13. Capillaries
Capillary flow provides
essential nutrients and
oxygen and removes
waste products.
– Only one-cell thick
Hydrostatic pressure
pushes the plasma into
the interstitial space.
– Filtration
14. Veins
Collect blood and return
it to the heart
Contains the vast
majority of the total
blood volume
Able to constrict in early
stages of hemorhage
16. Blood
Blood is the tissue that circulates within the
cardiovascular system
– A mixture of cells, proteins, water, and other
suspended elements
Blood Volume
– Average adult male has a blood volume of 7% of
total body weight
– Average adult female has a blood volume of 6.5%
of body weight
– Normal adult blood volume is 4.5–5 L
Remains fairly constant in the healthy body
18. Blood Components
Erythrocytes (RBC’s)
– The major blood
Contains hemoglobin
A molecule to which oxygen attaches
– Efficient transporter of oxygen from the lungs to
body cells.
21. Blood Components
Platelets
– Part of the body’s defense mechanism
– Formed in red bone marrow
– Work by swelling and adhering together to form
sticky plugs (initiating the clotting phenomenon)
27. Hemorrhage Control
External Hemorrhage
– External hemorrhage is relatively easy to
recognize and control.
Bleeding from small vessels can often be controlled by
firmly bandaging a dressing in place.
Fingertip pressure
– With careful application of direct pressure you can
halt virtually all hemorrhage.
29. Hemorrhage Control
External Hemorrhage (cont.)
– If you consider using a tourniquet, be extremely
cautious.
The need for a tourniquet is rare.
– In the absence of perfusion, lactic acid, potassium,
and other anaerobic metabolites accumulate
Will be released into the circulation when released
– Use a wide-band if considering use
30. 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
31. Internal Hemorrhage
Signs and symptoms that suggest significant
internal hemorrhage include:
– Bright red blood from mouth, rectum, or other
orifice
– Coffee-ground appearance of vomitus
– Melena (black, tarry stools)
– Orthostatic hypotension
Chronic hemorrhage may result in anemia
35. Stages of Hemorrhage
Stage 1
– 15% loss of CBV (circulating blood volume)
70 kg pt = 500–750 mL
– Compensation
Vasoconstriction
Normal BP, pulse pressure, respirations
Slight elevation of pulse
Release of catecholamines
Epinephrine
Norepinephrine
Anxiety, slightly pale and clammy skin
36. Stages of Hemorrhage
Stage 2
– 15–30% loss of CBV
750–1500 mL
– Early decompensation
Unable to maintain BP
Tachycardia and tachypnea
– Decreased pulse strength
– Narrowing pulse pressure
– Significant catecholamine release
Increase PVR
Cool, clammy skin and thirst
Increased anxiety and agitation
Normal renal output
37. Stages of Hemorrhage
Stage 3
– 30–40% loss of CBV
1500–2000 mL
– Late decompensation (early irreversible)
– Classic Shock
Weak, thready, rapid pulse
Narrowing pulse pressure
Tachypnea
Anxiety, restlessness
Decreased LOC and AMS
Pale, cool, and clammy skin
38. Stages of Hemorrhage
Stage 4
– >40% CBV loss
>1750 mL
– Irreversible
Pulse: Barely palpable
Respiration: Rapid, shallow, and ineffective
LOC: Lethargic, confused, unresponsive
GU: Ceases
Skin: Cool, clammy, and very pale
Unlikely survival
40. Geriatric Patients
Discussed in another chapter
Old people take beta blockers and other
medications that slow heart rate. May not
show typical signs of shock.
Break bones easily
Have curvy spines
Can’t hear very well
41. Pediatric Trauma
Discussed in another presentation
PALS CONCEPT:
70 + (2 X Patient’s Age) is cutoff for
hypotension in a pediatric patient
Compensate well, then decline rapidly
– (don’t circle the drain like adults)
42. Stages of Hemorrhage
Concomitant Factors
– Pre-existing condition
– 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)
43. Stages of Hemorrhage
Concomitant Factors
– Children
CBV 8–9% of body weight
Poor compensatory mechanisms
– Elderly
Decreased CBV
Medications
BP
Anticoagulants
44. Hemorrhage Assessment
Assessment of the hemorrhage patient is
directed at identifying the source of the
hemorrhage.
– Halt any serious and controllable loss.
Examine the nature of the injury.
46. Hemorrhage Assessment
Primary Assessment
– General Impression
Obvious Bleeding
– Mental Status
– CABC
– Interventions
Manage as you go
O2
Bleeding control
Shock
BLS before ALS!
47. Hemorrhage Assessment
Secondary Assessment
– 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
Search for signs of internal bleeding
Bleeding from body orifice, melena, hematochezia
Orthostatic hypotension
48. Hemorrhage Assessment
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
49. Hemorrhage Management
Assure that the airway is patent and breathing
is adequate.
– Maintain the airway and provide the necessary
ventilatory support.
– Administer high-flow oxygen.
Assure that the patient has a palpable carotid
pulse.
Care for serious (arterial and heavy venous)
hemorrhage, immediately after you correct
airway and breathing problems.
50. Hemorrhage Management
Direct Pressure
– Controls all but the
most persistent
hemorrhage
– If bleeding saturates
the dressing, cover
it with another
dressing
If ineffective, may be
necessary to
visualize wound to
apply pressure
directly to site
55. Specific Wound
Considerations
Head Wounds
– Presentation
Severe bleeding
Skull fracture
– Management
Gentle direct
pressure
Fluid drainage from
ears and nose
DO NOT pack
Cover and bandage
loosely
Neck Wounds
– Presentation
Large vessel can
entrap air
– Management
Consider direct
digital pressure
Occlusive dressing
56. Specific Wound
Considerations
Gaping Wounds
– Presentation
Multiple sites
Gaping prevents
uniform pressure
– Management
Bulky dressing
Trauma dressing
Sterile, non-
adherent surface to
wound
Compression
dressing
Crush Injury
– Presentation
Difficult to locate
source of bleeding
Normal hemorrhage
control mechanism
non-functional
– Management
Consider an air-
splint and pressure
dressing
Consider tourniquet
57. Transport Considerations
Consider rapid transport if:
– Suspected serious blood loss
– Suspected serious internal bleeding
– Decompensating shock
– If in doubt, rapid transport indicated
Other Considerations
– Sympathetic response
– Anxiety
59. Shock
Inadequate tissue perfusion
– Transitional stage between normal life, called
homeostasis, and death
– Can result from a variety of disease states and
injuries
– Can affect the entire organism, or it can occur at a
tissue or cellular level
63. Cellular Metabolism
ATP is a product of the cellular breakdown of
glucose
– Breakdown occurs in three steps
Glycolysis
Does not require oxygen
Produces pyruvic acid and 2 ATP’s
Kreb’s Cycle
Requires oxygen
Converts pyruvic acid into water, carbon dioxide and 2 ATP’s
Electron transport chain
Occurs in mitochondria
Results in the production of 32 ATPS
70. Oxygen Transport
Oxygen must uptake on the hemoglobin
molecule.
– Efficiently carries 97% of the oxygen
– Remaining 3% dissolves in plasma
The cardiovascular system then moves the
red blood cells from the pulmonary system,
through the heart, through the arterial system
and into the tissues.
71. Oxygen Transport
In the capillaries oxygen diffuses across the
capillary wall, into the interstitial fluid and then
to the cell.
– Internal respiration
72. Cellular Metabolism
The cardiovascular system is also
responsible to help maintain other elements
of the homeostatic environment
– Removal of CO2 and water
– Heat regulation
– Provides the glucose necessary for the cellular
metabolism
73. Digestion, Filtration, Hormone
Production, Excretion
The digestive system absorbs carbohydrates
and lipids (fats), moving them through the
portal system to the liver for processing.
The pancreas regulates blood glucose.
– Glucagon increases blood glucose
– Insulin decreases blood glucose
74. Digestion, Filtration, Hormone
Production, Excretion
Role of the Kidneys
– Regulating the body’s fluid/electrolyte balance
Excreting excess sodium, potassium, chloride, calcium,
bicarbonate, and magnesium
– Excreting the waste products of metabolism
– Excrete or retain water
75. Circulation
The cardiovascular system
– Responsible for assuring that the necessary
materials travel to and from the body’s cells
– Cardiac output
Preload, cardiac contractility, and afterload
Systolic blood pressure is most indicative of the strength
and volume of cardiac output
Lowest pressure in the arteries is the diastolic blood
pressure
78. Microcirculation
Venules and veins serve as collecting
channels and storage vessels (capacitance)
Normally contain 70% of the blood volume
Muscular movement aids in blood return to the
heart
79. Circulation
Respiration also facilitates blood return to the
heart
– Changes in pressure draws blood towards the
heart
Thoracoabdominal pump
In states of hypovolemia, blood return to the
heart is diminished
– Reduces cardiac output, arterial blood pressure,
and the body’s ability to direct blood flow to critical
organs
80. Cardiovascular
System Regulation
The human body is controlled by the
autonomic branch of the nervous system.
– Parasympathetic branch
– Sympathetic branch
These two systems act in balance
Many sympathetic nervous system activities
are aimed at defending the organism.
– These mechanisms may be detrimental in shock
states
86. Cardiovascular
System Regulation
Hormonal Regulation
– Epinephrine and norepinephrine are sympathetic
agents
Most rapid hormonal response to hemorrhage
Both have A1 properties
causes vasoconstriction
Epinephrine has beta-1 and beta-2 properties
B1= increased rate, strength, and conductivity
B2= broncodilation
87. Hormonal Regulation
Antidiuretic Hormone (ADH)
– Arginine Vasopressin (AVP)
– Released
Posterior pituitary
Drop in BP or increase in serum osmolarity
– Action
Increase in peripheral vascular resistance
Increase water retention by kidneys
Decrease urine output
Splenic vasoconstriction
200 mL of free blood to circulation
88. Hormonal Regulation
Angiotensin
– Released
Primary chemical from kidneys
Stimulus is lowered BP and decreased perfusion
– Action
Converted from renin into angiotensin I
Modified in lungs to angiotensin II
Potent systemic vasoconstrictor
Causes release of ADH, aldosterone, and epinephrine
91. Hormonal Regulation
Glucagon
– Release
Alpha cells of pancreas
Triggered by epinephrine
– Action
Causes liver and skeletal muscles to convert glycogen
into glucose
Gluconeogenesis
92. Hormonal Regulation
Insulin
– Release
Beta cells of
pancreas
– Action
Facilitates transport
of glucose across
cell membrane
Erythropoietin
– Release
Kidneys
Hypoperfusion or
hypoxia
– Action
Increases production
and maturation of
RBCs in the bone
marrow
93. Hormonal Regulation
Adrenocorticotropic hormone
– Stimulates the release of glucocorticoids from the
adrenal cortex
Increases glucose production
Reduces the body’s inflammation response
Prolongs clotting time, wound healing, and infection
fighting processes
Growth hormone
– Promotes the uptake of glucose and amino acids
in the muscle cells
94. The Body’s Response
to Blood Loss
As stroke volume decreases, cardiac output
decreases resulting in decreased systolic BP
– Carotid and aortic baroreceptors recognize this
decrease in blood pressure
Stimulate the cardiovascular center of the medulla
oblongata
Mechanisms compensate for small blood
losses
95. The Body’s Response
to Blood Loss
Cellular Ischemia
– Constriction of arterioles means that less and less
blood is directed to the noncritical organs
Results in hypoxia
– Anaerobic metabolism results
Followed by ischemia
96. Cellular Ischemia
If blood loss continues, waste products
accumulate and blood becomes acidic.
– Increase in depth and rate of respirations
– Decreased LOC
– Increased circulating catecholamines causes
anxiousness, restlessness, and possibly a
combative patient
– Decreased myocardial oxygen supply
97. Cellular Ischemia
If the blood loss stops, the blood draws fluid
from within the interstitial space
– Up to 1 L per hour
Kidneys reduce urine output
98. The Body’s Response
to Blood Loss
Capillary Microcirculation
– Sympathetic stimulation and reduced perfusion to
the kidneys, pancreas, and liver cause the release
of hormones
Angiotensin II causes reduced blood flow
– Perfusion is further limited to only those organs
most critical to life
More cells begin to use anaerobic metabolism for energy
= Increased acids
99. Capillary Microcirculation
The build-up of lactic acid and carbon dioxide
relaxes the precapillary sphincters
Postcapillary sphincters remain closed
Capillary and cell membranes begin to break
down
Red blood cells begin to clump together
– Rouleaux
102. Capillary Washout
Acidosis finally causes relaxation of the
postcapillary sphincters
Washout causes profound metabolic acidosis
and microscopic emboli
Body moves quickly and then irreversibly
toward death
103. Stages of Shock
Three stages:
– Compensated
– Decompensated
– Irreversible
Stages are progressively more serious
104. Stages of Shock
Compensated Shock
Size of container is reduced
– The body is capable of meeting its critical
metabolic needs through a series of
progressive compensating actions.
106. Stages of Shock
Decompensated Shock (Progressive)
– Mechanisms that compensate for blood loss fail
– Systolic BP drops significantly
– Vital organs are no longer perfused
– Patient displays a rapidly dropping level of
responsiveness
107. Stages of Shock
Irreversible Shock
– The body’s cells die.
– Cell membrane lyses.
– Toxic chemicals released.
– Aggressive resuscitation will be ineffective.
– The longer a patient is in decompensated shock,
the more likely he has moved to irreversible
shock.
108. Etiology of Shock
Shock can have many causes
Classifications according to origin:
– Hypovolemic,
– distributive
– obstructive
– cardiogenic
– respiratory
110. Distributive Shock
Distributive Shock
– Mechanisms that interfere with the ability of the
vascular system to distribute the cardiac output
– Causes
Neurogenic
Anaphylactic
Sepsis
112. Obstructive
Obstructive
– Results from interference with the blood flowing
through the cardiovascular system
– Causes
Tension pneumothorax
Cardiac tamponade
Pulmonary emboli
114. Etiology of Shock
Cardiogenic Shock
– Results from a problem with the cardiovascular pump
– Causes
Infarction
Disturbances in the cardiac electrical system
Failure of the valves
Cardiac rupture
Reduced cardiac pumping action
– May present with the signs and symptoms of
myocardial infarction or pulmonary edema
115. Etiology of Shock
Respiratory Shock
– Occurs when the respiratory system is not able to
bring oxygen into the alveoli and remove carbon
dioxide
– Causes
Flail chest
Respiratory muscle paralysis
Pneumothorax
Pulmonary edema
Tension pneumothorax
117. Etiology of Shock
Neurogenic Shock
– Results from an interruption in the communication
pathway between the central nervous system and
the rest of the body
– Causes
Spinal injury
Skin remains warm and dry above injury site
Head injury
Temporary or permanent
– Body’s compensatory mechanisms are often
affected
Tachycardia and increased diastolic are not present
118. Let’s Look at the #s
Type of Shock Heart Rate BP
Hemorrhagic/hypovole
mic
Cardiogenic
Neurogenic
Anaphylactic
Warm septic shock
Late septic shock
119. Had Enough Yet?
Cardiac Output: Heart rate X stroke volume
MAP = 1/3 (2 X diastolic + systolic)
SVR= MAP ÷ Cardiac Output
Type of Shock Cardiac Output SVR
Hemorrhagic/hypovole
mic
Cardiogenic
Neurogenic
Anaphylactic
Warm septic shock
Late septic shock
120. Shock Assessment
You must be able to recognize shock as early
as possible in your patient assessment.
Search out the signs and symptoms of shock
in each phase of the assessment process.
Carefully monitor for the development or
progression of shock.
122. Shock Assessment
Scene Size-up
– Analyze the forces that caused the trauma.
Possibility of both external and internal injury.
– Look for mechanisms that might result in internal
chest, abdominal, or pelvic injuries.
– Observe for external hemorrhage.
123. Shock Assessment
Initial Assessment
– Determine the patient’s level of consciousness,
responsiveness, and orientation.
– Assess the airway for patency and breathing for
adequacy.
Administer high-concentration oxygen.
– Note the heart rate and pulse strength.
Skin color and temperature.
124. Initial Assessment
Pulse oximetry
– If you note erratic or intermittent readings with the
device, suspect increasing cardiovascular
compensation.
Capnography
– Decreased ETCO2 levels
Reflect cardiac arrest, shock, pulmonary embolism, or
incomplete airway obstruction
– Increased ETCO2 levels
Reflect hypoventilation, respiratory depression, or
hyperthermia
125. Focused History and
Physical Exam
Vary with the patient’s priority as determined
by the initial assessment
Patients who have no significant mechanism
of injury : focused trauma assessment
Trauma patients who have signs or
symptoms of serious injury : rapid trauma
assessment
128. Rapid Trauma Assessment
Inspect and palpate the patient head to toe.
Pay special attention to the areas most likely
to produce serious, life-threatening injury.
Rule out the possibility of obstructive shock.
Set the patient’s priority for transport and for
injury care.
129. Detailed Patient Assessment
Consider the detailed physical exam only
after all priorities have been addressed and
the patient is either en route to the trauma
center or during prolonged extrication.
130. Ongoing Assessment
Perform serial ongoing assessments
– Mental status, airway, breathing, and circulation
– Perform the ongoing assessment every 5 minutes
in the serious trauma patient
Pay particular attention to the pulse rate and
pulse pressure
Check the adequacy and effectiveness of any
interventions you have performed
132. Airway and Breathing
Management
Positive end-expiratory pressure (PEEP) and
continuous positive airway pressure (CPAP)
Protect the airway with an oral airway, nasal
airway or possibly, endotracheal intubation
Provide pleural decompression as necessary
134. Fluid Resuscitation Basics
Warm fluid if possible
After 250-500 mL, check BP and lung sounds
Permissive hypotension -80 mmHg
Children- 20 mL/kg
BP cuff on IV bag or pressure infuser
Large bore IV
135. Fluid Replacement
The field treatment of choice for significant
blood loss in trauma is whole blood.
– Generally not practical in the field setting
– Most practical fluid for prehospital administration is
an isotonic crystaloid
Polyhemoglobins
– Contain either animal or human hemoglobin
– Prolonged shelf life
– Relatively inexpensive
– Efficacy not well established
136. Fluid Replacement
Isotonic Fluid Replacement
– The standard for shock treatment in the
prehospital setting
– Current approach to fluid administration
Begin fluid resuscitation when blood pressure falls to
below 75 percent of normal or about 90mmHg systolic.
Observe the patient’s level of consciousness and other
signs and symptoms.
137. Isotonic Fluid Replacement
Employ aggressive fluid resuscitation
– Use lactated Ringer’s solution or normal saline via
two lines
– Administer until blood pressure returns to 100
mmHg and the level of consciousness increases
In children, infuse 20 mL/kg of body weight
139. Isotonic Fluid Replacement
Consider the internal lumen
size of both the catheter and
the administration set
– Utilize largest bore possible
– Catheter length and fluid
pressure
Ideal catheter for the shock patient
is relatively short, 1 1/2" or shorter
Cautiously control fluid
– Maintain V/S
– don’t increase them
