioration
• Pulse oximetry
• End-tidal CO2 levels
34. Management
• C-ABCs of trauma
• Control hemorrhage (splint the limb!!)
• Obtain IV access and resuscitate with fluids and
blood
– 2 liters crystalloid for adults
– 20 cc/kg crystalloid x 2 for kids
• Blood vs. Crystalloid??
• Long term critical care management
35. Management goals AFTER securing the ABCs:
• stop the bleeding!
• restore volume!
• correct any electrolyte/acid-base disturbances!
36. Apply direct pressure:
• with gloved hand,
• sterile dressing(s).
Bleeding stopped? Yes
No
Elevate extremity:
• above victim’s heart,
continue direct pressure
Locate pressure point,
apply pressure:
• maintain direct pressure
over wound
Treat for shock:
• care for wound,
• seek definitive care
Bleeding stopped?
Bleeding stopped?
No
Bleeding from
extremity?
No
Apply tourniquet
(last resort)
Yes
No
Definitive therapy
37. • Apply pressure directly to wound
site:
– Gloved hand, dressing
– If dressing soaks thru, add
more gauze on top and press
harder
37
Direct pressure
Apply direct pressure:
• with gloved hand,
• sterile dressing(s).
Bleeding stopped? Yes
No
Elevate extremity:
• above victim’s heart,
continue direct pressure
Locate pressure point,
apply pressure:
• maintain direct pressure
over wound
Treat for shock:
• care for wound,
• seek definitive care
Bleeding stopped?
Bleeding stopped?
No
Bleeding from
extremity?
No
Apply tourniquet
(last resort)
Yes
No
Definitive therapy
38. • If possible, raise wound site
above level of victim’s heart
38
Elevate wound site
Apply direct pressure:
• with gloved hand,
• sterile dressing(s).
Bleeding stopped? Yes
No
Elevate extremity:
• above victim’s heart,
continue direct pressure
Locate pressure point,
apply pressure:
• maintain direct pressure
over wound
Treat for shock:
• care for wound,
• seek definitive care
Bleeding stopped?
Bleeding stopped?
No
Bleeding from
extremity?
No
Apply tourniquet
(last resort)
Yes
No
Definitive therapy
39. • Find proximal “pressure point”
and press on it
(radial, ulnar, brachial, axillary, femoral
arteries—not carotid)
• Apply direct pressure to site
39
Pressure points
Apply direct pressure:
• with gloved hand,
• sterile dressing(s).
Bleeding stopped? Yes
No
Elevate extremity:
• above victim’s heart,
continue direct pressure
Locate pressure point,
apply pressure:
• maintain direct pressure
over wound
Treat for shock:
• care for wound,
• seek definitive care
Bleeding stopped?
Bleeding stopped?
No
Bleeding from
extremity?
No
Apply tourniquet
(last resort)
Yes
No
Definitive therapy
40. • Apply band above injury site,
tighten to stop bleeding:
– Last resort—risky
– Note time of application
– Reassess frequently
40
Tourniquet
Apply direct pressure:
• with gloved hand,
• sterile dressing(s).
Bleeding stopped? Yes
No
Elevate extremity:
• above victim’s heart,
continue direct pressure
Locate pressure point,
apply pressure:
• maintain direct pressure
over wound
Treat for shock:
• care for wound,
• seek definitive care
Bleeding stopped?
Bleeding stopped?
No
Bleeding from
extremity?
No
Apply tourniquet
(last resort)
Yes
No
Definitive therapy
41. Volume Resuscitation
• Rapid Responder
– Give 500cc-1 Liter crystalloid rapid
improvement of BP/HR/Urine output
– < 20% blood loss
• Transient Responder
– Give 500cc-1 Liter crystalloid improves briefly
then deteriorates
– 20-40% blood loss
– Continue crystalloid infusion +/- Blood
42. • Non Responder
– Give 2 Liters crystalloid/ 2 units Blood no
response
– > 40% blood loss
44. Correction of any electrolyte/acid-base
disturbances
• Normalization of acidosis and oxygen consumption
are the best current indicators of adequate
resuscitation
• Base deficit and lactate level are good indications of
tissue perfusion
45. • Bicarbonate
• HCO3 combined with hydrogen ion to form water and
carbon dioxide
• CO2 diffuses into cells and worsens intracellular
acidosis
• It is not indicated for lactic acidosis from HS
• Best treatment of acidosis from HS is restoring
perfusion to ischemic tissue.
47. Multiple organ failure
• pt who survive HS but die in the hospital later usually
die of MOF or sepsis
• MOF results from systemic inflammatory response
• Duration and severity of HS correlate with incidence
of MOF
• Patients who get > 6 units of packed RBCs in the first
12 hours of HS resusitation have higher risk of MOF
48. Coagulopathy
• Hypothermia
– Most common cause of coagulopathy in HS
– Significant coagulopathy begins at 34o c
– Undetectable on lab tests of coagulation ,blood
warmed to 37 c before testing
Note that
Treat with warmed fluids and external rewarming
49. • Platelet dysfunction and deficiency
– Second most common cause
– Hypothermia cause plt dysfunction
– Thrombocytopenia is common is massive HS
– Degree of thrombocytopenia not correlated
directly with volume of blood loss
– Platelets transfusion
