3. INTRODUCTION TO
HEMORRHAGE AND SHOCK
ā¢ Hemorrhage
ā¢ Abnormal internal or external loss of blood
ā¢ Homeostasis
ā¢ Tendency of the body to maintain a steady and normal internal
environment
ā¢ Shock
ā¢ INADEQUATE TISSUE PERFUSION
ā¢ Transition between homeostasis and death
4. HEMORRHAGE
ā¢ Circulatory System
ā¢ Hemorrhage Classification
ā¢ Clotting
ā¢ Factors Affecting Clotting
ā¢ Hemorrhage Control
ā¢ Stages of Hemorrhage
ā¢ Hemorrhage Assessment
ā¢ Hemorrhage Management
6. HEART
ā¢ Cardiac Cycle
ā¢ The repetitive pumping action that produces pressure changes that
circulate blood throughout the body
ā¢ Cardiac Output
ā¢ The total amount of blood separately pumped by each ventricle per
minute, usually expressed in liters per minute
7. CARDIAC OUTPUT
ā¢ Normal cardiac output = 5 to 6 liters per minute
(LPM)
ā¢ Can increase up to 30 LPM in times of stress or
exercise
ā¢ Determined by multiplying the heart rate by the
volume of blood ejected by each ventricle during
each beat (stroke volume)
ā¢ CO is influenced by:
ā¢ Strength of contraction
ā¢ Rate of contraction
ā¢ Amount of venous return available to the ventricle
(preload)
8. CIRCULATORY SYSTEM (1 OF 4)
ā¢ Heart
ā¢ Autonomic nervous system
ā¢ Parasympathetic nervous system
ā¢ Slows rate
ā¢ Mediated by vagus nerve
ā¢ Sympathetic nervous system
ā¢ Increases rate
ā¢ Cardiac plexus
9. CIRCULATORY SYSTEM (3 OF 4)
ā¢ Arteries
ā¢ Tunica Adventitia
ā¢ Tunica Media
ā¢ Tunica Intima
ā¢ Arteriole
ā¢ Capillary: 7% of total blood volume
ā¢ Venule
ā¢ Vein
ā¢ Constriction returns 20% (1 liter) of blood to active
circulation
} 64% of blood volume
} 13% of blood volume
11. CIRCULATION (1 OF 2)
ā¢ Systolic Pressure
ā¢ Strength and volume of cardiac output
ā¢ Diastolic Pressure
ā¢ More indicative of the state of constriction of the arterioles
ā¢ Mean Arterial Pressure
ā¢ 1/3 pulse pressure added to the diastolic pressure
ā¢ Tissue perfusion pressure
12. CIRCULATION (2 OF 2)
ā¢ Vascular Control
ā¢ Increased sympathetic tone results in increased vasoconstriction
ā¢ Microcirculation
ā¢ Blood flow in the arterioles, capillaries, and venules
ā¢ Sphincter functioning
ā¢ Most organ tissue requires blood flow 5 to 20% of the time.
13. THE VASOCONSTRICTION IN
PERIPHERAL VASCULAR BDS
RESULTS IN THE
CHARACTERISTIC PALE, COLD
SKIN OF PATIENTS SUFFERING
FROM HYPOVOLEMIC SHOCK.
14. VASCULATURE
ā¢ Lined with smooth muscle.
ā¢ All vessels larger than capillaries have layers of tissues (tunicae).
ā¢ Maintains blood flow by changes in pressure and peripheral
vascular resistance.
15. STARLINGāS LAW OF THE HEART
ā¢ When the rate at which blood flows into the heart
from the veins (venous return) changes, the
heart automatically adjusts its output to match
inflow.
ā¢ The more blood the heart receives the more it
pumpsā¦
ā¢ Increased end diastolic volume increases contractility.
ā¢ Increases stroke volume.
ā¢ Increases cardiac output.
ā¢ Starling curves at any end-diastolic volume.
ā¢ Increased sympathetic input increases stroke volume.
ā¢ Decreased sympathetic input decreases stroke volume.
17. MICROCIRCULATION (1 OF 3)
ā¢ Can be divided into pulmonary microcirculation and peripheral
microcirculation.
ā¢ Pressure in each division is produced by the right and left heart,
respectively.
ā¢ Approximately 5% of the total circulating blood flow is always
flowing through capillaries.
19. CNS ISCHEMIA RESPONSE
ā¢ CNS ischemia response is activated when blood flow
to the vasomotor center of the medulla is decreased.
ā¢ In the presence of ischemia, the neurons within the medulla
stimulate the sympathetic nervous system.
ā¢ Sympathetic vasoconstriction can elevate arterial
pressure for as long as 10 minutes.
ā¢ The cerebral ischemia response functions only in
emergency situations.
21. BLOOD
ā¢ Blood Volume
ā¢ Average adult male has a blood volume of 7% of total body weight.
ā¢ Average adult female has a blood volume of 6.5% of body weight.
ā¢ Normal adult blood volume is 4.5ā5 L.
ā¢ Remains fairly constant in the healthy body.
24. PLASMA (1 OF 2)
ā¢ Approximately 92% water
ā¢ The liquid portion of blood
ā¢ Circulates salts, minerals, sugars, fats, and proteins throughout
the body
25. PLASMA (2 OF 2)
ā¢ Contains 3 major proteins:
ā¢ Albumin
ā¢ Most plentiful plasma protein
ā¢ Similar in consistency to egg whites
ā¢ Gives blood its gummy texture
ā¢ Helps keep water concentration of blood low enough to
allow water to diffuse readily from tissues into blood
ā¢ Globulins serve 2 main functions:
ā¢ Alpha and beta globulins transport other proteins
ā¢ Gamma globulins give people immunity to disease
ā¢ Fibrinogen
ā¢ Aids in blood clotting by forming a web of protein fibers
that binds blood cells together
26. OTHER FUNCTIONS OF PLASMA
ā¢ Proteins function as an acid or base to correct changes in blood
acidity.
ā¢ Can temporarily meet nutritional need of the body should the
body run short of food.
27. PROTEINS
ā¢ Account for 50% of the bodyās organic material
ā¢ Components of most body structures
ā¢ Roles in the chemical reactions in the body
ā¢ Specialized proteins are responsible for:
ā¢ Immune responses
ā¢ Coagulation
ā¢ Digestion of foodstuffs
ā¢ Metabolism of nutrients
ā¢ Many other functions
29. LEUKOCYTES (WBCS)
ā¢ Defend the body against various pathogens (bacteria, viruses,
fungi, and parasites)
ā¢ Produced in bone marrow and lymph glands
ā¢ Release reserves when pathogens invade the body
30. PLATELETS
ā¢ Part of the bodyās defense mechanism
ā¢ Formed in red bone marrow
ā¢ Work by swelling and adhering together to form sticky plugs
(initiating the clotting phenomenon)
32. FOUR STAGES
ā¢ Stage 1: Vasoconstriction
ā¢ Stage 2: Capillary and venule opening
ā¢ Stage 3: Disseminated intravascular coagulation
ā¢ Stage 4: Multiple organ failure
33. STAGE 1: VASOCONSTRICTION (1
OF 4)
ā¢ Vasoconstriction begins as minimal perfusion to capillaries
continues.
ā¢ Oxygen and substrate delivery to the cells supplied by these
capillaries decreases.
ā¢ Anaerobic metabolism replaces aerobic metabolism.
34. STAGE 1: VASOCONSTRICTION (2
OF 4)
ā¢ Production of lactate and hydrogen ions increases.
ā¢ The lining of the capillaries may begin to lose the ability to retain
large molecular structures within its walls.
ā¢ Protein-containing fluid leaks into the interstitial spaces (leaky
capillary syndrome).
35. STAGE 1: VASOCONSTRICTION (3
OF 4)
ā¢ Sympathetic stimulation produces:
ā¢ Pale, sweaty skin
ā¢ Rapid, thready pulse
ā¢ Elevated blood glucose levels
ā¢ The release of epinephrine dilates coronary, cerebral, and
skeletal muscle arterioles and constricts other arterioles.
ā¢ Blood is shunted to the heart, brain, skeletal muscle, and
capillary flow to the kidneys and abdominal viscera decreases.
36. STAGE 1: VASOCONSTRICTION (4
OF 4)
If this stage of shock is not treated by
prompt restoration of circulatory
volume, shock progresses to the next
stage.
37. STAGE 2: CAPILLARY AND
VENULE OPENING (1 OF 5)
ā¢ Stage 2 occurs with a 15% to 25% decrease in intravascular
blood volume. Heart rate, respiratory rate, and capillary refill are
increased, and pulse pressure is decreased at this stage. Blood
pressure may still be normal.
38. STAGE 2: CAPILLARY AND
VENULE OPENING (2 OF 5)
ā¢ As the syndrome continues, the precapillary sphincters relax with
some expansion of the vascular space.
ā¢ Postcapillary sphincters resist local effects and remain closed,
causing blood to pool or stagnate in the capillary system,
producing capillary engorgement.
39. STAGE 2: CAPILLARY AND
VENULE OPENING (3 OF 5)
ā¢ As increasing hypoxemia and acidosis lead to
opening of additional venules and capillaries, the
vascular space expands greatly.
ā¢ Even normal blood volume may be inadequate to fill the
container.
ā¢ The capillary and venule capacity may become
great enough to reduce the volume of available
blood for the great veins and vena cava.
ā¢ Resulting in decreased venous return and a fall in
cardiac output.
40. STAGE 2: CAPILLARY AND
VENULE OPENING (4 OF 5)
ā¢ Low arterial blood pressure and many open
capillaries result in stagnant capillary flow.
ā¢ Sluggish blood flow and the reduced delivery of
oxygen result in increased anaerobic metabolism
and the production of lactic acid.
ā¢ The respiratory system attempts to compensate for the
acidosis by increasing ventilation to blow off carbon
dioxide.
41. STAGE 2: CAPILLARY AND
VENULE OPENING (5 OF 5)
ā¢ As acidosis increases and pH falls, the RBCs may cluster
together (rouleaux formation).
ā¢ Halts perfusion
ā¢ Affects nutritional flow and prevents removal of cellular
metabolites
ā¢ Clotting mechanisms are also affected, leading to
hypercoagulability.
ā¢ This stage of shock often progresses to the third stage if
fluid resuscitation is inadequate or delayed, or if the shock
state is complicated by trauma or sepsis.
42. STAGE 3: DISSEMINATED
INTRAVASCULAR COAGULATION (DIC)
(1 OF 4)
ā¢ Time of onset will depend on degree of
shock, patient age, and pre-existing medical
conditions.
ā¢ Stage 3 occurs with 25% to 35% decrease in
intravascular blood volume. At this stage,
hypotension occurs. This stage of shock
usually requires blood replacement.
43. STAGE 3: DISSEMINATED
INTRAVASCULAR COAGULATION (DIC)
(2 OF 4)
ā¢ Stage 3 is resistant to treatment (refractory
shock), but is still reversible.
ā¢ Blood begins to coagulate in the
microcirculation, clogging capillaries.
ā¢ Capillaries become occluded by clumps of RBCs.
ā¢ Decreases capillary perfusion and prevents removal of
metabolites
ā¢ Distal tissue cells use anaerobic metabolism, and
lactic acid production increases.
44. STAGE 3: DISSEMINATED
INTRAVASCULAR COAGULATION (DIC)
(3 OF 4)
ā¢ Lactic acid accumulates around the cell.
ā¢ Cell membranes no longer have the energy needed to maintain
homeostasis.
ā¢ Water and sodium leak in, potassium leaks out, and the cells swell
and die.
45. STAGE 3: DISSEMINATED
INTRAVASCULAR COAGULATION (DIC)
(4 OF 4)
ā¢ Pulmonary capillaries become permeable,
leading to pulmonary edema.
ā¢ Decreases the absorption of oxygen and results
in possible alterations in carbon dioxide
elimination
ā¢ May lead to acute respiratory failure or adult
respiratory distress syndrome (ARDS)
ā¢ If shock and disseminated intravascular
coagulation (DIC) continue, the patient
progresses to multiple organ failure.
46. STAGE 4: MULTIPLE ORGAN
FAILURE (1 OF 2)
ā¢ The amount of cellular necrosis required to
produce organ failure varies with each organ and
the underlying condition of the organ.
ā¢ Usually hepatic failure occurs, followed by renal
failure, and then heart failure.
ā¢ If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo
changes that rapidly become irreversible.
ā¢ In this stage, blood pressure falls dramatically (to
levels of 60 mmHg or less).
ā¢ Cells can no longer use oxygen, and metabolism
stops.
47. STAGE 4: MULTIPLE ORGAN
FAILURE (2 OF 2)
ā¢ If a critical amount of the vital organ is
damaged by cellular necrosis, the organ soon
fails.
ā¢ Failure of the liver is common and often presents
early.
ā¢ Capillary blockage may cause heart failure.
ā¢ GI bleeding and sepsis may result from GI
mucosal necrosis.
ā¢ Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis.
ā¢ Pulmonary thrombosis may produce
hemorrhage and fluid loss into the alveoli.
ā¢ Leading to death from respiratory failure.
49. DEFINING SHOCK (1 OF 2)
ā¢ Shock is best defined as inadequate tissue perfusion.
ā¢ Can result from a variety of disease states and injuries.
ā¢ Can affect the entire organism, or it can occur at a tissue or
cellular level.
āThe rude unhinging of the machinery of Lifeā
Gross, 1877
50. DEFINING SHOCK (2 OF 2)
ā¢ Shock is not adequately defined by:
ā¢ Pulse rate
ā¢ Blood pressure
ā¢ Cardiac function
ā¢ Hypovolemia
ā¢ Loss of systemic vascular resistance
52. EXTERNAL HEMORRHAGE
ā¢ Results from soft tissue injury.
ā¢ Accounts for nearly 10 million emergency department visits
in the United States each year.
ā¢ Most soft tissue trauma is accompanied by mild
hemorrhage and is not life threatening.
ā¢ Can carry significant risks of patient morbidity and disfigurement
ā¢ The seriousness of the injury is dependent on:
ā¢ Anatomical source of the hemorrhage (arterial, venous,
capillary)
ā¢ Degree of vascular disruption
ā¢ Amount of blood loss that can be tolerated by the patient
53. INTERNAL HEMORRHAGE (1 OF 2)
ā¢ Can result from:
ā¢ Blunt or penetrating trauma
ā¢ Acute or chronic medical illnesses
ā¢ Internal bleeding that can cause hemodynamic instability
usually occurs in one of four body cavities:
ā¢ Chest
ā¢ Abdomen
ā¢ Pelvis
ā¢ Retroperitoneum
54. INTERNAL HEMORRHAGE (2 OF 2)
ā¢ Signs and symptoms that may suggest significant internal
hemorrhage include:
ā¢ Bright red blood from mouth, rectum, or other orifice
ā¢ Coffee-ground appearance of vomitus
ā¢ Melena (black, tarry stools)
ā¢ Dizziness or syncope on sitting or standing
ā¢ Orthostatic hypotension
55. Internal hemorrhage is associated with
higher morbidity and mortality than
external hemorrhage.
56. PHYSIOLOGICAL RESPONSE TO
HEMORRHAGE
ā¢ The bodyās initial response to hemorrhage is to stop bleeding by
chemical means (hemostasis).
ā¢ This vascular reaction involves:
ā¢ Local vasoconstriction
ā¢ Formation of a platelet plug
ā¢ Coagulation
ā¢ Growth of tissue into the blood clot that permanently closes and seals
the injured vessel
57. FICK PRINCIPLE
ā¢ A method for measuring cardiac output.
ā¢ The Fick principle assumes that the quantity of
oxygen delivered to an organ is equal to the
amount of oxygen consumed by that organ plus
the amount of oxygen carried away from that
organ.
ā¢ Used to estimate perfusion either to an organ or
to the whole body when oxygen content of both
the arterial and venous blood is known and
oxygen consumption is assumed to remain fixed.
58. HEMORRHAGE CONTROL
ā¢ External Hemorrhage
ā¢ Direct pressure and pressure dressing
ā¢ General management
ā¢ Direct pressure
ā¢ Elevation
ā¢ Ice
ā¢ Pressure points
ā¢ Constricting band
ā¢ Tourniquet
ā¢ May use a BP cuff by inflating the cuff 20ā30 mmHg above the SBP
ā¢ Release may send toxins to heart
ā¢ Lactic acid and electrolytes
60. INTERNAL HEMORRHAGE
CONTROL
ā¢ Hematoma
ā¢ Pocket of blood between
muscle and fascia
ā¢ UNEXPLAINED SHOCK is
BEST attributed to
abdominal trauma
ā¢ General Management
ā¢ Immobilization,
stabilization, elevation
ā¢ Epistaxis: Nose Bleed
ā¢ Causes: trauma,
hypertension
ā¢ Treatment: lean forward,
pinch nostrils
ā¢ Hemoptysis
ā¢ Esophageal Varices
ā¢ Melena
ā¢ Diverticulosis
ā¢ Chronic Hemorrhage
ā¢ Anemia
61. STAGES OF HEMORRHAGE
ā¢ 60% of body weight is fluid.
ā¢ 7% circulating blood volume (CBV) in men
ā¢ 5 L (10 units)
ā¢ 6.5% CBV in women
ā¢ 4.6 L (9ā10 units)
62. STAGES OF HEMORRHAGE
STAGE 1
ā¢ 15% loss of CBV
ā¢ 70 kg pt = 500ā750 mL
ā¢ Compensation
ā¢ Vasoconstriction
ā¢ Normal BP, pulse pressure, respirations
ā¢ Slight elevation of pulse
ā¢ Release of catecholamines
ā¢ Epinephrine
ā¢ Norepinephrine
ā¢ Anxiety, slightly pale and clammy skin
63. STAGES OF HEMORRHAGE
STAGE 2 (1 OF 2)
ā¢ 15ā25% loss of CBV
ā¢ 750ā1250 mL
ā¢ Early decompensation
ā¢ Unable to maintain BP
ā¢ Tachycardia and tachypnea
64. STAGES OF HEMORRHAGE
STAGE 2 (2 OF 2)
ā¢ Decreased pulse strength
ā¢ Narrowing pulse pressure
ā¢ Significant catecholamine release
ā¢ Increase PVR
ā¢ Cool, clammy skin and thirst
ā¢ Increased anxiety and agitation
ā¢ Normal renal output
65. STAGES OF HEMORRHAGE
STAGE 3 (1 OF 2)
ā¢ 25ā35% loss of CBV
ā¢ 1250ā1750 mL
ā¢ Late decompensation (early irreversible)
ā¢ Compensatory mechanisms unable to cope with loss of blood
volume
66. STAGES OF HEMORRHAGE
STAGE 3 (2 OF 2)
ā¢ Classic Shock
ā¢ Weak, thready, rapid pulse
ā¢ Narrowing pulse pressure
ā¢ Tachypnea
ā¢ Anxiety, restlessness
ā¢ Decreased LOC and AMS
ā¢ Pale, cool, and clammy skin
67. STAGES OF HEMORRHAGE
STAGE 4
ā¢ >35% CBV loss
ā¢ >1750 mL
ā¢ Irreversible
ā¢ Pulse: Barely palpable
ā¢ Respiration: Rapid, shallow, and ineffective
ā¢ LOC: Lethargic, confused, unresponsive
ā¢ GU: Ceases
ā¢ Skin: Cool, clammy, and very pale
ā¢ Unlikely survival
68. STAGES OF HEMORRHAGE
CONCOMITANT FACTORS (1 OF 2)
ā¢ Pre-existing condition
ā¢ Rate of blood loss
ā¢ Patient Types
ā¢ Pregnant
ā¢ >50% greater blood volume than normal
ā¢ Fetal circulation impaired when mother compensating
ā¢ Athletes
ā¢ Greater fluid and cardiac capacity
ā¢ Obese
ā¢ CBV is based on IDEAL weight (less CBV)
69. STAGES OF HEMORRHAGE
CONCOMITANT FACTORS (2 OF 2)
ā¢ Children
ā¢ CBV 8ā9% of body weight
ā¢ Poor compensatory mechanisms
ā¢ TREAT AGGRESSIVELY!
ā¢ Elderly
ā¢ Decreased CBV
ā¢ Medications
ā¢ BP
ā¢ Anticoagulants
70. HEMORRHAGE ASSESSMENT (1 OF 5)
ā¢ Scene Size-up
ā¢ Is it safe?
ā¢ BSI
ā Blood loss
ā¢ Law enforcement
ā¢ Mechanism of Injury/Nature of Illness
ā¢ Should only be used in conjunction with vital signs and other clinical
signs of injury to determine the probability of injury
ā¢ Number of Patients
ā¢ Need for Additional Resources
71. HEMORRHAGE ASSESSMENT
(2 OF 5)
ā¢ Initial Assessment
ā¢ General Impression
ā¢ Obvious bleeding
ā¢ Mental Status
ā¢ CABC
ā¢ Interventions
ā¢ Manage as you go
ā¢ O2
ā¢ Bleeding control
ā¢ Shock
ā¢ BLS before ALS!
73. HEMORRHAGE ASSESSMENT (4 OF 5)
FRACTURES AND BLOOD LOSS
ā¢ Pelvic fracture:
ā¢ Femur fracture:
ā¢ Tibia/fibula fracture:
ā¢ Hematomas and contusions:
2,000 mL
1,500 mL
500ā750 mL
500 mL
74. HEMORRHAGE ASSESSMENT
(5 OF 5)
ā¢ Ongoing Assessment
ā¢ Reassess vitals and mental status:
ā¢ Q 5 min: UNSTABLE patients
ā¢ Q 15 min: STABLE patients
ā¢ Reassess interventions:
ā¢ Oxygen
ā¢ ET
ā¢ IV
ā¢ Medication actions
ā¢ Trending: improvement vs. deterioration
ā¢ Pulse oximetry
ā¢ End-tidal CO2 levels
77. SPECIFIC WOUND
CONSIDERATIONS
(1 OF 2)
ā¢ Head Wounds
ā¢ Presentation
ā¢ Severe bleeding
ā¢ Skull fracture
ā¢ Management
ā¢ Gentle direct pressure
ā¢ Fluid drainage from
ears and nose
ā¢ DO NOT pack
ā¢ Cover and bandage
loosely
ā¢ Neck Wounds
ā¢ Presentation
ā¢ Large vessel can
entrap air
ā¢ Management
ā¢ Consider direct digital
pressure
ā¢ Occlusive dressing
78. SPECIFIC WOUND
CONSIDERATIONS
(2 OF 2)
ā¢ Gaping Wounds
ā¢ Presentation
ā¢ Multiple sites
ā¢ Gaping prevents
uniform pressure
ā¢ Management
ā¢ Bulky dressing
ā¢ Trauma dressing
ā¢ Sterile, non-adherent
surface to wound
ā¢ Compression
dressing
ā¢ Crush Injury
ā¢ Presentation
ā¢ Difficult to locate
source of bleeding
ā¢ Normal hemorrhage
control mechanism
nonfunctional
ā¢ Management
ā¢ Consider an air-splint
and pressure
dressing
ā¢ Consider tourniquet
80. SHOCK MANAGEMENT (1 OF 2)
ā¢ Airway and Breathing
ā¢ NRB
ā¢ PPV (overdrive respiration)
ā¢ ET
ā¢ CPAP
ā¢ PEEP
ā¢ Hemorrhage Control
ā¢ Fluid Resuscitation
ā¢ Catheter size and length
ā¢ Large bore
ā¢ 20 mL/kg of NS or LR
ā¢ Polyhemoglobins
ā¢ STABILIZE VITALS to SBP of 80 mmHg or 90 mmHg in head
injuries.
Any injury to the
head or torso is
ALSO considered an
injury to the spine.
81. SHOCK MANAGEMENT (2 OF 2)
ā¢ Temperature Control
ā¢ Conserve core temperature
ā¢ Warm IV fluids
ā¢ PASG
ā¢ Action
ā¢ Increase PVR
ā¢ Reduce vascular volume
ā¢ Increase central CBV
ā¢ Immobilize lower extremities
ā¢ Assess
ā¢ Pulmonary edema
ā¢ Pregnancy
ā¢ Vital signs